Abdominal Pain

Author: Dr Didier Palmer (Director, Emergency Department, Royal Darwin Hospital)

Topic Reviewers: Monica Ostigh (RAN, Jabiru Clinic); Dr Penny Roberts-Thomson (Nguiu
Clinic); Bernard Egan (RAN, Bulman Clinic); Robyn Dixson (RAN, Yirrkala, Barunga
clinics); Dr Teresa Yee (Oenpelli)

The section on abdominal pain is simply a representation of established medical practice. The
section’s aims are to:
• Be concise and user friendly
• Enable a structured history of the key points to be taken for decision making, documentation
and communication
• Provide a structured approach to examining for the key findings for decision making,
documentation and communication. In particular: tenderness verses peritonism; masses;
common locations for pain and their associated common diagnoses
• Guide ‘when to call the doctor’
• Guide initial management of common conditions
• Highlight common pitfalls
• Include ectopic pregnancy
• Include cardiac pain or pneumonia presenting as abdominal pain
• Be safe

Does this section achieve its goals? There is no evidence base for this section as it is a distillation
of many contributor’s experience and thoughts. A prospective study, or retrospective audit, to
compare outcome with initial history and examination and decision-making would be an
interesting test of its value and a guide to how it could be improved.

[Editor: There have been, or are, high rates of sexually transmitted infections (STIs) in most remote
Aboriginal communities (see details in the sections on STIs). We can expect that this will lead to higher
rates of ectopic pregnancy and pelvic inflammatory disease. Consequently, practitioners should have a
high index of suspicion for these conditions when assessing abdominal pain. Case note audits conducted of
some Central Australian communities by the Tri-State Sexual Health Unit, Alice Springs, in 2000 found
numerous cases of abdominal pain that were not appropriately investigated as possible cases of PID.]
 Anaphylaxis

Authors: Dr Claire McGrath (Emergency Dept ASH) and Dr Dan Ewald

Topic Reviewers: Dr Phil Ryson (Darwin, Yuendumu Clinic); Kim Machen (RAN,
Nhulunbuy CDC); Liz Stephenson (RAN, Nhulunbuy CDC); Robyn Dixson (RAN,
Yirrikala Clinic); Helen Collinson (RAN, Adelaide River)

The mainstay of treatment for anaphylaxis remains adrenalin, IV fluids and oxygen. The protocol
has been made to be consistent with that described in the immunisation handbook as this is likely
to have been a source of refresher training for many practitioners.

Early recognition of anaphylaxis is probably crucial to good outcomes, so more details of signs
and symptoms have been included than were in the third edition of the STM.

In this protocol the aim is to ask someone else to call for help and for the ‘ABC’ to be done
immediately. IV fluids should be given as a bolus of 20mls per kilo of Haemacel or N saline. It
should be noted that a tachycardia does not preclude the giving of adrenalin, as people are often
reluctant to give adrenalin if pulse is greater than 120. But the tachycardia is a sign of the severity
of the anaphylaxis and actually indicates that adrenalin is needed. The tachycardia often settles
after adrenalin is given.

If hydrocortisone is being given IV then the Phenergan should be given IV also. The dose is the
same IVI as IMI (0.5 mg/kg/dose).

All patients who need adrenalin must be sent to hospital. This is in case of relapse of the reaction
after initial response to adrenaline and detailed assessment of the likely cause.

IV adrenaline has been removed from the protocol in favour of repeated IMI adrenaline. This is
because people may wast time trying to get IV access in a person who needs adrenaline quickly
and because IV adrenaline is probably more likely to cause over stimulation of the myocardium
and infarct. Royal Darwin Hospital has had this occur with IV adrenaline (personal
communication, Dr Didier Palmer, director RDH A&E). IVI adrenaline is not part of the
Immunisation Handbook protocol.

One ml syringes have been recommended rather than insulin syringes or tuberculin syringes to try
to save on confusion, though the dose has been provided in ‘units’ as well.

Insulin syringes do not have removable needles, and the ones provided may not be long enough
for deep IM injection in other than the most lean people.
We believe that the two things that are likely to have the greatest impact on outcomes in
anaphylaxis management (rather than any difference in IMI vs IV administration of adrenaline)
will be:
• Having an anaphylaxis kit available when and where you need it
• Recognising the need to use it.
References
National Guideline Clearinghouse. The Management and treatment of anaphylaxis June 1998.
Rosen et al. Emergency Medicine. 4th edition. 2000.
NHMRC. The Australian Immunisation handbook. 7th edition.
 Assessing in Custody

Authors: Jane Vadivalo (Psychologist, Tangentyere Council); Dr Dan Ewald

Topic Reviewers: Bernard Egan (RAN, Bulman Clinic); Robyn Dixson and staff (Yirrkala
Clinic)

Importance of the topic

High rates of incarceration in the NT and in Indigenous populations
‘Despite the Royal Commission into Aboriginal Deaths in Custody’s (RCADIC) 339
recommendations, Indigenous people are still 14 times more likely to be imprisoned than non-
Indigenous Australians. In the Northern Territory, 72.8 per cent of the prison population is
Indigenous’ (ATSIC website).

Features which make this topic important for the CARPA STM are:
• Lack of a remote prison/police health service, so regular health service staff are often called
on to assess and treat people in police custody
• High rates of morbidity among prisoners, mental health, drug and alcohol problems, petrol
sniffing
• Fear amongst practitioners about this sort of work, particularly if they are not used to it:
violent patients, family pressures within the community, fear of payback, staff out of their
‘comfort zone’
• High rates of death in custody for Indigenous people

Though the Royal Commission into Aboriginal Deaths In Custody directed many of its
recommendations to the police and correctional services, there are a number of areas that are of
interest to health service staff, particularly in remote communities where they are the only source
of health expertise available. The extracts from the RCADIC report included here serve to
highlight the seriousness of the issues and some of the points at which health care and assessment
of those in custody is likely to break down or fail.

Also see separate topics on assessing self-harm and suicide risk, petrol and solvent sniffing,
alcohol abuse, depression, anxiety in the CARPA STM and in this reference book.

Background
The Royal Commission into Aboriginal Deaths In Custody found the following:

The cases involving deaths in police custody have clearly highlighted past inadequacies in
relation to the assessment of whether prisoners and detainees were at risk either through
illness, injury or self-harm, both at the time of reception at the watch-house and generally
throughout the period of custody. Both the instructions to police and the training of the
officers who were responsible for the care and safekeeping of prisoners were found to be
seriously deficient.

‘During the year ended 30 June 1997, 15 Indigenous people were reported to have died in all
forms of custody in Australia. Thirteen of those deaths were of Aboriginal people and two were of
Torres Strait Islanders. This was the first time over the 17 year period for which data are available
(since 1980) that any Torres Strait Islander person was reported as having died in custody. Eighty
non-Indigenous deaths in custody occurred.’ (RCADIC 5 Year Report 1996/97)

Health service staff do not need to feel responsible for all the recommendations reproduced here.
Ultimately, a prisoner’s welfare is the responsibility of the agency that is holding the person in
custody. Cooperation and communication between police and health services will be important to
adequately assess people in custody.

Involving an Aboriginal health worker in the assessment is likely to help identify important social,
psychological and health issues that might otherwise be missed. The request for an assessment of a
prisoner will probably be directed to a nurse or doctor, but this should not prevent a health worker
being involved.

While there is a body of literature on health in prisons, there is little evidence base to guide the
approach to attending prisoners in remote communities.

Tips and approach

In general terms practitioners should try to ensure that prisoners receive high quality health care.
The legal detention is not intended to deprive them of access to health care. A person recently
detained in a remote community is likely to be in a highly stressed state that may exacerbate any
existing physical or mental health problem. Be particularly alert to drug and alcohol issues, mental
health issues and how these may complicate or exacerbate their health or risk of harm.

Royal Commission into the Aboriginal Deaths in Custody

The following extracts from the overview and recommendations are from the Report by
Commissioner Elliott Johnston QC, AGPS, Canberra, 1991. Recommendations of particular
relevance to health services have been selected by CARPA authors/editor.

Recommendation 127
That Police Services should move immediately in negotiation with Aboriginal Health Services and
government health and medical agencies to examine the delivery of medical services to persons in
police custody. Such examination should include, but not be limited to, the following:

a. The introduction of a regular medical or nursing presence in all principal watch-houses in

capital cities and in such other major centres as have substantial numbers detained;
b. In other locations, the establishment of arrangements to have medical practitioners or trained
nurses readily available to attend police watch-houses for the purpose of identifying those
prisoners who are at risk through illness, injury or self-harm at the time of reception;
c. The involvement of Aboriginal Health Services in the provision of health and medical advice,
assistance and care with respect to Aboriginal detainees and the funding arrangements
necessary for them to facilitate their greater involvement;
d. The establishment of locally based protocols between police, medical and para-medical
agencies to facilitate the provision of medical assistance to all persons in police custody where
the need arises;
e. The establishment of proper systems of liaison between Aboriginal Health Services and police
so as to ensure the transfer of information relevant to the health, medical needs and risk status
of Aboriginal persons taken into police custody; and
f. The development of protocols for the care and management of Aboriginal prisoners at risk,
with attention to be given to the specific action to be taken by officers with respect to the
management of:
i. intoxicated persons;
ii. persons who are known to suffer from illnesses such as epilepsy, diabetes or heart disease
or other serious medical conditions;
iii. persons who make any attempt to harm themselves or who exhibit a tendency to violent,
irrational or potentially self-injurious behaviour;
iv. persons with an impaired state of consciousness;
v. angry, aggressive or otherwise disturbed persons;
vi. persons suffering from mental illness;
vii. other serious medical conditions;
viii. persons in possession of, or requiring access to, medication; and
ix. such other persons or situations as agreed.

Recommendation 128
That where persons are held in police watch-houses on behalf of a Corrective Services authority,
that authority arrange, in consultation with Police Services, for medical services (and as far as
possible other services) to be provided not less adequate than those that are provided in
correctional institutions.

Recommendation 129
That the use of breath analysis equipment to test the blood alcohol levels at the time of reception
of persons taken into custody be thoroughly evaluated by Police Services in consultation with
Aboriginal Legal Services, Aboriginal Health Services, health departments and relevant agencies.

Recommendation 130
That:
a. Protocols be established for the transfer between Police and Corrective Services of
information about the physical or mental condition of an Aboriginal person which may create
or increase the risks of death or injury to that person when in custody;
b. In developing such protocols, Police Services, Corrective Services and health authorities with
Aboriginal Legal Services and Aboriginal Health Services should establish procedures for the
transfer of such information and establish necessary safe-guards to protect the rights of
privacy and confidentiality of individual prisoners to the extent compatible with adequate
care; and
c. Such protocols should be subject to relevant ministerial approval.

Recommendation 131
That where police officers in charge of prisoners acquire information relating to the medical
condition of a prisoner, either because they observe that condition or because the information is
voluntarily disclosed to them, such information should be recorded where it may be accessed by
any other police officer charged with the supervision of that prisoner. Such information should be
added to the screening form referred to in Recommendation 126 or filed in association with it.

Recommendation 132
That:
a. Police instructions should require that the officer in charge of an outgoing shift draw to the
attention of the officer in charge of the incoming shift any information relating to the well
being of any prisoner or detainee and, in particular, any medical attention required by any
prisoner or detainee;
b. A written check list should be devised setting out those matters which should be addressed,
both in writing and orally, at the time of any such handover of shift; and
c. Police services should assess the need for an appropriate form or process of record keeping to
be devised to ensure adequate and appropriate notation of such matters.

Recommendation 133
That:
a. All police officers should receive training at both recruit and in-service levels to enable them to
identify persons in distress or at risk of death or injury through illness, injury or self-harm;
b. Such training should include information as to the general health status of the Aboriginal
population, the dangers and misconceptions associated with intoxication, the dangers
associated with detaining unconscious or semi-rousable persons and the specific action to be
taken by officers in relation to those matters which are to be the subject of protocols referred to
in Recommendation 127;
c. In designing and delivering such training programs, custodial authorities should seek the advice
and assistance of Aboriginal Health Services and Aboriginal Legal Services; and
d. Where a police officer or other person is designated or recognised by a police service as being a
person whose work is dedicated wholly or substantially to cell guard duties then such person
should receive a more intensive and specialised training than would be appropriate for other
officers.

Recommendation 134
That police instructions should require that, at all times, police should interact with detainees in a
manner which is both humane and courteous. Police authorities should regard it as a serious
breach of discipline for an officer to speak to a detainee in a deliberately hurtful or provocative
manner.

Recommendation 135
In no case should a person be transported by police to a watch-house when that person is either
unconscious or not easily roused. Such persons must be immediately taken to a hospital or medical
practitioner or, if neither is available, to a nurse or other person qualified to assess their health.

Recommendation 136
That a person found to be unconscious or not easily rousable whilst in a watch-house or cell must
be immediately conveyed to a hospital, medical practitioner or a nurse. (Where quicker medical
aid can be summoned to the watch-house or cell or there are reasons for believing that movement
may be dangerous for the health of the detainee, such medical attendance should be sought.)

Recommendation 137
That:
a. Police instructions and training should require that regular, careful and thorough checks of all
detainees in police custody be made;
b. During the first two hours of detention, a detainee should be checked at intervals of not greater
than fifteen minutes and that thereafter checks should be conducted at intervals of no greater
than one hour;
c. Notwithstanding the provision of electronic surveillance equipment, the monitoring of such
persons in the periods described above should at all times be made in person. Where a detainee
is awake, the check should involve conversation with that person. Where the person is sleeping
the officer checking should ensure that the person is breathing comfortably and is in a safe
posture and otherwise appears not to be at risk. Where there is any reason for the inspecting
 officer to be concerned about the physical or mental condition of a detainee, that person should
be woken and checked; and
d. Where any detainee has been identified as, or is suspected to be, a prisoner at risk then the
prisoner or detainee should be subject to checking which is closer and more frequent than the
standard.

Recommendation 138
That police instructions should require the adequate recording, in relevant journals, of
observations and information regarding complaints, requests or behaviour relating to mental or
physical health, medical attention offered and/or provided to detainees and any other matters
relating to the well being of detainees. Instructions should also require the recording of all cell
checks conducted.

Recommendation 144
That in all cases, unless there are substantial grounds for believing that the well being of the
detainee or other persons detained would be prejudiced, an Aboriginal detainee should not be
placed alone in a police cell. Wherever possible an Aboriginal detainee should be accommodated
with another Aboriginal person. The views of the Aboriginal detainee and such other detainee as
may be affected should be sought. Where placement in a cell alone is the only alternative the
detainee should thereafter be treated as a person who requires careful surveillance.

Recommendation 147
That police instructions should be amended to make it mandatory for police to immediately notify
the relatives of a detainee who is regarded as being ‘at risk’, or who has been transferred to
hospital.

Recommendation 150
That the health care available to persons in correctional institutions should be of an equivalent
standard to that available to the general public. Services provided to inmates of correctional
institutions should include medical, dental, mental health, drug and alcohol services provided
either within the correctional institution or made available by ready access to community facilities
and services. Health services provided within correctional institutions should be adequately
resourced and be staffed by appropriately qualified and competent personnel. Such services should
be both accessible and appropriate to Aboriginal prisoners. Correctional institutions should
provide 24 hour a day access to medical practitioners and nursing staff who are either available on
the premises, or on call.

Recommendation 151
That, wherever possible, Aboriginal prisoners or detainees requiring psychiatric assessment or
treatment should be referred to a psychiatrist with knowledge and experience of Aboriginal
persons. The Commission recognises that there are limited numbers of psychiatrists with such
experience. The Commission notes that, in many instances, medical practitioners who are or have
been employed by Aboriginal Health Services are not specialists in psychiatry, but have
experience and knowledge which would benefit inmates requiring psychiatric assessment or care.

Recommendation 152
g. The development of protocols detailing the specific action to be taken by officers with
respect to the care and management of:
i. persons identified at the screening assessment on reception as being at risk or requiring any
special consideration for whatever reason;
ii. intoxicated or drug affected persons, or persons with drug or alcohol related conditions;
iii. persons who are known to suffer from any serious illnesses or conditions such as epilepsy,
diabetes or heart disease;
 iv. persons who have made any attempt to harm themselves or who exhibit, or are believed to
have exhibited, a tendency to violent, irrational or potentially self-injurious behaviour;
v. apparently angry, aggressive or disturbed persons;
vi. persons suffering from mental illness;
vii. other serious medical conditions;
viii. persons on medication; and
ix. such other persons or situations as agreed.

Recommendation 156
That upon initial reception at a prison all Aboriginal prisoners should be subject to a thorough
medical assessment with a view to determining whether the prisoner is at risk of injury, illness or
self-harm. Such assessment on initial reception should be provided, wherever possible, by a
medical practitioner. Where this is not possible, it should be performed within 24 hours by a
medical practitioner or trained nurse. Where such assessment is performed by a trained nurse
rather than a medical practitioner then examination by a medical practitioner should be provided
within 72 hours of reception or at such earlier time as is requested by the trained nurse who
performed such earlier assessment, or by the prisoner. Where upon assessment by a medical
practitioner, trained nurse or such-other person as performs an assessment within 72 hours of a
prisoner’s reception it is believed that psychiatric assessment is required then the Prison Medical
Service should ensure that the prisoner is examined by a psychiatrist at the earliest possible
opportunity. In this case, the matters referred to in Recommendation 151 should be taken into
account.
 Bites: Human and animal

Author: Dr Claire McGrath (Emergency Department, ASH)

Topic Reviewers: Andrew Urquhart (RAN, Beswick Clinic); Dave Corstorpan (RAN,
Nyirripi Clinic); Vicki Gordon (RAN, Mutitjulu Clinic).

Comments
Most bites will be dog, cat or human (closed fist injuries usually). Rates of infection of bites vary
between 2–20% in dog bites, 15–50% in cat bites and 9–50% in human bites. This compares with
4–15% in simple lacerations.

Infection rates are higher in hand injuries, puncture wounds, wounds involving joints, tendons,
ligaments, or fractures, and wounds requiring debridement. People with diabetes, renal disease,
alcohol abuse, on steroids, splenectomised or with other causes of immuno-compromise have
higher risk of infection.

The single most important aspect of treatment is thorough wound cleaning. This is best done by
copious irrigation with normal saline. Wound cleaning by debriding, scrubbing etc. may also be
needed. The use of hydrogen peroxide, Betadine or liquids other than normal saline is no longer
supported as they cause more damage to tissues and impair wound healing.

Delayed primary closure (after 3–5 days) is advisable for wounds needing extensive debridement,
those with crush injury and wounds more than 6–8 hours old. The time period stated in the current
manual is 4–7 days contrary to most recommendations, which state 3–5 days. This is based on a
more cautious/conservative approach to the chance of infection developing in a wound that has
been closed.

Dog bites
Dog bites actually have a lower rate of infection than other bites. This is multifactorial and due to
wounds being larger and more accessible to cleaning, usually earlier presentation than other bites,
and slightly less virulent organisms. Dog bites of the face have a lower rate of infection than bites
elsewhere and so they can be cleaned and sutured if less than 12 hours old, unless extensive,
requiring plastic surgery, or deep structures are involved. The recommendation to extend the time
limit for facial wounds to 12 hours seems to be supported by this lower rate of infection.
Otherwise the 6–8 hour rule should still apply.

The recommendation in the fourth edition of the CARPA STM is for IMI procaine for five days
for all bite wounds, with addition of amoxicillin-clavulanic acid if signs of infection are present
after two days of treatment. The British guideline states (from a meta-analysis in 1994) that ‘if 100
patients with dog bites are given oral antibiotics, 84 would escape infection regardless of
treatment, 9 would become infected despite treatment, and 7 would avoid infection because of the
infection’.

It is difficult to quantify such numbers in Central Australia, but we know the rates of skin
infections are higher here than elsewhere. Best practice around the world is currently initial use of
oral amoxicillin-clavulanic acid. In fact the eleventh edition of the Australian Antibiotic
Guidelines recommends to use one dose of procaine IMI plus five days of Augmentin for all high
risk wounds.
Dr Gary Lum, Microbiologist at RDH suggested that because of the ‘compliance issue’, initial
treatment with procaine penicillin may well remain appropriate with the addition of blood cultures
at the first sign of fever and early commencement of oral amoxicillin-clavulanic acid. Animal
bites can contain organisms such as Capnocytophagia canimorsus, which can cause overwhelming
systemic infection. The addition of blood cultures enables growth of a pure culture of the
responsible organism rather than a wound swab, which will grow multiple organisms. A wound
swab should, of course, still be performed at this stage, i.e. at stage when infection is obvious.

Cat bites
Cat bites have a much higher rate of infection than other animal bites. This is because they are
more likely to be puncture wounds — which are therefore harder to access and clean — and also
are more likely to occur on the hand. The Pasteurella species, common to both dog and cat bites, is
more virulent than the other species found in dog bites, and is usually the sole organism. All the
literature therefore supports prophylactic antibiotics for all cat bites. Cat scratch disease is caused
by Bartonella henselae and does not require therapy unless the patient is severely
immunocompromised, e.g. HIV/AIDS. The preferred treatment is Roxithromycin 300 mg daily for
10 days or intravenous in severe disease.

Human bites
As stated human bites have a high rate of infection. The commonest injury is the closed fist or
punch injury (CFI). All punch injuries or wounds about the knuckles should be assumed to be CFI
and treated accordingly. They also grow mixed organisms, but more often include anaerobes and
gram negatives. The anaerobes are often beta-lactamase producing. All CFI should be left open,
i.e. dressed but not sutured. The wound should receive full and meticulous cleaning and twice
daily dressings of providone-iodine until the wound is clearly not infected; then use saline for
cleaning.

All CFI should have antibiotics, the first preference being amoxycillin-clavulanic acid. This
covers anaerobes so metronidazole is not necessary. If penicillin allergy exists then use
roxithromycin and metronidazole. All CFI should be considered for early referral for X-ray to
exclude fracture. All people with infected human bites of the hand should be hospitalised.

Human bites to other areas of the body should be treated like other wounds, i.e. wound irrigation,
debridement, and antibiotics for high risk wounds.

Mucosal lacerations where the teeth go through the lip or cheek to the outside should be irrigated
well. Prophylactic antibiotic antibiotics do not reduce the incidence of infection in mucosal bites
unless they are through and through lacerations. Penicillin remains the drug of choice.

Bibliography
Medline searched on keywords: dog bites, human bites, animal bites, antibiotics, wound
treatment.
UK Guidance Clinical Recommendation Bites-human and animal. July 1998.
Therapeutic Guidelines: Antibiotics. 11th edition. 2000.
Rosen P et al. Emergency Medicine. 4th edition.
Talan TA et al. Bacteriological analysis of infected dog and cat bites. NEJM 1999 Jan 14;
340(2):85–92.
Javaid M et al. Primary repair of dog bites to the face: 40 cases JRSociety of Medicine 1998 Aug;
91(8):414–6.
Smith PF et al. Treating mammalian bite wounds. Journal of Clincial Pharmacolocal Therpeutics
2000 Apr; 25(2):85–99.
Chen E et al. Primary closure of mammalian bites. Academic Emergency Medicine 2000 Feb;
7(2):157–61.
Bunzli WF et al. Current management of human bites. Pharmacotherapy 1998 Mar–Apr;
18(2):227–34.
 Bites: Snakes and spiders

Author: Dr Claire McGrath (Emergency Dept, ASH)

Topic Reviewer: Prof Bart Currie (Menzies School of Health Research)

Red-back spider bite

The CARPA STM as it stood in the third edition was adequate. In symptoms, however, abdominal
pain can be added, especially in children.

The antivenom can in fact be given up to several weeks following the bite. Ideally it should be
given in a hospital, but it is an incredibly safe antivenom and could be given in any reasonable
clinic that has basic resuscitation facilities. It should be considered for the larger clinics, especially
those that have an on-site doctor. The visiting doctor (DMO) also could take antivenom to a clinic
in a situation where the patient was reluctant to go to hospital or where there was doubt about the
diagnosis, as symptoms start to resolve within 30–60 minutes after administration of the
antivenom. The ASH-ED protocol is that any residual symptoms after 1–2 hours mandate repeated
antivenom until symptoms resolve. Recent experience has shown that in severe envenomation
symptoms can recur within days and do resolve with further treatment.

The toxin of the red-back spider moves very slowly and there is rarely a need to react emurgently.
Patients need to be reassured that it will not kill them (no-one has died since the introduction of
the antivenom) and the treatment can be delayed until the next day unless there are significant
systemic signs (e.g. hypertension, severe pain, severe vomiting). Not all patients will need to be
evacuated in the middle of the night, many can wait until first light or the day plane.

Snakebite
There are the same three most important venomous snakes in the Top End and in Central
Australia, so it is appropriate to have the same protocol throughout the NT.

Blood should be taken for whole blood clotting time as this can guide the doctor (who can take
antivenom out to the patient) and hospital emergency department, as it will save time waiting for
blood tests, prior to treatment. If the blood has not clotted after 20 minutes the doctor must be
informed. It may be helpful to look at the venipuncture site or cannula site for oozing.

If there is blood in the urine on dipstick this probably indicates rhabdomyolysis/myoglobinuria

(unless the person has had it documented before, e.g. has renal disease) and IV fluids should be
started at a rate of 10 ml per kilo as a bolus and then at a rate of 5 ml per kilo per hour. Urine
output needs to be monitored in these patients by insertion of an IDC and output maintained at 0.5
ml per kg per hour. The doctor should be informed of the haematuria as antivenom may need to be
taken to the clinic.

[Editor: The following extracts are from the review paper on snakebite by Currie (listed in references
below).]

The time course of envenoming

Figure 1 overleaf shows the progression of envenoming, with features depending on the snake
species.
• The early collapse and recovery, if present, are the first features (5–30 minutes).
 • Lymph node pain (tenderness on palpation may precede the symptom of pain), early non-
specific systemic features and haemostatic abnormalities (manifest by oozing bite site or
venepuncture sites, spitting blood, macroscopic or dipstick haematuria or prolonged glass
tube clotting time) usually begin from 30–120 minutes after the bite.
• Neuromuscular paralysis onset is often delayed for several hours, and occasionally even 24
hours, possibly due to tissue sequestration of venom in the extreme case. First aid with
bandaging and immobilisation may also delay onset. The classical pattern of taipan
envenoming without medical intervention is onset fours after the bite, followed by steady
progression for around 24 hours to a maximum deficit. Ptosis is followed by
ophthalmopelgia, then bulbar palsy and finally intercostal, then diaphragmatic, paralysis.
Limb weakness is usually less severe and may be not evident. Death adder course may be
faster (related to post-synaptic neurotoxins), but may also be delayed and less severe without
progression in mild cases.
• The potential delay in neurotoxicity onset, although unusual, justifies all cases of possibly
venomous snakebite in tropical Australia, Papua New Guinea and Irian Jaya being observed
medically, ideally in hospital, for 24 hours after the bite.
Figure 1: Australasian elapid envenoming

Important bedside tests

A urine dipstick: Positive for ‘blood’ can mean haematuria from consumptive coagulopathy,
haemoglobinuria from intravascular haemolysis or myoglobinuria from rhabdomyolysis, or a
combination of these.
A glass tube whole blood clotting test: This simple test can be very useful to demonstrate
procoagulant activity. A clot should normally be forming in the glass tube by 10 minutes. An
assay validated in the field is the 20WBCT, which simply determines whether or not a clot is
formed in the glass tube by 20 minutes.1 With brown snake envenoming it is not unusual for the
blood to remain completely unclotted.

Therapeutic issues
There is a large amount of documented clinical experience in management of Australasian elapid
envenoming, however a number of important uncertainties and controversies remain, justifying an
evidence-based approach to toxinology as well as toxicology.2

First aid
Despite impressive case reports there remains a lack of data on overall efficacy of pressure-
immobilisation and, despite it being central to all Australian snakebite protocols, it has still only
been correctly applied in 18%–53% of snakebites.3,4 The critical importance of strict
immobilisation has been reinforced by lymphoscintigraphy studies.5 Overseas, prospective patient
serum venom level studies have shown a pressure pad method of first aid to retard venom
absorption.6 Preliminary venom level studies in the Northern Territory support concerns that crepe
bandages become loose.7 Seven patients bitten by western brown snakes (Pseudonaja nuchalis)
had severe coagulopathy on presentation to hospital despite documented full pressure-
immobilisation.8 With the rapid onset of envenoming in brown snakebites (hypotensive collapse is
usually within 30 minutes) direct vascular absorption of some venom components may be
occurring, suggesting timing of first aid is critical.

Use of venom detection kits (VDKs)

The current VDK was released in 19919 and takes 25 minutes for a result. It should not be used to
determine whether antivenom should be given, but if antivenom is clinically indicated it may
enable monovalent antivenom to be used instead of polyvalent. Erroneous results occasionally
occur, especially if blood is tested rather than bite swab or urine.10 However, VDKs are very
useful if the positive result is a snake genus (e.g. ‘brown’) consistent with the patient’s clinical
syndrome and with the snake species known to be present in the region.

Use of monovalent antivenoms

Monovalent antivenoms should only be used in tropical Australia if: a) the (dead or alive) snake
brought to hospital with the patient is positively identified by a trained reliable expert and was
definitely the snake that bit the patient or b) the VDK result is consistent with the clinical findings
and the snakes in the region, as above. If there is uncertainty, polyvalent antivenom should be
used. Relying on local ‘experts’ to identify snakes is dangerous and incorrect identification can
have tragic consequences.11

Use of antivenom premedication

The use of subcutaneous adrenaline before antivenom as premedication against anaphylaxis is
controversial. A recent study from Sri Lanka showed a significant decrease in acute adverse
reactions to antivenom with use of subcutaneous adrenaline.12 However, antivenom reactions
occurred in 43% of controls in the study, a rate much higher than that now seen with the more
purified current Commonwealth Serum Laboratories (CSL) antivenoms. There appear to have
been no deaths from snake antivenom reactions in Australia for over 40 years.9,13,14 The concern
with routine use of adrenaline is that it may occasionally exacerbate bleeding in snakebite patients
with severe coagulopathy. The last five snakebite deaths from intracranial haemorrhage in
Australia were all given adrenaline before antivenom, although three had intravenous adrenaline
(which is not recommended).11,15 It was considered that the time course in the two given
subcutaneous adrenaline made a causal association unlikely.11 However it remains possible that
even subcutaneous adrenaline may occasionally be harmful, especially in the context of the severe
haemostatic abnormalities with brown snake envenoming, with intracranial haemorrhage usually a
fatal outcome if it occurs. With the very low rate of severe reactions to antivenom seen in
Australia and Papua New Guinea, and the ability of emergency medicine physicians to adequately
manage reactions that may occur, a policy of withholding premedication but always having
adrenaline drawn up and ready is now recommended by many authorities and is policy in the
Northern Territory. The primary role of adrenaline in any severe reaction that does occur is well
documented.16

Antivenom doses
The number of ampoules of antivenom used has been empirically determined over many years for
the various snake species. Although one ampoule of each of the CSL antivenoms was designed to
neutralise venom from an ‘average’ bite, based on milking venom from snakes13, it is clear that
larger doses are often required. This is especially evident for bites from brown snakes, where
venom yields are very variable and may be substantially larger than previously thought17. Animal
studies have suggested many ampoules of antivenom may be required for neutralisation of venom
components.18,19 However, for bites from death adders and mulga snakes clinical response has
usually been adequate after one or two ampoules of antivenom.7,20,21

While antivenom reverses the post-synaptic neurotoxicity from death adder venom, established
pre-synaptic damage from taipan venom is not reversed with antivenom.22,23,24,25 Adequate
antivenom may prevent deterioration in taipan envenoming by preventing further venom binding,
but recovery requires time for neurotransmitter pathway restoration, not necessarily more
antivenom. It appears that for taipan envenoming the timing of antivenom is especially important.
After four hours from the bite, giving more than one ampoule of antivenom usually has no
additional benefit.22,25 However, in a case series from Townsville larger doses of antivenom given
within several hours of taipan bites appeared effective in hastening neurological recovery.26 This
is consistent with reversal of early post-synaptic neurotoxicity while neutralising pre-synaptic
neurotoxins before binding. These findings have important financial implications for treatment in
Papua New Guinea, where the cost of antivenom is prohibitive and most patients present beyond
four hours from the bite.
There have now been a number of well-conducted studies overseas comparing either different
antivenoms or different doses of antivenom, using serial patient blood venom levels and clinical
criteria to assess comparative efficacy.27,28,29,30 Similar collaborative studies within Australia,
using serial venom levels before and after defined antivenom doses, would enable a more
objective understanding of antivenom dose requirements for the various Australasian elapids.

Treatment in the absence of antivenom

Anticholinesterase therapy, such as neostigmine, can be beneficial by competitively displacing
post-synaptically acting neurotoxins. It has been beneficial in reversing death adder neurotoxicity
in Papua New Guinea and should be considered, especially in remote locations in Irian Jaya and
Papua New Guinea where antivenom is not affordable or available.31 Prolonged use of pressure-
immobilisation with graded release has been considered useful for death adder envenoming in
Papua New Guinea and requires further study (J. Oakley, personal communication).

The distribution of potentially lethal terrestrial snakes in tropical Australia,

in decreasing order of bites seen in each region

Tropical Western Northern Territory Tropical Queensland

Australia
Pseudonaja nuchalis Pseudonaja nuchalis Pseudonaja textilis
Western brown snake Western brown snake Common (Eastern) brown
(Gwardar) (Gwardar) snake
Pseudechis australis Pseudechis australis Oxyuranus scutellatus
Mulga Mulga Taipan
Acanthophis spp. Acanthophis spp Pseudonaja nuchalis
Death adder Death adder Western brown snake
(Gwardar)
Oxyuranus scutellatus* Oxyuranus scutellatus* Pseudechis australis
Taipan Taipan
Mulga
Acanthophis spp. Death
adder
Tropidechis carinatus
Rough-scaled snake
Rhinoplocephalus
nigrescens
Eastern small-eyed snake
*Taipans have been found in the Top End of the Northern Territory and across to the Kimberley in north
Western Australia, but are very uncommonly encountered in these regions, with no recorded human bites.
Clinical syndromes of the major Australasian snakes
Early Local Tender Non– Myotoxicity Coagulopathy Neurotoxicity
Collapse swelling regional specific
lymph ‘systemic
nodes features’1

Brown ++ +/– +/– +/– – +++2 Yes

snakes
Mulga – ++ ++ ++ ++ +3 Yes
snake
Death – +/– +/– +/– – – ++4
adder
Taipans + +/– + + + +2 ++5
Rough- + +/– + + + +2 +
scaled
snake

Eastern – +/– + + + +/– ?

small-
eyed
snake
Papuan – +/– + + – + +
black
snake

New – +/– + + + +3 +4
Guinea
small-
eyed
snake

Whip – + +/– +/– – – -

snakes6
Tiger + + + + ++ +2 ++5
Snakes7

1
Abdominal pain, nausea, vomiting, headache
2
Predominantly procoagulant with fibrinogen depletion
3
Anticoagulant, no fibrinogen depletion, usually mild
4
Predominantly post-synaptic
5
Predominantly pre-synaptic
6
Not potentially lethal but common
7
Not in the tropics but included for comparison

References for extracts from: Currie BJ. Snakebite in tropical Australia, Papua New Guinea and
Irian Jaya. Emergency Medicine 2000; 12:285–94.

1 Warrell DA, Davidson NM, Greenwood BM, et al. Poisoning by Bites of the Saw-Scaled or Carpet
Viper (Echis carinatus) in Nigeria. Quarterly J Med 1977; 181;33–62.
2 Whyte IM, Buckley NA. Progress in clinical toxicology: from case reports to toxicoepidemiology. Med
J Aust 1995; 163;340–341.
3 Jamieson R, Pearn J. An epidemiological and clinical study of snake-bites in childhood. Med J Aust
1989; 150;698–702.
4 Jelinek GA, Hamilton T, Hirsch RL. Admissions for suspected snakebite to the Perth adult teaching
hospitals, 1979 to 1988. Med J Aust 1991; 155;761–4.
5 Howarth DM, Southee AE, Whyte IM. Lymphatic flow rates and first aid in simulated peripheral snake
or spider envenomation. Med J Aust 1994; 161;695–700.
6 Tun-Pe, Aye-Aye-Myint, Khin-Ei-Han, Thi-Ha, Tin-Nu-Swe. Local compression pads as a first aid
measure for victims of bites by Russell’s viper (Daboia russelii siamensis) in Myanmar. Trans R Soc Trop
Med Hyg 1995; 89;293–5.
7 Currie B, Richards A, Lawrie P, Jacups S, Theakson D, Warrell D. The Top End Prospective Snakebite
Study and unresolved issues for Australia and Papua New Guinea, Annual Scientific Meeting Autralasian
Tropical Health Conference. Tropical Millennium Bugs 23rd–26th June, 2000. Noosa, Queensland, 2000.
8 Currie B. A prospective study of snakebite in tropical Australia (abstract). Aust NZ J Med 1999;
29;602.
9 Sutherland SK. Antivenom use in Australia. Premedication, adverse reactions and the use of venom
detection kits. Med J Aust 1992; 157;734–9.
10 Mead HJ, Jelinek GA. Suspected snakebite in children: a study of 156 patients over 10 years [see
comments]. Med J Aust 1996; 164;467–70.
11 Sprivulis P, Jelinek G. Fatal intracranial haematomas in two patients with Brown snake envenomation.
Med J Aust 1995; 162;215–16.
12 Premawardhena AP, de Silva CE, Fonseka MM, Gunatilake SB, de Silva HJ. Low dose subcutaneous
adrenaline to prevent acute adverse reactions to antivenom serum in people bitten by snakes: randomised,
placebo controlled trial. BMJ 1999; 318;1041–3.
13 Trinca GF. The treatment of snakebite. Med J Aust 1963; 1;275–280.
14 Sutherland SK, Lovering KE. Antivenoms: Use and adverse reactions over a 12 month period in
Australia and Papua New Guinea. Med J Aust 1979; 2;671–4.
15 Tibballs J. Premedication for snake antivenom. Med J Aust 1994; 160;4–7.
16 Brown AFT. Therapeutic controversies in the management of acute anaphylaxis. J Accid Emerg Med
1998; 15;89–95.
17 Masci PP, Mirtschin PJ, Nias TN, Turnbull RK, Kuchel TR, Whitaker AN. Brown snakes (Pseudonaja
Genus): venom yields, prothrombin activator neutralization and implications affecting antivenom usage.
Anaesth Intens Care 1998; 26;276–81.
18 Tibballs J, Sutherland S. The efficacy of antivenom in prevention of cardiovascular depression and
coagulopathy induced by brown snake (Pseudonaja) species venom. Anaesth Intens Care 1991; 19;530–4.
19 Sprivulis P, Jelinek GA, Marshall L. Efficacy and potency of antivenoms in neutralizing the
procoagulant effects of Australian snake venoms in dog and human plasma. Anaesth Intens Care 1996;
24;379–81.
20 Lalloo DG, Trevett AJ, Black J, et al. Neurotoxicity, anticoagulant activity and evidence of
rhabdomyolysis in patients bitten by death adders (Acanthophis sp.) in southern Papua New Guinea.
Quarterly J Med 1996; 89;25–35.
21 Campbell CH. The death adder (Acanthophis antarcticus): the effect of the bite and its treatment. Med J
Aust 1966; 2;922–5.
22 Campbell CH. The taipan (Oxyuranus scutellatus) and the effect of its bite. Med J Aust 1967; 1;735–9.
23 Currie BJ, Theakston RDG, Warrell DA. Envenoming from the Papuan taipan (Oxyuranus scutellatus
canni). In: Gopalakrishnakone P, Tan CK, eds. Recent advances in toxinology research. Singapore: Venom
and toxin research group, 1992; 308–14.
24 Lalloo DG, Trevett AJ, Korinhona A, et al. Snakebites by the Papuan taipan (Oxyuranus scutellatus
canni); paralysis, haemostatic and electrocardiographic abnormalities and effects of venom. Am J Trop
Med Hyg 1995.
 Burns

Author: Dr Claire McGrath (Emergency Department, ASH)

Topic Reviewers: Dr Elizabeth Mowatt (Director, Emergency Department, ASH); Alison

Mustapha (burns nurse RDH)

The major problems with burn patients in remote areas remain fluid resuscitation, airway
management and dressings.

Fluid resuscitation volumes should still be calculated using the same formula (Modified
Parkland’s) as before i.e. 3–4 ml/kg/% body surface area burnt. Evidence has shown no preference
for one crystalloid over another (other than not Dextrose). Therefore use either Hartmann’s or
normal saline, i.e. as long as it is warm and salty and wet. In children, if transfer is delayed past 12
hours from time of burn, use 5% dextrose in half saline (add 25mls of 50% dextrose to a 500ml
bag of 2.5% dextrose and N/2 saline) Emergency Management of Severe Burns (EMSB) Course
Manual.

The best indication of adequacy of fluid resuscitation remains urine output. For consistency and
better outcome in adults this should be increased to 0.5 ml/kg/hour. Paediatric recommendations
are unchanged. If urine output is not adequate, give boluses of 5–10 ml/kg and/or increase the next
hour’s fluids to 150% of the planned volume (EMSB Course).

Airway burns and inhalation burns injury are a major concern for management at the clinic, the
RFDS plane and emergency department (ED). The problems occur in the first 12–36 hours and are
mainly due to massive airway oedema, causing airway obstruction. Maximal oedema occurs in
about 8–12 hours following small burns and 12–24 hours in major burns as part of the
physiological response to the burn injury above the larynx itself. This can occur much earlier and
relatively suddenly as IV fluids are poured in.

The problem that presents out bush is: How much fluid to give out bush before the RFDS arrive?
Any person with facial burns, singeing of nasal hair, eyebrows, eyelashes, black sooty sputum,
oro-pharyngeal burns, hoarseness, tracheal tug, stridor, wheeze, a burn in a confined space or
explosion should be assumed to have suffered an airway burn and /or inhalational injury and fluids
withheld until after urgent DMO/ED consultation. Also, persons with lower-facial and/or neck
burns are at risk of airway obstruction. These people should receive Code 1 Priority for evacuation
and a doctor who has experience in managing the airway should attend. If in doubt fluids should
be withheld or given at a slower rate. Remember:
A policy that results in intubation of all patients at potential risk for airway compromise can
be both foolish and dangerous. At the same time, it is recognised that intubation of patients
who are likely to develop unstable airways is necessary if transport times are long and if IV
resuscitation is initiated during transport. (Yowler & Fratianne, 2000)

Cooling remains an important first aid measure for up to three hours post burn, but should be
applied for 20 minutes — not 10 mins as in third edition (EMSB Course). For transport there is no
benefit from transporting with wet dressings, and may indeed be harmful, especially in children. A
dry dressing or ‘Gladwrap’ is appropriate for most burns patients who are being sent to hospital.
The advantages of ‘Gladwrap’ are that it is transparent, easy to apply, non-scary for children,
helps prevent hypothermia, and is easy to remove in ED. It helps relieve pain by occluding the air.
Obviously old, infected burns should be swabbed, cleaned with warm soapy water and have either
Duoderm or SSD applied. Clean superficial burns or dry partial thickness burns not requiring
hospital assessment should be covered with Fixomull or Hypofix. People with more than 5%
burns with significant blistering should be sent to hospital for debridement. SSD should not be
applied to the face. In general do not apply SSD to burns less than 24 hours old without consulting
ED or burns unit directly.

Bibliography
Medline search keywords: burns; fluid resuscitation; resuscitation; burns dressings; airway
problems and burns
Australian and NZ Burn Association. Emergency Management of Severe Burns (EMSB) Course
Manual. 5th Edition. 1996.
UK Clinical Guidance Recommendations. September 1998. ‘Burn/Scalds’.
Royal Adelaide Hospital Burns Unit Protocol.
Yowler JY, Fratianne RB. Current Status of Burn Resuscitation Clinics in Plastic Surgery Jan
2000; l27(1):1–10.
Holm C. Resuscitation in shock associated with burns. Tradition or evidence-based medicine.
Resuscitation 2000; 44:157–64.
Ramzy PI, et al. Thermal Injury. Critical Care Clinics, April 1999; 15(2):333–53.
Micak R, et al. Emergency management of paediatric burn victims. Paediatric Emergency Care
1998 Feb; 14(1):51–4.
Alderson P. Colloids versus Crystalloids for fluid resuscitation in critically ill patients. Cochrane
Database Systemic review, 2000. (@) CD000567.
Tanaka H, et al. Reduction of resuscitation fluid volumes in severely burned patients using
Ascorbic Acid administration: a randomised prospective study. Archives of Surgery 2000 March;
135(3):326–31.
Whitelock-Jones L et al. Inhalational burns in children. Paediatric Surgery International 1999;
15(1)50–5.
Fitzpatrick J, Cioffi WG. Ventilatory support following burns and smoke inhalation injury.
Respiratory Care Clinics North America 1997 March; 3(1):21–49.
Ang ES, et al. The role of alternative therapy in the management of partial thickness burns of the
face- experience with the use of moist exposed burn ointment of silver sulphadiazine. Annals
Academy of Medicine Singapore 2000 Jan; 29(1):7–10.
 DR ABC:
Emergencies and management of injuries

Author: Dr Rodney G Mitchell

Topic Reviewers: Prof Don Moyes (Head, Dept of Anaesthesia, The Queen
Elizabeth Hospital, Adelaide); Dr John Crozier (Surgeon, Dept of Trauma
Surgery, Liverpool Hospital, Sydney); Assoc Prof Peter Reilly (Dept of
Neurosurgery, Royal Adelaide Hospital); Dr Kerrie Jones (Emergency
Medicine physician, Royal Darwin Hospital); Prof Bart Currie (Dept
Infectious Diseases, Royal Darwin Hospital); Leone Radnedge (RAN,
Utopia); Dr Liz Mowatt (ASH ED, Lake Nash Clinic); Dr Phil Rayson (RDH)

[Editor: Rod Mitchell, formerly the senior DMO in Alice Springs, undertook this
review and revision of the DR ABC and injury protocols as a project for his
specialist training in anaesthetics. An edited version of his project report is presented
here]

Summary
This project has sought to evaluate and revise current guidelines for the management
of ‘DR ABC/ Emergencies’ and ‘Injuries’, as produced by CARPA for use in
rural/remote Australia. The evaluation involved a telephone survey of guideline
users and an audit of Royal Flying Doctor Flight Records. This was in order to
examine the degree of dissemination of the guidelines amongst rural/remote
practitioners, the degree of impact of the guidelines on current practise, the degree to
which current practise is moving towards guideline recommendation, and the level
of user satisfaction with the guidelines. It would seem that the guidelines are widely
disseminated, and that guideline users are generally satisfied with their content. The
extent of the impact of the guidelines on current practise, and the extent to which the
current practise is approaching the ‘best practice’ espoused in the guidelines are
more uncertain, though both appear generally positive. In response to the
information gleaned during the evaluation, the revised guidelines have incorporated
a new flow diagram for DR ABC, more illustrations, prompts to remind clinicians of
the need to consider the administration of oxygen and intravenous fluids, improved
accessibility to the common clinical scenarios, and less medical jargon.

Introduction
In response to a perceived need, CARPA has developed and refined a series of
protocols over the last fifteen years to deal with health issues that are common and/
or unique to the region. These protocols are presented in the CARPA Standard
Treatment Manual (STM). Two such protocols have evolved for the initial
management of loss of consciousness and the management of acute injuries. The
former appears at the front of the manual, and is set out in a DR ABC format. The
‘Injuries’ guideline is found amongst the more general protocols, and offers a more
comprehensive guide to treatment.

It was the purpose of this project to formally evaluate and rewrite these two
protocols.
The author of this project worked as a District Medical Officer in remote Central
Australia for the period 1994–99.

The guideline revision process

In the process of rewriting the CARPA ‘DR ABC/ Loss of Consciousness’ and
‘Injuries’ protocols, this review has endeavoured to adhere, where applicable, to the
principles outlined in the National Health and Medical Research Council (NHMRC)
publication A guide to the development, implementation and evaluation of clinical
practice guidelines (1998). This document outlines the guiding principles, offers
advice on guideline development, and considers pertinent legal issues.

The guiding principles

1. ‘Processes for developing and evaluating clinical practice guidelines should
focus on outcomes . . .’
Outcome measures for the DR ABC/Loss of Consciousness and Injuries protocols
have proved difficult to quantify. The evaluation process will be discussed in detail
later, but unfortunately the protocol has largely been driven by perceived, rather than
measurable, outcomes. Nonetheless, the desired outcome has clearly been to reduce
morbidity and mortality associated with sudden loss of consciousness and/or injury.

2. ‘Clinical practice guidelines should be based on the best available evidence and
should include a statement about the strength of their recommendations . . .’
There are multiple ‘emergency’ protocols in existence. The American Heart
Association Resuscitation Guidelines printed in ‘Circulation’ (August 2000)
represent a stated attempt to publish a consensus position based on the best available
evidence pertaining to cardio-pulmonary resuscitation. The DR ABC/Emergencies
protocol has thus been based on this document.

The ‘Injuries’ protocol has been based on the guidelines in the ‘Advanced Trauma
Life Support’ Instructors Manual (1997) and ‘The Management of Acute
Neurotrauma in Rural and Remote Locations’. For the sake of consistency, it has
been cross-referenced against the other ‘trauma protocols’ in use in remote Central
Australia. These include publications by the Top End Division of General Practice,
Council of Remote Area Nurses of Australia and the Royal Flying Doctor Service
(Central Division).

3. ‘The process of guideline development should be multidisciplinary and should

include consumers . . .’
The protocols being rewritten are used primarily by nursing staff and Aboriginal
health workers, and to a lesser extent by medical practitioners and laypersons. The
third edition was written by a medical practitioner (myself) and a registered nurse,
with extensive reviews by consumers. This edition has been rewritten solely by a
medical practitioner (myself). The review process has been multidisciplinary.

4. ‘Guidelines should be flexible and adaptable to varying local conditions.’

Whilst originally written for use in Central Australia, the CARPA STM has found
itself having to address an ever-widening readership. The use of the STM in the
tropics, and in other states, has required addressing issues not found in Central
Australia (e.g. jelly fish stings) and the addition of more area-specific information
(e.g. phone numbers). However, management principles of loss of consciousness
and injuries are for the most part universal, so no particular geographical
idiosyncrasies have needed to be addressed. The guidelines recognise that the
epidemiology of emergencies and injuries is different in Central Australia, with
higher rates of alcohol-related injuries, meningitis, and hypoglycaemia.

5. ‘Guidelines should be developed with resource constraints in mind . . .’

It is recognised that loss of consciousness/injury management equipment can be
expensive, and infrequently used in the setting of a remote clinic which treats
relatively few serious emergency cases. The protocols have avoided recommending
strategies that require the purchase of such equipment. Defibrillators, extrication
devices, certain airway management aids are therefore not included. Similarly, it is
hoped that the recommendation of relatively few drugs (particularly antibiotics) will
avoid wasteful expenditure.

6. Guidelines are developed to be disseminated and implemented taking into account

their target audience
. . .’ This has proved a particular challenge, as the STM is addressing a readership
representing a large spectrum of experience and academic qualifications. The
protocols are primarily intended for use by AHWs, medical practitioners and nurses.
Within each of these groups there is a further spectrum of expertise. The intention
has been that any individual can follow the protocols for as far as they feel
comfortable, with reminders of the need to seek more senior advice when necessary.

The CARPA STM is now widely used throughout rural/remote Australia.

Dissemination of the DR ABC/ Loss of Consciousness and Injuries protocols is
achieved through the success of the STM as a whole. The evaluation of the DR
ABC/Loss of Consciousness and Injuries protocols reveals a potential under-
utilisation of these protocols, particularly by doctors and AHWs. The reasons for
this are not clear, and almost certainly multi-factorial. The frequent comment ‘too
hard to understand’ raises difficult issues regarding literacy and training. In terms of
‘focus on outcomes’ there is of course little point in having a carefully prepared
protocol if nobody is using it!

7. ‘The implementation and impact of the guidelines should be evaluated.’

The current guidelines have been evaluated as part of the revision process. The
evaluation of the new guidelines should occur when the new edition of protocols is
updated in approximately four years time.
[Editor: An evaluation of the third edition of the CARPA STM was done in 2001. It found
strong support for the STM among all clinicians and for development of the reference book,
and found that every clinic visited in the NT (~50% of all clinics included) were using the
STM.]

8. ‘Guidelines should be revised regularly.’

The CARPA STM is rewritten every four years. Given the relatively slow rate of
significant changes to the management of DR ABC/injuries, at the level at which
these protocols are addressing them, this is seemingly an appropriate time frame.

Guideline development
The process that the revisions of the Emergencies/Injuries protocols have followed
has also been guided by the NHMRC recommendations.

The need for protocols dealing with emergencies/injuries is highlighted by the

continued high prevalence of injury-related deaths in isolated areas. There are
almost twice as many injury deaths in Australia’s most remote areas as elsewhere.
Between 1979 and 1995 injury was the most frequent cause of death for Northern
Territory non-Aboriginal males, and the second highest cause of death for
Aboriginal males. In terms of ‘years of potential life lost’, (because injury tends to
occur in younger people) in the NT in 1995 injury accounted for more years of life
lost than all of the years of life lost from the combined total of respiratory disease,
infectious disease, cancer, diabetes and renal disease. Of those deaths due to injury,
almost forty per cent were due to road transport injuries.

Of course, protocols are only part of the answer in addressing the high rate of injury-
related deaths, along with issues relating to alcohol consumption, excessive
speeding, lack of restraints, and getting medical teams to isolated areas rapidly.

When ideas for earlier editions of the STM were being canvassed, users expressed a
strong need for protocols outlining management of emergencies and injuries.

A multidisciplinary panel, the CARPA editorial committee, has already been

convened to oversee the revision of all the protocols contained within the manual.

The purpose of the guidelines is defined as to minimise morbidity/mortality related

to loss of consciousness from all causes, and morbidity/mortality related to injuries.
The guidelines are now intentioned for use by health staff in remote/rural areas,
including those beyond Central Australia. They provide a basis for early treatment,
and are quite clearly not exhaustive. The primary focus of the intended readership is
nursing staff and Aboriginal Health Workers, though the protocols are written such
that medical practitioners will find a level of knowledge consistent with what they
would be expected to provide in the early phases of treatment. The NHMRC
recommend that different versions of guidelines should be developed for different
audiences. This is a somewhat contentious issue regarding emergencies/injuries,
where the basic treatment principles remain the same, i.e. ‘ABC’. Certainly the
concept of a universal reference, which all clinic staff refer to, has proved a popular
model.

[Editor: ‘One book for all users’ was strongly supported by the evaluation of the third
edition of the STM in 2001.]

The formulation of the guidelines has occurred after reference to appropriate

resources (outlined above). After the initial draft, the guidelines have been widely
circulated for comments amongst consumers and a selection of interested ‘experts’.
The latter include one senior specialist from each of the disciplines of anaesthesia,
emergency medicine, trauma surgery, neurosurgery, and infectious diseases.

Dissemination and implementation of the guidelines will to a large extent rely on the
continued uptake and support of the CARPA STM that has occurred over the last
decade. This support in turn relies on the involvement of users in the development of
the protocols. The production of a wall chart displaying a DR ABC algorithm is
being considered. Health educators will continue to be encouraged to promote
practice policies in line with those appearing in the manual.

An evaluation mechanism is in place for the manual as a whole. Ideally, each

individual protocol would be evaluated, using health outcomes as end points, or
more pragmatically, as has occurred with this revision of the DR ABC/Emergencies
and Injuries protocols. Unfortunately, the resources are not available for this to
occur, so the future evaluation of these particular protocols remains uncertain. The
protocols will be revised in four years time, along with the rest of the manual.

[Editor: CARPA and other groups interested in the application of evidence-based health
care are working on ways to promote and monitor the implementation of evidence-based
guidelines. Simple mechanisms, applied at the local clinic level are likely to be important
such as quality assurance auditing of clinical practice as is already done in some settings.
Health service management practices that help to overcome barriers to implementation are
also very important]

Evaluation of the current guidelines for injury

Methods
In keeping with the recommendations proposed by the NHMRC in their publication
A guide to the development, implementation and evaluation of clinical practice
guidelines, the current edition of the DR ABC and Injuries guidelines have been
assessed for the following factors.

1. Guideline dissemination. An assessment was made as to the success of the degree

of dissemination. This was based on the number of copies sold and on a phone
survey of users, who were asked the following questions: ‘Have you ever read the
DR ABC protocol at the beginning of the manual?’; and ‘Have you ever read the
Injuries protocol in the middle of the manual?’

2. Whether or not the guidelines have contributed to any changes in clinical

practice. During the same phone survey respondents were asked the questions:
‘Have you read the DR ABC protocol during the time that the patient was in your
care?’; and, ‘Have you ever read the Injuries protocol during the time that the patient
was in your care?’ This does not directly address the question of whether or not the
guidelines changed clinical practice. It was felt that practitioners who are reading the
guidelines during the time they are actively treating a patient could reasonably be
assumed to be following its recommendations, thus progressing the stated aim of the
guidelines to minimise morbidity and mortality. I also believed that practitioners
may feel defensive if they were directly asked if the guidelines had changed their
management of any particular case, suggesting they had ‘forgotten’ something
important, and therefore bias the responses.

3. Whether or not clinical practice is moving towards the guidelines

recommendations. This involved consideration regarding what information was
important, but also accessible. To fully assess patient management prospectively
was beyond the resources available. To do so retrospectively would entail examining
patient notes in health clinics. Given the isolated nature of these clinics, this was not
logistically possible. The ethical dimensions of such a task is also problematic. I
considered examining hospital notes to try to ascertain the efficacy of pre-hospital
patient management, but felt that RFDS and/or St Johns Ambulance Service
interventions would obscure ‘bush’ management. I finally decided to review
eighteen months of ‘code 1’ (i.e. ‘medical escort required’) Royal Flying Doctor
Service evacuations from remote Central Australia into Alice Springs, as the RFDS
remains the common destination point for the majority of seriously injured patients
in Central Australia.
Rather than generally assess the patient management notes to ascertain the level
of care, I chose several markers. Given that the guidelines emphasis the need to
focus attention on the basic tenets of ‘ABC’ management, I decided to simply assess
the frequency of administration of oxygen, cervical spine protection, and
intravenous fluids, and whether the respiratory rate had been noted on the flight
record. If these basic strategies are being implemented, it demonstrates an
appreciation of the most important principles of trauma management.

Where these interventions had not occurred it was further assessed, on the basis of
the information available, whether they were indicated. For example, if a young
child was evacuated with a suspected head injury, but was fully alert, it was deemed
appropriate for the health worker not to have attempted to gain IV access. Where the
first people on the scene were laypersons, only first aid interventions were possible.

The RFDS records whether oxygen, cervical spine protection and intravenous fluids
are ‘commenced’ or ‘continued’, making this information relatively accessible. Of
course, the quality of the information gleaned is dependent on the quality of record
keeping.

4. Relevance, ease of access, clarity, how much information they contain, and
general user satisfaction. During the phone interviews, respondents were invited to
suggest weaknesses and possible improvements of the current guidelines.

The NHMRC also recommends an economic evaluation, but this was felt to be
outside the scope of this project.

The most critical question of ‘Have health outcomes changed?’ was given careful
consideration. A randomised control trial was deemed to be unrealistic. Thus, this
study has contented itself instead with evaluating the factors outlined above.

The phone survey was conducted by one person (myself) over a period of several
weeks, and included fourteen Aboriginal Health Workers, fourteen registered nurses,
and twelve doctors. The twelve doctors represent virtually the entire remote Central
Australia clinical medical workforce. The AHWs and nurses were primarily
practitioners with whom I have worked. The advantage of this approach is that I
believed I would obtain relatively honest answers, and all these practitioners are
experienced ‘bush staff’ with a good knowledge of information required to work in
remote areas.

The disadvantages are that more experienced practitioners are probably less likely to
refer to a protocol during an acute situation, thus biasing their responses, and the
survey sample quite clearly is not a ‘random’ selection.

Results
1. Dissemination of guidelines
Over eight thousand copies of the third edition of the CARPA STM have been sold.
The manual is officially endorsed as part of NT Department of Health and
Community Services’ policy. The manual has been bought by health clinics
throughout Central Australia, the Top End, northern South Australia, and remote
areas of Queensland and Western Australia

Medical practitioners were asked what resources they do use for dealing with
emergencies. All replied that foremost they rely on their own experience, which as a
group they felt very confident in. Several mentioned seeking help over the phone
from more senior colleagues. Two said they refer to the CARPA guidelines after
they have treated a patient, as a checking process.
The three cases of recorded tachypnoea (>30) were all recognised as being
significant chest injuries. Two patients had intercostal catheters inserted. The third
patient had two 14g IV cannulas inserted (oxygen saturation 74% on room air, three
days after a motorcycle accident on a remote cattle station, with significant chest
pain). It was elected to fly at ground level cabin pressure, as the flight nurse was not
comfortable inserting an intercostal catheter.

In light of the findings associated with reviewing these Code 1 records, a heading
entitled ‘All badly injured patients require oxygen and intravenous fluids’ will be
placed at the top of each page of the Injuries guidelines. The possibility of
incorporating a simple diagram of a patient receiving oxygen, intravenous fluids and
cervical spine protection — to be inserted at the top of each page — is also being
considered. The importance of measuring and recording the respiratory rate has been
further highlighted.

1. Protocol reading

Have you ever read the DR ABC protocol? (Number and (%) of respondents)
Aboriginal health worker Registered nurse Medical officer
Yes 4 (29%) 10 (71%) 8 (67%)
No 10 (71%) 4 (29%) 4 (33%)

Have you ever read the Injuries protocol?

Aboriginal health worker Registered nurse Medical officer
Yes 4 (29%) 12 (86%) 5 (42%)
No 10 (71%) 2 (14%) 8 (58%)

2. Impact on clinical practice

Have you ever read the DR ABC protocol during the time that you were actually
looking after a patient? (Number and (%) of respondents.)
Aboriginal health worker Registered nurse Medical officer
Yes 2 (14%) 4 (29%) 1 (8%)
No 12 (86%) 10 (71%) 11 (92%)

Have you ever read the Injuries protocol during the time that you were actually
looking after a patient?
Aboriginal health worker Registered nurse Medical officer
Yes 4 (29%) 11 (79%) 3 (25%)
No 10 (71%) 3 (21%) 9 (75%)

3. Concordance of clinical practice and guideline recommendations

Intervention Cases indicated Cases administered Cases not

administered
Oxygen therapy 52 24/52 (46%) 28/52 (54%)
Cervical spine protection 47 23/47 (49%) 24/47 (51%)
Intravenous therapy 51 39/51 (76%) 12/51 (24%)

4. Respiratory rate

Respiratory rate 0–13 14–30 >30 Not recorded

 Number of cases 1 (RR=10) 49 3 9

General user satisfaction

At the conclusion of the phone interview, respondents were asked if they had ‘Any
particular problems with, or suggestions for improving the protocols?’
No particular themes emerged as predominant. Several AHWs made comments
about difficulty interpreting the guidelines, and requested simpler language, and
more pictures/diagrams.

Discussion of results
The widespread sales of the manual have ensured that the protocols of interest have
been widely disseminated. Previous studies have confirmed the ubiquitous nature of
the CARPA STM in Central Australian health clinics.

AHWs are employed in the great majority of remote health clinics in Central
Australia. The fact that less than a third of those to whom I spoke had actually read
the guidelines suggests a failure in dissemination to this group (remembering that
they represent a more experienced cohort). This likely reflects literacy levels, a view
reinforced by frequent comments of ‘too hard to understand’, and ‘more pictures’.
These comments have been borne in mind in the writing of the new edition.
However, as one health worker educator has emphasised, ‘increasing the font size
may help but there is nothing you can do to make up for missing out on years of
basic education’. There is certainly merit to the concept of having more AHW input
into the writing of protocols.

These findings confirm that nurses are regular users of the guidelines, whilst AHWs
and doctors refer to it less frequently. Nurses by far see the bulk of patients in
remote clinics, so in that sense the guidelines are impacting on clinical practice.
However, in that medical practitioners are likely to be involved in the early stages of
a ‘DR ABC’ scenario, the guidelines are having little impact through doctors.
Increasing the readership amongst doctors may well prove difficult, as long as they
perceive no need to do so.

Where the number of recorded interventions is low it is difficult to know whether

this reflects a lack of intervention, or a lack of attention to recording. One patient
with an intercostal catheter was not recorded as receiving oxygen, whereas one
would assume that the practitioner with the skill to perform this intervention would
have the knowledge to appreciate the need for oxygen.

1.Oxygen therapy: Of those cases where oxygen therapy was seemingly

indicated, it was only recorded as having been administered pre-evacuation in
less than 50% of cases, indicating a potential lack of appreciation for this basic
manoeuvre.
2.Cervical Spine Protection: Of those cases where formal cervical spine
protection was apparently indicated, it was only recorded as having been
instituted in approximately 50%, similarly reflecting a potential short-fall in this
aspect of trauma management.
3. Intravenous therapy: Of those cases where IVT was seemingly indicated, it
was recorded as having been administered in 76%. Intravenous therapy is more
likely to be recorded as it recognised as a more invasive procedure than oxygen
therapy, which is sometimes overlooked as being ‘a given’. Furthermore,
 remote area staff are often aware of the need to ‘put in a drip’ in an emergency.
The rate of fluid administration, which is critically important, was not recorded.

The third edition CARPA guidelines suggest that a respiratory rate outside the limits
of 8–30/minute demands attention. It was pleasing that those cases with respiratory
rates outside these values were recognised as having significant chest injuries.

One practitioner, with many years of remote clinic experience, made a thoughtful
comment that the most common head injury seen is that of the drunk, aggressive
man bleeding heavily from a head injury, but the management of such an injury is at
the end of the Head Injury section. Principles of emergency management for severe
trauma (EMST) have been followed, thus management of this scenario details
careful attention to Airway, Breathing and Circulation, with subsequent advice on
GCS (Glasgow Trauma Scale), checking pupil responses, the use of Mannitol etc.
This is all very sound practice, but appears too wordy and cumbersome for the
isolated practitioner who wants immediate help with stopping the spurting arterial
bleeder in the semi-conscious inebriated patient with the often-attendant stress of
hovering distressed relatives. Thus, a balance must be struck between providing
what by the author is seen as ‘best practice’, and what by the consumer is perceived
as helpful, practical advice. If the consumer feels the advice is idealised, the protocol
will gather dust on the shelf

Similarly, the patient with the heavily bleeding limb causes frequent angst.
Previously, this was at the end of the ‘Circulation’ section, after information about
the recognition and treatment of hypovolaemic shock. Immediate management of
this scenario has been relocated to the beginning of ‘Circulation’.

Guideline revision
Through feedback from the evaluation process, the guideline revision has attempted
to address the following issues.
1. More flow diagrams and pictures. The DR ABC protocol for the immediate
management of sudden loss of consciousness now incorporates a flow diagram
with a series of yes/no options. Diagrams of life-threatening trauma conditions,
application of oxygen and hard collars, and pressure application to bleeding
points have been added.
2. Improved layout. As mentioned earlier, several remote area practitioners
expressed difficulties and frustration in rapidly finding advice on the
management of the common trauma scenarios they faced. (Examples included
the young man exsanguinating from the self-inflicted ‘sorry’ cut to the groin
and the inebriated patient bleeding profusely from a head wound.). In response
to these comments, the sections have been relocated to the beginning of the
‘Circulation’ and ‘Head Injury’ sections, respectively, to improve accessibility.
3. Attempts have been made to simplify the language used throughout. The use of
medical jargon has been minimised. The simple language of the manual has in
the past been identified as being critical to its success.
4. Potential inadequacies in the administration of oxygen and intravenous fluids
have been identified. These have sought to be addressed through the insertion
of a ‘prompt’ at the top of each page reminding readers ‘all badly injured
patients need oxygen and intravenous fluids’.
5. I have attempted to adapt the reference guidelines to local conditions whilst
still maintaining key policy directions. The two major issues have been the
sheer volume of the references, and the fact that they have been written
 primarily for doctors (and include in-hospital management). In addressing the
first issue, I have endeavoured to select only the fundamental steps, with little
expansion and detail. Addressing the latter issue has required simplifying
medical jargon, deleting procedures not applicable to non-medical staff, and
focusing on the pre-hospital care. Thus, for example, airway management is
confined to opening, clearing, securing with an oropharyngeal airway, and
applying oxygen. References to intubation and surgical airways have been
deleted.

Conclusions
This project has sought to evaluate the current guidelines in the CARPA STM for
the immediate management of sudden loss of consciousness and injuries. A formal
evaluation involving a randomised control trial was deemed beyond the scope of the
available resources. The evaluation, conducted through phone interviews of remote
area practitioners and reviewing RFDS flight records, provided some insight into the
degree to which the current guidelines have been disseminated and impacted on
clinical practice, to what extent clinical practice parallels guideline
recommendations, and identified perceived shortfalls.

Registered nurses, who conduct the majority of face-to-face clinical care in remote
Central Australia, usually have a copy of the guidelines, have at least read the DR
ABC guidelines, and have read and used the Injuries guidelines during clinical care.
Aboriginal Health Workers seem far less likely to have read or used the guidelines,
in keeping with their feedback that they find the guidelines too difficult to
understand. Medical Officers report little use of the guidelines.

Evaluation of how well current clinical practice parallels guideline recommendation

suggests that basic manoeuvres — such as oxygen administration, cervical spine
protection and initiation of IVT — are being under-utilised. This is of concern,
while recognising that the apparent shortfalls may in fact merely represent poor
record-keeping on RFDS flight charts, or that good reasons for not instituting these
therapies may have existed.

The guidelines have been rewritten bearing all of the above in mind. Whilst the
CARPA STM continues to enjoy widespread readership, the role of specific
guidelines for the management of sudden loss of consciousness and injuries is
supported, though their impact remains somewhat enigmatic.

The overall impact of the guidelines is dependent on their successful broader

integration with other aspects of clinical care, including peer review, continuing
medical education, and quality assurance.

Acknowledgements
This project has been supervised by Dr Dan Ewald, of the Centre for Remote Health,
Alice Springs. I am very grateful to him for his support and frequent solutions to
difficult issues encountered during this project.

My thanks go to the Royal Flying Doctor Service (Central Division) for making
available to me past flight records from Alice Springs.

I am indebted to Dr Nick Williams for forwarding to me his comprehensive

‘Evaluation of the CARPA Standard Treatment Manual’, which he compiled in
1994, and which has proved an invaluable resource.

Dr John Crozier has once again given much appreciated input into the clinical
content of the guidelines.

I am grateful to Prof Don Moyes, of the Department of Anaesthesia, The Queen

Elizabeth Hospital, SA, for his helpful advice.

I also acknowledge the National Health & Medical Research Council document A
guide to the development, implementation and evaluation of clinical practice
guidelines, which provided the basic template for the guideline revision that this
project has conducted.

References
1. National Health and Medical Research Council. A guide to the development,
implementation and evaluation of clinical practice guidelines. November 1998; 9.
2. Eddy DM. Practice Policies-What Are They? Journal of the American Medical
Association, 1990; 263:877–80.
3. National Health and Medical Research Council. A guide to the development,
implementation and evaluation of clinical practice guidelines. November 1998; 10.
4. Hampton C, Fallon C. CARPA Standard Treatment Manual and GSAT Adult
Chronic Disease Management Guidelines Evaluation Report, 2001.
5. American Heart Association. Guidelines 2000 for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care. Supplement to Circulation. 102
Aug 22, 2000.
6. The Neurosurgical Society of Australia. The Management of Acute Neurotrauma
in Rural and Remote Locations. Second edition. Feb 2000.
7. American College of Surgeons Committee on Trauma. Advanced Trauma Life
Support for Doctors, Instructor Course Manual. Sixth edition. 1997.
8. Thompson S, Dempsey K, Pearce M. Injury and Violence. The Health of
Territorians. Territory Health Services, 2001.
9. Williams N. An Evaluation of the CARPA Standard Treatment Manual 1994.
 Fits

Author: Dr Alison McCready (Anaesthetist, RDH)

Topic Reviewers: Prof Sam Berkovic and Dr Michael Harbord; Dr Steve Skov; Dr Peter
Tait; Dr Andrew White; Robyn Dixson (RAN, Yirrkala Clinic); Kenna Bistani (RAN, Pine
Creek); Peter Wordsworth (RAN, Barunga); Chris Binks (RAN, Lajamanu Clinic); Monica
Ostigh (RAN, Jabiru); paediatricians at RDH and ASH

Introduction
The remote-area nurse or Aboriginal health worker may have to deal with the stressful emergency
of the fitting child or adult, with no medical backup other than telephone advice. The main goals
of treatment are:
• Maintain adequate vital functions (oxygenation and circulation)
• Prevent systemic complications
• Terminate the seizure rapidly
• Minimise side effects of treatment
• Evaluate and treat any underlying causes.

Many seizures will terminate spontaneously, but drug treatment should be initiated if fitting
persists. Rapid control of fitting results in fewer complications. As a general rule, this should be
done if a fit lasts for more than three minutes in children or five minutes in adults. There are no
specific data to support the use of these times: they are the recommendations of neurologists. In
individual patients whose pattern of fits is well understood, it may be appropriate to wait longer if,
for example, they usually stop fitting within say ten minutes. Such patients should have an
individualised management plan in their case notes.

Recommended protocols should therefore be easy to follow, involve only one or two drugs and
have simply- calculated dosage regimens. Drugs should be administered by socially/culturally
acceptable routes.

As a general rule, a doctor should probably be consulted after any fit unless an individual
management plan indicates otherwise. The degree of urgency can vary. If the fit is not controlled
with one dose of anti-convulsant, or fitting is recurrent, consultation should be immediate. If the
fit ceases spontaneously, or is controlled with a single dose, some time can be spent in taking a
history and doing some investigations (e.g. blood glucose) as per ‘Further Management’.

Specialist medical terminology has been avoided where possible, or explained if it is used. Cross-
references have been given to other topics in the CARPA STM (e.g. Resuscitation, Meningitis)
rather than duplicate material unnecessarily.

This revised protocol follows the previous version where no change is necessary or advisable.
However, since the publication of the previous edition of the manual there have been
developments in the management of seizures, which are changing recommended practice.

When should a fit be treated?

The recommendation of the Working Group on Status Epilepticus of the Epilepsy Foundation of
America is that fits lasting more than 10 minutes should be treated. Australian neurologists
associated with the Epilepsy Society of Australia recommend three minutes in a child and five
minutes in an adult. These times are based on expert opinion and not on specific data.
In practice, it may take several minutes for fitting patients to get to the clinic or for health
personnel to reach the patient. The protocol therefore recommends that once health personnel are
in attendance, drug therapy be started after three minutes in a child or five minutes in an adult.
Most self-limiting generalized convulsions stop within 3 minutes, and almost all stop by 5
minutes from onset. Furthermore, early therapy is far more effective than is delayed therapy,
so the longer the seizures persist, the more difficult they are to stop. Therefore, patients
seizing for 10 minutes should be treated on the assumption that they are in (status
epilepticus).3

The ‘demise’ of paraldehyde

All injectable paraldehyde products have been discontinued in the USA due to lack of demand
(RDH Pharmacy database), and it is likely that this will also follow in Australia. Royal Darwin
Hospital Pharmacy currently supplies about 60–70 ampoules per year to remote-area clinics and
the NT Aerial Medical Service. This probably represents replacement of expired unused stock.
RDH Pharmacy anticipates difficulty in future supply of paraldehyde. The perceived ‘safety’ of
paraldehyde is probably incorrect; it seems just as capable of causing respiratory depression as the
benzodiazepines (RDH Pharmacy database, MIMS Annual). Its intramuscular use when diazepam
could not be used in this way was a major rationale for its use in previous editions of the manual.
The availability of midazolam makes paraldehyde redundant.

The ‘rise’ of midazolam

Control of fitting is not one of the current listed indications for midazolam in Australia. It is,
however, a potent anti-epileptic as well as anaesthetic/sedative, and there is a large volume of
current literature dealing with its use for this purpose. It is widely used throughout Australia for
the control of fitting. At the Women’s and Children’s Hospital in Adelaide there is a program to
train parents, other carers and teachers to use intra-nasal midazolam to control fits that occur
outside of hospital.

Intravenous or intra-osseous administration produces the quickest onset of action, and is the
preferred route in ideal circumstances. However, in contrast to diazepam, midazolam is water-
soluble at its preparation pH (3.5) and is therefore well absorbed after intra-muscular injection and
also across mucous membranes (oral, nasal or rectal). Its low pH causes pain/burning when given
intra-nasally in the conscious patient but this is of decreased relevance in a convulsing subject. It
has an unpleasant taste when given orally, but this is unlikely to be appreciated by a fitting patient.

At physiologic pH, midazolam becomes extremely lipophilic3 and therefore crosses the blood–
brain barrier readily for a rapid onset of action. Effects on the EEG have been reported within
minutes of IV administration, and control of fitting has also been achieved within minutes.
Elimination half-life is short (1.5–3.5 hours). Its metabolites are pharmacologically inactive.

Midazolam has successfully terminated seizures when other benzodiazepines have failed to do so,
and has also reportedly succeeded when barbiturates have been ineffective. It is not yet widely
accepted as a first-line drug, but increasing numbers of studies are advocating its use in this
respect.

Midazolam has a generally good safety record with respect to respiratory depression, but can
cause this, especially when combined with opioids or other CNS depressant drugs. Incidence of
side effects, when used on its own for sedation in the Emergency Department, is of the order of
2%. This is mainly transient respiratory depression, occasionally requiring short-term bag-and-
mask ventilatory support.
Medline searches on midazolam in fitting:
• ‘effects can be seen within 1 to 5 minutes of administration, and its anti-convulsive effects are
apparent as early as 5 to 15 minutes after administration’ in refractory status epilepticusa
• ‘Seizure arrest is usually attained within 5 to 10 min’ after IM useb
• Efficacy in controlling seizures is 79% (intranasal), 93 to 100% (intramuscular) and 100%
(intravenous) – (v) 28.6 to 100% (rectal) and 54 to 100% (IV) for diazepamc
• ‘Midazolam is relatively free of side effects when used alone’.d

Midazolam: cost and shelf life

Midazolam is supplied in the several preparations including:

15 mg in 3 ml Box of 5 $34.85 or $37.10 $6.97 to $7.42

per amp

5 mg in 5 ml Box of 10 $11.65 or $15.30 $1.12 to $1.53

per amp

5mg in 1 ml Box of 10 $15.30 $1.53

per amp

The 5mg in 1 ml preparation comes in both glass and plastic ampoules. The plastic ampoules are
those recommended by the Women’s and Children’s Hospital in Adelaide for use by lay persons,
as the top can be removed easily and the midazolam dripped into the patient’s nose.
Only one concentration should be stocked, to minimise confusion in calculation of dose and
dilution. Therefore, either the 15 mg in 3 ml or 5 mg in 1 ml preparations are recommended, as the
volumes required are more suitable for nasal, buccal or IM injection.
One box should be sufficient stock, if this can be replaced readily by regional pharmacy. Shelf
life is four years at 25°C, if protected from light (store in cupboard or drawer). Health centres that
do not use it within four years could arrange to exchange their stock with the local hospital
emergency or anaesthetics departments so that in-date stock is maintained without extra expense.

What dose to use?

The doses recommended in this protocol are slightly conservative with respect to those cited in
journals. Most journal articles deal with therapy in hospitals or epilepsy centres. The CARPA
STM is intended for a remote-area situation, where expertise in managing respiratory depression
may be limited. A lower dose will often terminate the fit, is less likely to cause respiratory
problems, and can be repeated after discussion with a doctor, if seizures continue or recur.
Drug doses are best calculated for children on the basis of body surface area; the next best
measure is body weight, which does not always correlate well with age. However, it is usually
difficult to weigh a fitting child and a recent weight may not be known. Therefore, for this
protocol, drug doses are presented in both a weight and age table. For the age table, weights are
assumed as given in the following table. In many remote communities, a high proportion of
children are lighter than children in urban settings.
Age Approx weight
3 mths to <6 mths 6 kg
6 mths to <1 yr 8 kg
1yr to <2 yrs 10 kg
2 yrs to <3 yrs 12 kg
3 yrs to <4 yrs 14 kg
4 yrs to <5 yrs 16 kg
Is there still a place for diazepam?
‘Diazepam is highly lipid soluble, and appears in the brain as quickly as 1 minute after (IV)
injection, with a median time to terminate a seizure of two minutes’.3 Its anti-epileptic effect lasts
for 20–30 minutes, and the dose may have to be repeated, or a longer-acting agent (phenytoin or a
barbiturate) given for recurrent fitting.

It is not well absorbed after IM injection. It is effective rectally, and guidelines for rectal use have
been published by a combined group of organisations with interest in epilepsy. However, its onset
of action is slower than via the IV route, and the incidence of respiratory depression may be
unacceptably high. Norris et al. reported that diazepam is associated with a 9% incidence of
respiratory depression (no doses quoted). ‘The use of diazepam as first-line therapy for children
with acute seizures needs to be reviewed’.10

The impression of working practitioners is that while rectal delivery of diazepam is (barely)
acceptable in children, it is not so in adults. Midazolam given either IM, nasally or buccally is
likely to be much more socially acceptable to most clients.

Diazepam in oral form should still be retained in the community pharmacy, for sedation of
disturbed/psychotic patients.

What is the most suitable route of drug administration?

Intravenous administration undoubtedly gives quickest onset of action and quickest control of
seizures, regardless of which anti-convulsive agent is used. An intravenous cannula should be
inserted in any fitting patient as soon as possible, but this may be difficult until the fit is
controlled.
Intra-osseous needles are becoming increasing available in remote communities, as are staff who
are trained to insert them. These needles may be an equally rapid and more reliable alternative to
IV in a fitting infant or child. They should be regarded as an interim emergency measure, and IV
access should be obtained as soon as possible.

When using IV or intra-osseous anti-convulsants, it is advisable to dilute the drug and give a
larger injected volume, thus overcoming the problem of having to flush the drug in with saline,
etc.

Intramuscular injection can be used for midazolam and phenobarbitone. Many remote-area health
staff would be comfortable with giving IM injections. Several articles now report success of IM
midazolam at least equal to IV diazepam. Five relevant articles are summarised below. Full
references are given at the end of this document.

Chamberlain JM et al.
24 children (age from birth–18 years) presenting to emergency departments with seizures longer
than 10 minutes were randomly allocated to receive either IM midazolam 0.2 mg/kg (maximum 7
mg) or IV diazepam 0.3 mg/kg (maximum 10 mg). Both regimens were effective (one treatment
failure in each group), but time to stopping seizures was 3.3 +/– 2.0 minutes for IM midazolam
versus 7.8 +/– 3.2 minutes for IV diazepam. The reason given was that without the need to obtain
IV access, administrations was more rapid.
[Editor: This study was done in hospital emergency departments, where IV expertise may be higher
than in a remote-area health centre. The IM route will probably perform even better in the remote setting]
Lahat E et al.
(Abstract only sighted)
Midazolam was given IM in 60 episodes of epilepsy in 48 children (four months to 14 years). In
64 episodes, seizures stopped 1–10 minutes after injection. Its use is suggested ‘specifically when
attempts to introduce an intravenous line in convulsing children are unsuccessful’.
Nasal midazolam is generally well absorbed. There is some concern that absorption could be
decreased by nasal secretions, as in URTI, but this does not seem to happen in most cases in
practice.5 The dose is drawn up into a syringe and any needle discarded. The drug is ‘dripped’
alternately into both nostrils, or ‘injected’ over 30 seconds. Midazolam ‘burns’ when given
nasally, but that should not be a problem in a fitting patient.
Buccal (oral) administration of midazolam is probably better; absorption is also good. The dose
is drawn up into a syringe, any needle discarded, and the end of the syringe inserted between the
cheek and the teeth for injection. The surface for absorption is larger than the nasal surface, and
the volume of fluid used should not be a problem in the oral airway. There is a small risk of
mucosal damage from the end of the syringe, and therefore blood in the airway; loose teeth could
also be knocked out with rough handling. The bitter taste would not be noticed by a convulsing
patient.

Scott RC et al.
79 episodes of severe epilepsy in 18 young people (5–22 years) in a residential centre were treated
with either rectal diazepam (10 mg) from a commercially-prepared pack, or buccal midazolam (10
mg). Some patients received both drugs in different episodes. Midazolam was effective in 75% of
episodes (diazepam 59%) in median time six minutes (diazepam eight minutes). However, there
was no significant difference between the drugs for efficacy, time to drug administration, from
administration to end of seizure, or total seizure length. The buccal route was found to be more
acceptable than rectal.
[Editor: Camfield PR: Journal of Pediatrics 1999; Vol 135: No.3: p 398–9 finds the study ‘sufficiently
convincing that I will slowly begin to alter my [neurological] practice’.]

Jeannet PY et al.
26 children treated (11 at home and 17 in hospital; two treated in both locations) for total of 125
seizures. 122 seizures (98%) stopped within 10 minutes (average 3.6 minutes). No serious adverse
side effects. Parents with experience of rectal diazepam found that nasal midazolam was easier to
use and that post-ictal recovery was faster.

Lahat E et al.
47 children (six months–five years) with febrile seizure lasting at least 10 minutes in a paediatric
emergency department were given either nasal midazolam 0.2 mg/kg or IV diazepam 0.3 mg/kg
(maximum dose of each 10 mg). Both drugs are equally effective at controlling seizures, but mean
time to starting treatment was significantly shorter with midazolam (3.5 +/- 1.8 minutes) than
diazepam (5.5 +/- 2.0 min). Time to cessation of seizures is also two minutes shorter with
midazolam (although IV diazepam acts more quickly, it takes longer to obtain IV access and
administer drug). No significant side effects in either group.

Rectal administration can be used for diazepam, midazolam or phenytoin. A modified device, such
as a butterfly needle with the ‘wings’ removed, must be used. There is a small risk of rectal
perforation. The nasal or buccal routes seem easier than rectal in a fitting patient (especially
adult), and more socially acceptable. The rectal route may be abandoned in the future.

Most studies on IM, oral and nasal midazolam involve small numbers of patients and are not
statistically strong (insufficient power due to low numbers of patients, difficulties with
randomisation in an emergency situation, etc.). Larger trials are needed before the evidence basis
for change is statistically strong. [Editor: Or perhaps a meta analysis.] However, clinicians and
departments are starting to alter their practice and protocols, and this would seem to be sufficient
reason for recommending a CARPA protocol that is simpler to administer, equally effective, and
possibly safer than the former edition.

When are other drugs needed?

Phenytoin (Dilantin) is the drug of choice for patients who fit after a head injury. Phenytoin can be
given IV, but must be given slowly (with ECG monitoring) to prevent cardiac arrhythmias. It
should probably be given only on the advice of a doctor, with careful specific instructions. It is
therefore not included in the flow chart. Phenytoin is about 50% effective in stopping seizures
when used on its own. The propylene glycol solvent can cause fitting and other side effects in very
young children.

Fosphenytoin (a phenytoin prodrug) is well absorbed after IM injection and is less irritant if
extravasation occurs via the IV route.

Some paediatricians prefer phenobarbitone as a first-line anti-convulsant in neonates and young

babies. Recommending phenobarbitone would introduce another drug to the community
pharmacy, which has a lower safety margin than midazolam in relatively inexperienced hands.

Evans D, Levene M
Detection and treatment of the underlying cause of the seizure is most important. The authors’
practice is to give anticonvulsants if there are three seizures per hour or more, or if any one seizure
lasts for three minutes or more. First-line treatment in their hospital is still phenobarbitone.
Second-line drug is clonazepam but ‘other benzodiazepines are also popular . . . Diazepam has an
extremely short duration of action with a risk of sudden respiratory depression and its use should
be avoided’. IV lignocaine may be effective.

Refractory status epilepticus may need large doses of barbiturates or propofol for control. This
will cause profound respiratory depression, needing endotracheal intubation and ventilatory
support, and so is generally unsuitable for community use.

The current protocol

The major change to this edition of the manual advocates nasal or buccal midazolam as the first-
line treatment for a fitting patient. The rationale for this is as follows:
1. Evidence from the literature that these routes are safe, effective and as quick or even quicker
in controlling fits than intravenous or intramuscular administration.
2. Increasing experience in a number of centres in Australia of these routes of administration,
which supports the literature.
3. The experience of the program in Adelaide where parents, other carers and teachers are
effectively and safely using nasal midazolam in out of hospital settings.

Paediatricians and adult physicians at both Royal Darwin and Alice Springs hospitals have
reviewed the protocol and consider it appropriate for use. Advice has also been received from
consultant neurologists, Prof Sam Berkovic and Dr Michael Harbord, who have considerable
experience with these uses of midazolam in both in and out of hospital settings.

Intramuscular or intravenous administration can still be used if practitioners feel more confident
with those routes and dosage recommendations are provided.

Diazepam is no longer recommended. There appears to be no advantage to the use of diazepam

and several in favour of midazolam.

It is recommended for known epileptics, particularly children, that a test dose of midazolam be
given in a controlled setting to establish the safety of the dose. Ideally, this would be done in a
hospital ward or outpatients but it could also be done in a community clinic with a doctor present
and the facilities to support respiration. The appropriate dose can then be written into a
management plan for the individual.

The dosages recommended in the table of doses according to age are based on a 0.2 mg/kg dose
for nasal or buccal administration, a 0.1 mg/kg for the intramuscular route and a rather low
estimate of the weight of a child in that range. This relatively lower dose was chosen to minimise
the risk of overdose. In addition, according to practitioners experienced in the use of nasal or
buccal midazolam, a relatively lower initial dose often suffices to control a fit, and if it does not a
small extra dose can be given.

Individual management plans

People with known epilepsy should have an individual management plan documented in their
casenotes. This should include details of how long to wait before initiating drug therapy, specific
doses to give, whether to always consult a doctor or not and instructions for follow-up
observations.

When should fits be investigated?

There is no body of evidence indicating a clear direction as to whether and when fits should be
investigated. Specialist opinion varies somewhat and may change. As a result of discussion with
specialists at Royal Darwin and Alice Springs hospitals, the following is recommended:
• Anyone who has had a fit for the first time should be sent to hospital for investigation
• Always talk to a doctor immediately
• The doctor should talk with the specialist on-call at the regional hospital about how soon the
patient should go in.

References
1. Chamberlain JM, Altieri MA, Futterman C, Young GM, Ochsenschlager DW, Waisman Y. A
prospective, randomised study comparing intramuscular midazolam with intravenous diazepam
for the treatment of seizures in children. Pediatr Emerg Care 1997; 13(2):92–4.
2. Evans D, Levene M. Neonatal seizures. Arch Dis Child Fetal Neonatal Ed 1998; 78:F70–F 75.
3. Hanhan UA, Fiallos MR, Orlowski JP. Status epilepticus. Pediatr Clin North Am 2001;
48(3):683–94.
4. Jeannet PY, Roulet E, Maeder-Ingvar M, Gehri M, Jutzi A, Deonna T. Home and hospital
treatment of acute seizures in children with nasal midazolam. Europ J Paediatr Neurol 1999;
3(2):73–7 (abstract only sighted).
5. Lahat E, Goldman M, Barr J, Bistrizer T, Berkovitch M. Comparison of intranasal midazolam
with intravenous diazepam for treating febrile seizures in children: prospective randomised study.
Br Med J 2000; 321(7253):83–6.
6. Lahat E, Aladjam M, Eshel G, Bistritzer T, Katz Y. Midazolam in the treatment of epileptic
seizures. Pediatr Neurol 1992; 8(3):21–6.
7. Rivera R, Segnini M, Baltodana A, Perez V. Midazolam in the treatment of status epilepticus
in children. Crit Care Med 1993; 21(7):991–4.
8. Scott RC, Besag FMC, Neville BGR. Buccal midazolam and rectal diazepam for treatment of
prolonged seizures in childhood and adolescence: a randomised trial. Lancet 1999; 353:623–6.
9. Somerville ER, Antony JH. Position statement on the use of rectal diazepam in epilepsy. Med
J Aust 1995; 163:268–9.
10. Norris E, Marzouk O, Nunn A, McIntyre J, Choonara I. Respiratory depression in children
receiving diazepam for acute seizures: a prospective study. Dev Med Child Neurol 1999 May;
41(5):340–3.

Medline search references

a. Hanley DF, Kross JF. Use of midazolam in the treatment of refractory status epilepticus. Clin
Ther 1998 Nov–Dec; 20(6):1093–05.
b. Towne AR, DeLorenzo RJ. Use of intramuscular midazolam for status epilepticus. J Emerg
Med 1999 Mar–Apr; 17(2):323–8. Review.
c. Rey E, Treluyer JM, Pons G. Pharmacokinetic optimization of benzodiazepine therapy for
acute seizures. Focus on delivery routes. Clin Pharmacokinet 1999 Jun; 36(6):409–24. Review.
d. Nordt SP, Clark RF. Midazolam: a review of therapeutic uses and toxicity. J Emerg Med 1997
May–Jun; 15(3):357–65. Review.
 Ischaemic Heart Disease/Chest Pain
Part 1: Acute chest pain

Author: Dr John Hester (former Top End DMO)

Topic Reviewers: Dr Steve Brady (ASH); Central Australian DMOs; Kenna Bistani (RAN,
Pine Creek); Monica Ostigh (RAN, Jabiru); Angela Peermen (RAN, Oenpelli Clinic); Kaz
Knudsen (RAN, WA); Patrick and Anne Cashman (RANs, Mt Liebig Clinic); Dy Kelaart
(RAN, Yuendumu Clinic)

Cardiovascular disease is Australia’s largest health problem. It kills more people than any other
disease and generates enormous costs for the Australian health care system. The major types of
cardiovascular disease are ischaemic heart disease (IHD), cerebrovascular accident (CVA),
peripheral vascular disease (PVD) and congestive heart failure (CHF). Rheumatic fever and
rheumatic heart disease are also very important and are encountered frequently in the Aboriginal
and Torres Strait Islander peoples.

IHD results in a heavy physical and emotional burden upon individuals and families. In 1996 it
accounted for 13% of the total disease burden in the country, 19% of premature mortality and 5%
of years of equivalent ‘healthy’ life lost through disease, impairment or disability.1
In 1998–99 there were 437,717 hospitalisations in Australia where cardiovascular disease was
the principal diagnosis (7% of all hospitalisations). Of these, IHD accounted for 158,131 of them.
Acute myocardial infarction then accounted for 33,908 of the 158,131 figure. Further sobering
information is that, during the same time, there was a total of 27,825 deaths from IHD, both in and
out of hospital.1

Trends in the rate of fatal and non-fatal myocardial infarction among males and females aged 35–
64 years of age have been monitored in Newcastle (NSW) and Perth (WA) as part of the World
Health Organization’s multinational Monitoring of Trends and Determinants in Cardiovascular
Disease (MONICA) project. Analysis of the data reveals that the rates of non-fatal heart attack
have fallen by between 2.5% and 3.7% per year during the period 1984–93. Similarly IHD death
rates have also declined by 4.3% per year among males and 4.1% per year among females for the
period 1987–98. Such declines have resulted in a total decline of 39% among males and 38%
among females during this 12 year period.

However, the above figures are for all Australians. Deaths from IHD were twice as high among
Indigenous Australians as among non-Indigenous Australians in 1996–98. In fact, the ratio
increases to six to eight times for those in the 25–64 age group.1 IHD is a major health issue in
Indigenous communities and the appropriate treatment of ischaemic chest pain is vital.

Definition
According to the American College of Cardiology (ACC) and the American Heart Association
(AHA), ischaemic heart pain is defined as chest discomfort that is:
• usually in the centre of the chest
• can feel like uncomfortable pressure, squeezing or fullness
• can involve one or both arms, the back, the neck and the jaw
• can be associated with dyspnoea, sweating, nausea or light-headedness2.
Such a situation needs an immediate response due to the possibility of myocardial infarction. As a
preliminary step, the National Heart Foundation of Australia (NHFA), The Cardiac Society of
Australia and New Zealand (CSANZ), the ACC and the AHA all stress prompt presentation to a
medical service for review. However, especially in Australian Indigenous communities, this may
be a problem. According to Ong & Weeramanthri3 the foremost problem is a person presenting to
the emergency department (ED) of a hospital. In both urban and rural areas Indigenous patients (I)
presented significantly later than non-Indigenous patients (N/I) (10 hrs 00 mins vs 3 hrs 26 mins).

However, if only rural Indigenous patients are considered, no statistically significant delay can be
found when comparisons are made with rural non-Indigenous patients for time to primary
presentation, ED presentation, first ECG or time of thrombolytic therapy. A caveat on these
statements is that many Indigenous patients cannot (or may not) accurately state when their pain
began. As such there may be a significant delay in Indigenous presentation to the health clinic, but
no study has yet confirmed this fact.

Unfortunately, no additional statistical comparison between rural and urban people was made in
the above-mentioned study.3 However, the raw figures indicate that the delay in presentation to an
ED (10 hrs 23 mins vs 6 hrs 00 mins (I) & 7 hrs 48 mins vs 2 hrs 48 mins
(N/I)) and the delay in provision of thrombolytic therapy (7 hrs 45 mins vs 2 hrs 45 mins (I) & 6
hrs 2 mins vs 3 hrs 3 mins (N/I)) are definitely areas that need improvement. Statistical
significance regarding the figures in this study would not be likely, but any delay greater than six
hours compromises the effectiveness of a thrombolytic agent.4 Improving patient knowledge
regarding when one should go to the clinic will have its benefits. However, it is the provision of
therapy earlier that will have the greatest benefit.

The management of ischaemic heart pain is an evolving process. Initial treatment with rest,
oxygen, aspirin and nitrates has been endorsed by the NHFA and the CSANZ in their document
Management of Unstable Angina Guidelines 20005 and the ACC/AHA document Guidelines for
the management of patients with Acute Myocardial Infarction: Executive Summary and
Recommendations 1999 Update.2

However, it is the utility of other agents that is generating much interest. The pathophysiology of
the acute coronary syndromes essentially involves thrombus critically obstructing blood flow
down a coronary blood vessel. Thrombus formation is secondary to plaque rupture. Plaque is the
material lining such vessels. It contains extracellular and intracellular lipid, collagen, connective
tissue matrix proteins and inflammatory cells. Foam cells are also present in plaque and produce a
large number of cytokines and inflammatory mediators. This inflammation is in response to
modification (probably oxidation) of low-density lipoproteins in the subendothelial space and to
local monocyte adhesion and migration. The basic sequence of events is that the collagen cap
overlaying the plaque is infiltrated by inflammatory cells and therefore broken down. (Rupture of
a plaque is most likely if it is eccentrically shaped and has a shallow, lipid-rich centre.) Exposure
of plaque contents or the development of eddy currents then activates various arms of the
coagulation pathway.

Unstable angina pectoris (UAP), non-ST elevation myocardial infarction (non-STEMI) and ST
elevation myocardial infarction (STEMI) comprise the acute coronary syndromes. As such all are
part of a continuum of escalating myocardial damage. Whether one has the more mild UAP or the
more severe STEMI relates to the extent of platelet aggregation, vasospasm and distal platelet
micro-embolization following plaque rupture. The quality of collateral flow to jeopardised
myocardium also determines how much damage is done. Currently it is thought that patients with
UAP or non-STEMI have a platelet-rich non-occlusive thrombus on a fissured or ruptured
atherosclerotic plaque, whereas those with STEMI usually have occlusive thrombus principally
made up of fibrin containing trapped erythrocytes.6
Evidence for individual medical therapies

Oxygen
Supplemental oxygen is usually given to all patients with an acute coronary syndrome. This is
especially indicated if the arterial saturation is less than 95%. Although there is no data on
morbidity or mortality reduction, experimental results suggest that ST elevation and ischaemic
injury are reduced.7,8 The reason for its use is that even uncomplicated patients can initially be
somewhat hypoxic due to ventilation-perfusion mismatch and the presence of extra pulmonary
fluid.9

Aspirin
Aspirin irreversibly inhibits cyclo-oxygenase, preventing platelet synthesis of thromboxane A2, a
potent vasoconstrictor and stimulator of platelet aggregation. The value of this anti-inflammatory
action, which acts to decrease the amount of plaque rupture and its sequelae, has been clearly
proven by several studies.7,10 It also reduces the rate of death or completed myocardial infarction
by about 50%.11 Unfortunately up to a third of patients are non-responder, but as a general rule
aspirin should be given to all patients unless there is an established allergy.

ADP-receptor antagonists
Clopidogrel is an ADP-receptor antagonist and is an option for those intolerant of aspirin. Its
chronic use has been evaluated in patients with UAP in the CURE Trial.12 It has none of the
neutropenia associated with the ticlopidine (no longer used) and less gastrointestinal bleeding than
that associated with aspirin. However, its high cost precludes it from replacing aspirin at the
moment.
[Editor: Dr Steve Brady adds; It is used in combination with aspirin in high-risk patients (CURE
Trial).]

Nitrates
All the nitrates have systemic and coronary effects. The systemic effects include venous pooling,
which reduces left ventricular preload and end-diastolic pressure, as well as causing a slight
decrease in afterload. The coronary effects include vasodilatation of normal and atherosclerotic
coronary arteries, an increase in coronary artery collateral flow and redistribution of flow from
subepicardial to subendocardial regions. As such they are ideally suited to managing acute
coronary syndromes.

There is both clinical and experimental evidence that nitrate therapy reduces infarct size, improves
regional wall motion and may prevent the left ventricular remodelling that occurs after a large
infarct.13,14 Combined data from randomized controlled trials of nitrate use in acute myocardial
infarction have also demonstrated a small but statistically significant reduction in mortality.15
Nitrate therapy is contra-indicated when the systolic blood pressure is less than 90mmHg or when
the heart rate is less than 60 beats/min. It is important to note that nitrates should be used with
extreme caution in patients with suspected right ventricular infarction. These patients depend
especially on ventricular preload to maintain cardiac output and so can be made very hypotensive
if nitrates are given.

ß-blockers
ß1 receptor blockade in the heart results in decreased cardiac work and myocardial oxygen
demand. Several clinical trials have demonstrated a reduction in recurrent ischaemia, re-infarction
and mortality when they have been used in the first hours of a myocardial infarct.16,17 However,
there are relative contra-indications to the use of ß-blockers and so their use in acute coronary
syndromes is not automatic. These relative contra-indications are a heart rate <60 beats/min,
systolic blood pressure <90mmHg, prolonged first degree or higher atrio-ventricular block, severe
chronic obstructive airways disease, asthma, severe peripheral vascular disease or diabetes
mellitus.
Calcium channel blockers
Calcium channel blockers have not been shown to decrease mortality in acute myocardial
infarction and may even be harmful to certain patient subsets.18 A ß-blocker is a more appropriate
option for most patients. However, if ß-blockers are contra-indicated and if there is no evidence of
heart failure or heart block, a heart-rate-slowing calcium channel blocker (diltiazem or verapmil)
may be used.5

Intervention
The primary goal of treatment in acute coronary syndromes is reperfusion of the infarct-related
artery in as short a time as possible. Swift reperfusion has been demonstrated to decrease
mortality19,20,21,22,23 and to preserve left ventricular function.24 Present strategies for acute
reperfusion include the use of thrombolytic agents and a variety of catheter-based interventions.

Thrombolytic therapy is the most widely used method to achieve acute reperfusion, and when
given within the first 12 hours from the onset of symptoms reduces mortality by approximately
30%.19,20,21,22,23 Further breakdown of the first 6 hours shows a relative mortality reduction of 30%
between 0 and 1 hour, 25% between 2 and 3 hours and 18% between 4 and 6 hours. Data
regarding use after 12 hours is limited and not encouraging, so the current recommendation
remains at use before 12 hours.

Having established that thrombolytics can save lives, the GUSTO IIb Trial25 attempted to establish
which is the superior treatment: coronary angioplasty or thrombolytic therapy. Figures from the
trial indicated that angioplasty was more successful than thrombolysis. However Practice
Registers in the USA suggest that outside of clinical trials, angioplasty is equal to and not
necessarily better than thrombolytic therapy.

These facts then behove us to seek the most effective and available treatment for persons in
remote areas who require treatment for their evolving myocardial infarct. Portable cardiac catheter
theatres or cardiovascular surgery units are not a possibility in rural and remote Australia.
Furthermore, any trained healthcare worker who can give an intravenous antibiotic can give a
thrombolytic agent. Hence, thrombolytic therapy is the only sound and ethically responsible
treatment for those who meet the indications for such intervention.

Indications for thrombolysis: 2,4,26

1. A >20 minute history of chest pain fitting ACC/AHA criteria
2. ST elevation in two or more contiguous leads (>1mm in limb leads or >2mm in chest
leads) or new Bundle Branch Block formation
3. Time to therapy is <12 hours

Contra-indications for thrombolysis

Much debate exists in the literature regarding which contra-indications are absolute and which
ones are relative. Only discussion with a relevant specialist at the time of a patient’s presentation
will clarify the situation.
Current contra-indications are:4
• Recent (<10 days) prolonged and vigorous external heart massage
• Known haemorrhagic diathesis
• Patients with current concomitant therapy with oral anticoagulants e.g. Warfarin
• Intracranial neoplasm, arteriovenous malformation or aneurysm
• Neoplasm with increased bleeding risk
• History of cerebrovascular accident
• Severe uncontrolled hypertension (>160mmHg Systolic and >100mmHg Diastolic) (Severe
hypertension on presentation can be treated with sub-lingual or oral nitrates.)
• Active peptic ulceration
 • Portal hypertension (oesophageal varices)
• Severe liver or renal dysfunction
• Acute pancreatitis, percarditis, bacterial endocarditis
• Diabetic haemorrhagic retinopathy or other haemorrhagic ophthalmic conditions
• Within three months of severe bleeding, major trauma or major surgery (e.g. coronary artery
bypass graft, intracranial or intraspinal surgery or trauma), obstetrical delivery, organ biopsy,
previous puncture of non-compressible vessels.

Intracranial haemorrhage is the most feared outcome in all studies. The incidence of such a
haemorrhage following a thrombolytic agent increases with age, particularly in patients with a
systolic BP >170, diastolic BP >95 or both, or if recombinant plasminogen activator r-PA has
27
been used.

Thrombolytics
There are currently three fibrinolytic agents available in Australia: Streptokinase; tissue
plasminogen activator t-PA (Alteplase); and recombinant plasminogen activator r-PA (Reteplase).

Streptokinase
Streptokinase was the first available fibrinolytic agent and has been shown to reduce mortality in
acute myocardial infarction. It saves approximately 25 lives per thousand patients treated21 and is
associated with an average risk of non-fatal intracerebral bleeding of about 3/1000. Streptokinase
decreases infarct mortality by 25% and is more efficacious the earlier that it is given. Usually it is
given as an infusion of 1.5 million units intravenously over 60 minutes. Of particular importance
is the fact that Streptokinase is a naturally occurring product of the streptococcus bacteria and will
induce antibody production.
Clinical problems related to Streptokinase include:
1. Hypotension due to vasodilatation. This may occur in up to a third of patients and is partly
dependent upon the speed of the infusion. Slowing the infusion or giving intravenous fluids
corrects the situation.
2. Rash or hives often occur. Also true anaphylaxis is always a possibility.
3. Antibodies develop within five days, peak at 14 days and can still be at a level that will
neutralize a standard dose of Streptokinase up to four years after the initial administration.28
4. Of major importance in Indigenous communities is the fact that a high rate of exposure to
streptococcal infections will lead a large number of people having antibodies. The levels of
anti-streptokinase IgG and streptokinase resistance in a subset of Aboriginal and non-
Aboriginal persons in the Northern Territory has been investigated by Urdahl et al.29 This
study demonstrated that Aboriginal adults exhibited levels of anti-streptokinase IgG and
streptokinase resistance that respectively were almost 20 and 15 times greater than the values
for non-Aboriginal adults. Furthermore, at any one time at least 23% of Aboriginal adults had
sufficiently high enough levels of streptokinase resistance to neutralize a standard 1.5 million
unit dose of Streptokinase. Thus Streptokinase is not recommended for use in Indigenous
communities.

Tissue plasminogen activator

t-PA is a recombinant form of tissue plasminogen. It has been shown to achieve improved re-
perfusion rates compared to Streptokinase. This then results in an extra 10 lives per thousand
patients treated being saved.30 However, it is also associated with a slightly higher rate of
intracranial haemorrhage producing one extra disabling stroke per thousand patients treated.30 It is
also very expensive. It is given as a 100mg dose infusion over 90 minutes.

Recombinant plasminogen activator

r-PA is a variant of t-PA produced by further genetic engineering. Basically it is non-glycosylated
and lacks three N-terminal domains in comparison to t-PA. As a result of these structural changes
it has a longer half-life (18 mins) compared to t-PA (four minutes). Also it has fibrin specificity
without fibrin binding. This characteristic allows superior penetration into a thrombus and slightly
faster thrombolysis compared to t-PA. (In contrast t-PA binds very tightly to fibrin at the surface
of a thrombus.) The main advantage of r-PA is that it can be given as a double bolus of 10 units 30
minutes apart. On the down side, it has been demonstrated that the incidence of haemorrhagic
strokes is increased with the use of r-PA, especially in those over the age of 75 years or
hypertensive.

Choice of agent
For most of Australia Streptokinase is the thrombolytic agent of first choice. However, the
widespread occurrence of streptococcal infection in Indigenous populations, the need for possible
repeat treatments in the future and its simpler bolus delivery method make r-PA the preferred
option for Indigenous people.
[Editor: Dr Steve Brady (ASH) adds that Tenectaplase (Tnk-tPA) is another thrombolytic agent that
may become the treatment of choice (single injection and probably lower rate of intracranial haemorrhage
than other tPAs — similar to historic levels with SK — see ASSENT 2 trial).]

Heparin
Heparin is an agent that binds with antithrombin, increasing its ability to inactivate factor Xa and
thrombin. Evidence of benefit from the use of unfractionated heparin alone for the treatment of
acute coronary syndromes is weak. A meta-analysis in 1996 of six previous randomized short-
term trials assessed the value of the addition of unfractionated heparin to aspirin for the treatment
of UAP in 1352 patients.31 There was a trend towards reduced death and myocardial infarction in
the patients receiving heparin. However, only four of the studies reported results to 12 weeks and
by then most of the benefit had been attenuated. It should be noted that heparin-induced
thrombocytopaenia syndrome (HITS) occurs in approximately 1–3% of patients.31

The use of heparin in combination with thrombolytics has been investigated in ISIS III and
GUSTO. In ISIS III32 there was no benefit of subcutaneous heparin in comparison to no heparin
with either streptokinase or t-PA. In GUSTO20 there was no advantage in intravenous over
subcutaneous heparin with streptokinase at either 30 days or one year. Thus, it can be postulated
that there is no advantage of using heparin with streptokinase.

Interestingly, the data for heparin with r-PA is similar. The 90 minute patency is similar with or
without heparin.33 However, the use of heparin with r-PA has been due to the HART study34
which demonstrated decreased coronary patency at 18 hours in patients not given heparin. The
European Co-operative Study by Rapold et al.35 was also influential because it demonstrated
heparin’s ability to completely prevent the creation of the cleavage peptide Fibrinopeptide A (a
marker of the action of thrombin on fibrin formation) that always occurs when r-PA is used alone.

The current ACC/AHA guidelines2 recommend an initial bolus of 60 units/kg (maximum of 5000
units) and an initial infusion of 12 units/kg per hour. An APTT of 50–70 seconds is ideal and
adjustment of the infusion rate may be required. Heparin should be used for a minimum of 24
hours.

Low molecular weight heparin

Low molecular weight heparins (LMWH) are created by the depolymerization of unfractionated
heparin. LMW heparins have several advantages over unfractionated heparin. These include a
greater activity against factor Xa than thrombin and a lesser degree of binding to plasma proteins
and endothelial cells. This then results in a more predictable dose-response relationship. Also, the
long half-life of approximately four hours after subcutaneous injection allows twice-daily
treatment. A further advantage is that the rate of HITS is lower when LMW heparins are used. To
date some trials have promoted LMWH over UFH36, but a definitive recommendation can not yet
be made.
 [Editor: Dr Steve Brady (ASH) adds LMWH enoxaparin but not other LMWH is the treatment of choice
based on ease of administration and two trials showing efficacy over unfractionated heparin. Post TnK-tPA
enoxaparin has shown at least similar and probably superior efficacy to unfractionated heparin, and again
may become treatment of choice due to ease of administration (ASSENT 3 trial).]

Other agents
Glycoprotein IIb/IIIa receptor Antagonists
Platelet aggregation is a central component of coronary thrombosis. The aggregation can be
stimulated by a variety of substances, but the final common mechanism is activation of the
glycoprotein IIa/IIIb receptor that is the platelet membrane receptor for fibrinogen.
Currently there are eight different glycoprotein IIa/IIIb receptor antagonists on the Australian
market. The agents most widely known are:
• adciximab (a monoclonal antibody that is an irreversible blocker)
• eptifibatide (a peptide)
• tirofiban (a non-peptide small molecule).

Results of studies involving these receptor antagonists have been variable. The use of tirofiban in
combination with aspirin and heparin vs aspirin and heparin alone in the PRISM-Plus study37 has
demonstrated a significant reduction in the endpoints of death and non-fatal infarction at seven
days and 30 days, but not at six months. Further studies are awaited.

Antibiotics
In a study by Gupta et al in 199738 serological evidence was found that Chylamydia pneumoniae is
associated with atherosclerosis. In fact, it was found that C. pneumoniae would localize in
coronary plaque and promote LDL-cholesterol oxidation. Leading on from this study, two reports
on the use of roxithromycin in patients with unstable angina revealed a decrease in ischaemic
events at 30 days39 and six months40. Given the prevalence of other chylamydial diseases in non-
Indigenous and Indigenous communities, this will be a topic of much interest during the years
ahead.

[Editor: A number of reviewers were concerned about giving thrombolytics without having facilities to
monitor (and defibrillate) the patients ECG for reperfusion arrhythmias. We put this question to Dr
Marcus Ilton, RDH cardiologist, who also put it to a large conference of cardiologists in Sydney in 2001.
He reports that no cardiologist could think of a reason to withhold thrombolytic treatment just because
there was no cardiac monitor. They were clear in their view that if you are confident that it is an acute
coronary syndrome, there was more danger of fatal arrhythmia from withholding thrombolysis than from
giving it.

The protocol stresses that thrombolysis should only be done if the clinic staff and consulting doctor are
confident/ comfortable with the procedure.

Some indication of magnitude of benefit from thrombolysis (within six hours compared to no thrombolysis)
is provided in the summary of evidence in Clinical Evidence*. Fifty-six people would have to be treated in
the acute phase to prevent one additional death (NNT = 56). The benefit is even greater in those with
anterior infarcts. The benefits persist, and possibly become greater over long-term follow up (possibly
through less heart failure from preserved myocardium). One RCT (n = 219) showed a 15% absolute risk
reduction for death at 12 years follow up (NNT = 7). The absolute benefit was about one third less in those
given thrombolysis 7–12 hours after onset of pain compared to <6 hours from onset.

There is an increased risk of stroke with thrombolysis. The estimated number needed to harm (NNH) for
one extra stroke was 250. The NNH for other major bleeding was 143.
*Shamir M, Urban P, De Benedetti E. Acute myocardial infarction in Clinical Evidence. BMJ Publishing
Group, 2001.]
References
1. Australian Facts 2001. Heart, stroke and vascular diseases. Publisher: Australian Institute of Health and
Welfare, National Heart Foundation of Australia and National Stroke Foundation of Australia. April 2001.
2. 1999 Update: ACC/AHA Guidelines for the Management of Patients with Acute Myocardial
Infarction: Executive Summary and Recommendations. Circulation 1999; 100:1016–30.
3. Ong M, Weeramanthri. Delay times and management of acute myocardial infarction in Indigenous and
non-Indigenous people in the Northern Territory. Medical Journal of Australia 2000; 173:201–4.
4. Rapilysin Questions and answers. Information for Healthcare Professionals. Product Information.
Roche Pharmaceuticals.
5. Management of Unstable Angina Guidelines — 2000. National Heart Foundation of Australia and
Cardiac Society of Australia and New Zealand. Medical Journal of Australia 2000; 173(supplement): S65–
S88.
6. Aroney C. Management of the acute coronary syndromes. Australian Prescriber 2001; 24(3):56–8.
7. Madias J, Hood W. Reduction of precordial ST-segment elevation in patients with anterior myocardial
infarction by oxygen breathing. Circulation 1976; 53(supplement):198–200.
8. Maroko P, Radvany P, Braunwald E et al. Reduction of infarct size by oxygen inhalation following
acute coronary occlusion. Circulation 1975; 52:360–8.
9. Fillmore S, Shapiro M, Killip T. Arterial oxygen tension in acute myocardial infarction: Serial analysis
of clinical state and blood gas changes. American Heart Journal 1970; 79:620–9.
10. Lincoff A, Topol E. Illusion of reperfusion: Does anyone achieve optimal reperfusion during acute
myocardial infarction? Circulation 1993; 87:1792–805.
11. Lewis H, Davis J, Archibald D, Steinke W et al. Protective effects of aspirin against acute myocardial
infarction and death in men with unstable angina: results of a Veterans Administration cooperative study.
New England Journal of Medicine 1983; 309:396–403.
12. Yusuf S, Fox K, Tognoni G et al. The Clopidogrel in Unstable Angina to Prevent Recurrent Events
(CURE) trial investigators. Effects of clopidogrel in addition to aspirin in patients with acute coronary
syndromes without ST-segment elevation. New England Journal of Medicine 2001; 345(7):494–502.
13. Jugdutt B, Warnica J. Intravenous nitroglycerin therapy to limit myocardial infarct size, expansion, and
complications: Effect of timing, dosage, and infarct location. Circulation 1988; 78:906–19.
14. Yusuf S, Collins R, MacMahon S et al. Effect of intravenous nitrates on mortality in acute myocardial
infarction: an overview of the randomized trials. Lancet 1988; 1:1088–92.
15. A randomized factorial trial assessing early oral captopril, oral mononitrate, and intravenous
magnesium sulphate in 58,050 patients with suspected acute myocardial infarction: ISIS-4. Lancet 1995;
345:669–85.
16. First International Study of Infarct Survival Collaborative Group: Randomized trial of intravenous
atenolol among 16,027cases of suspected acute myocardial infarction: ISIS-1. Lancet 1986; 2:57–66.
17. The MIAMI Trial research Group: Metoprolol in acute myocardial infarction: Patient population.
American Journal of Cardiology 1985; 56(SupplementG):1–57.
18. Furberg C, Psaty B, Mayer J. Nifedipine: Dose-related increase in mortality in patients with coronary
heart disease. Circulation 1995; 92:1326–31.
19. Gruppo Italiano per lo Studio Della Sopravvivenza nell’Infarto Miodardico (GISSI): Effectiveness of
intravenous thrombolytic treatment in acute myocardial infarction. Lancet 1986; 1:397–402.
20. The GUSTO Investigators: An international randomized trial comparing four thrombolytic strategies
for acute myocardial infarction. New England Journal of Medicine 1993; 329:673–82.
21. Second International Study of Infarct Survival Collaborative Group: Randomized trial of intravenous
streptokinase, oral aspirin, both or neither among 17,187cases of suspected acute myocardial infarction.
ISIS-2. Lancet 1988; 2:349–60.
22. Wilcox R, von der Lippe G, Olsson C et al. Trial of tissue plasminogen activator (t-PA) for mortality
reduction in acute myocardial infarction: The Anglo-Scandinavian Study of Early Thrombolysis (ASSET).
Lancet 1988; 2:525–30.
23. Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group. Indications for fibrinolytic therapy in
suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity
results from all randomized trials of more than 1000 patients. Lancet 1994; 343:311–22.
24. Braunwald E. Myocardial reperfusion, limitation of infarct size, reduction of left ventricular
dysfunction and improved survival: Should the paradigm be expanded? Circulation 1989; 79:441–4.
25. The GUSTO IIb Angioplasty Substudy Investigators. A clinical trial comparing primary coronary
angioplasty and tissue plasminogen activator for acute myocardial infarction: the Global use of Strategies
to Open Occluded Coronary Arteries in Acute Coronary Syndromes. New England Journal of Medicine
1997; 336:1621–8.
26. Ellis C, French J, White H. Thrombolytic eligibility. Australian and New Zealand Journal of Medicine
1998; 28:518–24.
27. Simmons M, Maggioni A, Knatterud G et al. Individual risk assessment for intracranial haemorrhage
during thrombolytic therapy. Lancet 1993; 342:1523–8.
28. Elliott J, Cross D, Cederholm-Williams S, White H. Neutralizing antibodies to streptokinase four years
after intravenous thrombolytic therapy. American Journal of Cardiology 1993; 71:640–5.
29. Urdahl K, Mathews J, Currie B. Anti-streptokinase antibodies and streptokinase resistance in an
Aboriginal population in northern Australia. Australian and New Zealand Journal of Medicine 1996;
26:49–53.
30. Aylward P, Hunt D et al. Reperfusion Therapy for Acute Myocardial Infarction – Guidelines. National
Heart Foundation of Australia, December 2000.
31. Oler A, Whooley M, Oler J, Grady D. Adding heparin to aspirin reduces the incidence of myocardial
infarction and death in patients with unstable angina. A meta-analysis. Journal of the American Medical
Association 1996; 276:811–15.
32. Third international study of infarct survival. ISIS-III. Lancet 1992; 339(8796):753–70.
33. Topol E, George B, Kereiakes D et al. A multi-center randomised controlled trial of intravenous tissue
plasminogen activator and early intravenous heparin in acute myocardial infarction. Circulation 1989;
79:281–6.
34. Hsia J, Hamilton W, Kleiman N et al. The Heparin-Aspirin Reperfusion Trial (HART) Investigators. A
comparison between heparin and low-dose aspirin as adjunctive therapy with tissue plasminogen activator
for acute myocardial infarction. New England Journal of Medicine 1990; 323:1433–7.
35. Rapold H, de Bono D, Arnold A et al for the European Cooperative Study Group. Plasma
fibrinopeptide A levels in patients with acute myocardial infarction treated with alteplase. Correlation with
concomitant heparin, coronary artery patency and recurrent ischaemia. Circulation 1992; 85:928–34.
36. Cohen M, Demers C, Gurfinkel E et al for the ESSENCE Study Group. A comparison of low-
molecular weight heparin with unfractionated heparin for unstable coronary artery disease. New England
Journal of Medicine 1997; 337:447–52.
37. Platelet Receptor Inhibition in Ischaemic Syndrome Management in Patients limited by Unstable Signs
and Symptoms (PRISM-PLUS) Study Investigators. Inhibition of the platelet glycoprotein IIb/IIIa receptor
with tirofiban in unstable angina and non-Q-wave myocardial infarction. New England Journal of Medicine
1998; 338:1488–97.
38. Gupta S, Leatham E, Carrington D et al. Elevated Chlamydia pneumoniae antibodies, cardiovascular
events and azithromycin in male survivors of myocardial infarction. Circulation 1997; 96:404–7.
39. Gurfinkel E, Bozovich G, Daroca A et al. Randomised trial of roxithromycin in non-Q-wave coronary
syndromes: ROXIS Pilot Study. ROXIS Study Group. Lancet 1997; 350:404–7.
40. Gurfinkel E, Bozovich G, Beck E et al. Treatment with the antibiotic roxithromycin in patients with
acute non-Q-wave coronary syndromes. The final report of the ROXIS Study. European Heart Journal
1999; 20:121–7.
APPENDIX

Evidence Summary: Immediate use of ß-blockers in acute myocardial infarction

Question
In people with acute myocardial infarction, does immediate use of ß-blockers — compared to
delayed use of ß-blockers — affect death or re-infarction rates?

Rationale for question

When people are treated for AMI in the community with thrombolysis we are uncertain as to
whether we should give ß-blockers at the same time or delay it until they reach hospital.

Inclusion criteria for studies reviewed

Randomised trials or systematic reviews comparing immediate (intravenous) ß-blockers with
delayed ß-blockers

Search strategy
(Acute and myocardial and infarction) and ({ß-blockers} or {ß-near-blockers}) and intravenous.

Results
Studies (quality and size)
No systematic review of this topic found in Cochrane or Pubmed. Only One RCT found. This trial
had been extensively referred to in all secondary sources.
The trial was ‘Roberts R, Rogers WJ, Mueller HS, Lambrew CT, Diver DJ, Smith HC et al.
Immediate versus deferred beta-blockade following thrombolytic therapy in patients with acute
myocardial infarction. Circulation. 1991; 83(2): 422–437.’
This was a randomized controlled trial in which the assessors were blinded comparing an
international group of 720 participants and 714 controls. Participants were given immediate
intravenous metoprolol followed by oral treatment whereas the controls had oral metoprolol
commenced at six days. The primary endpoint was global ejection fraction at discharge, and this
did not differ between groups. Secondary analyses included a combined end point of death and re-
infarction at six weeks. There was no significant difference between the groups with 7.2% of the
participants and 9.6% of the control group attaining this endpoint at six weeks.

Conclusion (estimated absolute effect size)

No differences between the groups were seen.

Comments
Death and re-infarction were secondary endpoints in this trial. The study size was calculated based
upon the primary endpoint rather than the secondary endpoints. However, this was a large trial,
and since there were more than 50 events in the control groups, this suggests that there would have
been more than an 80% chance of picking up a 50% difference in outcomes.

Implications for CARPA STM 4th edition

Recommend that there is no need for urgent commencement of ß-blockers and this can be
instituted during ongoing therapy at the hospital.

Reference
Roberts R, Rogers WJ, Mueller HS, Lambrew CT, Diver DJ, Smith HC et al. Immediate versus deferred
beta-blockade following thrombolytic therapy in patients with acute myocardial infarction. Circulation
1991; 83(2):422–37.
 Ischaemic Heart Disease/Chest Pain
Part 3: Chronic IHD

Editor: Christine Connors

Authors: This chapter is made up of extracts (with permission from the authors and
publisher) from W Walsh, I Ring, A Brown, A Boyden and S Couzos, ‘Ischaemic Heart
Disease’, in Aboriginal Primary Health Care: An evidence-based approach, second edition,
Oxford University Press, Melbourne. The authors acknowledge Prof Lindon Wing, Prof
Andrew Tonkin, Ass/Prof Stephen Colaguiri, and Ass/Prof David Sullivan.

[Editor: Readers can refer to the full chapter of the above mentioned work for detailed information on the
prevention and management of ischaemic heart disese, treatment goals and targets, case management,
program implementation, data collection and performance indicators.]

Implementation summary
Cardiovascular conditions, particularly ischaemic heart disease, are the major cause of death for
Aboriginal and Torres Strait Islander people.
Comprehensive primary health care, including broad population health education and ongoing
preventive care, and access to appropriate specialist and hospital services is fundamental, but not
sufficient, to bring about an improvement in cardiovascular health for Aboriginal and Torres Strait
Islander people. Approaches should also include the involvement of Aboriginal people and Torres
Strait Islanders in determining their own communities’ health priorities and how they will be
addressed, and in designing and delivering a range of services.

Burden of suffering
Diseases of the cardiovascular system are the biggest single cause of deaths and of excess deaths
for the Aboriginal and Torres Strait Islander population.1,2,3,4
Cardiovascular conditions account for 30% of both deaths and of excess deaths of Aboriginal and
Torres Strait Islander peoples. Over half (57%) of cardiovascular disease (CVD) deaths in the
Aboriginal and Torres Strait Islander population are due to ischaemic heart disease (IHD). Age-
specific CVD mortality rates for Aboriginal and Torres Strait Islander people are higher than for
the non-Indigenous populations throughout adult life and are seven to twelve times higher than the
overall Australian population in the 25–54 year age group.

The average age of death from CVD in Aboriginal and Torres Strait Islander people is 59
compared with 79 for the non-Indigenous population in 1998.5

Hospital admission rates of Aboriginal and Torres Strait Islander people for CVD are two to three
times higher than for the rest of the Australian population, with Indigenous males having higher
admission rates than females. The average age at admission was 47 years, almost 20 years
younger than for the total population in 1998–99.2,4

In the last thirty-five years the age-standardised mortality from IHD has fallen by 70% in the total
Australian population. Although there may have been some reduction in mortality from heart
disease in Indigenous females, there does not appear to have been a significant reduction in heart
disease mortality in Indigenous males between 1991–97.
Cardiovascular health comparisons with the Maori population in New Zealand and Native
Americans in the United States of America have demonstrated that IHD mortality is 1.5 times
higher in the Australian Indigenous population than in Maoris and 2.6 times higher than in Native
Americans. Mortality rates from IHD in Maoris fell from levels in 1974 (which were above the
current Australian Indigenous rates) to a third below those rates by 1990–94, suggesting that rapid
and sizeable reductions in IHD mortality in Indigenous populations are possible.6

There are some explanations for the greater and growing relative disadvantage faced by
Indigenous Australians in cardiovascular morbidity and mortality. There have been very large
increases in the prevalence of type 2 diabetes. This is a potent risk factor which more than doubles
the likelihood of developing IHD. Smoking rates are more than twice those of the non-Indigenous
population (51% compared to 23%).7

Obesity is also more common, with Indigenous Australians far more likely to have BMI >30 than
non-Indigenous Australians. In 1995, Indigenous Australian adults were more likely to be
physically inactive in their leisure time (42% females were inactive compared with 38% of males).

Conventional risk factors may only explain approximately 60–70% of the IHD burden. A number
of studies have demonstrated that psychosocial stress — including social isolation, poverty,
hopelessness and lack of empowerment — are associated with significant increases in the
prevalence of IHD.8,9,10,11 Lower socioeconomic status is also associated with increased levels
of high-risk behaviour and therefore increased prevalence of cardiovascular risk factors. The high
prevalence of IHD in low socioeconomic populations has also been related to suboptimal intra-
uterine development and low birth weight (LBW).11

Chronic psychosocial stress has also been related to prognosis in patients with IHD. The mortality
rate in those who have suffered acute myocardial infarction (AMI) is higher if depression is
present, as well as a lack of quality social support.12,13,14 Depression and psychosocial factors
(psychological traits such as hostility, depression and anxiety, work characteristics, and social
supports) also predict the development of CVD (myocardial infarction or coronary related death)
in initially healthy people, as shown in systematic reviews of cohort studies.15,16

Diagnosis of stable angina

It is important to have a high index of suspicion concerning symptoms suggesting angina, as
patients may confuse them with indigestion, unfitness and the like. Many patients may delay
seeking help from health providers until symptoms have become quite limiting. Initial
investigation is a twelve-lead electrocardiogram (ECG). This is often normal in those with stable
IHD. However, it may show non-specific ST-T wave changes or evidence of an old myocardial
infarction with the presence of Q-waves. The presence of an abnormal ECG significantly increases
the likelihood of the patient having IHD, especially in males. Chest X-ray is frequently not helpful
in the diagnosis of IHD as heart size is usually normal. The diagnosis of IHD in those with
suspected angina is usually confirmed with non-invasive exercise ECG, otherwise known as a
‘stress test’.

Some patients may present with atypical chest pain which has some features of angina but the
diagnosis is not clear. Stress testing is useful in these patients, as patients with non-cardiac cause
of chest pain would be expected to have normal exercise tests. Patients who develop early
symptoms of angina during exercise with marked ST-segment depression on the ECG are likely to
have multi-vessel disease and need more aggressive management. Patients who perform well with
minimal ECG changes at a good level of exercise have a good prognosis and can usually be
managed conservatively with medications only. In some cases the test is not diagnostic, or patients
may be unable to exercise adequately because of co-morbidity. In these cases nuclear stress
myocardial perfusion imaging (NSMPI) is very helpful as pharmacological provocation can be
used to induce myocardial ischaemia. An alternative is stress echocardiography.

Patients with stable symptoms should be referred for further assessment, including coronary
angiography, if: (a) their anginal symptoms are interfering with their normal lifestyle, or (b) they
have a moderately or strongly positive exercise ECG or evidence on NSMPI of significant
myocardial ischaemia.

A note on acute coronary syndromes

[Editor: Acute ischaemic heart disease is covered in an earlier chapter. Warren Walsh adds: ‘In short, the
current correct term is acute coronary syndromes, which are divided into ST segment elevation and non-ST
segment elevation acute coronary syndromes (ACS). ST segment elevation ACS is a medical emergency,
which requires the prompt administration of thrombolytic drug, out of hospital if necessary as described in
the chest pain protocol. Non-ST Segment elevation ACS includes unstable angina (UA) and non-ST
segment elevation myocardial infarction (NSTSEMI). The treatment of UA and NSTSEMI is the same.
These patients need admission to hospital but there is time to allow transfer.’]

Effectiveness of prevention
The prevention of IHD has been divided into the following two approaches. Primary prevention
strategies relate to interventions that may prevent the onset of IHD, especially in people who have
increased risk factors for CVD. Secondary prevention strategies relate to optimal strategies to
prevent further deterioration in those who have already been diagnosed with CVD, and who are
therefore at future risk of another cardiovascular event.

Primary prevention
[Editor: There is strong evidence supporting the impact of primary prevention. For information
about smoking cessation, weight reduction, diet changes and physical activity refer to the relevant
sections in this reference book or to Aboriginal Primary Health Care: An evidence-based
approach.]

Secondary prevention of coronary heart disease

A summary of the relative risk reduction in CV endpoints attributed to secondary prevention
interventions is shown in table 1 on the following page.

Crucial need for early detection of ischaemic heart disease

There is evidence that the prevalence of pre-existing and undiagnosed CHD, even in young
Aboriginal people (<37 years), is high.17 The rate of autopsy-examined sudden death attributable
to IHD was 5.5 times higher for Aboriginal people than for non-Aboriginal people in the NT.18 A
high prevalence of undiagnosed IHD was detected by ECG screening in one Kimberley population
survey.19 However, screening the Aboriginal and Torres Strait Islander population with ECG has
not been recommended and is unlikely to be useful. The use of an initial ECG in the assessment of
newly diagnosed clients with diabetes is recommended. Early detection will facilitate further
diagnostic investigations. An exercise ECG in clients with stable symptoms to investigate the
severity of ischaemia may improve outcomes if interventions occur at a time when the risk of
complication and progression is lower.

Modifying diet
There is evidence that advising people with CHD to eat more fish (fish oil or fish oil capsules),
fruit and vegetables, bread, pasta, potatoes, and olive oil (i.e. a more ‘Mediterranean’ diet) leads to
survival benefits.20 The evidence supporting a low fat or high-fibre diet in reducing mortality from
CHD is less compelling20, but there is strong evidence these interventions (including weight
reduction) can reduce CV risk factors such as hypertension, hyperlipidaemia and possibly prevent
diabetes.
There may be a need to advise moderation of alcohol intake because of its impact on diet and
weight. Studies have consistently shown that blood pressure increases in direct proportion to
alcohol intake, and reducing heavy alcohol consumption will reduce blood pressure.

Increasing physical activity

There is evidence from a number of systematic reviews that physical activity is effective in the
primary prevention of CHD.21 All people should aim to participate in moderate intensity physical
activity for 30 minutes or more on most or all days of the week for health benefit. The evidence
for the effectiveness of exercise alone to reduce CV outcomes in those with existing CHD is not
compelling. However, when combined in cardiac rehabilitation programs with other forms of
secondary prevention, physical activity significantly reduced CV mortality by 20–25%.20
Physical activity can increase the risk for sudden death, but this risk in the individual is
outweighed by the benefits. Healthy Aboriginal sportsmen aged 15–37 years in the NT had a 40
times higher risk of sudden death than their non-Aboriginal counterparts in Victoria in a cases
series from 1982–96.17 All deaths occurred in the hottest time of the year, and were attributable to
underlying IHD.

[Editor: Community strategies to reduce this risk include playing sport during cooler times of the day (late
afternoon, evening), installing lights at football fields, ensuring sufficient fluid intake both prior to and
during the games, avoiding alcohol the night prior to games, and local health staff providing health
education, including recognition of CVS symptoms, during preseason training.]

Psychological or stress management

There is some evidence to support the effectiveness of stress management using relaxation therapy
and other counselling strategies to reduce rates of AMI and death in people with CHD.20 In two
meta-analyses of randomised controlled trials, psycho-educational (health education and stress
management) programs for coronary heart disease patients yielded: reductions in cardiac
mortality; recurrence of myocardial infarction; and significant positive effects on blood pressure,
cholesterol, body weight, smoking behavior, physical exercise, and eating habits.22,23 The
applicability of these findings to Aboriginal and Torres Strait Islander populations is unclear,
given that social and emotional support can take a number of forms, and most determinants have
to do with socioeconomic disparities which are beyond the control of individuals.

Smoking cessation
The primary and secondary prevention of CV events has been demonstrated in many observational
studies. Patients with CHD who stop smoking reduce their risk of recurrent coronary events or
premature death by 50% compared with continuing smokers.20

Aspirin
Some of the strongest evidence for the prevention of further CV events in those with established
CHD pertains to the use of aspirin.24 Aspirin, even in relatively low doses reduces the risk of
serious vascular events in those with previous CV events (including AMI, angina) at doses as low
as 75 mg/day, which is as effective as higher doses.25 Unless contra-indicated, aspirin should be
given to all patients indefinitely with acute coronary events or for secondary prevention in patients
with chronic ischaemic disease. In those who are intolerant or allergic to aspirin alternative
treatment is available with the antiplatelet agent clopidogrel (300 mg loading dose, 75 mg daily).
Systematic review of trials have shown that clopidogrel is clinically equivalent to aspirin for
reducing cardiovascular risk without the gastrointestinal side effects of aspirin.26,27

ß-blockers
Data from pooled meta-analyses suggest that early intervention and long-term treatment of
patients following an acute coronary syndrome with beta-blockers significantly reduce the risk of
patients suffering death, cardiac arrest or another myocardial infarction.25 The American Heart
Association and the American College of Cardiology recommend the use of beta-blockers in all
patients without contra-indications, post AMI or acute coronary syndrome for an indefinite
period.28

ACE inhibitors
ACE inhibitors should be considered for all patients suffering an AMI within 24 hours of onset,
and continued for at least 5–6 weeks unless contra-indicated based on efficacy established in large
clinical trials.29 ACEi therapy as secondary prevention can reduce the rate of death, hospitalisation
for heart failure and recurrent AMI for those with evidence of left ventricular dysfunction (e.g.
heart failure).30

Recent randomised controlled trials show that even those without heart failure can benefit from
ACE inhibitor therapy.31 Treatment with ramipril was associated with significant declines in the
rates of death, AMI, stroke, coronary revascularisation, cardiac arrest and heart failure as well as
the risk of complications related to diabetes.

Controlling blood pressure

The benefits of treating hypertension in terms of reduced CVD mortality and morbidity are well
established from randomised controlled trial evidence.32
International and Australian blood pressure management guidelines emphasise that the
management of hypertension should not only be influenced by an individual’s blood pressure
level, but also take into account the factors that worsen an individual’s prognosis and increase the
absolute risk of adverse CV outcomes.32,33 The numerous intervention trials that have
demonstrated the clear benefits of blood pressure reduction in patients with hypertension in terms
of reduced CV morbidity and mortality have not necessarily been designed and/or powered to
determine blood pressure targets for intervention. The HOT study34, did investigate targets but
this showed no significant differences in CV outcomes between three blood pressure target groups
(diastolic blood pressure <90, 85, or 80 mmHg respectively). Subgroup analysis, however, did
demonstrate improved CVD outcomes in diabetics in the low target group.

Cholesterol-lowering agents
[Editor: There is very strong evidence for the benefit of lipid-lowering agents, particularly the
‘statins.’ The benefits and cost effectiveness are greatest for (but not limited to) secondary
prevention in those with existing ischaemic heart disease. For more detail on this see the chapter
on lipids in this book, or Aboriginal Primary Health Care: An evidence based approach.]

Integrating secondary prevention through cardiac rehabilitation

An important part of the post discharge management of CHD is enrolment in a cardiac
rehabilitation (CR) program where emphasis is on secondary prevention and health education.
There is now strong evidence, collated in a number of systematic reviews, that comprehensive risk
factor management extends overall survival, improves quality of life, decreases the need for
interventional procedures (such as angioplasty and bypass grafting) and reduces the incidence of
subsequent myocardial infarction. The most significant benefits of CR programs are a reduction in
longer-term mortality. Overseas studies have shown significant reductions in non-fatal reinfarction
rates of 61% and between 25–30% in total cardiac events for those who undertake CR (table 2).35

These ratings are dependent upon demonstration of benefits from randomised controlled trials
(1,2) and/or supported by observational studies (3). While all are supported by authoritative
opinion, none is solely dependent on such opinion (4).

The National Heart Foundation of Australia recommends that, unless contraindicated, CR and
secondary prevention programs should be offered to all patients with CVD.36 However, evidence
suggests that Aboriginal people access CR to a very limited degree compared to the non-
Aboriginal population.37

Case management
Stable angina
Risk factor modification (increased physical exercise, dietary modification including reduction in
fat intake, and smoking cessation) has been found to be effective in those with stable angina.38
Most patients require initiation of a statin drug for lipid control, since benefits have been shown
with patients who have a total cholesterol of 4 mmol/L or greater in patients with known CAD.39

Smoking is a powerful risk factor for coronary artery disease and cessation is essential. Aspirin
has been shown to be quite beneficial in stable angina.24

Beta-adrenergic blocking agents have also been demonstrated to improve ischaemic symptoms
and prognosis in acute coronary syndromes. Despite a lack of mortality trials using beta-blockers
in chronic stable angina there is no reason to believe why efficacy would not apply to these
patients.40
Calcium channel blockers may also be used in patients with chronic stable angina.41 These have
been shown to improve symptoms but there is controversy about their effect on prognosis. Long-
acting drugs such as verapamil or diltiazem, slow A-V conduction and hence heart rate, and have
been demonstrated to be very effective in providing symptomatic control. Long-acting nitrates are
also of benefit symptomatically. Topical nitrates are especially useful for nocturnal symptoms.
There is no evidence that nitrates improve prognosis but they do enhance symptomatic control.

Recent studies have suggested that ACE inhibitors may also be beneficial in patients with stable
IHD. A large study of the ACE inhibitor ramipril in patients who are at high vascular risk
demonstrated significant improvement in clinical outcome independent of blood pressure
reduction. ACE inhibitors are particularly beneficial in patients who have left ventricular
dysfunction post AMI or who have clinical heart failure. In the HOPE study of 9297 patients
without clinical heart failure, ramipril significantly reduced the risk of composite endpoint of
cardiovascular death, AMI and stroke from 17.7% to 14.1%, a relative risk reduction of 22%
(P<0.01). This is the first of the large ACE inhibitor trials in patients with chronic IHD and other
trials are currently in progress using other ACE inhibitors.42

Unstable angina
[Editor: These patients will present with increasing frequency or severity of angina. ECG shows
no ST segment elevation. Due to the high risk factor profile of many Aboriginal and Torres Strait
Islander people, patients presenting with unstable angina should be managed in consultation with
the appropriate specialist, and should be admitted to hospital for further investigation. Also see
note on acute coronary syndromes above.]

Patients need to have their future CV risk stratified for management purposes. Numerous studies
have now identified that elevated cardiac troponin I or T or CKMB, new or reversible ST segment
depression on ECG, and recurrent anginal symptoms are indicative of high risk. The presence of
clinical heart failure and depressed LV function (e.g. echocardiography) also signifies high risk.
These patients require referral to a tertiary centre for coronary angiography and consideration of
revascularisation.43 Three large randomised trials have shown significant reductions in the
combined endpoint of recurrent AMI, in-hospital mortality and hospital readmission when an
invasive approach is carried out in this high-risk population.44,45

Intermediate-risk patients are those with a history of previous myocardial infarction, previous
bypass surgery or coronary angioplasty and/or have diabetes. Aboriginal and Torres Strait Islander
patients who are at intermediate risk should also be referred for coronary angiography. Patients
who lack the above features, have normal cardiac markers or enzymes and a normal ECG are
deemed to be at low risk and can be managed locally without the need for referral to a tertiary
institution. These patients do not benefit from an invasive strategy.

Implementation of programs
There are clearly many barriers to the appropriate care of Aboriginal and Torres Strait Islander
clients with established cardiovascular disease. Whilst data is limited, there is evidence that
Aboriginal patients frequently delay presentation to hospitals with ST-segment AMI.46 Similar
differential delays were noted for the performance of diagnostic ECGs and the delivery of nitrate
therapy, heparin and lipid-lowering drugs.

The reasons for the delay in presentation are complex and relate to cultural, education and distance
factors. Typical AMI symptoms appear less likely to be recorded for Aboriginal and Torres Strait
Islander patients, often because of communication difficulties with mainstream health
providers.46,47

There is evidence that Aboriginal people are significantly less likely to undergo procedures such
as coronary artery bypass surgery or coronary angioplasty compared to the non-Aboriginal
population.45

The structure and benefits of cardiac rehabilitation (CR) programs both in Australia and overseas
have been reviewed48, yet there is little appraisal of the provision of cardiac services to Indigenous
population groups. During the development of CR services in the Top End of the NT, it was
demonstrated that only 8% of eligible clients admitted to the Royal Darwin Hospital were
recruited to rehabilitation services.49

A number of Cardiac Rehabilitation resources have been developed for use in rural, remote,
Aboriginal and Torres Strait Islander communities. The ‘Heart Story’50 is a manual developed for
health workers to use with Aboriginal people who are at risk or who have suffered a cardiac event.
‘Promoting heart health’51 is an educational resource manual for rural and remote health workers.
The Heart Health Manual training resource for Aboriginal health workers has recently been
released.52

There is insufficient evidence of the impact and potential benefits of targeted cardiovascular
prevention programs within remote Aboriginal communities or for the Aboriginal and Torres
Strait Islander population within larger metropolitan centres.

Between 1995 and 1998, a systematic treatment program was developed in a remote NT
Aboriginal community to modify renal and CV disease.53 The main focus of the trial included
health education about diet, exercise, health behaviours and medical therapy. The study found that
the introduction of a systematic treatment program was associated with improvements in blood
pressure, stabilisation of renal function, decreases in the rates of renal failure and all-cause
mortality (including cardiovascular deaths). It was concluded that a systematic approach to the
treatment of cardiovascular and renal disease risk factors, with screening and treatment algorithms
and clear goals was of tremendous value.

References
1.
Commonwealth Department of Health and Aged Care and Australian Institute of Health and Welfare
National Health Priority Areas Report: Cardiovascular Health 1998. AIHW Cat. No. PHE9. HEALTH and
AIHW, Canberra. 1999.
2.
The Health and Welfare of Australian Aboriginal and Torres Strait Islander People. ABS & AIHW,
2001. ABS. Catalogue No. 4704.0.
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 Ischaemic Heart Disease/Chest Pain
Part 2: Clinical management

Author: Dr Marcus Ilton (Cardiologist, RDH)

[Editor: The following is primarily an abridged summary of technical notes on the investigation and
management of chronic stable angina. Investigations have been given a rating of their use and value in
different settings of IHD management. A class 1 indication inplies there is substantial evidence and expert
agreement supporting the use of these investigations.
There is some overlap with Ischaemic Heart Disease Part 3: Chronic IHD, which covers the burden of
ischaemic heart disease, epidemiology and evidence base for recommended interventions all in some
detail. For more detail on the management of acute coronary syndromes, see Ischaemic Heart Disease
Part 1: Acute chest pain.

Pathophysiology
IHD is a complication of atherosclerosis. Atherosclerosis is a chronic inflammatory disease of the
arterial wall resulting from initial injury to the endothelial cells lining the artery. Injury is due to
combination of chemical and mechanical stress. Mechanical stress is from elevated blood
pressure. Chemical stress results from smoking, elevated cholesterol, and the alteration of proteins
as a consequence of elevated blood glucose (glycosylated proteins).

Clinical manifestations
Angina
Clinical syndrome is characterised by chest, jaw, shoulder, back and/or arm discomfort. It is
typically aggravated by exertion or emotional stress and relieved by anginine.

Chronic stable angina

• Exertional/emotional-induced discomfort in the chest, jaw, shoulder, back and/or arm
• Exertional/emotional-induced dyspnoea

Acute coronary syndromes

• Unstable angina
• Non-ST infarction
• Non-Q wave infarction
• Q wave infarct
• Sudden death

History and clinical examination

In patients presenting with chest pain a detailed symptom history, physical examination and
directed risk factor assessment needs to be performed. Need to determine the probability of
significant coronary artery disease and assess whether symptoms are chronic and stable or patient
has an acute coronary syndrome which requires immediate attention and intervention.
Low risk
• Non-cardiac pain
• No risk factors

Intermediate risk
• Atypical pain (probable angina)
• 1–2 risk factors

High risk
• >2 risk factors
• Typical pain
• Previous known coronary artery disease

Recent:
<30 days post myocardial infarction (heart attack)
<6 months post PTCA (balloon angioplasty with or without stent
<6 months post CABG (bypass surgery).
Patients with rest symptoms, recent onset of chest pains or increasing frequency of symptoms
need to be considered as potentially having an acute coronary syndrome and need to be treated
accordingly.

Definition of angina symptoms

Typical angina (definite)
• Substernal chest discomfort with a characteristic quality and duration that is provoked by
exertion or emotional stress and relieved by rest or nitroglycerin

Atypical angina (probable)

• Meets two of the above characteristics

Noncardiac chest pain

• Meets one of the typical angina characteristics

Risk factors
• Family history
• Smoking
• Hypertension
• Diabetes
• Dyslipidaemia, elevated cholesterol
• Post menopause

Investigations
ECG (Class 1 indication)
Rest ECG.
Rest ECG with pain:
• To determine cardiac rhythm, previous AMI, acute ST changes, evidence of left ventricular
hypertrophy
• Performed immediately if patient presents with chest pain, even if atypical; fax ECG for
doctor’s review
• 50% of patients with chronic stable angina will have a normal ECG; suggests normal rest left
ventricular function
• Repeat ECG with each visit
Blood chemistry
FBC (Class 1 indication)
Anaemia with haemoglobin less than 90 may result in angina at rest.
EUC (Class I indication)
Renal function
Electrolytes (potassium and magnesium); risk of arrhythmias.
Fasting blood sugar levels (Class I indication)
Diabetes is a major risk factor for coronary artery disease.
HbA1c in patients with known diabetes to assess diabetic control.
Lipids (Class I indication), total cholesterol, HDL, calculated LDL, triglycerides.
Thyroid function (Class II indication)
Hyperthyroidism may lead to increase in angina due to increased metabolism.
Patients with hypothyroidism may experience worsening of angina control with commencement of
thyroid replacement therapy.

Imaging
Chest X-Ray (Class I indication): Patients with signs and/or symptoms suggestive of: heart failure,
valve disease, aortic dissection.
Chest X-Ray (Class IIa indication): Patients with lung disease.

Cardiac investigations
Echocardiogram
• Assesses LV size, function, and presence of wall motion abnormalities suggesting previous
AMI
• Valve disease, including aortic stenosis that can cause angina
• LV hypertrophy with associated outflow obstruction that can also cause angina

Not routinely required for the investigation of patient with stable angina.
Patients with: (Class I indication) LV failure, Q waves, ventricular arrhythmia, systolic murmur
suggestive of aortic stenosis, mitral regurgitation, HOCM.
Patients with: (Class IIb indication) click or murmur suggestive of mitral valve prolapse.

Stress testing
Exercise ECG test
• Treadmill or bicycle exercise with ECG monitoring with or without imaging
• In the NT these test are only available in Darwin and Alice Springs
• Should be used in initial assessment, as important in risk assessment
• Without imaging (e.g. without echocardiography or nuclear scanning)

Class I indications
• For investigation of patients with intermediate pre-test probability of obstructive coronary
artery disease
• Includes patients with: complete RBBB, <1 mm ST depression at rest
• For risk assessment and prognosis during initial assessment

Class IIb indications

Patients with: high or low pre-test probability of obstructive coronary artery disease for age,
gender and symptoms
Patients taking digoxin with baseline ECG ST depression <1 mm
Patients with ECG criteria for LV hypertrophy and baseline ST depression of <1 mm
Cardiac stress imaging
Stress nuclear cardiac perfusion scan (previously called thallium scans, now myoview is used) or
stress echocardiography. Wherever possible exercise testing should be used as the most
appropriate form of stress as it provides the most information. The inability to perform an exercise
test is a strong negative prognostic factor in patients with chronic coronary artery disease. Other
forms of stress that are available in the NT are dobutamine or persantin. Nuclear cardiac perfusion
scans are available in Darwin. Stress echocardiography is not routinely available

Class I indications for exercise nuclear cardiac perfusion scan (or stress echo)
• To identify the extent, severity and location of ischaemia in patients who do not have LBBB
or ventricular paced rhythm who have an abnormal rest ECG or are on digoxin
• Patients with previous revascularisation with either angioplasty or CABG
• Patients with intermediate pre-test probability of CAD with >1 mm ST depression at rest or
pre-excitation (WPW syndrome)

Class I indications for persantin nuclear cardiac perfusion scan.

• Patients with LBBB or ventricular paced rhythm

Class IIb indications for stress imaging

• Exercise or dobutamine echocardiography in patients with LBBB
• Any form of stress imaging as initial stress test in patients with normal resting ECG and are
not taking digoxin

Angiography
Gives the most accurate anatomical assessment of coronary arteries as well as assessment of LV
function and mitral and aortic valve function. Is now available in Darwin as day procedure.

Class I indications
• Patients with disabling symptoms CCS symptoms Class III–IV
• Patients with high risk criteria on clinical assessment or after non-invasive testing regardless
of angina severity
• Patients who have survived sudden cardiac death or serious arrhythmia
• Patients with angina and symptoms and signs of heart failure

Class Ila indications

• Patients with an uncertain diagnosis after non-invasive testing in whom the benefit of a more
certain diagnosis outweighs the risk and cost of angiography
• Patients who are unable to undergo non-invasive testing due to disability, illness or morbid
obesity
• Patients with an occupational requirement for a definitive diagnosis
• Patients with inadequate prognostic information after non-invasive testing

CT calcium score
High resolution CT scan assessment of levels of coronary artery calcium is a good negative
predictor of cardiac events. This is a new technology and is not yet available in the NT.

Management of chronic angina

Acute management
See chapter on acute coronary syndromes.
Chronic management
The two primary objectives of treatment are to maximise survival by preventing heart attack and
death and to control symptoms (patient’s adequate quality of life). Treatment therefore involves
revascularisation where appropriate, control of symptoms with medication and secondary
prevention by targeting risk factors. Secondary prevention relates to patients who have already had
cardiac events (either exertional angina or acute coronary syndromes) and have had cardiac
investigation (such as angiography or revascularisation, such as angioplasty or coronary bypass
surgery). Management therefore involves identifying risk factors, lifestyle modification (including
education with regards to smoking, diet and exercise), intervention with medication and/or
revascularisation and ongoing monitoring of outcomes.

Control of risk factors

Risk modification significantly reduces primary and secondary events.

Smoking
Provide education and advice on the dangers of smoking. Consider use of patches, nicotine
chewing gum or other medications such as zyban. (Cessation of smoking has to be a priority.)

Hypertension
Normalising blood pressure significantly reduces cardiac events. Needs both lifestyle modification
and pharmacological intervention.
Recent trials have shown that in diabetic patients BP <130/80 improves survival.

Hypercholesterolaemia
Several trials have now shown a benefit, both primary and secondary prevention, of cardiac
events. For patients with highest risk (known coronary artery disease or previous cardiac) event
aim for: total cholesterol <4.0 mmol/L, LDL cholesterol <2.5 mmol/L

Diabetes
Prevention and early appropriate treatment of type 2 diabetes is important for both primary and
secondary care. (See diabetes chapter)

Medication
Antiplatelet medication
Aspirin
• 100–150 mg daily. Post angioplasty and stent 300 mg daily for four weeks
• Inhibitor of thromboxane induced platelet activation
• Non-reversible effect on platelets, therefore effect lasts up to 10 days until adequate numbers
of platelets have been naturally replaced
• Standard treatment in all patients with coronary artery disease
• Contraindications: allergy to aspirin, serious bleeding disorders, low platelet count

Clopidogrel
• 75 mg daily. Initial loading dose of 300 mg. The loading dose is given with aspirin in patients
suspected of having an acute coronary syndrome, usually within 24 hour of presentation
• Inhibits ADP-mediated platelet activation. Recent studies have shown improved survival in
combination with aspirin post-acute coronary syndrome
• Is used in combination with aspirin 300 mg daily for four weeks post-angioplasty with stent
• There is a slight increase in bleeding when used with aspirin
• Preferred alternative to aspirin if this medication is contraindicated
Ticlopidine
No longer in use due to drug-induced neutropenia.

ß-blockers
• Cardio-selective beta-blockers primarily affect B1 receptors and reduce angina by reducing
cardiac oxygen demand. Reduces heart rate, force and rate of contraction
• All patients with angina should be on a beta-blocker unless contraindicated or unable to
tolerate

Atenolol
• Once-a-day medication, 25 mg up to 100 mg daily
• Hydrophilic, therefore has better bioavailability than metoprolol, but dosage may have to be
altered in renal failure

Metoprolol
• Twice-daily dosage 12.5 mg BD up to 100 mg BD
• Lipophilic, therefore variable bioavailability
• Proven benefit in heart failure

Carvedilol
• Twice-daily dosage 3.125 mg BD up to 25 mg BD
• Has alpha 1-, as well as beta 1- and 2-, blocking effects
• Has proven benefit on survival in patients with heart failure (mainly used in this group)

Nitrates
GTN
• All patients with suspected obstructed coronary artery disease should have access to either
medication and be educated in their use
• Sublingual anginine 600 mcg 1–3 tablets/30mins
• Sublingual GTN spray 400 mcg 1–4 puffs/30mins

Isordil

Imdur
Long-acting mononitrate.
• 60–120 mg/day. Do not use as a BD dose as patients will develop tolerance and medication
will become ineffective

Nitrate patches
Long-acting 25–50 mg, eight hour medication-free, otherwise develop tolerance.

Calcium antagonists
Do not use short-acting dihydropyridines as may induce tachycardia and angina.
Diltiazem, Verapamil, Amlodipine, Nifedipine Oros.

ACE inhibitors
• Essential in treatment of patients with previous cardiac events, especially if impaired LV
function, diabetes and/or hypertensive. Also should continue to be used in renal failure,
especially diabetic nephropathy
• Ramipril, 1.25–10 mg daily
• Perindodril, 2–8 mg daily, long acting
Cholesterol-lowering medication
• HMG Co enzyme A reductase inhibitors:
• Atorvastatin, Simvastatin, Pravachol, Fibrinates, Gemfibrozil

Other anti-anginal medications

1. Perhexiline
Starting dose 100 mg daily (recommend only started by visiting physician or cardiologist).

Increases intracellular oxygen and ATP coupling (e.g. improves heart muscle use of oxygen) and
is used in patients with intractable angina and aortic stenosis. However, perhexiline has a long
half-life (1–40 days) and is subject to saturable (non-linear) pharmacokinetics, so that small
changes in dosage can produce disproportionate changes in plasma concentrations.

Perhexiline is also subject to genetic polymorphism (CYP2D6), and 5–10% of Caucasian patients
are poor metabolisers, achieving high plasma perhexiline concentrations with usual doses.
Monitoring is therefore recommended one week following commencement of dosing to detect
poor metabolisers with rapidly rising plasma perhexiline concentrations, followed up within 14
days to ensure concentrations are not continuing to rise, and then at three-monthly intervals, as
required.

If symptomatic response is inadequate using the above therapeutic range, increasing the dose to
achieve plasma perhexiline concentrations in the range 0.60–1.20 mg/L may provide additional
beneficial response. However, at this higher range monitoring for signs of toxicity (e.g. nausea,
dizziness and elevated liver function tests) is recommended.

Significant interactions include fluoxetine, paroxetine (possibly other CYP2D6 substrates),

amiodarone (increased risk of hepatotoxicity) and hypoglycaemic medications (increased insulin
sensitivity).

2. Nicorandil
Dose: 10–20mg daily. A nicotinamide nitrate with potassium channel-opening activity, is a
vasodilator used as an additional therapy in the treatment of angina pectoris. This compound has
been shown to possess several properties that have been proposed to be part of its antianginal
efficacy, including reductions in preload and overload, an increase in large coronary artery
diameter and an increase in coronary collateral blood flow.

Nicorandil has been described as a hybrid between nitrates and potassium channel activators.
Potassium channel activators cause smooth muscle relaxation and subsequent vasodilation by
increasing potassium flux through sarcolemma ATP-sensitive potassium channels. The drug is
therefore capable of acting as a balanced arterial dilator and venodilator; potassium channel
activation indirectly leads to calcium channel blockade and dilation of arterial resistance vessels,
while the nitrate moiety dilates venous capacitance vessels. In the clinical setting, the nitrate’s
activity is probably predominant. In association with the decrease in afterload following
nicorandil, the contractile responses during isovolumic contraction and relaxation improved
significantly, indicating that nicorandil does not demonstrate negative inotropic actions

Revascularisation
Class I indications
• CABG (coronary artery bypass surgery) or PTCA
• Left main stenosis
• Three vessel disease (benefit greater if EF <50%)
 • Two vessel disease with significant proximal left anterior descending CAD and either
abnormal LV function (ejection fraction<50%) or demonstrable ischaemia on noninvasive
testing
• PTCA for patients with two or three vessel disease with significant proximal left anterior
descending CAD, who have anatomy suitable for catheter-based therapy, normal LV
function, and who do not have treated diabetes
• PTCA or CABG for patients with one or two vessel without proximal left anterior descending
CAD but with a large area of viable myocardium and high-risk criteria on noninvasive testing
• In patients with prior PTCA, CABG or PTCA for recurrent stenosis associated with a large
area of viable myocardium and/or high-risk criteria on noninvasive testing
• PTCA or CABG for patients who have not been successfully treated (see text) by medical
therapy and can undergo revascularization with acceptable risk

Class IIa indications

• Repeat CABG for patients with multiple saphenous vein graft stenoses, especially when there
is: (i) significant stenosis of a graft supplying the left anterior descending coronary artery.
PTCA may be appropriate for focal saphenous vein graft lesions or multiple stenoses in poor
candidates for reoperative surgery, or (ii) PTCA or CABG for patients with one vessel
disease with significant proximal left anterior descending CAD

Class IIb indications

Compared with CABG, PTCA for patients with three or two vessel disease with significant
proximal left anterior descending CAD who have anatomy suitable for catheter-based therapy and
who have treated diabetes or abnormal LV function.

Class III Indications

• PTCA or CABG for patients with one or two vessel CAD without significant proximal left
anterior descending CAD who:( i) have mild symptoms that are unlikely due to myocardial
ischemia; or (ii) have not received an adequate trial of medical therapy and (a) have only a
small area of viable myocardium or (b) have no demonstrable ischemia on noninvasive
testing
• PTCA or CABG for patients with borderline coronary stenoses (50–60% diameter in
locations other than the left main) and no demonstrable ischemia on noninvasive testing
• PTCA or CABG for patients with insignificantcoronary stenosis (<50% diameter)
• PTCA in patients with significant left main CAD who are candidates for CABG

Note: PTCA is used in these recommendations to indicate PTCA and/or other catheter-based
techniques such as stents, atherectomy, and laser therapy.

Exercise program
Regular exercise has been proven to improve functional capacity and can have beneficial effects
on lipid profile as well.
 Marine Bites and Stings

Author: Dr Mark Little (Department of Emergency Medicine, Sir Charles Gairdner

Hospital, Perth)

Topic Reviewers: Prof Bart Currie (MSHR); Mike Barnes (Gove Hospital); Primrose
Underhill (RAN, Galiwin’ku Clinic)

Major box jellyfish (Chironex fleckeri) sting

The major box jellyfish, Chironex fleckeri, is the most dangerous jellyfish in the world. In
Australia it has killed 67 people. The last 10 deaths in the NT have all been children in remote
coastal communities, with the last Australian death being in a six-year-old child at Yarrabah, near
Cairns. The death is quick, usually within 20 minutes of the sting, and the patient often succumbs
on the beach. The mode of death is thought to be a cardiac death.

The major box jellyfish is found throughout tropical Australia, with cases being reported from
Gladstone (Qld), through to Broome in WA. The greatest numbers of cases occur in the NT. In the
NT, major box jellyfish stings have occurred in every month of the year, except one, where as in
Qld the jellyfish season is said to be October to May. It is believed that these jellyfish breed in the
estuaries then migrate to the ocean, being helped by the rainfall of the wet season. They have
never been found in the offshore waters around coral reefs, only in coastal regions.

The stinging mechanisms, the nematocysts, are located on the tentacles of the jellyfish. They are
like spring-loaded syringes, which explosively discharge toxic venom when activated, usually by
contact but also by remote factors. The venom of the major box jellyfish has not yet been
extensively characterized, although it is believed to have a cardiotoxic effect, dermatonecrotic
effect (skin damage) and haemolytic effect, although this has not been demonstrated clinically.

Clinically, the patient screams with sudden severe pain and has welts on his or her skin. There
have been reports of patients then running from the water and collapsing with a cardiac arrest.
There are at least three reports of patients arresting on the beach but surviving with prompt CPR.
In the latest case — near Cairns in 2002 — a child was pulseless after a major box jellyfish sting
and survived with prompt CPR performed on the beach.
Although the literature has many cases of death reported, most cases of major box jellyfish sting
are minor. In a 12 month prospective study looking at all cases of jellyfish sting presenting to the
Royal Darwin Hospital there were no deaths, none required antivenom and only one case of the 28
with major box jellyfish sting required opiate analgesia. Most did well with symptomatic
treatment.

The management of patients stung by the major box jellyfish is attention to airways, breathing,
and circulation, ensuring it is safe for the first aiders. Vinegar should be applied for at least 30
seconds to the sting site.

As the patient may be in pain, ice packs to the sting site may help. If not, oral or injectable
analgesics may need to be given. If the patient is in severe pain or is unstable then antivenom is
recommended.

Antivenom to the major box jellyfish (C. fleckeri antivenom CSL), was first made available in
1970. From 1970–81 CSL reported 73 patients receiving antivenom. It is made from sheep serum
and seems to have a low rate of allergic reaction. The current NT indications for use of antivenom
are:
a. severe pain unrelieved by opiate analgesia;
b. life threatening cardiac or respiratory
decompensation, or cardiac arrhythmia.

The antivenom can be given IM (dose of three ampoules) but it is preferable to give intravenously.
The intravenous dose is one ampoule diluted 1:10 in normal saline or Hartman’s solution, given
over 10 minutes. If the patient is in cardiac arrest then CPR should be continued, and IV
antivenom given as a quick push. Up to six ampoules should be given.

Current experimental work from Qld, as well as a review of the literature, supports the NT current
practice of not applying pressure immobilization bandages (PIB) for any jellyfish sting. There
does not appear to be any evidence to support its use and laboratory work suggests that PIB
increases the venom load delivered to the stung patient.

The sting should be treated as a burn to avoid secondary infection. Delayed reactions to major box
jellyfish stings are common, with patients developing an itchy rash 7–14 days after a sting. This is
thought to be a delayed hypersensitivity reaction and responds to topical steroid cream and oral
antihistamines.

Irukandji syndrome
Much interest in Irukandji syndrome has occurred over the last few years, heightened in 2002 with
the death of two tourists in north Queensland. Interestingly, both died from intracerebral
haemorrhage, believed due to the initial hypertension seen with Irukandji syndrome.

Irukandji syndrome was first described by Flecker, a Cairns radiologist, in 1952. He described that
after a short (up to 60 minutes) interval after a seemingly innocuous sting patients became unwell,
began vomiting, and suffered significant back, loin, limb and chest pain and sweating. Patients
have also been noted to be hypertensive and tachycardic. In 1961 Barnes captured two jellyfish,
now called Carukia barnesi, and demonstrated that these caused the Irukandji syndrome by
stinging himself, the duty lifeguard and his nine-year-old son. All three developed Irukandji
syndrome and were taken to Cairns Base Hospital for treatment. Since 1987 there have been
reports in the literature of patients with Irukandji syndrome developing pulmonary oedema, with
some patients requiring ventilation and inotrope support. It is now believed that more than one
jellyfish is responsible for Irukandji syndrome. Cases have occurred across tropical Australia,
although the majority of cases are reported from the Cairns region.

Nothing is known about the venom, and there is no antivenom. There are no significant data about
the biology of the C. barnesi or any other jellyfish that may be responsible for the Irukandji
syndrome.
In a one-year review of 62 Irukandji syndrome patients presenting to EDs in Cairns, 56%
presented within a three week period in December. The majority (76%) were stung at coastal
locations, and 61% required parenteral analgesia to relieve the pain. Other than two patients who
developed pulmonary oedema and needed critical care admission, all patients were discharged
home pain-free by 24 hours after admission.

It appears that a significant percentage of patients with ongoing pain from Irukandji syndrome
develop evidence of cardiac injury. In the summer 2001–02 Cairns Base Hospital treated 116
patients with Irukandji syndrome. Of these 22% developed abnormal troponin results (a marker
for cardiac injury). This group of patients also had abnormal ECGs, and eight had abnormal
cardiac echocardiographs showing reduced cardiac function. Reassuringly, 36% of all patients
presenting to ED with Irukandji syndrome were sent home that day, with another 47% being
discharged the next morning. Only 17% needed ongoing care in hospital, and all of these had
ongoing analgesia requirement.

First aid management involves the use of vinegar to the sting site. This prevents any further
nematocysts (the jellyfish stinging cells) releasing more venom. Pressure immobilization bandages
(PIB) are not recommended as research suggests that PIB may increase the amount of venom
introduced into the body.

These patients will be in severe pain and will need regular doses of opiod. There is debate about
which one to use. There are theoretical grounds not to use pethidine, however morphine or
fentanyl have been used. The patients who seem to develop cardiac dysfunction have ongoing
pain, and will need to be transferred to a centre where further investigations can be performed.
Pulmonary oedema seems to present within 10 hours of the sting, however there are reports of
patients developing this within three hours of a sting. These patients may require ventilation and
adrenalin as an inotrope. Clearly these cases are rare, and expert opinion should be sought.

Stonefish sting
The Synanaceia genus is found throughout tropical Australia, as well as in the Indo-Pacific region.
It is a particularly unattractive fish that is well camouflaged in coral or as a piece of rock. Usually
the unwary person either stands on the stonefish, or picks it up.

The venom apparatus of the stonefish are the dorsal spines, with each spine having two lateral
venom glands. This system is for defense of the stonefish and has nothing to do with capture of
prey. When the stonefish is threatened the spines become erect. If an object, such as a foot, is
pressed down on the dorsal spine then the venom gland has the venom forced into the object. The
venom has been demonstrated to have neurotoxic, myotoxic, cardiotoxic and cytotoxic effects on
experimental animals, however the major effect on humans is one of pain, probably as a result of
enzymes in the venom.

There have been no reported deaths from a stonefish sting in the Northern Territory, although
deaths have been reported in the Indo-Pacific region (e.g. the Seychelles), and there is a report of a
death in 1915 at Thursday Island, Queensland.

In a one-year period (July 1989 to June 1990) there were 25 cases of stonefish antivenom usage
reported to CSL. Four of these cases were from the NT, with the majority being from Queensland

Patients who have been stung by a stonefish know so almost immediately. They present with
severe local pain, often with the entry site of the spines visible. The pain is often worsened by the
application of a pressure immobilization bandage or tourniquet, and therefore is not
recommended.

The initial management should involve placing the affected limb in hot water, ensuring that the
water does not scald the limb. Often the pain is severe. Other options to reduce the pain include
local anaesthesia, either injected into and around the sting site or a regional block, such as a foot
block. The patients often will need an opiod injection, such as morphine or pethidine, and repeated
doses.

Fortunately, there is a horse-derived antivenom, which is used as an intramuscular injection. One

ampoule (2000 units) is said to neutralize 20 mg of venom, and each ampoule is recommended for
each two spine puncture sites visible. The antivenom is safe, and is recommended for nearly all
cases. As it is a horse-derived antivenom there is a small risk of anaphylaxis.
With any marine wound it is important to ensure the patient has adequate tetanus cover, and watch
for any evidence of retained spine or infection.

Stingray barb injuries

The stingray is the largest of the venomous fish, however it is the barb that is located on its tail
that produces the major injury to humans.

There is not a lot known about the venom of the stingray. Evidence from human stings suggests
that the venom associated with the barb produces tissue necrosis.

The most common mechanism of injury is when a human stands on the stingray in the shallows.
The tail of the stingray flips up and penetrates the lower limb of the person. Other injuries occur
when a stingray has been netted whilst fishing and the person is injured whilst trying to release the
stingray.

Most of the injuries produced by stingrays are minor. Fenner reported over 100 cases of stingray
injury from Queensland. All patients complained of pain and a wound, with most being treated
with symptomatic care. This included placing the limb in hot water, and/or infiltrating the wound
with local anaesthetic. As there have been reports of infections developing and the barb remaining
in the wound, it is important that the wound is examined for a retained barb, and washed or
scrubbed. Some patients have required antibiotic therapy.

Tragically, there have been two deaths reported in Australia due to stingray barbs. In both cases
the barb penetrated the left side of the chest and caused an injury to the myocardium. In one case a
12-year-old child died six days after a barb struck the left side of his chest. It is believed that the
toxin on the barb caused a chemical myocardial necrosis resulting in myocardial rupture.

Therefore, it is prudent that any person with a stingray barb injury to the chest or abdomen will
need a high index of suspicion for a significant internal injury, and should probably have their care
monitored by a surgical service.

Management of a stingray barb injury to the chest is to ensure no immediate threat to life. Treat
the wound ensuring bleeding and pain is controlled. The wound needs to be explored, ensuring
there is no retained barb, and scrubbed. An X-ray may be required to confirm the presence or
absence of a barb. Tetanus status should be checked and antibiotics may be required. If the wound
appears contaminated, it is safer to leave the wound open and review the wound in 24–48 hours.

Ciguatera poisoning
Ciguatera is an illness that develops from eating larger tropical fish. The toxin, ciguatoxin, is
produced by a dinoflagellate (algae), Ganbierdiscus toxicus, and the toxin accumulates in larger
fish as they eat the smaller fish. The toxin is tasteless and is not destroyed by heat. Symptoms of
ciguatera have occurred in tropical Australia, as well on tropical island communities where fish is
a very important part of the diet. From 1964–86 more than 19,000 cases were reported in French
Polynesia. With the ever-increasing export of fish throughout the world there have been reports of
ciguatera poisonings in non-tropical parts of the world.

There have been discovered a number of ciguatoxins, and the structure of these toxins is known.
Ciguatoxin is known to bind to sodium channels, and by this induces membrane depolarization.

Clinically a person with ciguatera poisoning presents initially with a gastrointestinal illness within
1–2 days of ingesting the offending fish. Usually the symptoms of vomiting, abdominal pain and
diarrhoea occur within 12 hours of ingesting the fish. Patients then develop parasthesia around the
mouth, hands and feet, myalgias, arthralgias, ataxia, and itching. The patients can also develop
temperature sensation reversal (hot things feel cold, cold things feel hot). Symptoms are worsened
with alcohol consumption. Hypotension and bradycardia is rare, and the quoted fatality rate is less
than 1%.

There is no specific treatment or antidote for this poisoning. If possible gastrointestinal

decontamination should be attempted using activated charcoal, but this may be difficult if the
patient is vomiting. Numerous drugs have been tried with limited success. Intravenous mannitol
has been described as the most effective treatment for ciguatera poisoning, especially acute
poisoning. Usually this is given in the dose of up to 1 g/kg over one hour, with some good
anecdotal success; however there has not been any randomized trials to confirm it effectiveness.
|Symptoms can last for days, and there have been cases with symptoms lasting for months.

Bibliography
Major box jellyfish
Williamson JA, Fenner PJ, Burnett J, Rifkin J, Eds. Venomous and poisonous marine animals: a medical
and biological handbook. Sydney: NSW University Press, 1996; 96–118.
OReilly GM, Isbister GK, Lawrie PM et al. Prospective study of jellyfish stings from tropical Australia,
including the major box jellyfish Chironex fleckeri. Med J Aust 2001; 175:652 – 5.
Sutherland SK, Tibballs J, Eds. Australian Animal Toxins. Second Edition. Melbourne: Oxford University
Press, 2001.
Currie B. Box-Jellyfish in the Northern Territory. The Northern Territory Disease Control Bulletin Sept
1998; 5(3):12–14.
Tibballs J, Williams D, Sutherland SK. The effects of antivenom and verapamil on the haemodynamic
actions of Chironex fleckeri (box jellyfish) venom. Anaesth Int Care 1998; 26:40– 5.
Maguire EJ. Chironex fleckeri (sea wasp) sting. Med J Aust 1968; 2:1137–8.
Pereira P, Carrette T, Cullen P et al. Pressure immobilisation bandages in first aid treatment of jellyfish
envenomation: current recommendations reconsidered. Med J Aust 2000; 173:650–2.

Irukandji syndrome
Little M, Mulcahy RF. A years experience of Irukandji envenomation in far north Queensland. Med J Aust
1998; 169:638–41.
Williamson JA, Fenner PJ, Burnett J, Rifkin J, Eds. Venomous and poisonous marine animals: a medical
and biological handbook. Sydney: NSW University Press, 1996.
Flecker H. Irukandji sting to North Queensland bathers without production of weals but with severe general
symptoms. Med J Aust 1952; 2:89–91.
Barnes J. Cause and effect in Irukandji stingings. Med J Aust 1964; 1:897–904.
Little M, Mulcahy RF, Wenck DJ. Life threatening cardiac failure in a health young female with Irukandji
Syndrome. Anaesth Int Care 2001; 29:178–80.
Sutherland SK, Tibballs J, Eds. Australian Animal Toxins. Second Edition. Melbourne: Oxford University
Press, 2001.
Pereira P, Carrette T, Cullen P et al. Pressure immobilisation bandages in first aid treatment of jellyfish
envenomation: current recommendations reconsidered. Med J Aust 2000; 173:650–2.

Stonefish sting
Williamson JA, Fenner PJ, Burnett J, Rifkin J, Eds. Venomous and poisonous marine animals: a medical
and biological handbook. Sydney: NSW University Press, 1996.
Sutherland SK, Tibballs J, Eds. Australian Animal Toxins. Second Edition. Melbourne: Oxford University
Press, 2001.
Stingray barb injuries
Fenner PJ, Williamson JA Skinner RA. Fatal and non fatal stingray envenomation. Med J Aust 1989; 151:
621–2.
Williamson JA, Fenner PJ, Burnett J, Rifkin J, Eds. Venomous and poisonous marine animals: a medical
and biological handbook. Sydney: NSW University Press, 1996; 96–118.
Sutherland SK, Tibballs J, Eds. Australian Animal Toxins. Second Edition. Melbourne: Oxford University
Press, 2001.

Ciguatera poisoning
Williamson JA, Fenner PJ, Burnett J, Rifkin J, Eds. Venomous and poisonous marine animals: a medical
and biological handbook. Sydney: NSW University Press, 1996.
Sutherland SK, Tibballs J, Eds. Australian Animal Toxins. Second Edition. Melbourne: Oxford University
Press, 2001.
 Meningitis

Author: Drs Peter Markey and David Peacock (Diseases Surveillance, Centre for Disease
Control, Darwin)

Topic Reviewers: Kaz Kundsen (RAN, WA); Prof Bart Currie (MSHR); Dr Jim Burrow
and Dr Keith Edwards; Dr Gavin Weaton (ASH); Prof David Brewster

Introduction
Acute meningitis is a serious disease with high rates of mortality and long-term morbidity. Early
treatment of bacterial meningitis improves outcomes and it is therefore important to treat suspect
cases presumptively prior to hospitalisation. This applies in any setting, but is even more
important in remote locations where admission to hospital might be delayed.

Meningitis may follow an acute or chronic course and the causes of these respective forms of the
disease differ. However, the indolent nature of the chronic form means that pre-hospital diagnosis
and treatment is often not possible. Thus it makes sense to target empirical treatment towards the
known causes of the acute meningitis and to match this with the local epidemiology of the
infection.

Epidemiology of meningitis in the NT

The authors are not aware of any studies done (after searching PubMed, NT CDC Bulletins and
inquiring through colleagues) examining the overall relative frequency of the causative agents of
meningitis in the NT. However, a study of the causative agent of 69 cases of childhood bacterial
meningitis (excluding the neonatal period) in the NT between 1985–89 revealed that 58% were
caused by Hib, 22% by pneumococcus and 16% were culture negative.1 Only two cases were
caused by meningococcus (with another two cases which were probable). This study also revealed
that the incidence rate of meningitis in Aboriginal children less than five years of age was 337/100
000 per year, or 5.69 times that of non-Aboriginal children.1

Looking at the rest of Australia, a study looking at the causes of paediatric bacterial meningitis in
South Australia between 1979–89 found that, out of 80 episodes, 60 (75%) were caused by Hib,
10 (12.5%) by pneumococcus, 4 (5%) by meningococcus, 3 (3.7%) by Group B strep and one each
by E. Coli, Moraxella and an enterococccus.2 Similar findings were reported over a similar time in
Western Australia.3

The three most common causes of meningitis are notifiable to the Centre for Disease Control. The
numbers of cases in the NT over the 12 years to 2001 of Hib and meningococcal disease is
depicted in the following figures.4
 It should be noted that these graphs include all
cases of meningococcal and Hib disease and
not just those of meningitis.

The following graph summarises recent data on

pneumococcal meningitis for which there is an
enhanced dataset in the NT.

In the 10 years to 2001 there were only four cases of Listeriosis, one case in 1994 and three in
2000.4

Aetiology and treatment

Most commonly acute meningitis is caused by viruses or bacteria. Other infectious agents such as
rickettsiae, yeasts, spirochetes, protozoa and helminths have also been recognised as causes. There
are also non-infectious causes such as tumours, drugs and connective tissue disease (SLE).5

The infectious causes* of meningitis which might be relevant in the NT are listed in table 1
below.5

Table 1: Potential infectious causes of acute meningitis in Northern and Central Australia
Viruses
Enteroviruses (Cocksackie and Echo viruses)
Mumps virus
Herpe sviruses
HIV
Adeno viruses
Parainfluenza viruses types 2 and 3
Influenza virus
Measles virus
Rickettsia
Scrub typhus (Orientia tsutsugamushi)

Bacteria
Haemophilus influenzae
Neisseria meningiditis
Streptococcus pneumoniae
Listeria monocytogenes
Streptococcus agalactiae (Group B strep)
Propionibacterium acnes
Staphylococcus epidermidis
Enterococcus faecalis
Escherichia coli
Klebsiella pneumoniae
Pseudomonas aeruginosa
Salmonella spp.
Nocardia spp.
Mycobacterium tuberculosis
Burkholderia pseudomallei

Spirochetes
Treponema pallidum
Leptospira spp.

Yeasts, protozoa and helminths

Cryptococcus neoformans
Naegleria fowleri
Angiostrogylus cantonensis
Strongyloides stercoralis
* An exhaustive list of causes would include pathogens not prevalent in Australia. Non-infectious causes
are rare and are not relevant to this exercise.

This list is not meant to reflect the local epidemiology of the disease; nevertheless, the most
frequent bacterial causes are similar to elsewhere in the country and the world, namely Neisseria
meningitidis, Streptococcus pneumoniae and Haemophilus influenzae type B. Less common
bacteria — which are more likely to be found in cases in the very young, very old or
immunocompromised — are Listeria monocytogenes, Group B streptococcus (neonates) and
Escherichia coli. Also, it is worth noting that several of the other potential causative agents listed
above cause non-meningitic disease in the NT at a higher rate than elsewhere in the country and
therefore we need to be aware of these as possible causes. These include TB, melioidosis,
salmonella, strongyloides, cryptococcus, syphilis, rickettsia and leptospirosis. Meningitis is a well
described manifestation of TB infection and there have been documented reports of melioid and
salmonella meningitis in remote communities in Australia.6,7

The most likely viral causes are the enteroviruses (such as Echo and Cocksackie viruses).5,8 The
yeast Cryptococcus neoformans can also cause meningitis, mainly, but not exclusively, in the
immunocompromised.8
Table 2 (opposite) gives a summary of the potential causes of non-viral acute meningitis in the NT
with recommended treatments.
As can be seen from the list in table 2, treatment with ceftriaxone and penicillin covers all the
main six bacterial causes and five out of the other 13 causes in the list.
Table 2: Potential causes of acute meningitis in the NT with a list of first-line treatments*

Agent First line antibiotic With penicillin allergy Reference/comments

Main recognised causes
Haemophilus influenzae Ceftriaxone or cefotaxime Antibiotic Guidelines
(ABGs)9, Mandell5
Neisseria meningiditis Benzylpenicillin or Ceftriaxone Mandell5, ABGs9,
ampicillin Meningococcal
guidelines10
Streptococcus pneumoniae Ceftriaxone or cefotaxime The addition of empirical
vancomycin in areas of
increased resistance is
recommended, but is
currently not applicable in
the NT. ABGs
Listeria monocytogenes Benzylpenicillin or Co-trimoxazole ABGs9, Mandell5
ampicillin
Streptococcus agalactiae Benzyl penicillin or Vancomycin Ceftriaxone acceptable in
(Group B strep) ampicillin penicillin allergy.
Mandell5
Escherichia coli Ceftriaxone or cefotaxime Mandell5
Other potential causes in NT1
Salmonella spp. Ceftriaxone or cefotaxime Price et al11
Burkholderia pseudomallei Co-trimoxazole and one of: ABGs9
Ceftazidime
Imipenem
Meropenem
Mycobacterium Isoniazid ABGs9
tuberculosis Ethambutol
RifampicinPyrazinamide
Treponema pallidum Benzylpenicillin Doxycycline ABGs9
Cryptococcus neoformans Amphotericin and ABGs9
flucytosine
Strongyloides stercoralis Invermectin or albendazole ABGs9
or thiabendazole
Orientia tsutsugamushi Doxycycline ABGs9
Leptospira spp. Benzly penicillin or Doxycycline ABGs9
doxycycline
Other bacterial causes
Staphylococcus Vancomycin Mandell5
epidermidis
Klebsiella pneumoniae Ceftriaxone or cefotaxime Brooks12
Pseudomonas aeruginosa Ceftazidime Mandell5
Nocardia spp Co-trimoxazole Brooks12
Enterococcus faecalis Ceftriaxone or cefotaxime Mandell5

* The risk here is theoretical and not based on any epidemiological study and therefore the
organisms are not listed in any order.
Changes for the 4th edition
In developing these guidelines, an important consideration has been deciding what level of
treatment is appropriate in the bush given the remoteness and lengthy transit times to secondary
centres. Specifically, is pre-hospital treatment (as recommended in other guidelines) sufficient or
should early hospital treatment be started prior to transfer? Transit times to hospital from
diagnosis depend on a multitude of things and can vary from 30 minutes to 12 hours; indeed, in
some circumstances evacuation is not possible for several days. Usually, though, the transit time
to a secondary centre (including the logistics) is 3–6 hours. Hence, even though in some
circumstances what would be referred to as ‘pre-hospital’ treatment (in other guidelines) would be
appropriate care, in other cases, and I would argue most others, it would be prudent to administer
‘early hospital’ treatment.

In reviewing the guidelines the following literature has been consulted:

ABG Writing group. Therapeutic Guidelines Antibiotic version 11. 2000. Therapeutic Guidelines Limited.
Melbourne.9
Communicable Disease Network Australia. Guidelines for the early clinical and public health management
of Meningococcal disease in Australia. 2001. Commonwealth Department of Health and Aged Care,
Canberra.10
Chin J.(Ed) Control of Communicable Diseases Manual. 2000. American Public Health Association.13
Mandell GL, Bennett JE, Dolin R. (Eds) Principles and Practice of Infectious Diseases. 2000. Churchill
Livingstone, New York.5
Brooks GF, Butel JS, Morse SA.(Eds) Jawtez, Melnick and Adelburg’s Medical Microbiology. 2001.
McGraw Hill, New York.12
Beaman MH, Wesselingh SL. Acute community-acquired meningitis and encephalitis. Med J Aust 2002;
176:389–96.8
Discussion via e-mail with Dr John Ferguson at Hunter Health who is revising the Central Nervous System
chapter of ABGs for the twelfth edition.
Discussion with colleagues.
Other articles as appear in the reference list.

Changes to the third edition of the CARPA STM

1. In the first table of symptoms and signs delete ‘headache’ from the bottom of the first column
entitled ‘in children under 2 years’ and insert ‘headache’ to the top of the second column
entitled ‘in older children or adults’.
Justification: I’m sure this just corrects a formatting error from the previous edition.
2. In the second table in the second column entitled ‘or any adult who:’ add ‘is very unwell’.
Justification: Meningitis should be on the list of causes of ‘being very unwell’ in adults just as
in children, because specific signs may be masked or difficult to elicit in the obtunded patient.
In addition, meningococcal (or pneumococcal) septicaemia is not covered elsewhere in the
manual, and treatment of these conditions as presumptive meningitis would be appropriate (see
below).
3. In the list of things under ‘If out bush, do the following:’, add ‘— take a throat swab’. This may
require reference to an additional paragraph in ‘How to do some lab tests’. [Editor: This is now
covered in the CRANA Clinical Procedures Manual] There should also be a proviso: ‘Treat the
patient even if you cannot do a throat swab’, as with blood cultures.
Justification: In the case of meningococcal or Hib disease there is often throat carriage and
isolation from the throat is possible. It is easier to do than blood cultures and the swabs are
likely to be easily available. However, national meningococcal guidelines state that the
sensitivity of throat swabs done in hospital is not diminished after pre-hospital treatment with
parenteral antibiotics, so on those grounds it would do no harm to wait until arrival in hospital.
 Nevertheless, in the remote setting with a greater possibility of delay before microbiological
assessment, one would think the more sites cultured the better. The editors may not think the
potential benefits here outweigh the work involved in explaining the technique.
4. Treatment for all ages should be: Ceftriaxone 50 mg/kg up to 2 g im/iv and benzylpenicillin 60
mg/kg up to 1.8 g im/iv. The third edition suggests benzylpenicillin only for those under three
months and at 30 mg/kg. New doses will mean a new table for benzylpenicillin.
Justification: There are several points to consider here:
i. Version 11 of the Therapeutic Guidelines: Antibiotic suggests:

• pre-hospital treatment with benzylpenicillin (60 mg/kg) or ceftriaxone (50 mg/kg)

• empirical early hospital treatment of ceftriaxone 60 mg/kg (or cefotaxime) and
benzylpenicillin 60 mg/kg (or amoxy/ampicillin), with the proviso ‘penicillin may be
omitted in patients aged between 3 months and 15 years because it is added to cover
Listeria . . .’
ii. National meningococcal guidelines suggest:

• pre-hospital treatment with benzylpenicillin (30–60 mg/kg) in cases of suspect

meningococcal disease with ceftriaxone as an ‘acceptable alternative’
• early hospital treatment is the same as recommended in the ABGs above.

The rationale for the addition of high dose benzylpenicillin is firstly that it is the treatment of
choice for meningococcal disease and secondly that it covers Listeria. In addition, because the
guideline is written to be used in the remote setting, it was thought appropriate that it cover the
‘early hospital treatment’ recommendations of both the reference guidelines. Editors and
reviewers may think otherwise. To be consistent with the ABGs we could omit penicillin in
immunocompetent patients between three months and 15 years old, but given the underlying
risk of immunocompromise in this middle group and the possibility of meningococcal disease it
seems both simpler and more appropriate to recommend a blanket treatment with both
antibiotics.

5. The recommendation for the use of ceftriaxone in patients with penicillin allergy should be
commensurate with that mentioned elsewhere in the manual and should override this one. My
recommendation is the following. After ‘If a previous severe reaction to penicillin has
occurred:’ insert ‘do not give the benzyl penicillin and discuss with the doctor before giving the
ceftriaxone.’ Omit the recommendation about vancomycin and chloramphenicol.
Justification: I note that other guidelines vary in their recommendation in this regard and that
the ABGs (V11) recommendation is contradictory (i.e. in some instances ceftriaxone is the
recommended substitute, while in other situations cephalosporins are contraindicated). There is
recent evidence to suggest that the risk of giving cephalosporins to patients who have IgE
hypersensitivity to penicillin is a lot less than previously estimated.14,15 For most of the
potential aetiological agents for which penicillin is the first line treatment, ceftriaxone has been
recommended as an appropriate substitute. The exception here is Listeria, for which co-
trimoxazole is recommended, and this is not usually available in the parenteral form in the
bush. As such a reasonable approach in patients with penicillin allergy is simply to omit the
penicillin but continue with the ceftriaxone. However, it may depend on the severity of the
allergy and the particular patient circumstances, so it was thought that the guideline need not be
proscriptive but to suggest discussing with a medical officer.

6. Under public health considerations the fifth point where it says ‘CDC or your own health. . .’
after rifampicin add ‘, ciprofloxacin or ceftriaxone’.
Justification: These are now standard as options for prophylaxis against meningococcal
disease.10
Other issues
While responding to a possible case of meningitis health practitioners may need to be aware of
other possible diagnoses. The price of having a simplified treatment manual for use in the bush is
the loss of detail which is required to cover other possible explanations for the group of symptoms
and signs with which patients may present. Future editors of the manual might keep these in mind
if they feel further expansion is necessary. The following are areas of interest.

Encephalitis
Encephalitis may present in a similar fashion to meningitis. Most of the causes are viral, and
presumptive treatment with acyclovir is not feasible in the bush setting. Non-viral causes include
Treponema, Cryptococcus, Mycobacteria, melioidosis and Listeria; most of these usually have a
subacute or chronic course.8 Listeria is covered by empirical anti-meningitis treatment.

Brain abscess
There is much overlap between the symptoms and signs of meningitis and those of a brain
abscess. Causative organisms vary and usually differ from those of meningitis. Nevertheless,
empirical treatment for brain abscess, according the ABGs V119, does include the two antibiotics
recommended for meningitis in this guideline and the third (metronidazole) could be given if the
clinical situation was suggestive and there was a prolonged delay getting to hospital. This needs to
be kept in mind.

Meningococcal septicaemia
Meningococcal disease often presents as overwhelming sepsis rather than meningitis and for this
reason the treatment of anyone who becomes suddenly very unwell with empirical anti-meningitis
antibiotics is appropriate. Whether a statement needs to be made to this effect in the guideline is
up to the editors.

Acknowledgments
The authors would like to acknowledge Prof Bart Currie, Dr Jim Burrow and Dr Keith Edwards
for their help in reviewing the guideline and document.

References
1. Hanna JN. Bacterial meningitis in children in the Northern Territory. (letter) Med J Aust 1989;
151:173.
2. Thomas DG. Outcome of paediatric bacterial meningitis 1979–89. Med J Aust 1992; 157:519–20.
3. Hanna JN, Wild BE. Bacterial meningitis in children under five years of age in Western Australia. Med
J Aust 1991; 155:160–4.
4. Centre for Disease Control, Northern Territory Department of Health and Community Services. May
2002. Notifiable Diseases Database.
5. Mandell GL, Bennett JE, Dolin R. (Eds) Principles and Practice of Infectious Diseases. New York:
Churchill Livingstone, 2000.
6. Woods ML, Currie BJ, Howard DM, et al. Neurological melioidosis: seven cases from the Northern
Territory of Australia. Clin Infect Dis 1992; 15:163–9.
7. Messer RD, Warnock TH, Heazlewood RJ, Hanna JN. Salmonella meningitis in children in Far North
Queensland. J Paediatr Child Health 1997; 33:535–8.
8. Beaman MH, Wesselingh SL. Acute community-acquired meningitis and encephalitis. Med J Aust
2002; 176:389–96.
9. ABG Writing group. Therapeutic Guidelines: Antibiotic. Version 11. Melbourne: Therapeutic
Guidelines Limited, 2000.
10. Communicable Diseases Network Australia. Guidelines for the early clinical and public health
management of Meningococcal disease in Australia. 2001. Canberra: Commonwealth Department of
Health and Aged Care.
11. Price EH, de Louvois J, Workman MR. Antibiotics for Salmonella meningitis in children. J
Antimicrobial Chemotherapy 2000; 46:653–5.
12. Brooks GF, Butel JS, Morse SA. (Eds) Jawtez, Melnick and Adelburg’s Medical Microbiology. New
York: McGraw Hill, 2001.
13. Chin J. (Ed) Control of Communicable Disease Manual. American Public Health Association, 2000.
14. Novalbos A, Sastre J, Cuesta J et al. Lack of allergic cross-reactivity to cephalosporins among patients
allergic to penicillins. Clin Exp Allergy 2001; 31(3):438–43.
15. Anne S, Reisman RE. Risk of administering cephalosporin antibiotics to patients with histories of
penicillin allergy. Ann Allergy Asthma Immunol 1996; 76(1):61.
 Near Hanging

Author: Dr Phil Rayson (RDH)

Topic Reviewers: Dr Kerrie Jones (A&E RDH); Malcolm Auld (RAN, Bonya Clinic); Kaz
Knudsen (RAN, WA); Kylie Harris (RAN, Docker River); Martin Kelly (RAN, Pukatja);
Pam Moll (RAN, Haasts Bluff)

Australia-wide, hanging is the second most common cause of suicidal death.2 Hanging is the most
prominent method of suicide among Top End Aboriginal males and females.3 Suicide rates among
young people are increasing, as is the popularity of hanging as a mode of suicide.4 Almost 90%
are males between the ages of 15–35 years. Indigenous Australians and those in legal detention are
at particular risk. About one-third have a history of psychiatric illness, and nearly 50% have a
history of drug (especially ‘ganja’) or alcohol abuse.1 Some communities appear to have no
incidence of hangings, while others have experienced near epidemic numbers of hangings and
near hangings, with numbers of ‘copy cat’ hangings occurring over short periods of time.2

Mechanism of injury
There were eighteen relevant references found after a Medline search using search terms
‘hanging’, ‘near hanging’, ‘non-lethal hanging’, and ‘attempted suicide’. Two review articles1,5
provided a comprehensive review of literature over the past 15 years focusing on pathophysiology,
clinical features and management.

One further study by a local psychiatrist provided additional local statistics and information.2

Survival without neurological damage is possible after attempted suicide involving near hanging.4
Initial neurological assessment is a very poor guide to final outcome (including fixed, dilated
pupils).1,4 The worst prognostic indicators are absent or agonal respiration, absent vital signs or the
need for resuscitation.1 Therefore, aggressive resuscitation should be attempted on all victims and
transfer to hospital performed if initial resuscitation is successful.

The patterns of injury are quite different to those seen in judicial hanging. Cervical spine injuries
are quite rare.1 Injury mainly arises through pressure on the neck veins and arteries. Compression
of the airway is less common. The external compression causes venous cerebral congestion,
hypoxic circulation and reduced arterial cerebral supply. If the person survives the initial event
they may succumb in hospital due to the severity of the initial hypoxic and ischaemic brain
injury.1

Pulmonary complications include pulmonary oedema (ARDS) and bronchopneumonia secondary

to aspiration. The oedema may be from a centrally mediated massive sympathetic discharge that
produces an intense generalised vasoconstriction and a fluid shift from the high resistance
systemic circulation to the low resistance pulmonary circulation. The other cause of pulmonary
oedema is secondary to negative intrathoracic pressures generated as the person attempts to inspire
through an obstructed airway.

Laryngeal injuries may occur. Thyroid cartilage fractures are the most common with fractures of
the hyoid bone and cricoid cartilage seen less often. Damage to these structures is more common
in those over 40 years due to calcification and where a narrow ligature has been used. Review
articles of large numbers of near hanging victims show that airway compromise, leading to
difficulty intubating, are extremely rare.1
Other neurological injuries include various spinal cord syndromes, focal cerebral deficits, transient
hemiparesis and larger infarctions. The nature of the initial insult is a diffuse brain injury so
myriads of deficits have been described. Various nerve palsies also occur. Cerebral oedema is
invariable present if there has been a significant injury.

Other described injuries include traction injuries to the carotid arteries where bleeding into the
vessel wall or intima occurs. This can lead to immediate or late obstruction to blood flow.
Hyperthermia, status epilepticus, subarachnoid haemorrhage, ruptured oesophagus and
pneumoperitoneum have all been described. Facial petechiae and subconjunctival haemorrhages
are common.

Management
First aid measures should follow the standard DR ABC resuscitation scheme.

Early management should include intubation if the person requires CPR, has a compromised
airway or has neurological compromise. Intubation should aim to cause minimal haemodynamic
instability and avoid any period of hypoxia. Cricoid pressure, in-line cervical stabilisation and
moderate positive end expiratory pressure (PEEP) should be used. All victims, whether intubated
or not, should be transported to hospital and observed for 24 hours as soft tissue swelling can
occur. The cervical spine should be protected even though fractures are extremely rare.
Management of cerebral oedema follows standard therapies for managing head injuries due to
other causes. These include nursing in a 30° head-up position, careful maintenance of
normocarbia, normoglycaemia, moderate fluid restriction and avoidance of hypotension.
Consideration should be given to performing a cerebral CT scan and carotid studies.

All victims will require psychiatric support. All staff and relatives involved in a near hanging
incident also require skilled counselling providing psychological and emotional support.

References
1. Adams, N. Near hanging. Emerg Med 1999; 11:17–21.
2. Parker, R. Suicide in the NT 1991–1998. Darwin: Health Library, 2000.
3. Cantor, C Baume, P. Access to methods of suicide: what impact? Aust NZ Journal of Psychiatry 1998;
32:8–14.
4. Kaki A, Crosby ET & Lui AC. Airway and respiratory management following non-lethal hanging. Can
J Anaesth Apr 1997; 44(4):445–50.
 Pain Relief

Author: Dr Didier Palmer (Director ED, RDH)

Topic Reviewers: Dr Liz Mowat (ED, ASH); Kenna Bistani (RAN, Pine Creek); Helen
Collinson (RAN, Adelaide River); Monica Ostigh (RAN, Jabiru); Dr Tim Semple (RAH
pain clinic)

Overview
Pain is a subjective feeling belonging to the patient, and only the patient can decide if pain has
been relieved. The successful management of pain involves a combination of several elements: a
proper attitude in approaching each patient as an individual; the ability to evaluate the degree of
pain; an understanding of pain physiology and analgesia pharmacology; and the clinical
application of this knowledge.1

There is a wealth of knowledge and research on pain relief but I will limit myself to a description
the main areas of relevance to our patients — the influence of ethnicity on pain management —
within which I will also discuss pain measurement tools and touch on pain theory. Detailed pain
physiology, analgesia pharmacology and the clinical treatment of pain is covered by standard
medical texts.

Influence of ethnicity on pain management

Introduction
There is no published research specifically examining pain management in the Australian
Aboriginal population; there is, however, a completed research project2 in preparation for
publication from the Royal Darwin Hospital’s emergency department and many papers of
relevance on population subgroups in the USA.

There is firm evidence of disparities in pain management between different ethnic groups. Part of
the rationale for this is that people from lower socioeconomic groups experience disparities for
many health related measures.3,4,5 Income alone, however, does not explain the differences in
outcome.6,7

Padianathan describes less analgaesia and less patient satisfaction of pain management in
Aboriginal patients presenting to an Australian tertiary emergency department compared to non-
Aboriginal patients.2 This disparity in acute pain management reflects the findings of two separate
studies by Todd et al. in an emergency department setting which found that Hispanic ethnicity and
African-American ethnicity were the strongest predictors of receiving no analgaesia for long bone
fracture after controlling for confounders (gender, language, insurance status).6,7 The same cross-
cultural trends have been found for chronic cancer pain12 and post-operative pain.13

Why do we have disparity in pain management? To examine this we have to deconstruct the
clinician– patient interaction:
 Pain experience

Pain expression

Pain assessment

Figure 1: The clinician–patient interaction

Pain experience
Do ethnic groups experience pain differently? Zatzick et al. reviewed 13 cross-cultural studies
(total of 42,933 subjects) from 1944–89 looking experimentally at the ability of people to
discriminate induced noxious stimuli.8 None of these studies found ethnic differences in the ability
to discriminate painful stimuli. The conclusion is that differences in pain expression and pain
behaviours do not have a neuro-sensory basis. None of the studies were on an Australian
Aboriginal population but there is no reason to believe that this population is significantly
different.

Pain expression
After experiencing pain the patient expresses pain related behaviours, including those involved
with seeking medical attention where the patient expresses his/her pain to a clinician. There is no
published research on the Australian Aboriginal population in this area. The world literature on
cross-cultural pain expression, many reviews of which are available9,10,11, leaves little doubt that
variations in pain related behaviour by ethnicity do exist, however, intra-ethnic variations are also
prominent and often more marked than inter-ethnic differences. Experience has shown that pain
expression in the Australian Aboriginal population may be different but has yet to be quantified.
This is a rich area for future research.

Pain assessment (pain measurement tools)

Introduction
There is no gold standard to objectively quantify this multi-dimensional, internal and personal
experience. Currently-used tools are uni-dimensional and often limited to quantifying severity. We
need to be able to measure pain because, without baseline measurement, we cannot assess the
response to treatment which is a complex endpoint not limited to ‘pain free’. There is also
mounting evidence that formal pain measurement reveals unrecognised and under-treated pain,
makes us aware of iatrogenic pain, improves pain management and reduces return visits.14,15,16

Gate control theory of pain

The Melzack et al. ‘gate control’ theory of pain17, although extensively modified since 1965,
remains the basis for our understanding of pain. Further work by Melzack with Casey in 196818
proposed a multi-dimensional model of pain experience, which included:
1. A sensory-discriminative dimension, corresponding to the classical view of pain perception
and associated with information on location, magnitude and temporal pattern of pain.
2. An affective-motivational dimension associated with aversion, fear and other emotional
components.
 3. A cognitive-evaluative dimension, where the significance and reaction to pain is determined
through the interaction of current sensory and affective dimensions of pain with higher
cognitive functions and previous experience.

Multi-dimensional pain assessment tools (research)

The only multi-dimensional tool for pain assessment in widespread use is the McGill Pain
Questionnaire.19 This tool takes 15–20 minutes to complete, and so is not useful in the clinical
environment, but is mentioned as it is an important and validated research tool across many
(Western) language groups.

Uni-dimensional pain assessment tools

The visual analogue scale (VAS) is the most commonly used pain assessment scale. Typically it
consists of a 10 cm line bounded by perpendicular stops and descriptors (figure 2).

Rate how severe your pain is now. Mark the line with one vertical slash.

No pain Unbearable pain

Figure 2: Visual analogue pain scale20

The score is read in centimetres from the left. Horizontal lines are preferred as scores tend to be
more normally distributed21 and placing adjectival descriptors or intermediate marks along the line
creates artificial clustering.20,21,22 Interestingly, Chinese subjects assess pain more accurately with
a vertical scale rather than the more usual horizontal scale so there appear to be cross-cultural
differences in interpretation.

There is a problem of determining what movement along the scale is clinically relevant rather than
statistically relevant. For example, do patients appreciate that a new medication produces a 0.75
cm reduction in their VAS? Data from a USA study suggests that a reduction in the VAS by 2.9
cm corresponds with the patient’s perception of adequate pain relief23, however this may be
different for different ethnic groups and has not been studied in the Australian Aboriginal
population.

VAS in the Australian Aboriginal population

One major problem is that not all adults understand the concept of the VAS as a graphical
representation of pain severity. Thus up to 11% of adults24 and 25% of the elderly25 are unable to
complete it. In unpublished research conducted in the Royal Darwin Hospital emergency
department2 the use of the VAS had to be abandoned in Aboriginal patients due to inability to
complete the scale. Further validation of the use of the VAS is required in the Australian
Aboriginal population.
[Editor: Some work carried out in Alice Springs Hospital found that an adaptation of a paediatric visual
pain scale worked well and influenced analgesia decision making. This is the set of faces reproduced in the
CRANA Clinical Procedures Manual, page 87. The protocol recommends its use where possible.]

Decision to treat
The final step in the clinician–patient interaction is the ‘decision to treat’. There are studies in
non-Aboriginal populations that show that even where there are interventions that improve pain
monitoring and relay that information to the physician there is no change in physician prescribing
practices or improving patient pain relief.26,27 There is also evidence to the contrary.14,15,16 This
highlights, but does not shed light on, the complex nature of the physician’s decision to treat.
More research is required in this area.

[Additional notes from Editorial Committee:

Pethidine has been removed from the protocol after advice from some experts that:
1. It is particularly problematic for leading to drug seeking behaviour
2. It is no better than morphine for analgesia
3. Concerns about use of morphine in ureteric or biliary colic are not well supported and should not
influence practice.
4. That concerns about use of pethidine in penetrating eye injury were not supported by any significant
evidence from the literature (more detail in the eye chapter).

The committee was also concerned about perceived high rates of use of paracetamol/codeine. This is not a
medical problem per se but may be unnecessarily leading to problems of opiate tolerance or dependence.
By recommending that ongoing use of codeine-paracetamol be reviewed by a doctor with a view to
assessing the need for tramadol or oxycodone, or SR morphine, it is encouraging the ongoing use of
codeine to be regarded as an ‘S8’ issue.

Dr Tim Semple from RAH pain clinic strongly supports the aim of not using paracetamol/codeine mixtures
to prevent drift into long-term use of strong pain medication use, tolerance, habituation, side effects
(including medication seeking behaviour) and reduced options for use in future pain episodes.

Paracetamol-codeine 8 mg is no longer mentioned, effectively discouraging its use. This is because the
editorial committee believe that it is tending to be over-used, with little analgesic advantage, higher rates
of side effects and, in some instances, likely tolerance and habituation. There is some supporting evidence
for this stance (limited analgesic role and increased side effects) for the 8 mg codeine combination from a
systematic review.28]

References
1. Ducharme J. Whose pain is it anyway? Managing pain in the emergency department. Emergency
Medicine 2001;13:271–3.
2. Padianathan N. Pain Management in the Royal Darwin Hospital emergency department. Presentation to
the scientific meeting of the Australasian College for Emergency Medicine, Canberra, 2000
3. Burstin H, et al. Socioeconomic status and risk for substandard medical care. JAMA 1992; 268:2383–
97.
4. Sorlie P, et al. Black–white mortality differences by family income. Lancet 1992; 340:346–50.
5. Khan K, et al. Health care for black and poor Medicare patients. JAMA 1994; 271:1179–84.
6. Todd K, et al. Ethnicity as a risk factor for inadequate emergency department analgaesia. JAMA 1993;
269:1537–9.
7. Todd K, et al. Ethnicity and analgaesic practice. Ann Emerg Med 2000; 35:11–16.
8. Zatzick D, et al. Cultural variations in response to painful stimuli. Psychosom Med 1990; 52:544–57.
9. Wolff B, et al. Cultural factors and the response to pain: a review. Am Anthropologist 1968; 70:494–
501.
10. Wolff B, et al. Ethnocultural factors influencing pain and illness behaviour. Clin J Pain 1985; 1:23–30.
11. Martinelli A. Pain and ethnicity: how people of different cultures experience pain. AORN J 1987;
46:273–8.
12. Cleeland C, et al. Pain and treatment of pain in minority patients with cancer. Ann Intern Med 1997;
127:813–16.
13. Ng B, et al. The effect of ethnicity on prescriptions for patient controlled analgaesia for post operative
pain. Pain 1996; 66:9–12.
14. Singer A, et al. Comparison of topical anaesthetics and vasoconstrictors vs lubricants prior to
nasogastric intubation: A randomised, controlled trial. Acad Emerg Med 1999; 6:184–90.
15. Cohen D. Effects of mandated pain scales on frequency and timeliness of analgaesic administration.
Acad Emerg Med 2001; 8:485.
16. Ducharme J. Emergency management of acute migraines: Is the headache really over? Acad Emerg
Med 1998; 5:899–905.
17. Melzack R, et al. Pain mechanisms: A new theory. Science 1965; 50:971–9.
18. Sensory, motivational and sensory control determinants of pain: A new conceptual model. In: Kenshalo
D (ed). The skin senses. Springfield,IL: Charles C Thomas, 1968; 423–43.
19. Katz J, et al. Measurement of pain. Surg Clin North Am 1999; 79:231–52.
20. Scott J, et al. Graphic representation of pain. Pain 1975; 2:175–84.
21. Sriwantanakul K, et al. Studies with different types of analogue scales for measuring pain. Clin
Pharmacol Ther 1983; 34:234–9.
22. McCormack H. Clinical applications of visual analogue scales: a critical appraisal. Psych Med
1988;18:1007–19.
23. Lee J, et al. Clinical meaningful values of the visual analogue scale of pain severity. Acad Emerg Med
2000; 7:550.
24. Kremmer E. Measurement of pain: Patient preference does not confound pain measurement. Pain 1981;
10:241–8.
25. Her K. Comparison of pain assessment tools for the use with the elderly. Appl Nurs Res 1993; 6:39–
46.
26. Ward S, et al. Patient satisfaction and pain severity as outcomes in pain management: A longitudinal
view of one setting’s experience. J Pain Symptom Manage 1996; 11:242–51.
27. Kravits R et al. Bedside charting of pain levels in hospitalised patients with cancer: A randomised
controlled trial. J Pain Symptom Manage 1996; 11:81–7.
28. de Craen AJM, Di Giulio G, Lampe-Schoenmaeckers AJEM, Kessels AGH, Kleijnen J. Analgesic
efficacy and safety of paracetamol-codeine combinations versus paracetamol alone: a systematic review.
BMJ 1996;313(7053):321–5.
 Poisoning

Author: Dr Didier Palmer (Director, RDH ED)

Topic Reviewers: Kenna Bistani (RAN, Pine Creek); Bernard Egan (RAN, Bulman Clinic)

The vast majority of poisoning requires conservative management with attention to the ABCDs,
fitting, and management of the unconscious patient. After the immediate event a psychosocial
evaluation is generally required.

The management of poisoning has seen some significant changes in the past 10 years with a move
to less intervention. For example, gastric emptying is rarely used and induced emesis (with ipecac)
is never used, in fact ipecac is no longer available in Australia. Activated charcoal also has a
decreasing role.
The 24-hour availability of poison information lines for giving high quality advice on all aspects
of care (seriousness of poisoning, what to look out for, required period and type of observation,
necessity of decontamination, specific treatment etc.) removes the need for any detailed discussion
of toxicology in this manual.
 Procaine Penicillin Reactions

Author: Colin Watson

Topic Reviewers: Dr Penny Roberts-Thomson (Nguiu); Angela Peermen (RAN, Oenpelli

Clinic)

Introduction
Procaine penicillin is listed as a treatment for a number of clinical conditions common in the
remote-area health practice. It is a drug frequently administered. The adverse reactions to procaine
penicillin are well documented in the literature. It is important that practitioners to be aware of
these potential reactions, be able to differentiate between the types of reaction and offer
appropriate treatment.

What is procaine penicillin?

Trade name: Cilicaine. An antibiotic
Presentation: 1.0 gram (1 million units) and 1.5 gram (1.5 million units).

What are the adverse procaine penicillin reactions?

There are three types of adverse reaction to procaine penicillin: severe allergic (anaphylaxis); faint
(vaso-vagal); and non-allergic (pseudoanaphylactic). Similarities between these reactions can
make diagnosis difficult. The clinical imperative is to exclude the life threatening anaphylactic
reaction. A person who collapses from shock (low blood pressure and rapid weak pulse) or
respiratory failure (from bronchospasm causing wheeze or angioedema causing respiratory
obstruction)1 following an injection of procaine penicillin should be treated for anaphylaxis. These
severe allergic reactions are rare.

In this protocol, non-allergic reactions include those reactions which are predominantly psychotic
in nature. In the previous protocol these were considered separate reactions. The literature
suggests that these reactions are essentially the same.2,3,10,12,21 In some of these non-allergic
reactions transient psychotic symptoms predominate. In others, symptoms may resemble an
anxiety attack or mimic anaphylaxis. The variation in clinical manifestation can be confusing,
however the clinical imperative remains one of excluding anaphylaxis.

Anaphylaxis
This is a potentially life threatening systemic allergic reaction, often explosive in onset, affecting
primarily respiratory and cardiovascular systems but capable of affecting virtually any organ
system.4,5,6 Anaphylaxis is a medical emergency and requires immediate treatment. The symptoms
of anaphylaxis result from the action upon one or more target organs, of chemical mediators
released by mast cells. The dramatic and potentially lethal consequences of systemic anaphylaxis
may include upper respiratory tract obstruction (laryngeal oedema), wheezing (bronchospasm) and
shock (vascular collapse).4
Recommendations
• Those administering medications have knowledge of anaphylaxis and its management.
• All clinics have anaphylaxis kits available, including appropriate drugs and information on
management of anaphylaxis. Oxygen and resuscitation equipment should be readily available.
• Expiry dates of drugs in these kits checked regularly.
• Information regarding management of anaphylaxis displayed in clinic treatment areas and
pharmacy.

Faint
This is the most common mimic of anaphylaxis. It is also known as a vaso-vagal reaction, which
is a transient vascular and neurogenic reaction characterized by pallor, nausea, sweating, and a
rapid fall in arterial blood pressure. These can result in a loss of consciousness. Vaso-vagal
reactions are usually associated with bradycardia as opposed to tachycardia seen in anaphylaxis.
Upper respiratory obstruction and bronchospasm are not usually seen in vaso-vagal reactions. This
reaction is most often evoked by emotional stress associated with fear or pain.4
Non-allergic reactions

These encompass a number of signs and symptoms. Anxiety, fear of imminent death, visual and
auditory disturbances, aggression, confusion, disorientation and restlessness, disturbances in taste,
cardio-vascular changes and partial or generalized epileptiform seizures are the principle
manifestations.2,7,10,21, 18 These signs and symptoms are rapid in onset and short in duration. They
usually appear immediately after intramuscular injection and resolve within 15–30 minutes.8

Since being first reported in 1948, this non-allergic reaction has been described frequently in the
literature and referred to variously as Hoigne’s Syndrome, Procaine Psychosis and
Pseudoanaphylactic reaction.2,9,13 No other preparation of penicillin is known to produce such
effects.2

Incidence of non-allergic reactions to procaine penicillin

The incidence of non-allergic reactions to procaine penicillin has been variously reported from
1:1000 to 3:1000 injections.10,11,12

The cause of non-allergic reactions to procaine penicillin

At present there are two theories regarding the cause of non-allergic procaine penicillin reactions.
The vascular theory was first proposed by Batchelor et al. in 195111, reporting on eight cases of
procaine penicillin reaction. The rapidity of onset and the report of metallic taste suggested partial
inadvertent intravenous injection. Hoigne, after whom this syndrome has been named, proposed
micro-embolisation of small vessels in the lungs and brain by micro-crystals of procaine penicillin
as the causative mechanism. Hoigne suggested that at the site of injection the crystals of procaine
penicillin penetrate venous circulation, which then lodged in pulmonary and cerebral vessels.
However, both autopsy and animal studies have failed to demonstrate micro-emboli in the brain,
although this absence may in part be due to the rapid solubility of procaine crystals.13
The toxic theory proposes that the reaction is caused by the toxic action of procaine on the central
nervous system.11,14 The body’s enzymatic system is capable of liberating procaine from the
procaine penicillin molecule. Procaine is metabolized by procainesterase to non-toxic metabolites.
Systemic toxic reactions may occur from the release of procaine after the administration of
procaine penicillin. Reduced plasma procainesterase activity may increase the likelihood of a
reaction by delaying hydrolysis of procaine with subsequent accumulation of toxic levels in the
systemic circulation.7,21

The toxic theory has been further developed by the hypothesis of limbic kindling. The
phenomenon of kindling has been described as the appearance of physiological and behavioral
responses to a repetitive stimulus that initially has no effect.24 The cumulative effect of this
stimulation is to lower the convulsive threshold and produce secondary stimulation of other
cerebral sites. The limbic system sometimes referred to as the ‘emotional brain’ is an interrelated
group of structures that are involved in regulation of the emotional state with accompanying
behavioral, physiological and psychological responses.13 Among the pharmacological agents, local
anaesthetics such as lignocaine, cocaine and procaine have been shown to induce behavioral
kindling in experimental animal studies.16 The same neuromuscular-central nervous system
syndrome noted in procaine reactions has been observed in patients receiving intravenous
lignocaine for the treatment of cardiac arrhythmias and in cocaine abuse.17 Specifically, procaine
has been shown to elicit a kindling-like pattern of seizure activity.13

Management
It is important to distinguish anaphylactic shock from the acute non-allergic reaction by
determining the absence of such clinical signs as angioedema, urticaria, bronchospasm, and
vascular collapse.18

Severe allergic reaction (anaphylaxis) is a medical emergency. The outcome is related to the
promptness of intervention. Resuscitation involves establishing an airway, ensuring that the
patient is breathing, and cardiopulmonary support as required. The cornerstone of anaphylaxis
management is adrenaline 1:1000. Adrenaline is a powerful cardiac stimulant which increases
systolic blood pressure, reduces diastolic pressure and increases heart rate. Adrenaline also has
antihistamine and broncho-dilating properties.19 Adrenaline has a rapid onset of action but short
duration. Adrenaline 1:1000 is given as a deep intramuscular injection using a 1 ml syringe. This
is to ensure accuracy of dose when giving small volumes of Adrenaline.

A vaso-vagal reaction or faint is treated by laying the patient flat and elevating their legs. By
doing this we are helping to correct the drop in blood pressure. Offer reassurance to allay anxiety.

Non-allergic reactions (no signs of circulatory collapse or respiratory distress) are treated with
oxygen only. Stimulation of cerebral cells by local anaesthetic agents will increase the metabolic
rate within these cells leading to greater oxygen demands. If oxygen demands are not met,
hypoxia of the cerebral cells will lead to increased carbon dioxide concentrations, which can cause
convulsions and cardiovascular collapse.20

Treatment may be initially difficult if the patient is extremely anxious. Agitation, restlessness and
aggression can be features of this reaction. Because of the potential for collapse and seizure it is
important to minimize the risk of injury. Getting the patient to sit or lay down may minimize this
risk.

It is very important to discuss these reactions with the patient, their relatives and health staff.
These reactions are frightening for all concerned. The patient or relatives may believe that the
needle was given incorrectly or that the wrong medicine was administered. These beliefs can be
quite destructive. It is important people are aware that these reactions sometimes occur, that the
exact cause is still being debated in the medical literature, and that the person who gave the needle
was not at fault.

Recommendations
• Correct storage. Procaine penicillin should be refrigerated. Storage at room temperature has been
shown to liberate additional free procaine.21 Check expiry date of drug prior administration.
Protect from light. Do not freeze. Discard solution if it appears discoloured.
• Lay the patient down to administer the procaine injection. This serves two purposes. Firstly, it
may reduce the chance of patient injury in the event of a reaction. Secondly, having the patient
lying down for procaine injection may reduce the chance of inadvertent intravascular injection.11
• Correct administration involves remixing components of procaine penicillin syringe, which can
separate with storage. Procaine penicillin is only administered by deep intra-muscular injection.
The needle is inserted in the upper outer quadrant of the buttock. The plunger must be
withdrawn and if any blood appears in the syringe immediately withdraw the needle and discard
the syringe.
• Discard any unused solution.
• Given the potential for adverse reactions to procaine penicillin, this drug should only be
administered within a clinic setting or where access to resuscitation equipment and drugs is
readily available.
• Report to pharmacy batch number of Cilicaine syringes which become occluded during
administration. Expelling air from the syringe and needle just prior to inserting the needle may
overcome this problem.

References
1. Walls R. Allergies and Their Management. Sydney: MacLennan &Petty, 1997.
2. Ilechukwu S, Pollock D. Pseudoanaphylactic Reaction to Procaine Penicillin and Kindling. Psychiatric
Journal University Ottawa 1987; 12(2):109–110.
3. Lankin D, Jewell G, Grinvalsky H, Fye D. Psychotic-Like Reaction to Procaine Penicillin G. 1983;
12(8):507–9.
4. Holgate S, Church M, Lichtenstein L. Allergy. London: Mosby, 2001.
5. Durham S (ed). ABC of Allergies. London: BMJ Books, 1998.
6. Altman L, Becker J, Williams P. Allergy in Primary Care. Philadelphia: WB Saunders Company, 2000.
7. Downham T, Cawley R, Salley S, Dal Santo G. Systemic Toxic Reactions to Procaine Penicillin G.
Sexually Transmitted Diseases 1978; 5(1):4–8.
8. Kryst L, Wanyura H. Hoigne’s Syndrome — Its course and symptomatology. J Maxillo-facial Surgery
1979; 7:320–6.
9. Kline C, Highsmith L. Toxic Psychosis Resulting from Penicillin. Annals of Internal Medicine 1948:
28:1057–8.
10. Galpin J, Chow A, Yoshikawa T, Guze L. Pseudoanaphylactic Reactions from Inadvertent Infusion of
Procaine Penicillin. Annals of Internal Medicine 1974; 81:358–9.
11. Batchelor R, Horne G, Rogerson H. An Unusual Reaction to Procaine Penicillin in Aqueous
Suspension. The Lancet 1951; 195–8.
12. Utley P, Lucas J, Billings T. Acute Psychotic Reactions to Aqueous Procaine Penicillin. Southern
Medical Journal. 1966; 59:1271–4.
13. Araskiewicz A, Rybakowski J. Hoigne’s Syndrome: A Procaine-induced Limbic Kindling. Medical
Hypotheses 1994; 42:261–4.
14. Bjornberg A, Selstam J, Acute Psychotic Reaction After Injection of Procaine Penicillin. Acta Psych Et
Neurol Scand 1960; 35(2):129–39.
15. Goddard G, Development of Epileptic Seizures Through Brain Stimulation At Low Intensity. Nature
1969; 214:1020.
16. Post R, Kopanda R, Lee A. Progressive Behavioral Changes During Chronic Lidocaine Administration.
Life Science 1975; 17:943–50.
17. Araszkiewicz A, Rybakowski J. Hoigne’s Syndrome, Kindling and Panic Disorder. Depression and
Anxiety 1997; 4:139–43.
18. Landis B, Dunn L, Adverse Toxic Reaction to Aqueous Procaine Penicillin. Nurse Practitioner 1984;
41–3.
19. Mims Annual. St Leonards: MediMedia Australia, 1999.
20. Moore D, Bridenbaugh L. Oxygen: The Antidote for Systemic Toxic Reactions from Local Anaesthetic
Drugs. JAMA 1960; 174(7):102–7.
21. Kraus S, Green R. Pseudoanaphylactic Reactions with Procaine Penicillin. Cutis 1976; 17:765–7.
 Acute Chest Infections in
Children
1–5 Years of Age

Author: Assoc Prof Paul Torzillo (Medical Director, Nganampa Health Service)

Topic Reviewers: Malcolm Auld (RAN, Bonya Clinic); Leone Radnedge (RAN,
Utopia); Deb Beaver (RAN, Bagot clinic); Dr Ian Dumbrell (Port Keats)

The CARPA treatment guidelines are partly based on WHO guidelines aimed at
children in developing countries.1,2 However, they have significant
differences to the WHO algorithms because of local circumstances. In
particular the WHO guidelines are primarily aimed at preventing death. In
Central Australia mortality rates are much lower than in developing
countries and efficient evacuation is usually possible for sick children.

Most children with acute chest symptoms will have infection with bacteria,
virus or sometimes both.
The most important decisions are:
1. Which children are likely to have bacterial infection and therefore
need antibiotics?
2. Which children are sick enough to need evacuation?

The international literature suggests that S. pneumoniae is the most common

pathogen in childhood pneumonia, but that H. influenzae is also important.3,4
It is very likely that S. pneumoniae is the major cause of pneumonia in
Central Australian children. A study of invasive pneumococcal disease in
Central Australia has shown that children in this region have the highest
rates of this disease in the world literature.5

A study of the aetiology of pneumonia in hospitalised children in Alice

Springs supports a prominent role for S. pneumoniae, but also demonstrates
that nearly half these children had evidence of viral infection, and co-
infection may also be common.6

Research in developing countries has shown that in settings where X–ray is

not available respiratory rate is the best clinical predictor of pneumonia.7
A major problem with this respiratory rate ‘cut-off’ is that it lacks
specificity and will lead to over-diagnosis of bacterial pneumonia, and
hence increased use of antibiotics in children who do not have bacterial
infection.7,8 This problem is likely to be worse in populations where viral
infection and wheeze syndromes are common. However, this approach provides
the safest option for managing these children because there are no clinical
signs which can exclude the presence of bacterial infection. Studies to
determine the optimum cut-off respiratory rate demonstrate that increasing
the cut-off increases the specificity but lowers sensitivity. In children
one and up to five years a respiratory rate of 40 or more provides a
sensitivity of 71 to 87 per cent and a specificity of 72 to 85 per
cent.9,10,11,12

Studies of lower chest wall indrawing (defined as inward movement of the

lower chest wall on inspiration) have shown it to be a predictor of severe
pneumonia.7 However, the sign must depend on compliance of chest wall,
degree of airway obstruction and consequent generation of intra-thoracic
pressure swings. Predictably, chest indrawing can be seen in conditions
such as bronchiolitis which may be due to viral rather than bacterial
infection. Therefore, its value as a predictor of severity in pneumonia
will vary with the incidence of severe bronchiolitis in the population
being serviced.

Wheeze can occur in children with bacterial pneumonia and bacterial co-
infection can occur in Respiratory Syncytial Virus and other viral-related
bronchiolitis syndromes.13,14 Therefore, it is not possible to distinguish
viral bronchiolitis from pneumonia on clinical signs alone.

Fever is an obvious candidate as a predictor of infection requiring

antibiotic treatment. However, it has not been shown to reliably
distinguish between viral and bacterial infection. In a study of 90 infants
presenting with bronchiolitis, El–Radhi15 found that fever was more likely
to be present in those with severe disease and in those with radiological
evidence of pneumonia. This study identified fever, defined as a single
reading >38.0°C or two consecutive readings of >37.8°C, in 28 children
(31%). The children who presented with fever had a longer hospital stay and
a more severe illness than other children. Weber et al.16, in a study of
bronchiolitis in The Gambia, found that the mean temperature of children
with a positive blood culture was significantly higher than those with a
negative blood culture. However, Cherian et al.17 found no clinical
predictors of X–ray consolidation in 114 Indian children with
bronchiolitis.

Benzyl penicillin, procaine penicillin and amoxicillin all have activity

against both S. pneumoniae (SP) and H. influenzae (HI). There is some
evidence that, at least for SP, achieving blood levels above the mean
inhibitory concentration (MIC) for significant periods of time is important
in antibiotic efficacy18, although at least one important clinical trial has
failed to demonstrate this association.19 Both benzyl penicillin and
procaine penicillin given intra-muscularly will achieve serum levels
greater than the MIC for pneumococci even with intermediate level
resistance (0.1 to 1.0 µg/ml).20 Benzathine penicillin and other long-acting
penicillins achieve only very low serum levels and should not be used for
pneumonia. They are likely to be ineffective and to facilitate resistance.20

The effectiveness of oral amoxicillin in the Central Australian setting is

not clear. Some recent studies from Pakistan provide some basis for
decision making. These studies are all in non–severe pneumonia i.e.
children who do not have chest indrawing or any other signs of severity.
Oral amoxicillin given three times a day in a dose of 15 mg per kg is
effective19 in childhood pneumonia although failure rates in recent studies
have been in the order of 16 per cent.21 In addition compliance with three
times a day oral therapy is obviously problematic.
 A recent study has shown that a three day course of three times a day
amoxicillin is as effective as five days.22 Twice daily amoxicillin is as
effective as twice daily cotrimoxazole but with a failure rate of over
16%.21 Currently studies are underway to determine if increasing the dose of
Amoxicillin will decrease failure rate. The high rate of chronic lung
disease in Central Australian Aboriginal children23 raises further concerns
about the impact of duration of therapy on long-term outcome. On the basis
of existing evidence it would appear that oral therapy should not be
considered first-line treatment option. If the health care worker does not
consider parenteral therapy possible, then amoxicillin in a dose of 25–30
mg/Kg per dose two or three times daily (depending on the health care
worker’s estimate of compliance) is a reasonable second-line therapy
option.

There are many issues to consider in the treatment of fever in young

children. These issues are extensively reviewed elsewhere.24,25

In summary, fever may be beneficial to the host with infection. Animal

studies show that moderate fever improves immune response. A series of
animal studies reviewed by Shann25 demonstrate a worse outcome in febrile
animals treated with paracetamol or aspirin compared to placebo. Except in
children with cardiac or respiratory failure, fever is not harmful unless
greater than 41°C. Febrile convulsions are thought to occur in response to
an initial rapid rise in temperature and so paracetamol is unlikely to be
beneficial. The only relevant clinical trials suggest no benefit with the
use of paracetamol in preventing convulsions. Finally, paracetamol has been
shown to have only a modest effect in reducing distress and discomfort
associated with infection.

Overall, very little toxicity has been associated with paracetamol therapy
for fever in children. Thus, although anti-pyretic treatment seems
relatively safe in the setting of acute respiratory infection, it is
reasonable to restrict its use to children with axillary temperature over
38.0°C.21

References
1. WHO Programme for the Control of Acute Respiratory Infections. Acute respiratory
infections in children: Case management in small hospitals in developing countries: A
manual for doctors and other senior health workers. Document WHO/ARI/90.5 (1990).
2. WHO Programme for the Control of Acute Respiratory Infections. Management of the
Child with Cough (training module), revised 1991.
3. Selwyn BJ. The epidemiology of acute respiratory tract infection in young children:
comparison of findings from several developing countries. Coordinated DATA Group of
BOSTID Researchers. Rev Infect Dis 1990; 12(8):S870–888.
4. Shann F. Etiology of severe pneumonia in children in developing countries. Paed Inf
Dis 1986; 5(2):247–51.
5. Torzillo PJ, Hanna JN, Morey F, Gratten M, et al. Invasive pneumococcal disease in
central Australia. Med J Aust 1995; 162:182–6.
6. Torzillo PJ, Dixon J, Manning K, Gratten M, et al. Aetiology of acute respiratory
infection in central Australian Aboriginal children. Paediatr Infect Dis J 1991;
18:714–21.
7. Mulholland EK, Simoes EAF, Costales MOD, McGrath EJ, Manalac EM, Gove S. Standardised
diagnosis of pneumonia in developing countries. Paediatr Infect Dis 1992; 11:77–81.
8. Brewster DR, Pyakalyia T, Hiawalyer G, O’Connell DL. Evaluation of the ARI program: a
health facility survey in Simbu, Papua New Guinea. PNG Med J 1993; 36:285–96.
9. Shann F, Hart K, Thomas D. Acute lower respiratory tract infections in children:
possible criteria for selection of patients for antibiotic therapy and hospital
admission. Bulletin WHO, 1984; 62:749–51.
10. Campbell H, Byass P, Lamont AC, Forgie IM, et al. Assessment of clinical criteria
for identification of severe acute lower respiratory tract infections in children.
Lancet 1989; 1:297–9.
11. Cherian T, Simoes E, John TJ, Steinhoff MC, John M. Evaluation of simple clinical
signs for the diagnosis of acute lower respiratory tract infection. Lancet 1988
July16; 125–8.
12. Mulholland EK, Simoes EAF, Costales MOD, McGrath EJ, Manalac EM, Gove S.
Standardised diagnosis of pneumonia in developing countries. Pediatr Infect Dis J
1992; 11:77–81.
13. Ghafoor A, Nomani NK, Ishaq Z, et al. Diagnosis of acute lower respiratory tract
infections in children in Rawalpindi and Islamabad, Pakistan. Rev Infect Dis 1990;
12(Suppl8):S907–14.
14. Forgie IM, O’Neill KP, Lloyd–Evans N, et al. Etiology of acute lower respiratory
tract infections in Gambian children; I Acute lower respiratory tract infections in
infants presenting at the hospital. Pediatr Infect Dis J 1991; 10:33–41.
15. El-Radhi AS, Barry W, Patel S. Association of fever and severe clinical course in
bronchiolitis. Arch Dis Child 1990; 81:231–4.
16. Weber MW, Dackour R, Usen S, et al. The clinical spectrum of respiratory
syncytial virus disease in The Gambia. Pediatri Infect Dis J 1998; 17:244–30.
17. Cherian T, Simoes EA, Steinhoff MC, et al. Bronchiolitis in tropical south India.
Am J Dis Child 1990; 144:1026–30.
18. Drusano GL. Role of pharmacokinetics in the outcome of infections. Antimicrob
Agents Chemother 1988; 32:289–97.
19. Straus WL, Qazi SA, Kundi Z, et al. Antimicrobial resistance and clinical
effectiveness of Cotrimoxazole versus amoxicillin for pneumonia among children in
Pakistan: randomised controlled trial. Lancet 1998; 352:270–4.
20. Shann F, Linnemann V, Gratten M. Serum concentrations of penicillin after
intramuscular administration of procaine, benzyl and benethamine penicillin in
children with pneumonia. J Pediatr 1987; 110:299–302.
21. Catchup Study Group. Clinical efficacy of cotrimoxazole versus amoxicillin twice
daily for treatment of pneumonia: a randomised controlled trial in Pakistan. Arch Dis
Child 2002; 86:113–18.
22. Mascot study group. Clinical efficacy of three days versus five days oral
amoxicillin for treatment of childhood pneumonia: a multicentre double-blind clinical
trial in Pakistan. Lancet 2002; 360:835–41.
23. Chang A, Masel JP, Boyce NC, Wheaton G, Torzillo PJ. Evaluation of central
Australian children with chronic suppurative lung disease. Submitted for publication.
24. The management of fever in young children with acute respiratory infections in
developing countries. Programme for the control of acute respiratory infections.
Geneva: WHO, 1993.
25. Shann F. Paracetamol: when, why and how much. J Paeditr Child Health 1993; 29:84–
5.
 Acute Chest Infections in
Children 3–12 Months

Author: AB Chang (Flinders University NTCS, Alice Springs Hospital)

Topic Reviewers: Dr Penny Roberts-Thomson (Nguiu); Dr Teresa Yee (Oenpelli

Clinic); Malcolm Auld (RAN, Bonya Clinic); Rin Riemersma (RAN, Finke); Leone
Radnedge (RAN, Utopia); Dr Ian Dumbrell (Port Keats)

Introduction
Respiratory health is an important consideration in Indigenous Australians,
as the burden of respiratory disease remains high.1,2 Australian Bureau of
Statistics data based on Northern Territory (NT), Western and South
Australia shows that respiratory illness was the second highest cause of
death in adult Indigenous males and females.1 Within the NT, in the 0–4
years age group, recently published data indicates that respiratory disease
is still the leading cause of preventable mortality with rates of five
times that of non-Aboriginal Territorians.3 While mortality data is
important, data on morbidity — and hence the burden of disease in the
community — is crucial. However, it is difficult to obtain population
information on morbidity which can be defined in many ways. Hospital
morbidity data (with its limitations) is often used as a measure of the
level of ill health in the population.2 In the NT, respiratory diseases
again top the list with rates of 399.1 admissions per 1000 population
[Editor: ‘average’ of one infant in four admitted each year for resp
infection!] in the 4–51 weeks age group and 84.8 in the 1–4 years age group
(1993–97).2 In Central Australia, the number of separations for pneumonia in
1997–2000 was 418–533 per year, giving a hospitalisation rate of 30–38 per
1000 children per year. This is significantly higher than that reported
elsewhere (Pacific Islanders in Auckland 14 per 1000, Fiji 1.7 per 1000,
USA 0.5–1 per 1000).4 Based on these figures alone, the management of acute
respiratory infections is important and highly relevant for remote and
rural health practitioners.
Respiratory infections are manifested in different ways in infants and
children, although there is a considerable amount of overlap. This chapter
is restricted to those aged between 3–12 months and to the four most
commonly seen infective respiratory illnesses in this age group. Previous
editions of the CARPA STM have focused mainly on the detection and
management of acute bacterial pneumonia. The 4th edition of the CARPA STM
has added the dimension of detection of respiratory sounds. Should the
practitioner be unsure of these sounds, bypassing of this section is
recommended, and the user should proceed directly to assessing the
respiratory rate. In addition, the previous edition recommends the use of
physiotherapy and bronchodilators in infants with bronchiolitis. New
evidence (levels 1 and 2) do not support this approach and has been removed
from the 4th edition (see Bronchiolitis, below).
The management of croup, bronchitis and pertussis are not discussed in
this section as they are far more common in the toddler age group. Brief
statements specifying the peculiarities in infants with these infections
are made below.

Literature review and discussion

Why children are different from adults
The respiratory system like any other system undergoes a process of
maturation in infancy and childhood. While external features such as
walking and talking are obviously developing, the developmental process of
internal features such as control of the respiratory system, respiratory
muscles, thoracic cage and glandular development of the respiratory tree,
are often forgotten by adult-focused practitioners. These various factors
result in the young child’s basal respiratory state lying closer to the
fatigue threshold and, thus, predispose a child to develop respiratory
failure earlier than adults.5
Another aspect of paediatric respiratory disease is the influence of
prenatal factors and when insults to the system occur, growth potential can
be lost.6 In the respiratory system it has been well documented that lower
respiratory infections (LRTI) in children can lead to later respiratory
morbidity, chronic lung disease and lung function abnormalities.7,8,9,10,11,12 In
adenovirus and many viral ALRIs, the young child has an increased risk of
developing lung function abnormality.8,13 Management should arguably be
intensive in children, as it is now increasingly appreciated that
inflammatory disease processes may impair lung growth in addition to
accelerated respiratory function decline in later years.14,15,16

Major risk factors for development of respiratory failure

Infants with decreased respiratory reserve are more likely to develop
severe respiratory distress and respiratory failure. Clinically, these
infants are identified by the presence of significant past history of
prematurity associated with respiratory distress, previous mechanical
ventilation, congenital cardiac defects, chronic neonatal lung disease,
known respiratory disease or immunodeficiency.17,18 Extra caution should be
exercised when these infants develop any respiratory infections as the
disease process is more likely to rapidly progress to a severe state.17,18

Classification of respiratory infections in young children

Upper respiratory tract infections (including ‘cold’, otitis media,
pharyngitis etc.) will not be discussed in this section.
Lower respiratory tract infection, (LRTI), including:
• Pneumonia
• Bronchiolitis
• Croup
• Bronchitis
• Pertussis

Diagnosis of a lower respiratory tract infection

In infants, Campbell and colleagues reported that a high fever (>38.5°C),
vomiting and refusal to breast-feed were the best predictors of acute
pulmonary lobar consolidation.19 Vomiting and refusal to feed will lead to a
degree of dehydration; the severity will depend on the length of the acute
illness and the intesity of the illness. Thus, any infant who is dehydrated
should be urgently referred and discussed with a doctor.
 Respiratory rate should be counted over 60 secs (not 30 secs as in third
edition of CARPA STM) as it has been shown that counting respiratory rate
over a shorter period leads to different results.20,21 Periodic breathing is
normal in infants and becomes less pronounced with increasing age.22 In
infants and children respiratory rate is physiologically dependent on the
activity level (awake vs asleep, feeding etc.), sleep state, gender, age,
arousal level among other factors.22,23,24 Thus, measuring respiratory rate in
a consistent manner (over 60 secs) and state (calm state) is important.25 In
pathological situations, respiratory rate has been shown in some studies to
be a good discriminator of upper vs lower respiratory tract infection as
assessed by trained field workers.26 The use of respiratory rate for
management purposes has largely been based on studies for detection of
pneumonia and has not been validated for conditions such as bronchiolitis
and croup.
Chest in-drawing as a sign of severe LRTI has been shown to be a
reliably detected sign by health workers. However, it may not necessarily
be a good discriminator for severe LRTI in all community settings.19
Campbell and colleagues warn against the use of hospital-based data of
chest in-drawing in the community.19
Oximetry is a valuable clinical tool and the presence of hypoxaemia
(SpO2 <95) is highly clinically important in the context of a child with
respiratory illness. However, the use of oximetry in children is not as
straightforward as it is in adults and, like any other instrument, must be
interpreted in the context of the clinical state of the child. For accurate
measurement in children it is essential to obtain a good trace on the
pulse-meter (should always be displayed and clinics should choose an
oximeter that displays the pulse), use an appropriate probe that is not
placed too tightly and placed on a well perfused limb. Movement artefacts
must always be considered. Single instantaneous SpO2 may not reflect the
true reading in children and the trend over several minutes is more
reliable. In very darkly pigmented individuals, the readings may be
erroneously high.27

Audible respiratory sounds

These can be divided into inspiratory or expiratory sounds. Typically
inspiratory sounds are generated from extra-thoracic lesions and expiratory
sounds from intra-thoracic lesions. When either is severe enough, a bi-
phasic (both inspiratory and expiratory) sound may be audible.
Wheeze is a high-pitched musical sound that is characteristically in the
expiratory phase. The commonest cause of wheeze in infancy is bronchiolitis
(see below). Stridor is a high pitched monophonic musical sound, and the
commonest cause in infants over nine months is viral
laryngotracheobronchitis. Paroxysmal cough is classically due to pertussis.
Grunting is an expiratory sound and the noise is generated when
expiration occurs against a partially closed glottis. The presence of
grunting is always significant and almost always is a sign of involvement
of the respiratory system (though not always necessary). Infants grunt to
increase airway pressure and thus preserve or increase functional residual
capacity.

Limitations of the STM protocol

The suggested CARPA STM protocol, in line with the WHO protocol, is heavily
reliant on elevated respiratory rate as a criterion for the presence of
chest infection in children. The use of respiratory rate thresholds is
however limited by how it is measured, e.g. state of child, length of
observation, as outlined above. There is no correlation between respiratory
rate and hypoxaemia28, and the use of respiratory rate is more reliable in
children over 12 months than in infants (<12 months).19

Management of chest infections in children

Pneumonia
The best predictor of the cause of paediatric pneumonia is age, and in the
first two years of life viruses are most frequently implicated.28 Guidelines
for practical diagnosis and treatment of paediatric pneumonia are
available.28,29 The CARPA STM is based on WHO recommendations in which the aim
is largely to prevent death from bacterial infections30, as well as local
historical influences. Penicillin is the antibiotic of choice for
management of paediatric pneumonia and five days of treatment is the
commonly used length of treatment. There is a dearth of randomised
controlled trials to guide antibiotic choice, length of treatment, and
administration method.
All children with pneumonia (irrespective of where they are treated)
should be closely followed up for a clinical response. Cough should cease
after 3–4 weeks and, if cough is persistent, the child should be managed
aggressively until the cough totally clears. In a yet unpublished study in
Central Australia, 19.7% of those who were followed up following lobar
pneumonia had a new diagnosis on follow-up. The majority of these had
chronic suppurative lung disease.

Bronchiolitis
There are many causes of wheeze in infancy, of which the most common in
those with a first episode of wheeze is bronchiolitis. Infants with
recurrent wheeze should always be referred for further assessment. This
section does not cover those with recurrent wheeze. Any infant with wheeze
and other concurrent risk factors (outlined above) requires extra
precautions and should be discussed with the doctor. Evidenced based
reviews for the management of bronchiolitis are available.31,32 The previous
CARPA STM protocol for wheeze in infants suggests the use of
bronchodilators. However, new level 1 evidence does not recommended routine
use of bronchodilators for first-time wheezer.31,32 The use of bronchodilators
has been associated with deterioration, including oxygen desaturation
(level 2 evidence).31 Chest physiotherapy is also not recommended (level 2
evidence), as it is associated with clinical deterioration.31
The management of bronchiolitis is largely supportive with oxygen
therapy (when SpO2 is <93% and fluid/nutritional support. Thus, transfer to
hospital is necessary when: (a) these are required (b) the infant should be
observed if he/she has major risk factors or (c) the infant is likely to
deteriorate.

Croup
Anecdotally croup is uncommon in remote Indigenous communities. Stridor in
any infant, especially in those under six months of age, requires careful
evaluation: croup is uncommon in this age group and the stridor is more
likely because of a congenital airway lesion in association with a upper
RTI.
Bronchitis
Bronchitis is manifested by the presence of a cough and the child is
otherwise usually well. Viral infections are the commonest cause of this
infection, but secondary infection may occur. As early and heavy
nasopharyngeal colonisation has been shown in some remote Indigenous
communities33, secondary infection may be more common in this setting. When
the cough persists for longer than 2–3 weeks, a chronic condition should be
suspected and bacterial infection considered.34

Pertussis
Infants with pertussis do not usually have a whoop and the infection is
usually manifested by presence of paroxysmal cough. In between these
episodes of cough the infant looks well. The young infant may present with
apnoea without cough paroxysms. Any infant under six months with pertussis
should be closely observed and closely monitored, as there is an increased
risk of apnoea and death in this age group. It would therefore be necessary
to transfer any infant under six months to the closest hospital for
monitoring. Indications for admitting those over six months include
cyanosis during paroxysms and excessive vomiting.35 Management for those not
requiring admission into hospital is otherwise supportive. There is no role
for cough suppressants or bronchodilator therapy.35

Stabilisation of an infant with respiratory distress

Infants’ respiratory basal states physiologically lie closer to the
respiratory muscle fatigue threshold and therefore develop respiratory
failure earlier than older children and adults.5 Stabilisation of an infant
prior to transfer to minimise the risk of respiratory failure is important
in the remote setting. Recommendations for stabilisation are:
• Oxygen use. Hypoxaemia and hypercapnia leads to increased muscle
fatigue and, if these abnormalities exist because of pulmonary disease,
a vicious cycle of deterioration occur.36 Oxygen should be commenced
using nasal prongs of an appropriate size at 0.5–1.5 L/min.
Alternatively, face masks at a minimum of 4 L/min could be used.
• Minimal handling. Handling an infant may upset the infant leading to
increased cardiorespiratory demands that are already compromised,
causing further hypoxaemia. Mechanisms for minimal handling include
sitting the infant on the carer’s lap and avoiding unnecessary
manipulations such as venesection and suctioning.
• Erect or semi-erect position. The supine position decreases airway
patency and functional residual capacity.37 To optimise lung volumes,
airway patency and respiratory muscles, the erect or semi-erect
position is recommended. Effectively this means sitting the infant on
the carer’s lap with the infant resting against the carer’s chest or
carrying the infant against the carer’s chest.

• Avoid feeds. When an infant has severe respiratory distress,

aspiration of feeds can occur and lead to further deterioration. In the
young infant, the balance of precipitating aspiration and hypoglycaemia
and further dehydration must be considered. Ultimately it depends on
severity of distress and length of time to transfer/admission of the
infant.
• Hydration. Interventions for optimising this must be balanced with
expertise of IV insertion, degree of dehydration, severity of
 respiratory distress, avoidance of handling the infant, and length of
time to transfer/admission of the infant.

References
1. Australian Bureau of Statistics. Mortality of Aboriginal and Torres Straits Islander
Australians. [3315.0]. Australian Bureau of Statistics, 2000.
2. d’Espaignet ET, Kennedy K, Paterson BA, Measey ML. From infancy to young adulthood:
health status in the Northern Territory. Darwin: Territory Health Services, 1998.
3. Dempsey KE, Condon JR. Mortality in the Northern Territory 1979–1997. Darwin:
Territory Health Services, 1999.
4. Grant CC. Pneumonia in children: becoming harder to ignore. N Z Med J 1999; 112:345–
7.
5. Gaultier C. Developmental Anatomy and Physiology of the Respiratory System. In:
Taussig LM, Landau LI, editors. Pediatric Respiratory Medicine. St Louis: Mosby Inc.,
1999; 18–37.
6. Stick S. Pediatric origins of adult lung disease. 1. The contribution of airway
development to paediatric and adult lung disease. Thorax 2000; 55:587–94.
7. Chang AB, Masel JP, Masters B. Post-infectious bronchiolitis obliterans: clinical,
radiological and pulmonary function sequelae. Pediatr Radiol 1998; 28:23–9.
8. Becroft DM. Bronchiolitis obliterans, bronchiectasis, and other sequelae of
adenovirus type 21 infection in young children. J Clin Pathol 1971; 24:72–82.
9. Laraya-Cuasay LR, DeForest A, Huff D, Lischner H, Huang NN. Chronic pulmonary
complications of early influenza virus infection in children. Am Rev Respir Dis 1977;
116:617–25.
10. Penn CC, Liu C. Bronchiolitis following infection in adults and children. Clin
Chest Med 1993; 14:645–54.
11. Cooreman J, Redon S, Levallois M, Liard R, Perdrizet S. Respiratory history
during infancy and childhood, and respiratory conditions in adulthood. Int J
Epidemiol 1990; 19:621–7.
12. Johnston ID, Strachan DP, Anderson HR. Effect of pneumonia and whooping cough in
childhood on adult lung function. N Engl J Med 1998; 338:581–7.
13. Weber MW, Milligan P, Giadom B et al. Respiratory illness after severe
respiratory syncytial virus disease in infancy in The Gambia [see comments]. J
Pediatr 1999; 135 :683–8.
14. Tiddens H, Silverman M, Bush A. The Role of Inflammation in Airway Disease.
Remodeling. Am J Respir Crit Care Med 2000; 162:7S–10.
15. Bush A, Tiddens H, Silverman M. Clinical implications of inflammation in young
children. Am J Respir Crit Care Med 2000; 162:S11–S14.
16. Stockley RA. Role of bacteria in the pathogenesis and progression of acute and
chronic lung infection. Thorax 1998; 53:58–62.
17. Clark SJ, Beresford MW, Subhedar NV, Shaw NJ. Respiratory syncytial virus
infection in high risk infants and the potential impact of prophylaxis in a United
Kingdom cohort. Arch Dis Child 2000; 83:313–6.
18. Altman CA, Englund JA, Demmler G, Drescher KL, Alexander MA, Watrin C, Feltes TF.
Respiratory syncytial virus in patients with congenital heart disease: a contemporary
look at epidemiology and success of preoperative screening. Pediatr Cardiol 2000;
21:433–8.
19. Campbell H, Byass P, Lamont AC, Forgie IM, O’Neill KP, Lloyd EN, Greenwood BM.
Assessment of clinical criteria for identification of severe acute lower respiratory
tract infections in children. Lancet 1989; 1:297–9.
20. Simoes EA, Roark R, Berman S, Esler LL, Murphy J. Respiratory rate: measurement
of variability over time and accuracy at different counting periods. Arch Dis Child
1991; 66:1199–203.
21. Berman S, Simoes EA, Lanata C. Respiratory rate and pneumonia in infancy. Arch
Dis Child 1991; 66:81–4.
22. Hoppenbrouwers T, Hodgman JE, Harper RM, Hofmann E, Sterman MB, McGinty DJ.
Polygraphic studies of normal infants during the first six months of life: III.
Incidence of apnea and periodic breathing. Pediatrics 1977; 60:418–25.
23. Hoppenbrouwers T, Hodgman JE, Harper RM, Sterman MB. Respiration during the first
six months of life in normal infants: IV. Gender differences. Early Hum Dev 1980;
4:167–77.
24. Hoppenbrouwers T, Harper RM, Hodgman JE, Sterman MB, McGinty DJ. Polygraphic
studies on normal infants during the first six months of life. II. Respiratory rate
and variability as a function of state. Pediatr Res 1978; 12:120–5.
25. Gove S, Kumar V. Simple signs and acute respiratory infections. Lancet 1988;
2:626–7.
26. Campbell H, Byass P, Greenwood BM. Simple clinical signs for diagnosis of acute
lower respiratory infections. Lancet 1988; 2:742–3.
27. Yorgin PD, Kyoo HR. Gas Exchange and acid-base physiology. In: Taussig LM, Landau
LI, editors. Pediatric Respiratory Medicine. St Louis: Mosby Inc., 1999; 212–43.
28. Jadavji T, Law B, Lebel MH, Kennedy WA, Gold R, Wang EE. A practical guide for
the diagnosis and treatment of pediatric pneumonia. CMAJ 1997; 156:S703–S711.
29. Nelson JD. Community-acquired pneumonia in children: guidelines for treatment.
Pediatr Infect Dis J 2000; 19:251–3.
30. Methodology for a multicenter study of serious infections in young infants in
developing countries. The WHO Young Infants Study Group. Pediatr Infect Dis J 1999;
18:S8–16.
31. Evidence-based guidelines for the medical management of infants one year of age
or less with a first time episode of bronchiolitis. http://www.guideline.gov
32. Kellner JD, Ohlsson A, Gadomski AM, Wang EEL. Bronchodilators for bronchiolitis.
The Cochrane Library 2001.
33. Gratten M, Manning K, Dixon J, Morey F, Torzillo P, Hanna J, Erlich J, Asche V,
Riley I. Upper airway carriage by Haemophilus influenzae and Streptococcus pneumoniae
in Australian aboriginal children hospitalised with acute lower respiratory
infection. Southeast Asian J Trop Med Public Health 1994; 25:123–31.
34. von Mutius E, Morgan WJ. Acute, Chronic and Wheezy Bronchitis. In: Taussig LM,
Landau LI, editors. Pediatric Respiratory Medicine. St Louis: Mosby Inc., 1999; 547–
56.
35. Shebab ZM. Pertussis. In: Taussig LM, Landau LI, editors. Pediatric Respiratory
Medicine. St Louis: Mosby Inc., 1999; 693–702.
36. Henning R, South M. Respiratory Failure. In: Taussig LM, Landau LI, editors.
Pediatric Respiratory Medicine. St Louis: Mosby Inc., 1999; 404–30.
37. Nunn JF. Applied Respiratory Physiology. London: Butterworths, 1993.
 Anaemia in Children

Authors: Karen Edmund; Barbara Paterson; Andrew White. (First written 2001,
revised by Andrew White 2002)

Topic Reviewers: Brad Palmer (RN-CDC Darwin); Monica Ostigh (RAN, Jabiru
Clinic); Bernard Egan (RAN, Bulman Clinic); Helen Collinson (RAN, Adelaide
River); Monica Harris (RAN, locum); Kaz Knudsen (RAN, WA); Kylie Harris (RAN,
Docker River); Pam Moll (RAN, Haasts Bluff); Dyan Kelaart (RAN, Yuendumu
Clinic); Vicki Gordon (RAN, Mutitjulu Clinic); Dr Ian Dumbrell (Port Keats)

Introduction
Additional evidence about screening, diagnosis and treatment for childhood
anaemia has emerged since the third edition of the CARPA STM was completed.
This background paper attempts to document past and emerging evidence
for screening, diagnosis and treatment of anaemia in children aged 0–14
years living in rural and remote communities of the NT, and makes
recommendations for NT remote area protocol development, further
investigation and research. This is not a complete literature review.
The areas covered by this discussion paper are as follows:
1. Prevalence of anaemia and iron deficiency in the NT
2. Physiology of iron deficiency and iron deficiency anaemia
3. Types of anaemia in NT remote area Aboriginal children
4. Causes of iron deficiency and iron deficiency anaemia
5. Consequences of iron deficiency and iron deficiency anaemia
6. Diagnosis of iron deficiency and iron deficiency anaemia
7. The use of the HemoCue haemoglobinometer as a screening and a
diagnostic test
8. Treatment of iron deficiency anaemia .

Anaemia is a major public health problem. The high prevalence of iron

deficiency anaemia (IDA) in remote area Aboriginal children mandates a
population-based approach. Consideration must be given to population-based
interventions for the prevention (by high dietary iron intake and
minimisation of infections) and management of IDA.

Prevalence of anaemia and iron deficiency in the NT

There are a number of reports of the prevalence of anaemia in Aboriginal
children in Northern Australia.2–8 Only five NT papers describe the use of
venous blood and laboratory analysis to determine anaemia (Hb<110 g/L)
prevalence.2–5 Two of these studies (in children aged six months–six years in
remote area Top End communities) reported the prevalence of anaemia to be
42–52%.2,5 The other three studies were in hospitalised Top End children aged
six months to three years. These studies reported prevalence rates of 21–
40%.3,4 Other published studies of children aged 0–5 years living in remote
area Aboriginal communities in the Kimberley region of Western Australia
report anaemia prevalence between 20–60%.6,7 The NT growth assessment and
action nutritional survey in October 2000 (unpublished data Epidemiology
Branch, THS) used the HemoCue haemoglobinometer to screen 2590 children
aged 0–4 years. The prevalence of anaemia (Hb <110 g/l) ranged from 20–65%
across different communities. The prevalence in all children aged 0–4 years
was 43% in the Top End and 52% in Central Australia. School-aged screening
haemoglobinometer data were available for the Top End only. A total of 1802
Top End children aged 5–14 years were screened in 1999, with an estimated
anaemia prevalence of 19%. Haemoglobinometer data from the Katherine
district of the NT in 1993 estimated anaemia prevalence of 39%.8
There has been one Top End hospital-based study that determined the
prevalence of IDA. This study analysed blood samples in 161 children aged
five months–10 years admitted to Royal Darwin Hospital (RDH) in 1993. IDA
was diagnosed on the basis of FBE, blood film and iron studies. This study
described 48% (77/161) of children as anaemic (Hb <110 g/L) and 40%
(64/161) had IDA. Of the anaemic children, 83% (64/77) had IDA (Ingrid
Bucens, unpublished data). There are no other published studies of IDA
prevalence in the Top End of the NT and no known Central Australian
studies.

Physiology of iron deficiency and iron deficiency anaemia

Humans are inefficient in absorbing iron from plant sources. Much of the
world’s population has a diet from which sufficient iron cannot be obtained
to meet physiological requirements, especially in infancy, early childhood
and pregnancy when demands are the highest. Iron requirements are mean
daily intakes (RDIs) of: infants (0–6 months) 0.5 mg/day if breastfed, 3
mg/day if formula fed; 7–12 month olds 9 mg/day; young children 6–8 mg/day;
lactating women 12–16 mg/day.9,10
Iron requirements are higher for infants who were premature or growth
restricted at birth, as stores are lower and growth is more rapid. Normal
term infants have stores to maintain iron for about four months. Iron in
non-haem form usually makes up most of the iron for infants. Absorption is
variable and varies with iron stores and other components in the diet. Non-
haem iron absorption is increased by ascorbic acid, meat, fish and poultry,
and decreased by bran, polyphenols, oxylates, phytates, vegetable fibre,
tannins and phosphates.9–13 Ascorbic acid, such as in orange juice, more than
doubles the absorption of non-haem iron.9,11,12 Tea is reported to decrease the
absorption of non-haem iron by up to 75%.9,12 (This means that changing a
child from having tea to juice with the meal could increase absorption
eight times). Haem iron is much better absorbed and less influenced by
other components of the diet. Haem iron itself increases non-haem iron
absorption. Iron in breast milk is about 0.5–1 mg/L and absorption is high
(about 50%). Iron in cow’s milk is also 0.5–1 mg/L but absorption is only
about 10%.11,12
Infection blocks iron usage, affects iron utilisation and can decrease
haemoglobin levels by 5–10 g/L.2,9 However, it usually causes a normochromic
normocytic anaemia and does not cause iron deficiency as such.2, 9 In the
Kruske Top End anaemia study2, children given intramuscular iron had a rise
in haemoglobin to 110 g/L by six weeks, but many children dropped their
haemoglobin levels to below 105 g/L at 12 weeks due to infection in spite
of adequate iron. These infections were frequently trivial viral
infections, as well as more severe bacterial or chronic infections. Of
note, the mean cell volume (MCV) of a red blood cell can take up to three
months (the life span of red cells) to regain a normal volume. Thus, a dual
population of microcytic-hypochromic and normal red cells circulate in
children treated with adequate iron who have recurrent infections.9 This was
also described in the Kruske study.2 (See section on diagnosis of IDA for
further information about MCV and other blood film appearances).

Recommendations
• Dietary iron deficiency and recurrent viral or bacterial infections are
the most significant risk factors for IDA in NT Aboriginal children.
• Key nutritional advice for families with children should be:
– Encourage the intake of meat, fish, chicken and green leafy vegetables
– Reduce tea intake during meals
– Increase orange juice during meals
– Acute, recurrent and chronic infections may be the reason for a slow Hb
response to supplemental iron
– Acute, recurrent and chronic infections must be looked for in children
with anaemia
– Acute, recurrent and chronic infections must be treated early and
appropriately.

Types of anaemia in NT remote area Aboriginal children

IDA is the predominant type of anaemia in remote Aboriginal children.
Recent Top End studies (one community-based, one hospital-based) report 83–
88% of anaemia being due to IDA.2 (Bucens, unpublished data.)
Children are also at risk of folate deficiency anaemia, which is usually
dietary in origin. This may coexist with IDA but may also occur without
iron deficiency. Recent NT studies indicate that folate deficiency is rare
in remote area Aboriginal children. A recent RDH study estimated that 0.6%
(1/161) of remote area Aboriginal children were folate deficient. A Top End
community-based study estimated the prevalence of folate deficiency to be
9.8% (5/51).2 In Central Australia, 5% of children admitted to hospital over
a 20 month period because of gastroenteritis were folate deficient
(personal communication, Jim Thurley). B12 deficiency also appears to be
rare.2 (Bucens, unpublished data.) Other types of anaemia are also rare in
remote area Aboriginal children.2–4 The contribution of Vitamin A and other
micronutrients to anaemia in NT remote area children is currently unknown.

Causes of iron deficiency and iron deficiency anaemia

Iron deficiency can be due to: low iron stores at birth; inadequate iron in
the diet; chronic infection; or losses due to diarrhoea, parasites or cow’s
milk feeding.13,14 In Australian Aboriginal children iron deficiency is felt
to be due to late introduction and insufficient intake of iron-rich solids
in breastfed children, low birth weight and parasite and worm
infestation.2,6,15 There is no published data that examines dietary intake
patterns and the relative contributions of diet to anaemia in NT remote
area Aboriginal children. There is also little evidence about the role of
worms and parasites in the aetiology of anaemia in Top End Aboriginal
children and there are no published intervention trials. The only data
known to the authors are shown in table 1. The only other available
information is the clinical impression that there has been minimal change
in Top End anaemia prevalence in children aged 0–4 years despite widespread
community deworming programs over the last 10 years.
In Study 1 the stool specimens were analysed within two hours, thus the
results are likely to be accurate.16 However, the sample size for this study
is unknown. Study 2 may have underestimated the worm load due to the stool
collection method.17 The prevalence of helminths in Study 3 (D. Brewster
unpublished data) is also likely to be an underestimate, as most NT
children with diarrhoeal disease and worms are likely to have been fully
dewormed prior to admission to hospital as per standard NT protocols for
diarrhoeal disease and poor growth in children.
Hookworm is a well known cause of IDA worldwide.9 Thirty years ago it was
not uncommon for NT Aboriginal infants to present shocked with haemoglobin
levels of 35 g/L due to acute gastrointestinal blood loss due to acute
heavy hookworm infestation.18 Fortunately, this is now extremely rare
(personal communication, A. Walker). In 1995, hookworm infection was
reported by Provic19 to be ‘endemic’ in the Top End of the NT with
Ancylostoma duodenale likely to be the sole species. There have been
widespread Top End community deworming programs using Pyrantel and
albendazole since that study, thus hookworm prevalence is likely to have
decreased since that time. Prevalence of hookworm in the three recent local
studies are shown in table 1. A recent study in an Aboriginal community in
tropical Western Australia found that the highest mean number of parasite
species and the highest prevalence of A. duodenale (93%) was in children
aged 5–14 years.6 Sustained control programs appear to have eradicated
hookworms from Queensland.19
Only heavy infestations of Trichuris trichuria have been reported to
cause iron deficiency.20,21 In contrast, mild Trichuris infestations are well
known to cause significant growth faltering.22 In Jamaican children, iron
deficiency anaemia was associated with heavy Trichuris infections that had
over 10 000 eggs per grams of faeces, but not with less intense
infections.20 In Panama egg loads greater than 5000 eggs per grams of faeces
were associated with anaemia in children, but not lower worm burdens.21
Joint infestations with mild to moderate load of Trichuris and hookworm
were also more likely to cause anaemia than hookworm alone.21
Strongyloidiasis causes malabsorption, diarrhoea and growth faltering.23,24
More severe Strongyloides malabsorption can cause nutritional anaemia.
However, these children should have significant diarrhoea and will not be
asymptomatic.23,24
Giardiasis causes malabsorption, diarrhoea and growth faltering.25,26
Malabsorption with more severe and prolonged giardiasis can cause
nutritional anaemia.25,26 There is no published data on NT Giardia prevalence
or its association with IDA in the NT.
Maternal IDA has also been shown to affect newborn babies. Infants of
IDA mothers have lower iron stores at birth and higher rates of anaemia in
the first months of life.27,28
Table 1: Prevalence of helminth infestations in Top End adults and
children, 1993–98

Study 1 Study 2 Study 3

East Arnhem Pilot screening Aboriginal
island program in a Top children admitted
Aboriginal End Aboriginal to Royal Darwin
community16 community17 Hospital
Year of study 1997 1997 1993–98
Number of stool Unknown 28 5324
specimens
analysed
Age range ‘Whole community, Adults, age not Children aged 0–
including stated 14 years
children’
Hookworm 25% 3.6% 0.8%
Trichuris 88% 25% 3.4%
Strongyloides 15% 3.6% 3.5%

Recommendations
• Dietary iron deficiency and recurrent viral or bacterial infections are
likely to be the most significant risk factors for IDA in NT Aboriginal
children.
• Data is not sufficient to decide on the prevalence of hookworm or
Trichuris in the NT or the contribution of hookworm or Trichuris to
anaemia in the NT.
• A prevalence study which examines the relative contribution of parasites,
worms and diet to IDA in remote area Aboriginal children should be
conducted in the Top End and Central Australia

Consequences of iron deficiency and iron deficiency anaemia

There is a postulated link between IDA and delayed psychomotor development.
Correlational studies have mostly found associations between IDA and poor
cognitive and motor development, and behavioural problems. Two examples of
this type of reports are: 1) mild iron deficiency has been shown to be
associated with low infant developmental scores29; and 2) studies of iron
deficient adolescents show comparably lower test scores for academic
performance, (including vocabulary, reading knowledge, use of reference
material, arithmetic concepts and problem solving) and students are more
disruptive, irritable and restless in the classroom.30
Longitudinal studies show that children with anaemia in infancy continue
to have poorer cognition, school achievement and more behaviour problems in
later childhood.31–33 However, these uncontrolled observational studies do not
allow causal inference from being made, as there is evidence that anaemia
is associated with socioeconomic disadvantages which are independent
factors in poor cognitive development.
A review of therapeutic trials on the effect of iron deficiency on
cognitive development of children was published in 2001.34 In children older
than two years most studies showed clear benefit from iron treatment (four
studies), and benefit was highly likely in the three studies compared, with
two studies where no benefit was shown. Very few RCT trials in children
under two years were identified and there is no good evidence from RCT that
short-term iron treatment benefits development in iron-deficient infants.
In several studies identified, anaemic children failed to catch up to non-
anaemic children with iron treatment. However, longer follow-up and larger
studies are required before firm conclusions can be drawn.
Iron deficiency also leads to reduced cell mediated immunity and
neutrophil activity, but whether this leads to increased risk of infectious
disease is not clear.35,36

Diagnosis of iron deficiency and iron deficiency anaemia

Iron deficiency
The best way to diagnose iron deficiency is with the full blood examination
(FBE) and blood film.13 With early iron deficiency the only feature will be
increased red cell distribution width (RDW), an index of variation in red
cell size (anisocytosis).9,14 With early depletion of iron in the bone marrow
the RDW increases (>14.5% is abnormal).9,12 Increased RDW is more sensitive
than serum iron, transferrin, total iron binding capacity, ferritin,
haemoglobin or red cell size in the diagnosis of iron deficiency.9,13,14 When
red cells become iron deficient the mean cell volume (MCV) reduces
(microcytosis).12 Transferrin receptor levels are an accurate method of
determining iron levels.37 However, this test is not currently available in
the NT. An increase in haemoglobin after a therapeutic trial of
administration of iron is another indicator of iron deficiency. An increase
of 10 g/L is convincing evidence.9,14

Iron deficiency anaemia

The World Health Organisation (WHO) states that anaemia should be diagnosed
at a haemoglobin level of less than 110 g/L.12 This is the most common
convention adopted worldwide.8,9 The third edition of the CARPA STM stated
that anaemia should be diagnosed when the haemoglobin is less than 100 g/L.1
Clinical examination is a poor indicator of IDA. Unless the IDA is
severe there will be no clinical features.9 The best way to diagnose IDA is
also with the FBE and blood film.13 With IDA, as well as anaemia, there will
be microcytosis (low MCV) and increased RDW. There are also other
morphological abnormalities seen on the blood film, such as pencil cells.9,14
With increased levels of iron deficiency there may also be reduced serum
iron, reduced serum ferritin and increased iron binding capacity, and red
cell protoporphyrin.9,14 However, these iron studies are not useful in
children who are subject to chronic infection. False positives and false
negatives are commonly found due to the increased inflammatory load.13
Transferrin receptor levels are likely to be more accurate,37 but are not
available in the NT.

Recommendation
• Anaemia should be defined as Hb <110 g/L
• Only the full blood examination and blood film are needed to diagnose iron
deficiency and IDA
• Iron studies are misleading in the diagnosis of IDA and are best omitted.

The use of the HemoCue haemoglobinometer as a screening and a

diagnostic test
The HemoCue haemoglobinometer as a screening test
A finger prick blood sample tested on various types of haemoglobinometer
has been routine practice in screening for anaemia in the NT for the past
30 years. Currently the HemoCue haemoglobinometer is used. IDA, as tested
on the HemoCue hemoglobinometer, is considered against the WHO criteria for
a screening test below.38
IDA is an important health problem for Aboriginal children in the NT due
to its high prevalence and important sequelae. The natural history of IDA
is also well understood.9,10,14 Iron deficiency is the early precursor stage
where there is depletion of the body’s iron stores prior to the development
of anaemia.9,10,14 Ideally, iron deficiency should be identified and treated
before it develops into anaemia. In reality current practice aims to treat
anaemia at an early stage, i.e. mild anaemia, rather than treating later on
when the anaemia is severe enough to cause symptoms.
The HemoCue haemoglobinometer, which is currently in use in NT health
centres, has been demonstrated to be a reliable and valid method of
screening for anaemia. The HemoCue haemoglobinometer is also simple, quick
and easy and is a more acceptable test than a venous blood sample. There
should be a suitable test, i.e. a test with high sensitivity, specificity
and positive and negative predictive values. Mills and Meadows39 found that
the HemoCue haemoglobinometer used to detect anaemia had a sensitivity of
85% and specificity of 94% after compensation for a fixed positive bias.
Calibration with a single standard specimen (as per operating manual
recommendations) or with four standard specimens did not uncover this bias.
To allow for operating errors of the Coulter Counter and the HemoCue
haemoglobinometer they recommended using at least 30 measurements from a
range of standard specimens. Their adjustment for machine bias was made by
determining the mean difference between HemoCue results and Coulter Counter
results in the laboratory taken from a finger prick blood sample. Other
evaluations of the HemoCue haemoglobinometer found it easy to use with
readings comparable to those of the laboratory Coulter Counter for venous
and capillary blood specimens (correlation coefficients between 0.89 and
0.99).40,41
Recent local data has been obtained from an anaemia iron treatment study
in children aged six to 59 months in a remote area Aboriginal community in
1999.2 Paired (capillary and venous) (n=141) blood samples were taken from
each child and analysed for anaemia (Hb<110g/L). Capillary samples were
measured by the community HemoCue and venous samples were measured by a
laboratory based Coulter Counter model-M. Analysis of these paired data has
demonstrated that the HemoCue had a sensitivity of 91% and a specificity of
88% compared to the venous Coulter measurements when used to detect anaemia
(Sue Kruske, unpublished data). Confidence intervals have not yet been
constructed for these data. Of note, only 24 out of 141 children in this
sample did not have anaemia, thus the confidence intervals for the
specificity test are likely to be wide. Further validation of the HemoCue
haemoglobinometer in remote communities in the NT is recommended with a
larger non-anaemic group.
The positive and negative predictive values (PPV and NPV) of any test
vary with the prevalence of the condition.42 Using our local data, we have
calculated that the positive predictive value of the HemoCue in detecting
anaemia (Hb<110g/L) in NT remote Aboriginal children aged under five (with
50% anaemia prevalence) will be 88% and the negative predictive value will
be 91%. These values indicate that anaemia will be over-diagnosed by 12%
and under-diagnosed by 9% if the HemoCue is used in communities with
anaemia prevalence of 50%. These are quite reasonable values for a
screening test but are only achievable when the HemoCue is used strictly
according to the manufacturer’s instructions. The PPV and NPV drop quite
significantly when the anaemia prevalence reaches less than 20%. Further
validation of the HemoCue is recommended with a larger non-anaemic sample
size.
In the Northern Territory there are adequate facilities to diagnose and
treat anaemia. All rural and remote health centres have a HemoCue
haemoglobinometer and each test costs approximately $1 for the use of the
cuvette (personal communication, DHCS). The haemoglobinometer, HemoCue
cuvettes, iron and albendazole are part of the normal NT health centre
imprest system and budget. Medicare currently funds formal FBE testing
(Medicare rebate for an FBE as of 3/97 is $14.65). Public and private
laboratory services are available to investigate anaemia if considered
necessary. If all Aboriginal children of school age were to have annual
screening for anaemia then approximately 12 000 children would be screened
every year.43 The cost of false positive screening tests for 10%, 20%, 30%
and 40% prevalence of anaemia would be $28,700, $12,892, $8,790, and $5,625
respectively.

The HemoCue haemoglobinometer as a diagnostic test

The CARPA STM third edition recommended that venous blood be taken for FBE
if the Hb is below 80g/L and treatment depends on the FBE result.1 The
alternative would be to use the HemoCue as a diagnostic test, treat on the
HemoCue result and not perform an FBE. There is evidence to support using
the HemoCue for diagnosis of IDA. If we use the local data as described
above, the haemoglobinometer has a very high predictive value where the
prevalence of anaemia is high (as in remote area Aboriginal children in the
NT). Approximately 80–90% of the children with true anaemia will have IDA2
(Ingrid Bucens, unpublished data) thus making the PPV and NPV for IDA high
also. Near-patient testing and diagnosis also has the advantage of allowing
immediate results and explanations to be given to the patient, and
treatment can be started without having to wait for laboratories to confirm
the diagnosis. In rural and remote health centres the time from taking the
blood specimen to the result reaching the health centre can be 2–3 days.
Loss to follow-up is also common.
The haemoglobinometer should not be used to diagnose anaemia in children
at risk of ‘complicated anaemia’ (i.e. children aged under six months,
children with a Hb<90g/dl, children with cardiac failure, tachycardia or
tachypnoea, children with signs or symptoms that indicate non dietary
anaemia e.g. hepatosplemomegaly, and children who have IDA that does not
resolve with treatment). These children should always have an FBE and film
to diagnose anaemia. Iron therapy should always be started immediately and
medical review should also be arranged.

Recommendations
• The HemoCue haemoglobinometer is an acceptable screening tool for
detection of anaemia in remote area Aboriginal children living in
populations where the anaemia prevalence is >20%.
• Further validation of the HemoCue is recommended with a larger non-anaemic
sample size
• The HemoCue haemoglobinometer is an acceptable diagnostic tool for anaemia
in remote area Aboriginal children living in populations where the anaemia
prevalence is >20% who are aged >6 months
• Iron treatment can be instituted on the basis of the result of the HemoCue
haemoglobinometer in children aged >6 months
• A laboratory venous FBE and film should be performed:
 – If the Hb on the HemoCue haemoglobinometer is <90 g/l in children aged
>6 months
– If the Hb on the HemoCue haemoglobinometer is <110 g/L in children aged
under six months
– The Hb appears to be refractory to iron therapy and not increasing when
rechecked in one month
– In children who have any other abnormal features
– In children living in populations where the anaemia prevalence is
<20%.

o The manufacture’s instructions for the HemoCue haemoglobinmeter

should be followed carefully
o A follow-up Hb measurement should be performed one month after
treatment is commenced
o If the Hb has not increased in one month a formal FBE and film
should be performed
o Any questions or concerns about the diagnosis or treatment for
anaemia should be directed to the responsible medical officer

Treatment of iron deficiency anaemia

Principles of managing the individual child with IDA include: treatment of
disease contributing to the iron deficiency; administration of supplemental
iron; replenishment of stores; and provision of maintenance amounts of
iron. There is no place for dietary therapy alone in the treatment of iron
deficiency. Dietary intake is important in the prevention of IDA and to
maintain haemoglobin levels after treatment.
Given the high prevalence of IDA in NT remote area children
consideration must be given to community wide interventions for the
prevention and management of IDA.

Hookworm and Trichuris treatment to treat anaemia in NT remote area

children
Current practice in the Top End of the NT is to treat anaemia with three
days of albendazole. This guideline was developed assuming that the major
helminths implicated in anaemia in the NT were hookworm and Trichuris.
However, this evidence is in doubt (see above). Single dose albendazole is
effective in treating hookworm and reducing anaemia.44–46 Trichuris treatment
requires three days of albendazole for significant reduction in worm load.47–
50

Current practice in the Top End of the NT is to treat growth faltering

with three days of albendazole. This guideline was developed assuming that
the major helminths and parasites that caused growth faltering are
Strongyloides, Giardia, hookworm and Trichuris. This evidence is much more
robust.22–24,26,51
Many remote area NT children have both growth faltering and anaemia.
Management of these children becomes complicated if there is one
antihelminth regimen for growth faltering and a different antihelminth
regimen for anaemia. We consider that there is not adequate evidence to
change current practice and further investigation is needed.
Giardia and Strongyloides treatment to treat anaemia in NT remote area
children
Strongyloides may cause anaemia, but these children will also have
significant diarrhoea.23,24 Empirical treatment for unproven Strongyloides
without diarrhoea or growth faltering is thus not recommended. If
Strongyloides is isolated from faeces then albendazole is recommended daily
for three days.52
[Editor: Ivermectin is the preferred treatment for proven strongyloides
(for people over five years old) in the fourth edition of the CARPA STM.
There is an approximately 20–40% higher cure rate with ivermectin than
albendazole. However, ivermectin is mainly recommended for proven cases of
strongyloides, which is a different clinical situation to presumptive
treatment on the basis of anaemia. Ivermectin is not a good treatment for
the other important helminth infections that are more likely to be the
cause of anaemia. This is discussed in detail in the Worms-Strongyloides
chapter of the Reference Book.]

Giardia can be isolated from asymptomatic persons, thus the detection of

Giardia lamblia in stools is not necessarily pathogenic.27. We do not
recommend its empirical therapy for anaemia.

Iron treatment for anaemia

Effective treatment is available in the NT as oral (Fergon) or
intramuscular iron (Ferrum H).

Oral iron
Formulation. Fergon is made up of ferrous gluconate 60 mg/ml. Nine
milligrams ferrous gluconate is equivalent to 1 mg elemental iron thus
Fergon = 6.6 mg elemental iron per ml.52
Dose. The dose for treatment of iron deficiency is 1 ml/kg/day or 1 ml/kg
twice per week.2,10,52,53 Twice weekly-supervised regimens have been used
successfully in the NT2 and elsewhere.53,54 All regimens require that
treatment should continue for three months to enable stores to be
replenished. 2,10,52–54 During and after treatment adequate iron must be
received in the diet to maintain stores.10 Doses have been calculated for
remote area use based on 1 ml/kg of Fergon which contains 60 mg ferrous
gluconate per ml. These doses are shown in table 2.
Side effects and problems. Problems with oral iron treatment may include:
mild gastrointestinal symptoms; toxicity in overdose; treatment duration of
three months; poor palatability; and frequent vomiting.2,10,14 In practice few
side effects have been reported. Oral iron should be dispensed in small
amounts in child-proof containers to prevent accidental ingestion.

Table 2: Oral iron (Fergon) doses

Weight kg Dose
5–9 5 ml
10–14 10 ml
15–20 15 ml
*Iron tablets (FGF 1 tablet daily) may be easier in older children.

Intramuscular iron
Formulation. Ferrum H is an iron polymaltose complex with 100 mg iron/2 ml.
Imferon is an iron dextran with 100 mg elemental iron/2 ml.52 Only Ferrum H
is used in the NT.
Dose. Several different dosage calculations are quoted.

1. CARPA STM third edition doses are calculated using the formula:
Iron dose (mg) = weight in kg x desired rise in Hb (g/dl) x 3.
The source of this formula is unknown.
2. ‘Standard paediatric dosing’ in many children’s hospital handbooks
(including at RDH) is based on the following formula:
Iron dose (mg) = weight in kg x (15 – existing Hb g/dl) x 3.
The source of this formula is the paediatric haematology textbook edited
by Wintrobe.14 However, when we tried to find the primary source for the
formula from Wintrobe the reference given was wrong. We have contacted the
editors and are awaiting further information. The rationale Wintrobe
provides for the formula is that the total dose is calculated from the
amount of iron needed to restore the haemoglobin deficit plus an
additional amount to replenish the stores.
3. The manufacturer of Ferrum H (Vifor International) states the formula
used for calculation of the iron doses displayed in their product
information is the following:
Iron dose (mg) = weight in kg x (target Hb–current Hb g/l) x 0.24 + (15 x
weight).
The source of this is MIMS52 and a German paper.55 The rationale behind the
formula is that the iron dose = iron deficit = haem iron deficit + iron
reserve deficit. 0.24 is derived from: iron component of haemoglobin =
0.34%, blood volume = 7% body weight and 1000 is conversion factor from g
to mg (i.e. 0.0034 x 0.07 x 1000 = 0.24). Iron reserve deficit is
calculated using the formula 15 mg/kg if weight is up to 34 kg. This is a
conservative estimate derived from the calculation of adult stores of iron
being approximately 1200 mg for men and 800 mg for women.56 The doses
quoted in MIMS are obtained from Formula 3 using 130 g/L as the target Hb.

Formula 3 appears to have the clearest rationale and evidence base.

However, calculated doses are higher than those obtained from using
formulas 1 and 2. We have recommended doses that are a simplification of
the manufacturer’s recommendations. (We have given conservative doses from
the dosing chart in MIMS for each weight and haemoglobin range, and made
recommendations that Hb is checked in four weeks and further iron given if
necessary.) These doses are displayed them in table 3.
The prescribed dose per injection stated in the CARPA STM is 1.5ml given
on alternate days.1
The manufacturer (Vifor International) recommends 0.5 ml for children
weighing 0–5 kg, 1.0 ml for children weighing 5–10 kg and 2.0 ml for
children weighing greater than 10 kg. The manufacturer states that these
are the maximum doses that should be given per injection and per day. We
are currently contacting the manufacturers to ascertain the reasons for
this decision. Limiting the volume per injection is likely to reduce the
incidence of abscess formation and skin staining. However, limiting the
volume administered per day (and not allowing multiple sites for injection
on one day) does not make sense given that doses of 5–10 mls are
administered over a number of hours via the intravenous route in hospital
for children who have severe IDA. Health centre reviews would be reduced if
a larger volume of IM Ferrum H was authorised for administration at each
visit. We have, however, recommended following the manufacturers
guidelines.
Site. Buttock injections are not recommended in children.57–60 This is because
of the concern about the lack of muscle mass, sciatic nerve damage,
neurovascular bundle damage and the high incidence of local reactions.
Deltoid injections are also not recommended in children aged less than 12
months. This is again because of the concern about lack of muscle mass,
neurovascular bundle damage and the high incidence of local reactions. The
anterolateral thigh is the only endorsed site for vaccination in infants
under 12 months. Either the anterolateral thigh or the deltoid region is
acceptable for children aged 13 months and over, although the anterolateral
thigh remains the recommended site.57–60
Side effects. Problems with intramuscular iron therapy include anaphylaxis
and staining of the skin.10,14 Iron dextran (Imferon) has been estimated to
cause acute hypersensitivity reactions in 0.2–3% of patients.10,14,61,62 Iron
polymaltose (Ferrum H) is reported to have lower side effects.10,14 Vifor
International (the manufacturers of Ferrum H) keep an international safety
database. They have had only six cases of anaphylaxis reported in the past
10 years after both intravenous and intramuscular administration. Using
sales of the product they estimate an incidence of anaphylaxis of
<0.00000015% (personal communication, Maxine Orr, Sigma Pharmaceuticals Pty
Ltd). There are numerous recent reports in the literature about the safe
and effective use of parenteral iron.63–65 Wintrobe states quite clearly (1999
edition, p 1001)14 ‘indications for parenteral iron therapy include (a)
unable to tolerate iron compounds when given orally, (b) repeatedly fails
to heed instructions or is incapable of accepting or following them.’ A
recent American paper states similar indications.66
Intramuscular iron therapy has been associated with increased risk of
septicemia67, thus current recommendations are to avoid the use of oral or
intramuscular iron to children with a fever >38°C or signs of any systemic
infection.

Table 3: Intramuscular (ferrum H) iron doses

Weight (kg) Haemoglobin level in g/dL

7–9 9–11
5–7 3 mL 2 mL
8–10 4 mL 3 mL
11–13 6 mL 4 mL
14–16 7 mL 6 mL
17–19 9 mL 7 mL

Recommendations
• The high prevalence of IDA in remote area Aboriginal children mandates a
population-based approach. Consideration should be given to community wide
interventions for the prevention and management of IDA
• If a child in the Top End is found to be anaemic they should continue to
be given three days of daily albendazole. There is insufficient evidence
to change the current practice of deworming for both hookworm and
Trichuris as treatment for anaemia
• A community-based study, which examines the prevalence and load of
Trichuris and hookworm in NT Aboriginal remote area children should be
 performed in Central Australia and the Top End of the NT. If Trichuris egg
loads are found to be >5000 eggs/ml then the rationale for treating
anaemia with three days of albendazole will be established
• Empirical therapy for Strongyloides or Giardia in a child with anaemia is
not recommended
• If a child has growth faltering or significant diarrhoea then empirical
treatment for Strongyloides is recommended (albendazole daily for three
days [Editor: or ivermectin if more than five years old])
• If Strongyloides is isolated with or without anaemia or growth faltering
then albendazole is recommended daily for three days.
• If Giardia is isolated in a child with growth faltering or anaemia then
metronidazole TDS for seven days is recommended
• The following oral or intramuscular iron regimens are safe and effective,
provided compliance is ensured.
Oral: twice weekly supervised oral iron for three months, daily
unsupervised oral iron for three months. Doses as per table 2.
Intramuscular Ferrum H into anterolateral thigh. Total dose as per table
3. Given daily with maximum daily doses 0.5 ml (0–5 kg), 1.0 ml (5–10 kg)
and 2.0 ml (>10 kg) per injection and per day.
• The decision about which iron regimen to choose should be made in
conjunction with the child’s family and after consideration of health
centre resources.
• Oral or intramuscular iron should not be given to children with fever
>38?C or signs of any systemic infection

Acknowledgments
We would like to acknowledge the help of Sue Kruske and Brad Palmer in
preparing this paper.

[Editor: There is limited evidence of folate deficiency, and it is thought

to be uncommon. However, the editorial committee thought that it was
reasonable to give folate to those children with more severe anaemia (Hb<9
g/dL) who are the most likely to be malnourished in a more general sense.
We did not believe it was worth extra visits to the clinic so it should be
combined with the visits programmed for the iron treatment. It is probably
far more important to ensure that the child has an ongoing good diet in
general.
Timing of follow-up and length of treatment with oral iron: usually
three months of oral iron will be needed to restore significant iron
deficiency — this is of course dependent on the severity, how much iron is
provided in the child’s usual diet and how many of the prescribed doses are
missed. There is also some uncertainty in the haemocue result — so some
kids may be less deficient than initially assessed. We considered saying
check after two or three months of oral treatment — but went for one month
so that compliance etc. could be checked at that time. If the result after
one month is over the cut off level, although the child may be still iron
deficient, we suggest ceasing the iron and checking at the usual six month
intervals (and encouraging diet containing iron in all).]

Summary of recommendations
Policy and protocol development
• Anaemia is a major public health problem. The high prevalence of iron
deficiency anaemia (IDA) in remote area Aboriginal children mandates a
 population-based approach. Consideration must be given to population-based
interventions for the prevention (by high dietary iron intake and
minimisation of infections) and management of IDA
• Dietary iron deficiency and recurrent viral or bacterial infections are
the most significant risk factors for IDA in NT Aboriginal children
• Key nutritional advice for families with children should be:
Encourage the intake of meat, fish, chicken and green leafy vegetables
–
– Reduce tea intake during meals
– Increase orange juice during meals

• Acute, recurrent and chronic infections may be the reason for a slow Hb
response to supplemental iron
• Acute, recurrent and chronic infections must be looked for in children
with anaemia
• Acute, recurrent and chronic infections must be treated early and
appropriately
• Only the full blood examination and blood film are needed to diagnose iron
deficiency and IDA
• Iron studies are misleading in the diagnosis of IDA in remote area
Aboriginal children and are best omitted
• The HemoCue haemoglobinometer is an acceptable screening tool for
detection of anaemia in remote area Aboriginal children living in
populations where the anaemia prevalence is >20%
• The HemoCue haemoglobinometer is an acceptable diagnostic tool for anaemia
in remote area Aboriginal children living in populations where the anaemia
prevalence is >20% who are aged over six months
• Iron treatment can be instituted on the basis of the result of the HemoCue
haemoglobinometer in children aged over six months
• A laboratory venous FBE and film must be performed:
– If the Hb on the HemoCue haemoglobinometer is
<90 g/L in children aged over six months
– If the Hb on the HemoCue haemoglobinometer is <110 g/L in children aged
under six months
– The Hb appears to be refractory to iron therapy and not increasing when
rechecked in one month
– In children who have any other abnormal features
– In children living in populations where the anaemia prevalence is <20%.

• The manufacturer’s instructions for the HemoCue haemoglobinometer should

be followed carefully
• A follow-up Hb measurement should be performed one month after treatment
for IDA commences
• If the Hb has not increased in one month a formal FBE and film should be
performed
• Any questions or concerns about diagnosis or treatment for anaemia should
be directed to the responsible medical officer
• Data is not sufficient to decide on the prevalence of hookworm or
Trichuris in the NT or the contribution of hookworm or Trichuris to
anaemia in the NT.
• In the Top End: If a child is found to be anaemic they should continue to
be given three days of daily albendazole.
• Empirical therapy for Strongyloides or Giardia in a child with anaemia is
not recommended
 • If a child has growth faltering or significant diarrhoea then empirical
treatment for Strongyloides is recommended (albendazole daily for three
days)
• If Strongyloides is isolated with or without anaemia or growth faltering
then albendazole is recommended daily for three days.
• If Giardia is isolated in a child with growth faltering or anaemia then
metronidazole TDS for seven days is recommended
• The following oral or intramuscular iron regimens are safe and effective
provided compliance is ensured:
– Supervised oral: twice weekly oral iron for three months, daily
unsupervised oral iron for three months. Doses as per table 2.
– Intramuscular Ferrum H into anterolateral thigh. Total dose as per table
3. Given daily with maximum daily doses 0.5 ml (0–5 kg), 1.0 ml (5–10
kg) and 2.0 ml (>10 kg) per injection and per day.
• The decision about which iron regimen to choose should be made in
conjunction with the child’s family and after consideration of health
centre resources
• Oral or intramuscular iron should not be given to children with fever
>38°C or signs of any systemic infection.

Research
• Data is not sufficient to decide on the prevalence of hookworm or
Trichuris in the NT or the contribution of hookworm or Trichuris to
anaemia in the NT.
• A prevalence study which examines the relative contribution of parasites,
worms and diet to IDA in remote area Aboriginal children should be
conducted in the Top End and Central Australia
• Further validation of the HemoCue is recommended with a larger non-anaemic
sample size
• A community-based study, which examines the prevalence and load of
Trichuris and hookworm in NT Aboriginal remote area children should be
performed in Central Australia and the Top End of the NT. If Trichuris egg
loads are found to be >5000 eggs/ml then the rationale for treating
anaemia with three days of albendazole will be established.

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 Asthma in Children

Author: Dr Anne Chang (formerly ASH respiratory paediatrician)

Topic Reviewers: Dr Andrew White (ASH); Yuendumu Clinic staff; Dr Andrew Bell
(KWHB); Nicola Ross; Andrew Urquhart (RAN, Beswick Clinic); Dr John Hester
(DMO); Dr Steven Skov (DMO); Dr Therea Yee (Oenpelli); Kaz Knudsen (RAN, WA);
Rin Riemersma (RAN, Finke); Leone Radnedge (RAN, Utopia); Vicki Gordon (RAN,
Mutitjulu); Monica Ostigh (RAN, Jabiru); Leila Kennett (RAN, Fregon); Dr Ian
Dumbrell (Port Keats)

Introduction
Asthma was thought to be rare in most rural/remote Indigenous communities1
but more recent data has shown that this is indeed erroneous in some areas.2
Therefore, the management of childhood asthma in the acute and non-acute
settings is relevant for remote and rural health practitioners.
Furthermore, it has also been recently shown that there is considerable
room for improving the management of childhood asthma in a remote
community.3
Asthma is a growing health problem for children and adults world-wide,
with marked regional variation in the prevalence of asthma both between and
within countries.4 Australian children have some of the highest known
prevalence rates of asthma, ranging from 24.6% for the 6–7 year olds and
29.4% for the 13–14 year olds.5 Amongst Aboriginal and Torres Strait
Islander children in rural and remote communities the prevalence of
childhood asthma varies, rates from 0% to 16% have been reported.2
The prevalence of asthma in many remote areas is unknown. In an
Indigenous rural community in Western Australia, Bremner and colleagues
described a high prevalence (24%) of wheeze in female patients under the
age of 18 years.6 Williams and colleagues7 reported that in Western
Australia, where Indigenous status has been collected as part of the
hospital record for several years, the admission rate for asthma was higher
for Indigenous than non-Indigenous children (rate ratios for Indigenous
versus non-Indigenous children ranged from 1.4 to 5.3).
While recognising that hospitalisation data are not a good proxy for
prevalence, the Western Australian data suggest that serious asthma
requiring hospitalisation is more common among Indigenous children. This is
consistent with overseas studies that found the prevalence of asthma to be
higher in economically disadvantaged groups.8 However, on the contrary, data
from the Northern Territory suggests higher annual hospitalisation rates
per 1000 population for non-Indigenous children with a principal diagnosis
of asthma: between 2.6 and 4.7 for Indigenous children and non-Indigenous
as being 5.5.9 Remoteness of the Indigenous children in this latter study
may have lead to bias with an under- estimate with respect to
hospitalisation of Indigenous children. Its results are also limited by the
retrospective nature of the study and the gross calculation of rates. In
addition, the belief that asthma in Indigenous children is non-existent1,
and infectious disease is the dominant illness, may have lead to an
underestimation of asthma diagnosis10 as a comorbidity.
 In the Torres region (far north Queensland) asthma was the commonest
childhood respiratory illness seen by a specialist paediatric respiratory
service.11
Asthma management guidelines with an evidence based approach are widely
available nationally and internationally.12,13 This section will cover the
salient points of asthma in paediatrics with particular reference to remote
Indigenous communities. An education flipchart specifically for Indigenous
people is available from the NT Asthma Foundation and asthma pamphlets for
Indigenous communities have been developed by the NSW Asthma Group.

Literature review and discussion

What is wheeze and asthma?
There are many causes of wheeze in children, and not all that wheezes —
even in the older child — is asthma. Several phenotypes of childhood asthma
and wheeze have been recognised14 and an asthma-like illness is sometimes
present with an underlying respiratory disease like bronchiectasis and
bronchiolitis obliterans.15 The definition of asthma is varied depending on
the purposes for which it was being sought.16
The general definition for asthma is applicable only to the children
over six years. This definition incorporates the concept of asthma as
primarily a disease of airway inflammation in which eosinophils and mast
cells are prominent, producing recurrent episodes of wheeze associated with
increased bronchial hyper-responsiveness and reversible airway limitation.16
In a large longitudinal study, Martinez and colleagues have shown that
almost two-thirds of children who wheeze before age three do not have
asthma, and called this group ‘transient early wheezers’.17 The diagnosis of
asthma is indeed not always straightforward.13 For the practitioner, the
symptoms of clinical asthma are recurrent episodes of wheeze associated
with shortness of breath and chest tightness relieved by beta-2 agonists.
Cough may or may not be significantly present in children with asthma, and
cough alone (cough without any other features of asthma) is a poor marker
of asthma in children.18

Asthma and chronic lung disease

Asthma-like illness can coexist in a variety of chronic respiratory illness
such as bronchiectasis, bronchiolitis obliterans, ciliary dyskinesia,
cystic fibrosis and chronic neonatal lung disease.15 The first two
conditions are not uncommon in remote Indigenous children.
The estimated prevalence of bronchiectasis in Central Australia is 2.7
per 1000 children (unpublished) and in another as yet unpublished follow-up
study of Indigenous children hospitalised for pneumonia, the prevalence of
asthma-like illness after 12 months follow-up was 6.6%. Recognition of
asthma in conjunction with these illnesses is important, as asthma-like
illness is a known predictor of early mortality in children with
bronchiectasis.19 Under-treatment of reactive airways disease (RAD) can lead
to later significant morbidity and contribute to the prevalence and
morbidity of adult chronic airway obstructive disease.20
A recent study in south-west England has described that the cumulative
incidence of asthma 68 months after admission with childhood pneumonia was
45%.10 This study raises the possibility that children presenting with
pneumonia-like illness may have unrecognised asthma.
Isolated cough in children: is it asthma?
Many aspects of paediatric medicine and treatment differ significantly from
adult medicine, and paediatricians world-wide repeatedly warn against the
extrapolation of adult data to children.21,22 The symptom of isolated cough is
no different and adult data is not applicable in children.23,24 In children
isolated cough (non-productive cough without any other symptoms and signs)
is uncommonly asthma.18

Paediatric versus adult asthma

While adult asthmatics share some common features with childhood asthma,
there are also significant differences25, These include differences in the
importance of airway hyper-responsiveness26, induction of disease, natural
history and prognosis27, appropriate device usage, pathophysiology25,
associations with wheeze14, co-morbidities and psychosocial issues.25 There is
a need for children with asthma to be managed differently from adults with
asthma and for practitioners to appreciate this difference.
Also, in paediatrics, parental reporting is heavily relied on. This is
particularly important in paediatrics where careful history taking to
differentiate the nature of respiratory sounds is paramount to accurate
clinical diagnosis. For respiratory noises, although the repeatability of
wheeze has been shown to be highly reliable28, parental perception of wheeze
may be significantly different to that of clinicians, especially in
communities where English is not the first language.29,30

Asthma and socio-economic determinants

There is overwhelming evidence that poverty is a contributor to asthma
exacerbations and severity.31,32 Different research groups argue that cultural
differences (cultural barriers to self-care), communication difficulties
(different ethnic groups use different words to describe symptoms) and
doctor–patient interactions can partially explain why asthma affects
different minority groups differently.31,33 Rona pointed out in his recent
review that, to date, there is lack of consistent evidence that some
aspects of poverty cause asthma.32

Management of asthma in children

Acute management of paediatric asthma
International and national guidelines are widely available. 12,13,34,35 The
suggested management in the STM has been adapted locally. In remote
communities current standard recommendations for spacer use may be limited
by availability of appropriate spacers, personnel preference and experience
of personnel. Where possible, the use of a beta-2 agonist with spacer in
mild-to-moderate asthma is advocated and has been shown to be as equally
efficacious as nebulisers in acute asthma.13 Indeed, it maybe more suitable
in remote communities where the jet nebulisers maybe old, or the nebuliser
bulb aged, both limiting intra-thoracic aerosol deposition.
The respirable particle size influences intra-thoracic aerosol
deposition and is dependent on flow generated by the nebuliser, the volume
of solution in the nebuliser and nebuliser bulb type.36 Ideally the jet
nebuliser should be driven by a 6–8 L/min flow, have >3 ml of nebulising
fluid and an efficient nebuliser utilised (such as Sidestream or Pari
nebulisers).
 Spacers, like nebulisers, should be maintained correctly. Spacers should
be cleaned regularly (at least weekly for individual use and in between
patients). To increase efficiency of drug delivery, spacers should be
washed in warm soapy water and left to dry, without wiping the inside of
the spacers.13

Non-acute management of asthma

Goals of management of childhood asthma
This has been extensively reviewed by the National Asthma Campaign37 and the
evidence is available on-line.37 The six steps with local adaptation are:
• Step 1: Assess asthma severity. Assess overall severity when the
patient is stable, not during an acute attack: (a) infrequent episodic
asthma, (b) frequent episodic asthma, (c) persistent asthma (see
below).
• Step 2: Achieve best lung function. Treat with intensive asthma therapy
until ‘best’ lung function is achieved and back titrate to the lowest
dose that maintains good symptom control and best lung function. Note:
lung function testing cannot be reliably performed in children under
six years and assessment of ‘best lung function’ in young children is
dependent on history. Children with frequent and persistent asthma will
require anti-inflammatory therapy (cromolyns or steroids).
• Step 3: Maintain best lung function. Identify and avoid trigger
factors, this includes inappropriate medications.
• Step 4: Maintain best lung function. Optimise medication program: treat
with least number of medications and minimum doses necessary; ensure
patient understands the difference between ‘preventer’, ‘reliever’ and
‘symptom controller’ medications; take active steps to reduce the risk
of adverse effects from medication.
• Step 5: Develop an Action Plan (see p 85). In situations where self-
management is possible, discuss and write an individualised plan for
the management of exacerbations.
• Step 6: Educate and review regularly. Ensure carers (and children where
possible) understand the disease, rationale for their treatment and —
where possible — how to implement their asthma action plan; and
emphasise the need for regular review even when asthma is well
controlled.

Classification of asthma in children

In paediatrics, asthma severity is classified on clinical findings and
spirometry13,27

Asthma medications and devices

Asthma medications
Broadly divided into:
• ‘Relievers’: most blue in colour (salbutamol, terbutaline, fenoterol,
ipratropium)
• ‘Preventers’: most are earth colours or autumn colours (beclomethasone,
budesonide, fluticasone, nedocromil, sodium cromoglycate)
• ‘Symptom controllers’: most green in colour (salmeterol, eformoterol,
theophylline).

Devices and choices

A variety of devices are available and choice is dependent on:13,16,38,39
 • Age (see below)
• Personal preference (older child may prefer selecting their device e.g.
accuhaler versus turbuhaler)
• Disease severity (those with severe asthma may not be able to generate
sufficient inspiratory flow for adequate intra-thoracic deposition)
• Side effects experienced (dry powder devices may cause recurrent sore
throats in some)
• Availability in community
• Locality (humidity and possibility of device falling into water may
limit use of turbuhaler)
• Acuteness of problem
Spacers must be used correctly

Devices
• Pressured Metered dose inhalers (pMDI)
– with large or small volume spacer
– breath-activated devices
• Dry powder devices (Turbuhaler, Accuhaler, aeroliser)
• Oral medications (theophylline, leukotriene modifiers; should only be
used after consultation with specialist)
• Nebulisers
 Infrequent Frequent Persistent
episodic episodic
Frequency of More than 6 <6 weeks apart Attacks <6 weeks
episodes weeks apart apart
Interval symptoms Symptoms rare Increasing • Daytime
• Early morning between between symptoms symptoms >2
symptoms attacks attacks days/week
• Nocturnal • Nocturnal
symptoms symptoms >1
night/week
Attack type usually not Attacks more Multiple
severe troublesome hospital
admissions
Examination Normal Normal May be abnormal
between episodes
Lung function Normal Normal May be abnormal
between episodes
Treatment: Beta 2 As needed only As needed As needed
agonists
Anti- No Yes: Start with Yes: Usually
inflammatories cromones require inhaled
(Preventers) corticosteroids
Symptom No Maybe Usually
controllers

Route of <2 Years 2–6 Years 6–8 Years 8 Years and

administration older
pMDI, small Yes Yes
volume spacer
+ mask
pMDI and large Yes Yes
volume spacer
Turbuhaler* Possible Yes
Accuhaler* Possible Yes
pMDI (alone) Yes
but preferably
with spacer
Autohaler Possible
(little role
in children)
Aerolizer* Possible Yes
Nebuliser in Yes Yes Yes Yes
acute asthma
 Asthma action plan
The objective of having an asthma action plan is for empowerment of people
with asthma. In Indigenous communities the use of this may be limited and
the ability of the family/carer to utilise it should be evaluated before
assumptions of self-management are made. Explaining the plan to the carers
and asking the carer to self-record the plan in a way that is understood by
them may be more appropriate than the readily available prescriptive Asthma
Action Plans (available from pharmaceutical industries, state and national
asthma organisations). The paediatric component has been endorsed by the
Australian Paediatric Respiratory Group and, unlike the adult version, does
not include the use of peak flows.12 Briefly, the plan involves recognition
of an asthma deterioration, noted by the different colours — green (when
well), yellow (asthma getting worse), orange/red (asthma is
severe/emergency) — and steps that the child and carer/parent should take
under each circumstance. The evidence of this approach has been outlined in
the National Asthma Campaign’s on-line publication.37

[Editor: We believe that there are additional reasons to encourage the use
of asthma action plans in the CARPA STM. Some of these are logical
extensions of the rationale for having the STM itself. These include
helping to ensure early treatment for acute asthma, consistent treatment in
the face of high staff turnover, standardised treatment leads the patients
to encouraging the clinic staff to follow the protocols (reinforcement).
Dexamethasone versus hydrocortisone: Either can be used for severe
asthma, dexamethasone has a longer half-life (once a day vs four times a
day), and in IM doses is a smaller volume. We do not know of any direct
comparison RCTs.]

References
1. Bauman A. Lastest statistical trend. A decade of coordinated asthma management in
Australia. National Asthma Campaign 1998; 7–8.
2. Valery PC, Chang AB, Shibasaki S, Gibson O, Shannon C, Masters IB. High prevalence of
asthma in five remote Indigenous communities in Australia. Eur Respir J 2001;
17:1089–96.
3. Chang AB, Shannon C, O’Neil MC, Tiemann AM, Valery PC, Craig D, Fa’afoi E, Masters
IB. Asthma management in Indigenous children of a remote community using an
Indigenous health model. J Paediatr Child Health 2000; 36:249–51.
4. Sterk PJ, Buist SA, Woolcock AJ, et al. The message from the World Asthma Meeting.
The Working Groups of the World Asthma Meeting, held in Barcelona, Spain, December 9–
13, 1998. Eur Respir J 1999; 14:1435–53.
5. Robertson CF, Dalton MF, Peat JK, Haby MM, Bauman A, Kennedy JD, Landau LI. Asthma
and other atopic diseases in Australian children. Australian arm of the International
Study of Asthma and Allergy in Childhood. Med J Aust 1998; 168:434–8.
6. Bremner PR, de Klerk NH, Ryan GF et al. Respiratory symptoms and lung function in
aborigines from tropical Western Australia. Am J Respir Crit Care Med 1998; 158:1724–
9.
7. Williams P, Gracey M, Smith P. Hospitalization of Aboriginal and non-Aboriginal
patients for respiratory tract diseases in Western Australia, 1988–1993. Int J
Epidemiol 1997; 26:797–805.
8. Mielck A, Reitmeir P, Wjst M. Severity of childhood asthma by socioeconomic status.
Int J Epidemiol 1996; 25:388–93.
9. Whybourne A, Lesnikowski C, Ruben A, Walker A. Low rates of hospitalization for
asthma among Aboriginal children compared to non-Aboriginal children of the top end
of the northern territory. J Paediatr Child Health 1999; 35:438–41.
10. Clark CE, Coote JM, Silver DA, Halpin DM. Asthma after childhood pneumonia: six
year follow up study. BMJ 2000 Jun 3; 320(7248):1514–16. 2000; 320:1514–6.
11. Swingler GH, Hussey GD, Zwarenstein M. Randomised controlled trial of clinical
outcome after chest radiograph in ambulatory acute lower–respiratory infection in
children. Lancet 1998; 351:404–8.
12. Asthma Management Handbook. National Asthma Campaign. 1998.
13. Royal Children’s Hospital Asthma Best Practice Guidelines. Melbourne: Royal
Children’s Hospital, 1999.
14. Silverman M, Wilson N. Wheezing phenotypes in childhood [editorial; comment].
Thorax 1997; 52:936–7.
15. Zhang L, Irion K, Kozakewich H, Reid L, Camargo JJ, da Silva PN, Silva FA.
Clinical course of postinfectious bronchiolitis obliterans. Pediatr Pulmonol 2000;
29:341–50.
16. Warner JO, Naspitz CK, Cropp GJA. Third International Pediatric Consensus
Statement on the Management of Childhood Asthma. Pediatr Pulmonol 1998; 25:1–17.
17. Martinez FD. Definition of pediatric asthma and associated risk factors. Pediatr
Pulmonol Suppl 1997; 15:9–12.
18. Chang AB, Asher MI. A review of cough in children. J Asthma 2001; 38:299–309.
19. Field CE. Bronchiectasis: a long term follow-up of medical and surgical cases
from childhood. Arch Dis Child 1961; 36:587.
20. Ulrik CS, Backer V, Dirksen A. A 10-year follow up of 180 adults with bronchial
asthma: factors important for the decline in lung function. Thorax 1992; 47:14–
8.
21. Smyth RL. Research with children. BMJ 2001; 322:1377–8.
22. Sinaiko AR, Daniels SR. The use of short-acting nefedipine in children with
hypertension: Another example of the need for comphrehensive drug tesing in
children. J Paediatr 2001; 139:7–9.
23. McKenzie S. Cough — but is it asthma? Arch Dis Child 1994; 70:1–2.
24. Chang AB. State of the Art: Cough, cough receptors, and asthma in children.
Pediatr Pulmonol 1999; 28:59–70.
25. Busse W, Banks-Schlegel SP, Larsen GL. Childhood- versus adult-onset asthma. Am
J Respir Crit Care Med 1995; 151:1635–9.
26. Wilson N, Silverman M. Bronchial responsiveness and its measurement. In:
Silverman M, editor. Childhood asthma and other wheezing disorders. London:
Chapman & Hall, 1995; 142–74.
27. Phelan PD, Olinsky A, Oswald H. Asthma: classification, clinical patterns and
natural history. Baillieres Clin Paediatr 1995; 3:307–18.
28. Luyt DK, Burton PR, Simpson H. Epidemiological study of wheeze, doctor diagnosed
asthma, and cough in preschool children in Leicestershire. BMJ 1993; 306:1386–
90.
29. Cane RS, Ranganathan SC, McKenzie SA. What do parents of wheezy children
understand by ‘wheeze’? Arch Dis Child 2000; 82:327–32.
30. Cane RS, McKenzie SA. Parents’ interpretations of children’s respiratory
symptoms on video. Arch Dis Child 2001; 84:31–4.
31. Partridge MR. In what way may race, ethicity or culture influence asthma
outcomes? Thorax 2000; 55:175–6.
32. Rona RJ. Asthma and poverty. Thorax 2000; 55:239–44.
33. Hardie GE, Janson S, Gold WM, Carrieri-Kohlman V, Boushey HA. Ethnic
differences: word descriptors used by African-American and white asthma patients
during induced bronchoconstriction. Chest 2000; 117:935–43.
34. Robinson TD, Celermajer DS, Bye PTP. How to stop ACE-inhibitor-induced cough.
Lancet 1997; 350:3–4.
35. Verberne AA. Managing symptoms and exacerbations in pediatric asthma. Pediatr
Pulmonol Suppl 1997; 15:46–50.
36. Hess D, Fisher D, Williams P, Pooler S, Kacmarek RM. Medication nebulizer
performance. Chest 1996; 110:498–505.
37. Coughlan J, Wilson A, Gibson PG. Evidence-based Review of the Australian Six
Step Asthma Management Plan. NSW Health 2000; http://www.nationalasthma.org.au.
38. Gillies J. Overview of delivery system issues in pediatric asthma. Pediatr
Pulmonol Suppl 1997;15:55–8.
39. O’Callaghan C. Delivery systems: the science. Pediatr Pulmonol Suppl 1997;
15:51–4.
 Babies Under 3 Months Old
Who Are Sick

Author: Dr Anne Jacquari (ASH paediatrician)

Topic Reviewer: Dr Ian Dumbrell (Port Keats)

Clinical assessment of young babies is difficult and often causes anxiety

in health professionals. There may be non-recognition of ‘warning signs’,
and history is obviously observer dependent. Patterns of behaviour are
still emerging in the young infant and it may be difficult for a parent to
decide if non-specific symptoms, such as irritability or fussy feeding, are
outside the realm of normal.
Illness in this age group is often due to infection but congenital
abnormalities of heart, gut, kidneys, and inborn errors of metabolism may
also manifest in this period, with presenting signs and symptoms very
similar to those of sepsis. Conversely, the septic child may present
without fever or be hypothermic. Although empiric management must be aimed
at common, treatable conditions, such as bacterial infection, it is
important to consider other diagnoses.

Assessment of the young sick baby

It has been formally recognised for many decades that the manifestation of
serious illness — including bacterial infection — in young babies is non-
specific, and that clinical assessment alone even by experienced clinicians
may not have high sensitivity or specificity.1,2 Several baby illness
checklists and infant observation scales have been developed over the years
to try to provide a framework of markers of serious illness in febrile and
afebrile infants, with relative weighting of the most relevant findings via
a scoring system.1,3,4
The Yale Observation Scale (Appendix 1) is dependent on observer grading
of the quality of cry, reaction to parent stimulation, state variation (see
description in the Yale observation scale in appendix 1), colour, hydration
and response to social overtures. However, validation of this approach in
very young babies has not always been successful. One such study using the
Yale Observation Scale in febrile babies aged 29–56 days found that — of
the infants who had positive bacterial cultures of blood, urine, stool or
spinal fluid — 67% had observation scores indicative of a well-appearing
child.2 The Young Infant Observation Scale includes items from both history
and examination, such as feeding, respiratory status, CNS/arousal, GI/fluid
status and skin (colour, perfusion, rash) (Appendix 2).4 The most useful
items from this checklist in distinguishing an infective outcome are listed
as being affect, respiratory status and peripheral perfusion.
Clinical assessment of young babies should include a thorough history
and full examination, including objective measures of temperature, heart
and respiratory rates and oximetry where possible. However, literature and
experience suggest one can only be partially reassured when a young febrile
baby appears well clinically, as bacterial infection may still be present.2
The threshold for further observation and investigation must therefore be
low in the <3 month age group.

Infection in the young infant

In the first few months of life, infection may be congenital or acquired in
the neonatal or post-neonatal period. This has implications for the CARPA
region where there are high rates of STI and maternal infection, and where
antenatal information may not always be available. Late onset Group B
streptococcal disease and neonatal herpes infection may both occur several
days to several weeks after birth.5 Studies in the Top End looking at
postnatal colonisation with pneumococcus in particular show a marked left
shift (younger) in the curve for Aboriginal babies, with presumed increased
susceptibility to developing early bacterial infection.6,7 Babies in this age
group are also incompletely immunized, as the first dose of HIB,
pneumococcal vaccine and DTPa are given at the age of two months.
The young infant has poor immune system ability to localise infections,
and finding one focus does not preclude infection in other sites e.g.
coexistence of pneumonia or urinary tract infection with meningitis.8
Although a baby with bacterial infection may initially appear well,
progression of disease may be very rapid, hence the low threshold for early
empiric antibiotic treatment in situations where full investigation must be
postponed. Choice of antibiotic should take into account both gram-positive
and gram-negative organisms, and should be given parenterally.5,9 A third
generation cephalosporin — such as cefotaxime or ceftrixone — will usually
cover the most likely bacterial organisms in the CARPA region setting in
the first instance (local data, microbiology, Alice Springs Hospital). Late
onset neonatal infection with Listeria monocytogenes, though rarely found
in Alice Springs over the last several years, can cause meningitis. Hence
benzylpenicillin or ampicillin is added as a second agent in the <3 month
age group.
Viral infections, though less specifically treatable than bacterial
infections, may also be life-threatening in young babies. Often, morbidity
is secondary to respiratory infection, but overwhelming viraemia may also
occur. Even if a viral aetiology is suspected, empiric antibiotics should
be given to a sick infant in a setting where access to laboratory and
radiology services is not immediately available. Other management is
supportive with particular attention to respiratory management if these
symptoms predominate.
Whether viral or bacterial, gastrointestinal infections may be rapidly
dehydrating in infants and should always be taken seriously, especially if
both vomiting and diarrhoea are present. Compensatory mechanisms, such as
colonic reabsorption of fluid, are poor in the first several months of
life.10 Electrolyte and acid-base disturbance are common in Aboriginal
babies with moderate gastroenteritis, and hypokalaemia in particular may be
life-threatening. The blood glucose level should also be checked in the
small baby who has been unable to feed because of vomiting or poor
responsiveness. GI upset may be a manifestation of sepsis or viraemia
rather than a specific GI focus of infection. Gram-negative sepsis may
exist concurrently with gastroenteritis, and if a baby is very sick,
empiric antibiotic cover is indicated.
 Non-infective causes of serious illness in young infants
Although less common, other causes of illness should be considered in this
age group as congenital conditions may manifest in the first several weeks
of life. Cardiac failure may be difficult to differentiate clinically from
respiratory disease or sepsis. Relatively minor infection may have
devastating sequelae in children with certain inherited inborn errors of
metabolism. Gut obstruction at any level may present with vomiting, bilious
or otherwise, without diarrhoea, and an incarcerated inguinal hernia needs
urgent surgical attention. Undiagnosed renal abnormalities often present
with urinary tract infection, but may have associated electrolyte
abnormalities. Envenomation, e.g. from red-back spider bite, may present
with a constellation of signs that is difficult to interpret, and history
may not be forthcoming unless a witness was present.
Although initial management will almost always include cover for sepsis,
other urgent treatment — especially in surgical cases — may be lifesaving,
so thorough assessment is important.

References
1. Bonadio WA. The history and physical assessments of the febrile infant. Pediatric
Clinics of North America February 1998; 45(1).
2. Baker et al. Failure of infant observation scales in detecting serious illness in
febrile, 4 to 8 week old infants. Pediatrics June 1990; 85(6).
3. McCarthy et al. Observation scales to identify serious illness in febrile children.
Pediatrics November 1982; 70(5).
4. Bonadio et al. Reliability of observation variables in distinguishing infectious
outcome of febrile young infants. Pediatr Infect Dis J 1993; 12.
5. Mandell et al. Principles and Practice of Infectious Diseases. 4th Edition. 1995.
6. Leach et al. Bacterial colonization of the nasopharynx predicts very early onset and
persistence of otitis media in Australian Aborigines. Paediatr Inf Dis J 1994;
13:983–9.
7. Torzillo P & Grattan M. Conjugate pneumococcal vaccines for Aboriginal Children in
Australia. MJA October 2000; 173(2).
8. Davies EG. Manual of Childhood Infections. British Paediatric Association, 1996.
9. Paediatric Decision Making. 3rd Edition. Berman, 1996.
10. Decker Butzner, J. Colonic function of the infant: effects of development,
malnutrition and injury. Presentation. Karachi: Commonwealth Congress on Diarrhoea
and Malnutrition, 1997.
APPENDIX 1
Yale observation scale

Observation Normal (1) Moderate Severe impairment

variable impairment

Quality of cry Strong, normal Whimpering or Weak or moaning

tone or content, sobbing or high- pitched
not crying

Reaction to Cries briefly Cries on and off Continual cry or

parent then stops or hardly responds
stimulation content, not
crying

State variation If awake, stays Eyes close Fails to sleep or

awake or if briefly when cannot be aroused
asleep and awake or awakes
stimulated wakes with prolonged
up quickly stimulation

Colour Pink Pale extremities Pale or cyanotic

or acrocyanosis or mottled or
ashen

Hydration Skin normal, eyes Skin, eyes normal Skin doughy or

normal and mucous and mouth tented and dry
membranes moist slightly dry mucus membranes
or sunken eyes

Response (talk, Smiles or becomes Brief smile or No smile,

smile) to social alert becomes alert anxious, dull,
overtures briefly expressionless or
cannot be alerted

Total score ranges from 6 to 30

APPENDIX 2
Young infant observation scale

Observation variables

1. Level of activity:
Spontaneously active, vigorous (1)
Diminished spontaneous activity (3)
No spontaneous activity, or active only with painful stimulation
2. Level of alertness:
Fully awake, or asleep but awakens quickly, alerts fully (1)
Lethargic, arouses with difficulty, alerts briefly (3)
Won’t alert or arouse (5)
3. Respiratory status, effort:
No impairment, vigorous (1)
Mild – moderate respiratory compromise (tachypnoea, retractions or grunting) (3)
Respiratory distress with inadequate effort (apnoea, respiratory failure) (5)
4. Muscle tone:
Strong (1)
Diminished (3)
Weak, limp (5)
5. Peripheral perfusion:
Pink, warm extremeties (1)
Mottled, cool extremeties (3)
Pale, shock (5)
6. Affect:
Smiles and/or not irritable (1)
Irritable, consolable (3)
Irritable, won’t console (5)
7. Feeding pattern (offer infant a feed):
Strong suck, eager to feed (1)
Feeds briefly, weak suck (3)
 Diarrhoeal Disease

Author: Prof David Brewster

Topic Reviewers: Andrew White (paediatrician, ASH); Janet Fletcher (RAN,

Ngukurr Clinic); Kenna Bistani (RAN, Pine Creek); Bernard Egan (RAN, Bulman
Clinic); Helen Collinson (RAN, Adelaide River); Rin Riemersma (RAN, Finke); Mt
Leibig Clinic staff; Leone Radnedge (RAN, Utopia); Deb Beaver (RAN, Bagot
Clinic); Monica Ostigh (RAN, Jabiru); Vicki Gordon (RAN, Mutitjulu Clinic); Dr
Ian Dumbrell (Port Keats)

Summary
1. Use oral rehydration solution (ORS) for mild to moderate dehydration
(sugar or rice-based).
2. Use rapid IV rehydration over four hours with Ringer’s lactate
(Hartmann’s solution) for moderate-severe dehydration.
3. Start re-feeding early with appropriate feeds (avoid prolonged
fasting).
4. Severe dehydration, acidosis and hypokalaemia are complications of
gut damage, leading to lactose intolerance in Aboriginal children.
5. Oral tilactase may help (Lact-easy 10 drops with each feed) for
breastfed infants with positive stool reducing substances, or if you
suspect lactose intolerance.
[Ed: This recommendation was not supported by the editorial committee
due to limited evidence of effectiveness in community settings and an
expectation that it would be impractical.]
6. Avoid inappropriate use of antibiotics, anti-diarrhoeal medications
and nasogastric tubes.
7. Zinc and vitamin A supplements are recommended for persistent
diarrhoea and malnutrition.

Prevalence
Between 1991 and 1995, NT Indigenous infants (aged under one year of age)
had an infant mortality rate of 22.5 per 1000 live births, which is over
three times the average of the NT non-Indigenous population.1 The overall
annual hospitalisation rate for Aboriginal children in the Top End is
extremely high, at about 1.4 admissions per child under two years. With
regard to diarrhoeal disease alone, Aboriginal children have a much higher
rate of hospitalisation than non-Aboriginal children. Between 1993 and
1997, the annual diarrhoeal admissions rate for Top End Aboriginal infants
was 334 per 1000 compared to 20 per 1000 for non-Aboriginal infants, a 16-
fold higher rate. For children one to four years old, the equivalent rates
were 119 per 1000 for Aboriginal children and 10 per 1000 for non-
Aboriginal children, or about a 12-fold higher admission rate.2 These
admission rates in Aboriginal children may have been falling over the last
decade (e.g. for children 0–2 years of age, the rate fell from 4063 per 18
034 population in 1986–88 to 2301 per 13 957 in 1997–98), although this
apparent decrease may be due to changes and errors in coding (Alan Ruben,
pers. comm.). There has been no decrease in health centre visits for
diarrhoea over that time.3 In addition to the high diarrhoeal admissions
rates Aboriginal children also have a longer length of stay for diarrhoeal
disease, which averages about nine days compared to three days in non-
Aboriginal children.
Aboriginal children hospitalised for diarrhoea also have high rates of
co-morbidities, including lower respiratory infections (e.g. pneumonia,
bronchiolitis) (24%) skin diseases (scabies, pyoderma) (27%), chronic
suppurative otitis media (25%), urinary tract infections (15%), and
bacteraemia (5%).4,5 This is a reflection of the generally higher burden of
disease in Aboriginal children, including very high rates of bacterial
colonisation of the upper respiratory and GI tracts.
Aboriginal children hospitalised with diarrhoea have rates of severe
complication which are much higher than non-Aboriginal children, and
include moderate to severe dehydration (affecting 67% of RDH admissions),
acidosis (61%) and hypokalaemia (65%).5 These complications are due to
severe intestinal mucosal damage as reflected in high intestinal
permeability ratios, with the loss of brush border lactase exacerbating
osmotic diarrhoea when there is a high lactose diet, such as in breast
milk. Lactose malabsorption was documented in 42% and lactose intolerance
(positive stool reducing substances) in 30% of diarrhoeal cases in
hospitalised children who are breastfed.5
A randomised trial in Darwin showed that a low osmolality lactose-free
milk formula (De-Lact) resulted in less diarrhoea and more weight gain than
O-Lac or Alfaré formulas.6 There is only anecdotal evidence that oral
tilactase (Lact-Easy drops) with each breast feed reduces the severity of
lactose intolerance in breastfed children with acute gastroenteritis. The
main problem with its effectiveness is the short time of exposure of the
enzyme to breast milk lactose when given to infants after breastfeeding.
Ideally, breast milk should be expressed, the drops added, wait 30 minutes
for the lactose to be hydrolysed and then fed to the infant.
The most frequently isolated enteric pathogens in Aboriginal children
hospitalised with diarrhoea in Darwin are enteroaggregative E. coli
(EAggEC) (29%), rotavirus (27%), enteropathogenic E. coli (EPEC) (17%),
Salmonella species (11%), Cryptosporidium (7%) and Strongyloides (7%). Note
that the prevalence of intestinal worms, such as hookworm and dwarf
tapeworm (H. nana), was very low, and they do not cause diarrhoea. Whipworm
(Trichuris) was found in about 3% of children and did not cause either
diarrhoea or bowel damage. We documented giardiasis in only 6.8% of
controls and 3% of diarrhoeal cases, which may be an underestimate due to
the lack of sensitivity of stool microscopy, but giardiasis did not make a
major contribution to either severe disease or abnormal permeability in our
diarrhoeal subjects.7 It may be contributing to the tropical enteropathy in
healthy Aboriginal children but is not a major cause of poor growth.8–10
The importance of intestinal parasites (e.g. hookworm, whipworm) on
Aboriginal child health is often exaggerated, and published studies11–15 are
not representative of the current situation in view of the widespread use
of albendazole in many communities. However, Strongyloides is still an
important cause of acute diarrhoea5,16, but other intestinal parasites have
little public health importance.
Stool microbiology is often requested in Aboriginal children with
diarrhoea. However, its usefulness is often questioned, because it seems
not to affect clinical decision-making and E. coli probes are not available
routinely. The addition of diagnostic tests for diarrheagenic E. coli to
standard stool microbiological testing increased the rate of specific
diagnosis from 53% to 75% in Aboriginal children at Royal Darwin Hospital.
52% (66/127) of Aboriginal diarrhoeal admissions had a pathogenic E. coli
species isolated, although multiple pathogens were isolated from 34% of
children and no organism from 25%.7
The Infectious Diseases Guidelines of America recommend selective
testing of stool microbiology in children hospitalised with moderate to
severe diarrhoea (length of stay >3 days) for both individual patient care
and public health purposes, particularly for E. coli 0157 due to its role
in haemolytic uraemic syndrome.17 In view of these findings, we would argue
that E. coli probes on stool should be a funded routine investigation in
hospitalised Aboriginal children in northern and Central Australia. After
all, if E. coli species were associated with over half of diarrhoea in
southern Australia, it would now be a routine investigation like rotavirus.
Out of the common enteric pathogens, rotavirus causes transient but
severe intestinal mucosal damage associated with acidosis and lactose
intolerance. Cryptosporidium causes severe and prolonged mucosal damage
whereas Strongyloides is more likely to occur in malnourished children, but
both Cryptosporidium and Strongyloides cause hypokalaemia, which is
associated with high levels of nitric oxide production, indicative of gut
inflammation.16 The organisms associated with the most severe intestinal
mucosal damage on admission are Cryptosporidium, EAggEC and rotavirus, but
only Cryptosporidium causes continuing mucosal damage after clinical
recovery.5
Healthy Aboriginal children without diarrhoea have higher permeability
ratios than non-Aboriginal children, indicating the presence of tropical-
environmental enteropathy syndrome.4,5 Overseas studies have shown that this
is related to overcrowded living conditions and poor hygiene, with
bacterial contamination of food and water.18 It has been found in poor
developing country settings to contribute to almost half of the failure to
thrive from malabsorption, particularly of carbohydrates.19,20 Poor
environmental conditions have also been documented in tropical Australian
Aboriginal communities.21 Failure to thrive, faltering growth, stunting and
nutritional microcephaly are common problems in Aboriginal community
children.22,23 Improving hygiene and living conditions would be likely to
reduce the transmission of enteric pathogens and improve the underlying
mucosal damage. This would reduce the severity of diarrhoeal disease in
communities so that it could be managed with oral rehydration without the
need for referral to hospital. It would also reduce the nutritional
consequences of carbohydrate malabsorption.

Diagnosis
As a symptom, diarrhoea is a more reliable indicator of acute
gastroenteritis than most other symptoms in children, such as cough, fever,
shortness of breath or wheeze for respiratory illnesses (pneumonia,
asthma). The diagnosis of acute gastroenteritis is even more specific if
the stools are watery and green with >3/day and the illness lasts for at
least 2–3 days. However, diarrhoea may be a non-specific symptom of other
non-enteric infections, such as urinary tract infections in infancy and
upper respiratory tract infections. Severe vomiting — which is bile-stained
or projectile — and severe abdominal pain are unusual in acute
gastroenteritis, so need to have surgical conditions considered, especially
in infancy (e.g. intestinal obstruction, pyloric stenosis,
intussusception).24
Dysentery is defined as the presence of blood and mucus in diarrhoeal
stools. Compared to most developing country settings, dysentery is much
less common among Aboriginal community children, since it accounts for <5%
of diarrhoeal cases in Darwin. The most likely cause of dysentery is
Shigella which can cause outbreaks of severe bloody diarrhoea. Haemolytic-
uraemic syndrome (HUS) is caused by a shiga-like toxin produced by
enterohaemorrhagic E. coli (EHEC). This results in a haemolytic anaemia
(typical blood film appearance) and acute renal failure. It causes severe
disease but is fortunately rare, although outbreaks can occur. Antibiotic
treatment of diarrhoeal disease may cause harm, since it makes HUS more
likely with EHEC and prolongs the duration of carriage of Salmonella.17

Assessment of dehydration
The risk factors for dehydration are: 1) young age due to the increased
surface area to body volume ratio, resulting in increased insensible fluid
loss; 2) a milk diet, due to the risk of osmotic diarrhoea and the large
protein load, which causes a high renal solute load; and 3) bottle feeding
rather than breastfeeding.25 Clinical assessment of dehydration has low
sensitivity, and signs only become present with moderate to severe
dehydration (?5%). A Melbourne study found that poor capillary return was
the most reliable clinical sign of dehydration.26 An American study found
that the four signs which were the best predictors of dehydration were: a
capillary refill time >2 seconds; absent tears; dry mucous membranes; and
ill general appearance.27 Capillary refill time is a useful sign of
dehydration but can be affected by fever, ambient temperature (air
conditioning) and age.28 Other studies have found laboratory tests generally
insensitive in assessing hydration, but bicarbonate, urea, creatinine and
uric acid have been the most helpful results.29,30
The percentage weight loss is a relatively objective measure of
dehydration. It does require accurate measurement on the same scale with
the child undressed. The initial weight is subtracted from rehydration
weight and taken as a percentage of the rehydration weight. For example, a
rehydrated child weighing 10 kg who was 9 kg on admission would be 10%
dehydrated. The two weights should be taken at the same time of day, but
not more than 24 hours apart to exclude changes from loss of subcutaneous
tissues due to the catabolic state.
Studies in Darwin have found a relatively low level of agreement between
clinical assessment of dehydration and percentage weight loss (kappa
agreement 0.30 and Pearson correlation 0.56). Clinical dehydration
correlated better with a low bicarbonate and reflected how sick the child
appeared. The percentage weight loss tended to underestimate the degree of
dehydration because of ongoing losses from osmotic diarrhoea. It could
potentially overestimate the degree of dehydration if the child were given
excessive IV fluids and developed puffy eyes. Note that the degree of
clinical dehydration may be underestimated in obese children and
overestimated when children are wasted or septic. Urinary output and
specific gravity are helpful to confirm that a child has been adequately
rehydrated and is passing frequent urine of low specific gravity.
[Editor: At the time of presenting to a clinic with diarrhoea, many
children will have a recent routine weight recorded in their notes. As long
as this is a weight from a time when they were well, and is recent (a week
or so), then it can be used to estimate dehydration. This has been retained
in the fourth edition protocol.]

Management
Rehydration
Oral rehydration with an appropriate solution is a highly effective means
of rehydration, which uses the principle of glucose-facilitated sodium
transport.24,31 A NSW study found that oral rehydration was under-utilised in
Australian children with diarrhoea.32 Oral rehydration is time consuming for
caregivers, particularly with vomiting. Vomiting usually resolves and can
be managed with small, frequent amounts of oral rehydration solution (e.g.
5 mL every two minutes)24, but this requires a compliant and motivated
mother.
The optimal concentration of an oral rehydration solution is
approximately 60 mmols/L of sodium, 20 mmol/L of potassium, 110 mmol/L
(2.5%) of glucose and an osmolality of about 220.33,34 Soft drinks, juices and
similar solutions tend to be too hypertonic and low in electrolytes.
Cereal-based oral rehydration solutions (e.g. rice) have not been shown to
have a definite benefit in non-cholera diarrhoea compared to glucose-based
oral rehydration solution34, but there is anecdotal evidence that it may be
more palatable. However, the most likely reason for a child refusing to
drink oral rehydration solution because of the taste is because he/she is
not actually dehydrated. Dehydrated children will not refuse to drink oral
rehydration solution because of taste.
An important advance in rehydration has been the change to rapid
rehydration over four hours, except for rare causes of severe
hypernatraemia. This was introduced as best practice by WHO in the 1980s,
but has only been adopted by developed countries in the last few years.24,31
Rapid intravenous rehydration with Ringer’s lactate (Hartmann’s solution)
is now best practice for moderate to severe dehydration, or when oral
rehydration is inappropriate or fails. The only contra-indications to a
trial of oral rehydration therapy are shock, coma, ileus and severe
hypokalaemia. Rapid rehydration aims to correct the child’s deficit over
four hours. Thus, a 10 kg child who is 10% dehydrated would receive one
litre of Ringer’s lactate over four hours. Although no studies have
specifically compared rapid rehydration to slower rehydration, a number of
studies have found rapid rehydration to be successful.35 There is no
evidence of a benefit from the addition of bicarbonate to rehydration
solutions36–38, however this has never been tested in Aboriginal children.
This is of interest because they tend to have extremely high rates of
acidosis with acute gastroenteritis (raising the possibility of a role for
bicarbonate). Note that oral rehydration contains 10 mmol/L of citrate as
base and Ringer’s lactate contains 40 mmol/L of lactate as base. No study
has compared Ringer’s lactate to 0.9% normal saline for rehydration, but
most recommendations in paediatrics prefer Ringer’s lactate for
rehydration, although the Advanced Paediatric Life Support and ICU
guidelines favour normal saline.39 Note that alkalosis (e.g. pyloric
stenosis) is a relative contraindication to the use of Ringer’s lactate.
There is a continuing controversy about the use of colloid (e.g.
albumin) versus crystalloid (e.g. Ringer’s lactate) solutions for volume
replacement in critically ill patients. A systematic review40,41 did not
support the use of colloids for volume replacement and this issue is now
the subject of an Australian multicentre trial in adults. Colloids have
never been standard treatment for rehydration so are best avoided in
diarrhoea.

Early feeding
The duration of diarrhoea can be reduced by 0.43 (0.12–0.74) days by early
feeding of children with acute gastroenteritis, which also has added
nutritional benefits.42 The best foods to be introduced in the treatment of
acute gastroenteritis are complex carbohydrates (e.g. rice, wheat, bread,
and cereals) yoghurt, fruit and vegetables. Fatty foods or high sugar foods
— such as tea, juices or soft drinks — should be avoided.31

Anti-diarrhoeals
The current evidence does not support the use of anti-diarrhoeal drugs,
such as Loperamide, opiates, anti-cholinergic agents or bismuth
subsalicylate. None of the guidelines recommends their use. The only
generally accepted diarrhoeal indication for the use of antibiotics is
dysentery, particularly the acute phase of Shigella infection or a
Salmonella enteric infection with fever in the very young infant. Co-
trimoxazole would be the oral drug of choice since there are concerns about
resistance to amoxycillin, and norfloxacin is not approved for use in
children.
There is specific and effective treatment for giardiasis with tinadazole
or metronidazole, which is worth treating in cases of persistent diarrhoea.
Only half of cases will be picked up on stool microscopy, so treatment
without a stool result is acceptable in persistent diarrhoea (>10 days).
Albendazole for three days is only a moderately effective treatment for
Strongyloides, and needs to be repeated a week later. Follow-up with repeat
stool examination is important in these children in view of the dangers of
chronic strongyloidiasis (e.g. with steroid treatment). Albendazole is also
effective for Trichuris and hookworm, although they are not causes of acute
diarrhoea. Other than the above, there is no evidence of a benefit for
treating watery diarrhoea with antibiotics, indeed, there is a distinct
disadvantage in that it prolongs the carrier state for Salmonella and could
induce haemolytic uraemic syndrome in a child carrying an
enterohaemorrhagic E. coli.

Zinc and vitamin A

Zinc treatment reduces the duration and severity of acute and persistent
diarrhoea.43 Daily low dose zinc supplements also have an important
preventive action against diarrhoea.44 There is good evidence of a benefit
of vitamin A in reducing mortality in measles45, but the evidence in
diarrhoeal disease is still conflicting, although it probably reduces
episodes of persistent diarrhoea.46 Large doses of vitamin A (e.g. 200 000
IU/3-monthly) and prolonged high dose zinc (10 mg/kg for three weeks) are
potentially dangerous. There are interactions between micronutrients — such
as zinc, iron and vitamin A — which are still unclear47,48, but local dietary
and infectious circumstances may change the effectiveness of micronutrient
therapy in different settings.
A recent study of combined zinc and vitamin A synergistically reduced
the prevalence of persistent diarrhoea and dysentery.49 Although zinc was
associated with a significant increase in acute lower respiratory
infection, this adverse effect was reduced by the interaction between zinc
and vitamin A. There are many studies under way examining this question so
we need to await better evidence. In terms of folic acid for the treatment
 of diarrhoea, an unpublished study by Jim Thurley at Alice Springs Hospital
found some benefit for folic acid in diarrhoea, but two randomised
controlled trials have found no benefit compared to placebo.46,50

[Editor: At the moment ‘Liquid Zinc’ is the only suitable formulation

available but it has the problems of needing large volumes (15 ml) for
small children, and poor taste. We hope to find a better alternative
formulation in the future. This may need to be prepared by regional
pharmacies. RDH pharmacy grinds up 50 mg tablets into a suspension, though
the shelf life is only seven days in the refrigerator.]

New treatments
There are some interesting novel therapies for diarrhoea under
investigation. Racecadotril is an inhibitor of enkephalins (endogenous
opioid peptides) that causes decreased intestinal hypersecretion. A
Peruvian study showed a decreased duration and severity of diarrhoea in
children in the Racecadotril-treated group.51 Gum arabic is a soluble
polysaccharide fibre with proabsorptive properties which affects intestinal
nitrous oxide (NO) and potassium channels, and may improve sodium
absorption in diarrhoea.52,53 Nitazoxanide is a new broad-spectrum
antimicrobial agent which has been shown to be effective against
giardiasis, amoebic dysentery and cryptosporidiosis.54,55 Rifaximin is a non-
absorbable antibiotic which is effective in the treatment of small bowel
bacterial overgrowth.56 Finally, probiotics — such as Lactobacillus GG
(healthy germs) — have been shown to shorten the course of diarrhoeal
disease, particularly in rotavirus infection.57 This is currently the
subject of a trial at Royal Darwin Hospital, since the benefits in
Aboriginal children who are breastfed with bacterial diarrhoea are
uncertain.

[Editor: The recommendation to change formula-fed babies with persisting

diarrhoea to a lactose-free formula is based on the high prevalence of
lactose intolerance seen in hospitalised babies with gastroenteritis. An
alternative option would have been to recommend testing all formula-fed
babies with persisting diarrhoea for reducing substances as evidence of
lactose intolerance. We felt this was probably difficult to do in remote
practice, and most such babies should be tried on a de-lact formula anyhow.
Testing urine M/C/S for possible UTI in children with persisting
diarrhoea has been dropped from the fourth edition protocol. The rate of
proven UTI with acute diarrhoea or FTT is 15–20% in hospital. The most
practical and reliable test is a fresh bag urine for nitrites (dipstick).
Sending a bag urine for culture is likely to be a waste of time, with a
very high false positive rate.
The recommendation to collect a daily stool specimen for three days for
M/C/S has been dropped because it is usually difficult to get stool
specimens from Aboriginal patients, and because the additional yield from
two more specimens is limited. Stool cultures miss over 35% of pathogens
anyway by not checking E. coli probes. The treatment protocol includes
treating for Giardia anyhow.]

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intestinalis and Entamoeba histolytica or E. dispar: a randomized, double-blind,
placebo-controlled study of nitazoxanide. J Infect Dis 184:381–4 (2001).
56. Corazza GR, et al. Non-absorbable antibiotics and small bowel bacterial overgrowth.
Ital J Gastroenterol 24:4–9 (1992).
57. Guandalini S, et al. Lactobacillus GG administered in oral rehydration solution to
children with acute diarrhea: a multicenter European trial. J Pediatr Gastroenterol
Nutr 30:54–60 (2000).
 Ear Disease in Children

Author: Dr Paul Torzillo

Topic Reviewers: Kathy Bethune (Audiologist, CAAC); Dr Allan (ENT Surgeon ASH);
Juanita Sheerwood; Peter Morris (MSHR Darwin); Dr Penny Roberts-Thomson
(Nguiu); Kenna Bistini (RAN, Pine Creek Clinic); Vicki Gordon (RAN, Mutitjulu,
Santa Teresa clinics); Dr Ian Dumbrell (Port Keats); Vivian Hammond (RAN,
Amata); Murray Sneesby (RAN, Mimili)

The CARPA STM treatment protocols for ear disease are heavily based on a
recent systematic review of existing evidence on the management of otitis
media and a subsequent document on Recommendations for Clinical Care
Guidelines on the Management of Otitis Media.1,2 The second of these
documents provides a brief summary of evidence on all issues covered in the
treatment protocols and should be utilised as the primary resource document
for health care workers in the field. The documents are available from the
Office for Aboriginal and Torres Strait Islander Health, Commonwealth
Department of Health and Ageing. A further useful document is the General
Guidelines for Audiological Practice with Indigenous Australians prepared
by a special interest group of the Audiological Society of Australia.3

Definitions
The CARPA STM utilises the definitions used in the Recommendations for
Clinical Care Guidelines.2 These are:
Otitis media: Refers to all forms of inflammation and infection of the
middle ear.
Otitis media with effusion (OME): Presence of fluid behind the eardrum
without any symptoms or signs of acute otitis media.
Acute otitis media (AOM): Presence of fluid behind the eardrum (plus at
least one of the following: bulging eardrum, recent discharge of pus, and
ear pain) are the most reliable indicators of AOM.
Recurrent acute otitis media: The occurrence of three or more episodes of
acute otitis media in a six-month period.
Acute otitis media with perforation (AOM with perforation): Discharge of
pus through a perforation (hole) in the eardrum within the last six weeks.
Chronic suppurative otitis media (CSOM): Persistent discharge of pus
through a perforation in the eardrum for at least six weeks despite
appropriate treatment for AOM with perforation.
Dry perforation: Presence of a perforation in the eardrum without any
signs of discharge or fluid behind the eardrum.
Otitis externa (also known as ‘tropical ear’ or ‘swimmer’s ear’):
Infection of the ear canal associated with pain, swelling and discharge.
This is not a form of otitis media.

Natural history
In remote communities it is clear that the onset of ear disease generally
occurs in the first few weeks to few months of life. By 12 months of age
the vast majority of these children have ear disease of one form or
another. Persistent or recurrent disease is common.

Diagnosis
The age category with the highest prevalence of ear disease is very young
children. Examining the ears in very young children is difficult and often
requires considerable expertise. In addition, the diagnosis of middle ear
disease with an intact ear drum is dependent on both quite expert otoscopy
as well as appropriate hearing tests. All these factors mean that accessing
specialist services is an important part of a primary care approach to ear
disease in rural and remote communities. In particular, this means an
audiologist, but also means finding ways for the population you service to
access a specialist ENT consultative service.

Encouraging facial hygiene

There are no specific intervention studies that demonstrate that hygiene
practices improve rates of ear disease or lead to improvement in existing
ear disease. The technique of ‘blowing, breathing and coughing’ is used in
a number of remote schools. It has not been established to impact on ear
disease but this, together with frequent face and hand washing, clearly has
implications for a range of infectious diseases in children and so it is
quite reasonable to support these activities, even in the absence of a
clear evidence based impact on ear disease.

Cleaning the external ear canal

Both tissue wicks and syringing are used to clean ears. There are no
definitive data to say which is the preferred technique. The tissue wick
technique takes time and may need several wicks or ‘spears’ before the
canal is clean. The ear canal should be visualised to ensure the canal has
been cleaned. Syringing should be done gently with warm water. There are no
studies that compare water, saline or dilute Betadine solutions. There is
no evidence that Betadine is harmful, and some experts prefer its use to
any other solution for syringing. Therefore, it is quite reasonable for
staff to use dilute Betadine if available.

Limits to the effectiveness of medical treatment

Although the protocols do outline a treatment approach for most ear
conditions the evidence for some of these is not particularly strong, and
even where it does exist the ‘effect size’ is not large. A good example of
this is the evidence for ear toilet and topical antibiotic drops in the
treatment of chronic suppurative otitis media. Although the recommendations
are based on the result of a meta analysis of trials, essentially these
recommendations depend heavily on one single trial performed in Kenyan
school children. In this study the treatment resulted in about 50% of
children with an ear which was dry (i.e. no longer discharging) as well as
about 15% of children in whom the perforation had healed. However, even
these limited benefits occurred only after 16 weeks of therapy. Therapy for
one or two weeks resulted in a much smaller number of dry ears. Obviously,
in most service settings it would be impossible to deliver therapy
continuously for 16 weeks and so the likely impact of these protocols will
be less than it was in the study setting.5
There is some evidence that quinolone topical eardrops will be more
effective than other antibiotics in the treatment of ear disease, but a
definitive position on this issue awaits trials that are currently
underway. There is however good evidence that intravenous or intramuscular
Ceftazidime given twice daily is effective in the treatment of chronic
suppurative otitis media. In the studies performed this has required
hospitalisation for a period of 2–3 weeks. Obviously, this will be an
option that is extraordinarily difficult for most remote area Aboriginal
children, but it does need to be remembered as a possible therapy in
particular children.
[Editor: A recently published multicentre RCT compared the effectiveness
of topical ciprofloxacin (0.3%; CIP) with the usual framycetin (0.5%),
gramicidin, dexamethasone (FGD) eardrops (5 drops twice daily for nine
days) as treatments for chronic suppurative otitis media (CSOM) in
Aboriginal children. Both groups also received povidone-iodine (0.5%) ear
cleaning. Of those 75% followed up (n=111), the ciproflaxicin group had
significantly higher rates of dry ear at 10–21 days (absolute difference
24.6%) but no change in perforation size or hearing was shown.
At this stage ciprofloxacin is not licensed for suppurative otitis media
but this may change.
(Couzos S, Lea T, Mueller R, Murray R, Culbong M. Effectiveness of
ototopical antibiotics for chronic suppurative otitis media in Aboriginal
children: a community-based multicentre, double-blind randomised controlled
trial. MJA 2003; 179(4):185–190)]

Hearing and audiological interventions

A child with bilateral OME will usually have a hearing loss of around 25
decibels, but it may be more than 40 decibels (a hearing loss of 25
decibels means that normal talking will be very soft. This may disadvantage
the child in speech, language development and learning).2
CSOM causes the greatest level of conductive hearing loss in high-risk
populations. It is usually associated with a hearing loss of around 35
decibels, but may progress to erode the whole eardrum and cause hearing
loss of around 60 decibels.2 People communicating with a hearing-impaired
person should be advised to speak slowly (and clearly) after gaining their
attention in well-lit conditions. Seating at the front of the class,
increased use of visual prompts and interventions that reduce background
noise are appropriate (e.g. carpets, quiet heating and air-conditioning
systems). Hearing aids are strongly recommended for children with
persistent bilateral hearing loss greater than 35 decibels. Ongoing
audiological and educational support is essential.2

Removing hard wax

Olive oil has been recommended by many sources, including the Australian
medicines handbook. A study comparing the in-vitro effect of olive oil,
sodium bicarbonate solution (as in the protocol) and Cerumol found that
olive oil had no effect on a lump of hard ear wax, Cerumol had dispersed
half the wax at 30 hours and the sodium bicarbonate solution had dispersed
the wax in one hour.7 Given that it is about 1000 times cheaper than the
commercial product, it is recommended. A dropper bottle with a quarter
teaspoon sodium bicarbonate in 10 ml water will be sufficient for many
treatments.
[Editor: Discussion of the use of amoxycillin twice a day rather than
three times a day for middle ear infection is included in the chapter on
antibiotic doses.
The author, Paul Torzillo, was the chair of the technical advisory group
for the development of the National Guidelines prepared by the Menzies
 School of Health Research ear team. Consequently, they have had a lot of
direct and indirect expert review. The ‘big issue’ was that optimal care
involves a huge amount of referral and specialist care and assessment,
which is not available. The protocols in the fourth edition of the CARPA
STM are a compromise to make it more ‘doable.’
There was some discussion during the revision of the ear protocols as to
the importance of cleaning out ears blocked with wax or pus. It makes sense
that an open ear canal will improve hearing, and this is likely to be a
very good thing to encourage in all children with runny ears. However,
Torzillo and Boswell looked at the change in hearing in 22 children before
and after cleaning out the canal and found no difference. This is contrary
to the everyday experience of the audiologist at CAAC clinic in Alice
Springs (Kathy Bethune, pers. comm.) where she sees significant
improvements in hearing thresholds after cleaning. The difference may be
the extent to which the middle ear structures have been destroyed by
chronic infection. If there are no middle ear structures then an open ear
canal may make less difference. Further, the pus itself is probably
ototoxic and erodes the middle ear structures.
It is unlikely that clinic staff will have the capacity to clean these
children’s ears daily or more often. Families should be encouraged to do it
whenever possible, and in some instances schools may be involved.]

References
1. Systemic review of existing evidence and primary care guidelines on the management of
otitis media in Aboriginal and Torres Strait Islander populations. National
Aboriginal Community Controlled Health Organisation 2001. Canberra: Office for
Aboriginal and Torres Strait Islander Health, Commonwealth Department of Health and
Aged Care.
2. Recommendations for clinical care guidelines on the management of Otitis Media in
Aboriginal and Torres Strait Islander populations. 2001. Canberra: Office for
Aboriginal and Torres Strait Islander Health, Commonwealth Department of Health and
Aged Care.
3. General guidelines for audiological practice with Indigenous Australians. June 2001.
Richmond, Victoria: Audiological Society of Australia.
4. Boswell JB, Niehuys TG. Patterns of persistent otitis media in the first year of life
in Aboriginal and non-Aboriginal infants. Ann Otol Rhinol Laryngol 1996; 105:893–900.
5. Smith A, Hatcher J, McKenzie I, Thompson S, et al. Randomised controlled trial of
treatment of chronic suppurative otitis media in Kenyan school children. Lancet 1996;
348:1128—33.
6. Nelson JD. Chronic suppurative otitis media. Pediatr Infect Dis J 1988; 7(6):446–8.
7. Kamien M. Which cerumenolytic? Aust Family Physician 1999; 28(8):817.
Growth and Malnutrition (Failure
to Thrive)

Authors: Prof David Brewster (RDH); Dr Andrew White (Central Australian

paediatrician)

Topic Reviewers: Heather Greive (GAA CASN); Dr Andrew White; Katie Roids (RAN,
Barunga), Dr Ian Dumbrell (Port Keats)

[Editor: The following chapter is divided into three parts. ‘Part 1:

Malnutrition in Aboriginal children’ and ‘Part 2: Growth monitoring for
action’ are authored by Dr David Brewster. ‘Part 3: Measurement of head
circumference: Discussion’ is authored by Dr Andrew White.]

Summary
1. Growth failure is the principal manifestation of malnutrition in
children.
2. Normal growth variations and errors in charting must be recognised and
not labelled as malnutrition.
3. Anthropometric assessment can differentiate wasting and stunting.
4. A detailed history, physical exam and assessment for psychosocial
deprivation are important.
5. The most common dietary problem in Aboriginal children is insufficient
weaning foods.
6. In the primary care setting, major organic disease is uncommon (<5%) and
can usually be suspected on clinical assessment.
7. Routine hospitalisation with an expensive laboratory work-up to exclude
rare causes is considered inappropriate medical practice in the absence
of other manifestations of illness.
8. Dietary improvement with home visits can improve growth in some
community children.
9. Micronutrient supplements (zinc and vitamin A) have improved growth in
children living in poor circumstances.

Part 1: Malnutrition in Aboriginal children

Key features
Malnutrition principally affects young children during the weaning period
(4–24 months), i.e. those who are not yet able to feed themselves. The
great majority of malnourished children in any community suffer from mild
or moderate energy deficiency, and will not be recognised as undernourished
by the casual observer because the only clinical manifestation will be
growth retardation. Stunting will not be recognised unless the child’s
growth is charted and compared with normal standards. These children look
like healthy children of a younger age, so mothers are usually not
concerned about the child’s health.
Parental ignorance of the importance of adequate feeding in the weaning
period, in maintaining health, and lack of knowledge of hygiene are
important contributing factors. Malnutrition and infection are synergistic
in the hospital context, so a child who is malnourished is more prone to
infections. These further impair his nutritional state by depressing his
appetite and increasing the demand on his reserves of protein and energy.
In the community context, promoting catch-up growth after diarrhoeal
disease will break the cycle of malnutrition-infection.
Many Aboriginal community children have ‘tropical enteropathy syndrome’
due to intestinal mucosal damage from living in a contaminated environment
with poor hygiene circumstances. Consequently, they may not demonstrate the
expected catch-up growth between episodes of diarrhoea unless a special
effort is made to increase their intake of weaning foods during
convalescence.
The important deficiencies are usually energy, protein and iron.
Specific deficiencies may complicate the clinical picture, though these are
not often clinically florid (e.g. vitamin A, zinc, folate). If malnutrition
is present from early infancy, particularly if it follows intrauterine
growth retardation, it may permanently affect brain growth and mental
function, leading to individuals who do not reach their potential.
Prolonged periods of iron deficiency and poor head growth (microcephaly)
make this more likely.

Prevalence
It is well recognised that Aboriginal children in the Northern Territory
have a higher burden of disease, with higher admission rates and longer
lengths of hospital stay than other children in the Territory. Ruben and
Walker estimated a minimum prevalence of malnutrition of 20% (weight/height
or height/age >2 standard deviations below the NCHS standard) in children
0–2 years of age living in the Darwin rural region, with microcephaly very
commonly accompanying malnutrition.1,2 According to WHO/FAO criteria for
developing countries a community nutritional intervention is warranted when
the prevalence of acute malnutrition in children under five years is >10%,
or 5–9% with aggravating factors.3

Tropical enteropathy
The GI tract is extremely susceptible to effects of malnutrition, enteric
infections and bacterial contamination.4 Abnormal permeability ratios due to
tropical enteropathy have functional significance in that they explained a
major part (40%) of the growth faltering in Gambian children.5,6 Thus,
mucosal damage measured by permeability ratios is clearly an important
contributor to ill health in children on borderline diets in contaminated
environments.7 In children in developing countries permeability testing has
been used to assess the impact of various nutritional, infectious,
environmental and dietary factors on gut integrity. For example, studies in
Malawi, Central Africa, showed the superiority of a milk-based diet over
local cereals in rehabilitating children with kwashiorkor8,9, and that tube-
feeding resulted in more rapid weight gain than oral feeds.10 Studies on
Aboriginal children at Royal Darwin Hospital have shown that the severe
complications of diarrhoeal disease (acidosis, hypokalaemia, lactose
intolerance) are associated with high permeability ratios and high nitric
oxide excretion from gut damage.
Although breastfeeding rates are high and continue into the second year
of life, there is insufficient intake of complementary foods in the first
2–3 years of life. Once children lose weight with diarrhoeal disease or
other infections it is difficult for them to regain it on the usual weaning
diet of low energy density, particularly in view of the underlying
enteropathy. Frequent or recurrent infections increase energy needs and
cause anorexia, making catch-up growth even more difficult. This is
compounded by high rates of bacterial colonisation and small bowel
bacterial overgrowth, as well as environmental enteropathy with
disaccharide intolerance. The vicious cycle of malnutrition-infection
increases the severity of infections and the need for hospitalisation.
Recent evidence indicates that malnutrition in utero and early childhood
may increase the risk of heart and kidney diseases.11,12

Health and nutrition promotion

Child nutrition faces a number of problems before its key health
promotional messages can reach a receptive audience. The first is that
malnutrition is largely silent and does not present in obvious ways like
diarrhoea, pneumonia, or renal failure. The only obvious manifestations may
be growth retardation — particularly stunting and microcephaly, which do
not make the child ill — and so the mother may not recognise its importance
in increasing morbidity. However, there is some evidence that stunting,
microcephaly, iron deficiency and borderline zinc and vitamin A status
during the vulnerable brain growth spurt (0–2 years) have serious
detrimental consequences for immune, intestinal and cognitive functions,13–20
although the evidence is interpreted differently by different reviewers.21,22
Just as anti-smoking campaigns that preached cancer risks had little
impact, we believe that isolated nutrition educational approaches will not
reach a receptive audience in communities until the potential benefits are
demonstrated to carers and communities. This has been the experience of
nutritional rehabilitation programs and other health programs, i.e. that
promotional activities need to be integrated with nutritional interventions
and are ineffective in isolation.23 In addition communities must also
recognise malnutrition as a problem and then be assisted and supported to
address the issue, including appropriate development of community education
resources (which can take a variety of forms). The community also needs to
build capacity to address these issues by appropriate training, increasing
knowledge and skills in this area and the availability of appropriate food
sources.
The ‘Improving Growth Promotion in the NT’ project is using a community
development approach in child growth promotion, funded by the CRC for
Aboriginal and Tropical Health. Preliminary findings suggest that there are
important differences in perceptions between health providers and parents
of the causes of poor child growth, including the role of illness and
caring, appropriate weaning times, and ways of knowing whether a child is
growing well. For example, health service providers generally focus on
reducing the prevalence of illness and improving nutrition, whereas
Aboriginal community members see caring for children as being central to
improving child growth. This project argues that the process of supporting
community members through a community development process, although time-
consuming, is likely to lead to the implementation of appropriate community
growth promotion strategies. Whether this can be demonstrated by convincing
outcomes remains to be seen.
There is little good evidence about sustainability of programs in
Aboriginal communities. The Minjilang study24 does indicate the importance
of community participation. The NT Department of Health and Community
Services (DHCS, formerly Territory Health Services) are committed to
growth, assessment and action (GAA) and the Strong Women, Strong Babies,
Strong Culture programs. The latter was alleged to have positive health
outcomes in relation to low birth weight, although there are methodological
weaknesses to the study.25 The key to sustainability is the demonstration of
an effective implementation and improved outcomes that are obvious to the
community, so that continuing community participation will be assured:

The immediate expense of nutrition programs and broader interventions

should be considered a critical investment in the future . . . Steps
taken today to combat malnutrition and its intellectual effects can go
a long way towards improving quality of life — and productivity — of
large segments of a population and thus of society as a whole. 26

When the adverse socioeconomic circumstances of a child’s environment

cannot be easily changed, providing adequate nutrition during the weaning
period of early childhood will lessen the disadvantages and deficits
engendered by poverty. There is a window of opportunity at this age for an
effective intervention because it corresponds to the most vulnerable period
of rapid somatic growth and also the brain growth spurt.27–31 Follow-up
studies of community nutrition programs have demonstrated long-term
benefits on intellectual and physical function.32–37 There can be little doubt
that a community nutrition project targeted at the vulnerable weaning diet
is a more effective health services model for improving malnutrition during
the vulnerable weaning period (4–18 months) than hospital admission.
The experience with large scale integrated nutrition projects has shown
that integrated, well-managed and targeted programs of nutrition education,
food supplements and health services were most effective.3,38–42 The lessons
for us from extensive international experience with therapeutic nutrition
programs are the need to:
• Enter into partnership with communities to respect their cultural
values, while ensuring close supervision and good management of the
project
• Target children with faltering growth during the weaning period
• Include an educational component to promote appropriate diets for
children at home and
• Use a commercial high energy therapeutic supplement initially,
containing a range of nutrients.

The most common reasons for unsuccessful programs are:

• Ration sharing (‘leakage’)
• Not reaching the most vulnerable families
• Use of a low energy or unacceptable supplement
• Lack of micronutrients and
• Poor management of the project.

It is well known that a low energy weaning diet (e.g. Weetbix, potato)
alone will not be sufficient for rapid catch-up growth during convalescence
from an enteric infection. In the past, children have been sent to hospital
for a high energy milk diet by nasogastric tube. It makes more sense to
provide high energy nutritional therapy to children with significant
failure to thrive within the community rather than at the hospital. The
nutritional weaning therapy Fortisip is already being used in some
communities. Each 200 mL of Fortisip has 1270 kJ of energy (1.5 kcal/mL),
and contains: protein 10 g (13% of energy as protein), vegetable oil 13 g
(39% of energy), carbohydrates 35.8 g (mainly as maltodextrin and sucrose,
48% of energy), vitamins A (666 iu), B, C, D, E and K, niacin and folic
acid, with a sodium content of 160 mg, potassium of 300 mg, and an
osmolarity of 390 mOsmol/L.
Finally, it is the strong clinical impression of paediatricians in the
NT that nutritional growth retardation in Aboriginal children occurs
predominantly in the weaning period between 4–24 months and is due to an
inadequate weaning diet (other than breast milk). This is also the major
contributor to iron deficiency anaemia, since breast milk alone is
insufficient to satisfy energy and iron requirements over most of that
period. It is therefore important to focus on the weaning period and an
improved weaning diet in any effort to address nutritional problems of
Aboriginal community children in the Top End. Similarly, the strong
correlation of female literacy or educational levels with child health and
mortality43 is clearly relevant to Aboriginal children.

Terminology
A confusing array of terms and classifications are used to describe
malnutrition. In this discussion, we focus on undernutrition, excluding
both obesity and specific nutrient deficiencies. In the developed world
malnutrition is usually described as ‘failure to thrive’ (FTT), which means
growth retardation or low weight-for-age. Although FTT usually refers to a
child below the third percentile for weight-for-age. This cut-off tends, on
one hand, to identify genetically small children with transient growth
deceleration due to an infection and, on the other hand, to miss
significant weight loss in a bigger child. Consequently, FTT should be seen
as growth deceleration or crossing growth percentiles, particularly falling
through two percentile spaces (e.g. from 50–75th percentile to 10–25th
percentile) on the growth chart.
Children who are underweight may also be classified as ‘wasted’ or
‘stunted’. Stunting, or short stature, is defined as a height-for-age below
two standard deviations below the mean (Z-scores), but it needs to be
appreciated that about 3% of normal children will grow on or below this
cut-off. If a stunted child has had two height measurements at least a year
apart then the height velocity can also be charted. For example, the third
percentile for height velocity in boys of 7 to 12 years of age is about 4
cm/year. Where stunting is due to undernutrition, it represents chronic
malnutrition. Wasting, on the other hand, represents more acute
malnutrition and is measured as a low weight-for-height. Wasting means a
child is thin, and severe wasting is called ‘marasmus’. The other form of
severe malnutrition is ‘kwashiorkor’ (which is rarely seen in Australia)
and is characterised by oedema, hypo-albuminaemia, dermatitis and fatty
infiltration of the liver. Although some underweight children will be both
wasted and stunted, many do not satisfy criteria for either wasting or
stunting and are merely underweight for age.

Anthropometric indices
Growth measurements and charting are essential in investigating a child
with possible malnutrition. Key measurements are weight (kg), length or
height (cm) and head circumference (cm). For growth charting, length is
measured in children <24 months and height thereafter, because there is a
mean difference of about 1.5cm between height and length, and growth charts
change from length to height at 24 months. Anthropometric assessment alone
is not a good indicator of nutritional status in children with oedema and
hypo-albuminaemia (kwashiorkor). Accuracy of measurements is essential,
particularly for length/height. Errors in measurement are very common and
one always needs to consider this as the explanation for anthropometric
indices that do not fit the clinical appearance of the child.
What growth standard should be used? Until recently, the conventional
answer was the National Centre for Health Statistics (NCHS) growth curves,
which are the basis of growth charts used in Australia. However, these are
based on North American children, most of whom were bottle fed, so they may
not be appropriate for breastfed children. New international growth curves
are being developed which should also be used in Australia, and will
probably be introduced soon. Revised American (www.cdc.gov/growthcharts)
and European growth curves (www.eurogrowth.org) have been published
recently which are more appropriate for breastfed children. Aboriginal
children have the same growth potential as non-Aboriginal children, so it
would be wrong to conclude that growth faltering was ‘normal’ for them.
Correction of age must be made for prematurity until 18 months with head
circumference, until two years for weight and until 40 months for height.44
Routine growth monitoring is a key component of infant and child health
services. It has come under scrutiny in recent years in both the developing
and developed world, and criticised as a waste of valuable time and causing
unnecessary parental anxiety. A systematic review found no reliable
evidence of a benefit.45 [Editor: This is discussed further in Part 2
below.] A UK consensus meeting recommended that infants need only be
weighed at birth and with immunisations and surveillance checks, with only
those causing clinical concern weighed and measured thereafter.46 In
settings where only mild malnutrition is seen, weight-for-age alone may be
the most appropriate anthropometric index.47 These issues are best decided
at a regional level on the basis of the existing evidence and local
circumstances.

Clinical assessment
All children being investigated for malnutrition should have a complete
history and physical examination. The history will establish whether the
child was pre-term or low birth weight due to intrauterine growth
retardation. Clinical assessment also needs to establish whether there are
signs or symptoms of organic disease. A dietary history, developmental
assessment, observations of parent/child interaction and assessment of
family stress dysfunction or neglect are also important. It is always worth
ensuring that the infant formula is being correctly prepared and not
diluted as a cost saving device, that excessive fruit juice is not
replacing milk, that low energy ‘diet’ foods are not being given because of
erroneous health beliefs or food fads, and that restricted diets for
alleged food allergies are not causing inadequate energy or micronutrient
intake. If there are problems in any of these areas, more detailed
assessment with the assistance of a dietician or other allied health
professional should be considered.

Normal growth variants

In investigating a child with possible malnutrition it is important not to
cause undue parental anxiety by incorrectly labelling a child with normal
nutritional status. Errors in measurement or charting are one pitfall as
mentioned previously. Infants show considerable variability in the early
weeks, with 5% shifting up or down in percentiles as part of normal
growth.46 This is often referred to as ‘catch-up’ growth, with intrauterine
growth retardation or ‘catch-down’ adjustments in early infancy. In the
latter case, breastfeeding problems need to be considered without causing
unnecessary anxiety to a breastfeeding mother.
Familial short stature is a common normal variant and unnecessary
parental anxiety can be avoided by adjusting for mid-parental height,
although it can be misleading unless allowance is made for regression to
the mean.48 Constitutional growth delay occurs in a sub-group of mostly boys
whose height falters between three and 36 months with delayed bone age, so
ultimately they attain normal adult height. Studies have found that
‘constitutional growth delay’ tends to be used for middle class families
whereas ‘failure to thrive’ is more likely to be used for poor families
with the same degree of growth retardation.46 Children commonly have weight
loss and anorexia accompanying infections, particularly diarrhoea, but this
is followed by catch-up growth provided the child receives a diet of
adequate protein and energy density.

Organic vs non-organic causes

Historically, FTT was divided into organic and psychosocial aetiologies.
Major organic disease is found in <5% of community cases of FTT, and can
mostly be diagnosed from signs and symptoms accompanying the growth
failure. Furthermore, even with organic disease, FTT may be due to poor
nutrition in addition to the disease process. Non-organic causes imply poor
emotional or physical nurturing, which is often classified as reactive
attachment disorder, but infant temperament and difficult feeders may also
be factors in poor growth. Abuse, neglect or deprivation is likely to
result in malnutrition, but these only account for 5–10% of FTT cases in
developed countries. Many consider this organic/ psychosocial dichotomy
obsolete since most cases are of mixed aetiology.

Undernutrition
Undernutrition is a factor in up to two-thirds of cases of growth
retardation in childhood, and the degree of wasting and poor dietary intake
may often not be recognised. Caregivers may often not appreciate the high
energy needs of infants and toddlers, which are considerably higher than
adults on a body weight basis. They may also not appreciate the need for
catch-up growth after illness, and if the child’s intake does not increase
after illness he may not demonstrate any catch-up growth but continue to
grow along the percentile to which he has have fallen during the illness.

Laboratory tests
The tendency to order many tests to exclude an underlying organic disease
needs to be avoided as it has a very low yield. Abnormal test results aided
the diagnosis in only 16% of inpatients with FTT and only 0.8% (39/4880) of
tests were helpful.49 Vomiting was often associated with organic disease.
Wright46 suggests doing the following screening tests: full blood count;
thyroid function tests; urea and electrolytes; anti-endomysial antibodies;
mid-stream urine; chromosomes in girls (to exclude Turner syndrome); and
chest X-ray, sweat test, HIV serology and Mantoux test if appropriate.
These screening tests are only done to exclude pathology, most of which is
evident clinically. There are no early reliable laboratory tests of
nutritional status, since serum albumin, cholesterol, triglycerides and ß-
carotene are unreliable or late signs of nutritional deficiency. Similarly,
levels of zinc or vitamin A may be unreliable because serum levels do not
always change in parallel with body stores. The general experience with
 investigating children with malnutrition is that laboratory studies not
suggested on the basis of the initial clinical examination are rarely
helpful.

Trial of therapy
Children with growth retardation in the primary health care setting rarely
need hospital admission or dietary supplement, but can be managed in the
primary care setting in the first instance. For example, a recent
randomised control trial in the UK found a significant benefit for a
health-visitor led intervention, with a fifth of children showing
improvement after dietary advice50, although two other randomised trials
failed to document a growth benefit of home visits.51,52 With more severe
degrees of malnutrition the most important investigation in the hospital
context is a trial of feeding and close observation of the parent/child
interactions and feeding pattern. Hospitalisation is much less effective in
finding an underlying cause of malnutrition than in providing an
environment to assess dietary intake, feeding techniques and parent-child
interactions.

Conclusion
Managing the child with malnutrition relies heavily on growth charts but
must remain aware of normal variations in growth, as well as the all too
common errors in measurement. All children investigated for malnutrition
should have a full history and physical examination — with particular
emphasis on signs and symptoms of organic disease, a dietary history,
developmental assessment and assessment of the parent-child interaction —
looking for family dysfunction, stress or neglect. The tendency to do an
extensive battery of laboratory investigations to exclude the long list of
differential diagnoses associated with malnutrition is not appropriate but
there may be a need for selective tests to exclude organic disease
suggested in the clinical assessment.
Hospitalisation should be largely reserved for wasting and infection-
associated malnutrition. For milder cases, follow-up after dietary advice
with home visits (if feasible) can be done in the primary health care
setting, with a need for paediatric referral only for cases who are more
severely affected or who are not responding to therapy.
Supplements of vitamin A and zinc have been found in overseas studies to
benefit children with malnutrition and persistent diarrhoea. Finally, the
main focus in Aboriginal children should be on improving the intake of
weaning foods and better hygiene and environmental living conditions in
communities. The high prevalence of malnutrition in the weaning period in
Aboriginal communities demands a preventive nutritional intervention
program that would focus on the weaning diet, micronutrients (including
iron) and hygiene.

References
1. Skull SE, Ruben AR & Walker A. Malnutrition and microcephaly in Australian
Aboriginal children. Med J Aust 166:412–14 (1997).
2. Ruben AR & Walker A. Malnutrition among rural Aboriginal children in the Top End
of the Northern Territory. Med J Aust 162:400–3 (1995).
3. Anonymous. Food and nutrition in the management of group feeding programmes.
Nutrition Programmes Service. FAO Food Policy and Nutrition Division. FAO. Food Nutr
Pap 23 Revis 1:1–185 (1993).
4. Bhan MK. Pediatric Gastrointestinal Diseases: Pathophysiology, Diagnosis,
Management. Walker WA, Durie PR, Hamilton JR, Walker-Smith JA & Watkins JB (eds):
867–78 (Mosby, St Louis,1996).
5. Lunn PG, Northrop Clewes CA & Downes RM. Intestinal permeability, mucosal injury,
and growth faltering in Gambian infants. Lancet 338:907–10 (1991).
6. Northrop Clewes CA, Lunn PG & Downes RM. Lactose maldigestion in breast-feeding
Gambian infants. J Pediatr Gastroenterol Nutr 24:257–63 (1997).
7. Kukuruzovic R & Brewster DR. Small bowel intestinal permeability in Australian
Aboriginal children. J Pediatr 2001.
Ref Type: In Press.
8. Brewster DR, Manary MJ, Menzies IS, Henry RL & O’Loughlin EV. Comparison
of milk and maize-based diets in kwashiorkor. Arch Dis Child 76:242–8
(1997).
9. Brewster DR, Manary MJ, Menzies IS, O’Loughlin EV & Henry RL. Intestinal
permeability in kwashiorkor. Arch Dis Child 76:236–41 (1997).
10. Brewster DR, Manary MJ & Graham SM. Case management of kwashiorkor: an
intervention project at 7 Nutritional Rehabilitation Centres in Malawi. Eur J Clin
Nutr 51:139–47 (1997).
11. Godfrey KM & Barker DJ. Fetal nutrition and adult disease. Am J Clin Nutr
71:1344S–1352S (2000).
12. Barker DJ. The long–term outcome of retarded fetal growth. Clin Obstet Gynecol
40:853–63 (1997).
13. Lozoff B, Jimenez E & Wolf AW. Long-term developmental outcome of infants with
iron deficiency. N Engl J Med 325:687–94 (1991).
14. Williams J, et al. Iron supplemented formula milk related to reduction in
psychomotor decline in infants from inner city areas: randomised study. Br Med J
318:693–7 (1999).
15. Ashworth A, Morris SS, Lira PI & Grantham-McGregor SM. Zinc supplementation,
mental development and behaviour in low birth weight term infants in northeast
Brazil. Eur J Clin Nutr 52:223–7 (1998).
16. de Andraca I, Castillo M & Walter T. Psychomotor development and behavior in
iron-deficient anemic infants. Nutr Rev 55:125–32 (1997).
17. Grantham-McGregor SM & Fernald LC. Nutritional deficiencies and subsequent
effects on mental and behavioral development in children. Southeast Asian J Trop
Med Public Health 28 Suppl 2:50–68 (1997).
18. Lozoff B, Wolf AW & Jimenez E. Iron-deficiency anemia and infant development:
effects of extended oral iron therapy. J Pediatr 129:382–9 (1996).
19. Moffatt MEK, Longstaffe S, Besant J & Dureski C. Prevention of iron deficiency
and psychomotor decline in high-risk infants through use of iron-fortified infant
formula: a randomised clinical trial. J Pediatr 125:527–34 (1994).
20. Idjradinata P & Pollitt E. Reversal of developmental delays in iron-deficient
anaemic infants treated with iron. Lancet 341:1–4 (1993).
21. Morley R & Lucas A. Nutrition and cognitive development. Br Med Bull 53:123–134
(1997).
22. Grantham-McGregor SM & Ani C. A review of studies on the effect of iron
deficiency on cognitive development in children. J Nutr 131:649S–666S (2001).
23. Beaton, GH & Ghassemi H. Supplementary feeding programs for young children in
developing countries. Am J Clin Nutr 35:864–916 (1982).
24. Lee AJ, Bonson AP, Yarmirr D, O’Dea K & Mathews JD. Sustainability of a
successful health and nutrition program in a remote Aboriginal community. Med J
Aust 162:632–5 (1995).
25. Mackerras DE. Evaluation of the Strong Women, Strong Babies, Strong Culture
Program. 1–76. 1998. Darwin: Menzies School of Health Research. Menzies Occasional
Papers 2/98.
26. Brown JL & Pollitt E. Malnutrition, poverty and intellectual development. Sci Am
274:38–43 (1996).
27. Dobbing J. Boyd Orr memorial lecture. Early nutrition and later achievement. Proc
Nutr Soc 49:103–118 (1990).
28. Dobbing J & Sands J. Comparative aspects of the brain growth spurt. Early Hum Dev
3:79–83 (1979).
29. Dobbing J. The later growth of the brain and its vulnerability. Pediatrics 53:2–6
(1974).
30. Dobbing J. Nutrition and the developing brain. Lancet 1:48 (1973).
31. Dobbing J. Vulnerable periods of brain development. In: lipids, malnutrition &
the developing brain. Ciba Found Symp :9–29, 9–29 (1971).
32. Grantham McGregor SM, Walker SP, Chang SM & Powell CA. Effects of early childhood
supplementation with and without stimulation on later development in stunted
Jamaican children. Am J Clin Nutr 66:247–53 (1997).
33. Powell CA, Walker SP, Himes JH, Fletcher PD & Grantham-McGregor SM. Relationships
between physical growth, mental development and nutritional supplementation in
stunted children: the Jamaican study. Acta Paediatr 84: 22–9 (1995).
34. Grantham-McGregor SM, Powell C, Walker S, Chang S & Fletcher P. The long-term
follow-up of severely malnourished children who participated in an intervention
program. Child Dev 65:428–39 (1994).
35. Elizabeth KE & Sathy N. The role of developmental stimulation in nutritional
rehabilitation. Indian Pediatr 34:681–95 (1997).
36. Haas JD, et al. Nutritional supplementation during the preschool years and
physical work capacity in adolescent and young adult Guatemalans. J Nutr 125
Suppl:1078S–1089S (1995).
37. Pollitt E, Watkins WE & Husaini MA. Three-month nutritional supplementation in
Indonesian infants and toddlers benefits memory function 8 y later. Am J Clin Nutr
66:1357–63 (1997).
38. Berg A. Malnutrition: What can be done? The Johns Hopkins University Press,
Baltimore (1987).
39. Habicht JP, Martorell R & Rivera JA. Nutritional impact of supplementation in the
INCAP longitudinal study: Analytic strategies and inferences. J Nutr 125
Suppl:1042S–1050S (1995).
40. Alderman MH, Wise PH, Ferguson RP, Laverde HT & D’Souza AJ. Reduction in young
child malnutrition and mortality in rural Jamaica. J Trop Pediatr 24:7–11 (1978).
41. Heikens GT, Schofield WN, Christie CD, Gernay J & Dawson S. The Kingston Project.
III. The effects of high energy supplement and metronidazole on malnourished
children rehabilitated in the community: morbidity and growth. Eur J Clin Nutr
47:174–191 (1993).
42. Golden MH, Briend A & Grellety Y. Report of meeting on supplementary feeding
programmes with particular reference to refugee populations. Comite Scientifique
Consultatif de Nutrition, Action Internationale Contre la Faim. Eur J Clin Nutr
49:137–145 (1995).
43. Caldwell JC. Routes to low mortality in poor countries. Popul Dev Rev 12:171
(1986).
44. Schwartz ID. Failure to thrive: an old nemesis in the new millennium. Pediatr Rev
21:257–64 (2000).
45. Garner P, Panpanich R & Logan S. Is routine growth monitoring effective? A
systematic review of trials. Arch Dis Child 82:197–201 (2000).
46. Wright CM. Identification and management of failure to thrive: a community
perspective. Arch Dis Child 82:5–9 (2000).
47. Raynor P & Rudolf MC. Anthropometric indices of failure to thrive. Arch Dis Child
82:364–5 (2000).
48. Wright CM & Cheetham TD. The strengths and limitations of parental heights as a
predictor of attained height. Arch Dis Child 81:257–60 (1999).
49. Berwick DM, Levy JC & Kleinerman R. Failure to thrive: diagnostic yield of
hospitalisation. Arch Dis Child 57: 347–51 (1982).
50. Wright CM, Callum J, Birks E & Jarvis S. Effect of community based management in
failure to thrive: randomised controlled trial. Br Med J 317:571–4 (1998).
51. Raynor P, Rudolph MC, Cooper K, Marchant P & Cottrell D. A randomised controlled
trial of specialist health visitor intervention for failure to thrive. Arch Dis
Child 80:500–6 (1999).
52. Black MM, Dubowitz H, Hutcheson J, Berenson HJ & Starr-RHJ. A randomized clinical
trial of home intervention for children with failure to thrive. Pediatrics 95:807–
14 (1995).

Part 2: Growth monitoring for action

Routine growth monitoring is a key component of infant and child health
services. It has come under scrutiny in recent years in both the developing
and industrialised world, and criticised as a waste of valuable time and
causing unnecessary parental anxiety. The Nyeri Declaration on Growth
Promotion for Child Development1 expressed concern that weighing and
charting of millions of children in the developing world had not been
followed by appropriate action. It recommended that growth monitoring be
accompanied by assessment, analysis and action.
However, a systematic review found no reliable evidence of a benefit
from growth monitoring.2,3 A UK consensus meeting recommended that infants
need only be weighed at birth and with immunisations and surveillance
checks, with only those causing clinical concern weighed and measured
thereafter. In settings where only mild malnutrition is seen, weight-for-
age alone may be the most appropriate anthropometric index.4
For school age children, screening for short stature with a single
precise measurement using standard techniques and a reliable stadiometer
has been recommended, taking the 0.4th percentile as the cut-off, which is
particularly oriented to detecting Turner’s Syndrome and growth hormone
deficiency.5 American recommendations are that children should have routine
supervisory health visits with weight, height and head circumference
measured at one, two, four, six, nine, 12 and 15 months, and weight and
height at 18 months, and annually from two to five years. These issues are
best decided at a regional level on the basis of the existing evidence and
local circumstances.
For routine screening in a high-risk setting (like NT Aboriginal
children) the GAA program recommends approximately monthly weights in the
first three years and then six-monthly to school entry, length/height
measurements about six-monthly to school entry, and head circumference
three times in the first six months of age.6 A retrospective review of
health centre records from 11 remote Aboriginal communities in the Top End
recommended against annual growth screening of school children since it did
not pick up new cases of growth failure.7 Twenty-one per cent of the four to
10-year-old children measured were malnourished (weight/age below -2 Z-
scores), with 51.4% stunted, 40.7% wasted and 7.9% both wasted and stunted.
It is important to detect poor growth prior to school age. The mean age
(range) of onset of growth faltering is 6.6 (3.5–12) months for stunting
and 8.9 (7.5–18) months for wasting. Hence, the critical period for linear
 growth is the first two years of life, so growth monitoring needs to focus
on this age group and follow up ‘at risk’ children closely.

References
1. Anonymous. Growth Promotion for Child Development: Proceedings of a colloquium in
Nyeri, Kenya, May 12–13, 1992. Ottawa: International Development Research Centre,
1993.
2. Garner P, Panpanich R, Logan S. Is routine growth monitoring effective? A
systematic review of trials. Arch Dis Child 2000; 82:197–201.
3. Panpanich R, Garner P. Growth monitoring in children. The Cochrane Database of
Systematic Reviews 1999; 2:1–14.
4. Raynor P, Rudolf MC. Anthropometric indices of failure to thrive. Arch Dis Child
2000; 82:364–5.
5. Hall DM. Growth monitoring. Arch Dis Child 2000; 82:10–5.
6. Anonymous. Growth Assessment Action Resource Pack. Darwin: Territory Health
Services, 1999.
7. Paterson BA, McKinnon CP, Edmond KM. A review of annual growth screening in
Aboriginal schoolchildren in Australia. J Paediatr Child Health 2001; 37:18–23.
8. Paterson BA. Evaluation of the school screening program in the rural Aboriginal
communities of the Katherine district of the Northern Territory. Menzies School of
Health Research, University of Sydney: MPH Thesis, 1995; 1–134.

Part 3: Measurement of head circumference: discussion

Published recommendations
Hall1 recommends to measure after birth, then at 6–8 weeks. Further
measurements are indicated if:
1. The head circumference (HC) line is crossing percentiles upwards,
and there are no symptoms of hydrocephalus, but only for four weeks
after which immediate referral for evaluation should be made if
abnormal1; or
2. The child is being evaluated for concerns about growth or
development.
NHMRC guidelines 1993: Measure at birth, seven days (or at discharge
from hospital) and then at 6-8 weeks.2. NHMRC guidelines on child
health surveillance are being revised at present and any details
will not be provided in advance 3.

Published evidence about head growth

• Large head can be caused by hydrocephalus, subdural effusion, subdural
empyaema and various syndromes (Soto’s, Alexanders etc.). Microcephally
can be caused by chromesomal or genetic abnormalities, congenital
infections, congenital toxins (alcohol etc.), craniosynostosis.
• Head circumference below the third percentile is perfectly compatible
with normal intelligence, but with lower measures abnormal development
becomes more common.4 Small-for-gestational age babies at birth remain
shorter and lighter and have smaller head circumferences than normal for
gestational age babies.5
• Early malnutrition was shown to be associated with poor head growth in
three studies.6,7,8
• There is also evidence that poor early nutrition affects cognitive
function. However, other factors (including poverty) may be involved, and
the relationship may be due to specific micronutrient deficiency rather
than protein/calorie malnutrition.9,10,11
• A relationship between wasting (but not stunting) and microcephally
independent of interuterine growth retardation (IUGR) was shown in a study
of Aboriginal children at RDH; there was no relationship between
microcephally and stunting. This study does not prove a causal relationship
between nutrition and head growth.12

Issues
1. What is the purpose of measuring head circumference?
• In the first few months of life as a screen — which will lead to
investigation for causes of small or large head.
• To allow identification of particular children with nutritional
problems where intervention will make a difference to the individual.
(Microcephaly will be a late and insensitive feature of undernutrition)
• In older children as an indicator of nutritional status of a
population (i.e. prevalence of microcephally). However, weight-for-age,
height-for-age and weight-for-height are better measures.13

2. What could be the positive outcomes of HC monitoring?

• Indicating that poor nutrition in early life has implications for
brain growth, psychomotor development and intellectual function.

3. What could be the negative outcomes of HC monitoring?

• Head circumference is an insensitive indicator of intellectual
function and many individuals with lower HC have normal IQ. Families
could be made unnecessarily concerned about their child’s developmental
potential based on HC.
• Aboriginal health researchers in history have been caricatured as
‘skull measurers’, and head circumference reporting can be offensive
and provoke sensationalist and racist publicity.14,15

Recommendations
• Measure HC at birth and then at 1–2 months of age. Any abnormalities
detected should be referred immediately for assessment and
investigation.
• Consider further measurements at six and 12 months, although the
evidence for benefit is not very strong.
• Measurement of HC should be part of the medical review of children who
are identified and referred because of poor growth or development
• Further measurements (on a population level) are not indicated and may
be harmful.

References
1. Hall DMB. Health for all children (2nd ed). Oxford: Oxford Medical Publications,
1991.
2. NHMRC. Review of child health surveillance and screening.
Commonwealth of Australia, 1993; 157–9.
3. Callen P. NHMRC, deputy director, Health advisory section, personal
communication, Jan 2001.
4. NHMRC. Review of child health surveillance and screening.
Commonwealth of Australia; 157–9.
5. Hediger ML, Overpeck MD, Maurer KR, et al. Arch Pediatr Adolesc Med
1998; 152:1225–31.
6. Sathy N, Elizabeth KE, Nair MKC, Sugunu Bai NS. Indian Pediatr 1990;
28:255–8.
7. Stoch MB, Smythe PM. Does undernutrition during infancy inhibit
brain growth and subsequent intellectual development? Arch Dis Child 1963;
38:546.
8. Winick M, Rosso P. Head circumference and cellular growth of the
brain in normal and marasmic children. J Paediatr 1969; 74:774.
9. Gorman K. Malnutrition and cognitive development: evidence from
experimental/quasi-experimental studies among the mild-to-moderately
malnourished. J Nutr 1995 Aug; 125(8 Suppl):2239S–2244S. Review.
10. Grantham-McGregor S. A review of studies of the effect of severe
malnutrition on mental development. J Nutr 1995 Aug; 125(8 Suppl):2233S–
2238S. Review.
11. Allen L. The nutrition CRSP: what is marginal malnutrition, and does
it affect human function? Nutr Rev 1993 Sep; 51(9):255–67. Review.
12. Skull SA, Ruben AR, Walker AC. Malnutrition and microcephaly in
Australian aboriginal children. Med J Aust 1997 Apr 21; 166(8):412–4.
13. WHO. Physical status: the use of and interpretation of
anthropometry. WHO technical report series 854. Geneva: WHO, 1995; 175.
14. Thomas DP, Andeson P. Malnutrition and microcephaly in Australian
Aboriginal children. Med J Aust 1997 Nov 17; 167(10):554.
15. Torzillo PJ. Politicised Aborigine health research. Med J Aust 1997
Nov 17; 167(10):555–6.
 Head Lice Management

Author: Keith Edwards (Community Paediatrician, CDC)

Topic Reviewers: Dave Corstorpan (RAN, Nyirripi Clinic); Dr Christine Connors

(RDH)

Head lice are tiny wingless insects (2–3 mm) that vary in colour from cream
to brown. They are found attached to the hair near the scalp and are harder
to see than nits. Nits is the common name for the small eggs that are laid
by head lice. They are the size of a grain of salt, yellow-white in colour
and are hard and gritty in texture. They are found glued to the hair near
the scalp. Common places are behind the ears, back of the neck and the
fringe. Dead nits are often black in colour and are found well away from
the scalp.

Biological/life cycle facts about head lice infections

• Nits are laid within 1–2 mm of the human scalp.
• Nits take between 7–10 days to hatch.
• Newly hatched nymphs become adults nine to 12 days later.
• Nits will only hatch when kept at a high temperature and moist
environment, as in the scalp.
• Nits die quickly on furniture, clothes and hairbrushes.
• Head lice spread from one person to another by close head-to-head
contact in most cases.
• Head lice can spread by sharing hats and brushes, but this is less
common.
• Head lice do not transmit HIV or hepatitis B infections.
• Rare diseases — such as typhus, trench and relapsing fever — can be
transmitted by head lice.
• Head lice infections cause itching, which may in turn cause poor
sleep and behaviour problems.
• Itching often causes scalp sores due to secondary bacterial
infection.
• Head lice are most commonly found in primary school children due to
close personal contact.
• Adults may have head lice without being aware of the infection.
• Cleanliness does not prevent head lice: anyone can catch them.
• Head lice infections do occur in cycles in the community.
• The last big outbreak in the Top End of Northern Territory was 1994–
95.
• 50% of primary school children were affected in the last big
outbreak.
• A warm and humid environment favours hatching and survival of head
lice.
• Head lice are more common in the wet season and ‘build-up’.
Head lice treatments
(Dodd CS. Interventions for treating head lice (Cochrane Review). In: The
Cochraine Library, Issue 1, 2002.Oxford: Update Software)
• No evidence that one approved chemical lice treatment has any
greater effect than another.
• Permethrin, synergised pyrithrin and malathion have all been shown
to be effective in the treatment of head lice.
• Resistance to treatments has emerged since trials performed, and
this varies with location.
• Physical treatment methods have been shown to be ineffective in
completely treating head lice.
• Other ‘natural’ treatments have not been formally studied but are
known to be more toxic.
• ‘Rotation’ model replaced by ‘mozaic’ model because of resistance
and the fact that all treatments are available over the counter.

Reasoning/evidence for CARPA head lice management protocol

Head lice infestation is a very common problem in the NT and I feel that
the existing five lines in the third edition (two are repeated!) does not
give enough guidance. The reasons/evidence for each component of the
suggested new edition section are given below. The management flow chart
could be used as an adjunct or could replace the written section with some
additions.
Asking about previous treatment and whether any other members of the
family are affected is the initial step. This allows you to decide which
lice treatment to use (permethrin or malathion) and also whether other
members of the family need treatment. It makes most sense that all members
of the family are treated at the same time, otherwise lice may spread back
to the person who has already been treated.
Looking for live lice by combing with a fine tooth comb is the next step
as this will tell you whether the person requires chemical treatment or
not. We know that many people are over-treated with chemical treatments
when only nits are found in their hair. If there is an ongoing infection
requiring treatment then live lice should be present. Over-treatment with
chemicals is known to cause irritation of the scalp and can be the cause of
itching. It is important therefore to only use chemicals when they are
needed. If nits only are found, many of these may be ‘empty shells’. Those
eggs that are viable are resistant to chemical treatment and only if they
hatch and produce live lice should chemical treatment be commenced.
Looking for sores is important as these are usually infected with
staphylococci or streptococci and are equivalent to ‘impetigo’. They
require treatment as post streptococcal glomerulonephritis may occur, as
may acute rheumatic fever. Furthermore, the presence of sores may also
cause itching and be mistaken for an ongoing head lice infection resulting
in further chemical treatment and further irritation.
Do treat with 1% permethrin when live lice are found because this is the
chemical treatment with the least likelihood of toxicity and is as
effective as other chemical treatments. Lotions and shampoos require
different application methods because of their differing physical
properties and strengths.
Do perform fine tooth combing with hair conditioner if available. The
hair conditioner allows the comb to slide through the hair more easily and
also ‘stuns’ the head lice making them easier to catch. The comb teeth
should be 0.25 mm apart otherwise the lice will not be caught effectively.
The double advantage of combing is that it allows confirmation of the need
for chemical treatment and it allows the identification of resistance to
chemical treatments and the need to change to another. There is some
evidence that reducing the numbers of live lice assists cure by chemical
treatment. If chemical treatment is performed without washing off hair
conditioner, it is less effective at killing lice. Family members should be
taught how to fine comb hair as this needs to be repeated every few days in
those affected and the workload would be too great for clinic staff to do
this.
Do advise parents to inform the school, as other children should be
checked at the same time to avoid this child being reinfected. Lice
checking days may be organised by the school in conjunction with parent
groups.
Follow-up. A repeat treatment with 1% permethrin is essential at about
seven days as more nits will have hatched since the previous treatment.
Nits are not killed by the treatment so if the second treatment is not
given at the right time, the infestation will recur.

[Editor: There were a wide range of experiences and opinions expressed in

the editorial committee about the approach to head lice management in
Aboriginal communities. We felt that it was a given that there was an
Australia-wide long lasting epidemic of head lice, not confined to
Aboriginal communities. Where there is an ongoing high prevalence, it is
not realistic to expect to be able to eradicate head lice from a family as
the originally proposed protocol had suggested. In these cases ongoing
management (control) without eradication will be the goal.
Notifying the health service and school was removed, as it is not
realistic for the school or health service to respond in a meaningful way
in the CARPA regions. However, if a person lives in a community without
locally endemic head lice, then there is a good case for taking measures to
decrease spread to other people. The main practical application of this is
in withdrawing a child from school or childcare until they have been
treated.
If a person or family is moving from an endemic community to a non-
endemic setting, then they should attempt to eradicate head lice before the
move.
The result is that the head lice protocol in the STM has been
significantly altered from that originally offered. It is included here for
those seeking to eradicate head lice from an individual or family.]

Head lice protocol for eradication

Ask:
• About previous treatment.
• Other members of the family affected.

Look for:
• Live lice by combing thoroughly with a fine tooth comb.
• Finding nits (eggs) only does not require chemical treatment.
• Scalp sores.
Do
• Treat with 1% permethrin (pyrifoam, quellada, lyclear); follow
packet instructions.
• Lotion should be rubbed in and washed out 12 hours later with
regular shampoo.
• Head lice shampoo should be combed through the hair with a fine
tooth metal comb and washed out 10 minutes later.
• Perform thorough hair combing with a fine tooth metal comb (teeth
0.25 mm apart).
• Teach family members how to do this.
• Head down over spread paper, one section at a time.
• Apply hair conditioner (if available) before combing.
• Repeat combing by family at home every few days until no more live
lice found.
• Always wash out hair conditioner before using chemical head lice
treatment.
• Treat scalp sores if present in the same way as impetigo
• Examine and treat other affected members of the family at the same
time.

Advise on prevention issues:

• Weekly hair and scalp checks with nit combs for all the family.
• Do not share brushes, combs, hats or pillows.
• Keep long hair tied back or cut hair short.
• Inform school if a child is affected so that other children can be
checked and treated.

Follow-up
Review after seven days and repeat 1% permethrin treatment. If live lice
are still present, encourage family to continue combing every few days.
Review after a further seven days, and if live lice are still present:
• Change treatment to 1% malathion or 0.5% malathion in an alcohol
base.
• Recommend continued combing every second day.

Review after a further seven days, if live lice are still present:
• Check that treatment has been done correctly.
• Consider reinfection as cause.
• Contact medical officer for advice.

Head lice management flowchart (next page)

Head lice management flowchart
 Nappy Rash (Nappy Dermatitis)

Author: Dr Ian Dumbrell

Nappy rash is a common ailment of infancy. Paediatri-cians and primary care

workers both encounter this problem relatively frequently. There is some
Level 2 evidence to guide interventions for nappy rash. No level 1,2, or 3
evidence relating to diagnosis of different causes of napkin dermatitis
could be found.
The appearance of the rash roughly relates to the causes of napkin
dermatitis as seen in the table below.

Comments on recommendations in the protocol

Keeping the nappy area dry
All nappy rashes are made worse by an element of contact irritant
dermatitis from prolonged contact with urine and faecal enzymes, so keeping
the nappy area dry is relevant to the treatment of all nappy rash. Some
communities strive to reduce the use of disposable nappies because of the
infection hazard posed by dirty nappies left in the street and yards. All
the trials of intervention recommended2 using disposable nappies over cloth
nappies because of the superior ability of disposable nappies to keep the
nappy skin area dry, and the ability of disposable nappies to actually
reduce the load of Candida sp. So, despite the possible public health risk,
whilst not making a community-wide recommendation for all babies to use
disposable to prevent nappy rash, it seems reasonable to advocate limited
use of disposable nappies to treat established nappy rash.
Some authors recommend not using nappies for brief periods, where
feasible, to help treat contact irritant napkin dermatitis. Baby faeces can
be highly infectious, and in the context of over-crowded housing and poor
hygiene it is probably reasonable to avoid recommending going without
nappies, even though not wearing nappies may well help relieve a nappy
rash. It may however promote the spread of gastroenteritis through the
household (average household occupancy in Port Keats is 15 per house (pers.
comm., Terry Bullemor, Town Clerk, Port Keats)). Parents in communities may
well choose this option in any case. Use of barrier cream — such as zinc
and castor oil — and avoidance of baby wipes are recommended by most
authors.

Classifying cause of nappy rash by appearance

The schema followed here is an amalgamation of the diagnostic
recommendations of various authorities, and represents a consensus of their
views.

Choice of anti-fungal and steroid creams

There is universal recommendation of 1% hydrocortisone because more potent
topical steroids can cause skin atrophy if used in the nappy area. The
recommendation to never use these steroids is a bit dogmatic, but in
keeping with the style of brevity and clarity adopted by the CARPA STM.
Most authors recommend 1% clotrimazole, rather than mycostatin, which may
 be cheaper and marginally more effective than clotrimazole. However, there
is no evidence base for this distinction, and since most remote clinics
often only stock one topical anti-fungal (and this is usually clotrimazole)
clotrimazole is recommended for use in the protocol. Because contact
irritant napkin dermatitis (even with super-infection with Candida sp.)
will often clear simply by keeping the skin of the nappy area dry, the
protocol recommends holding off on the topical 1% hydrocortisone and 1%
clotrimazole in the first instance.

On not elaborating the causes of ‘flexural’ napkin dermatitis

Some babies with seborrhoeic dermatitis or psoriasis will have a rash over
other parts of the body, and some will not respond to the simple generic
treatment outlined in the protocol, needing tar-based ointments etc.
However, in a lot of cases a specific diagnosis is not needed because, in
practice, these skin diseases often will respond to such simple measures.
If they do not, this contingency is covered by the recommendation ‘talk
with a doctor if rash is not improving’.

Appearance Rash on Rash also Jacquet’s/Erosive:

convexities, but involving glazed, red shiny
sparing flexures flexures, or skin, with punched
primarily in out erosions; or
flexures any other
blistering
Cause Contact irritant Candida sp. +/- Can indicate a
dermatitis Seborrhoeic degree of neglect,
dermatitis, or just severe
psoriasis, and disease.
other primary Blistering can
skin diseases mean Staphlococcal
bullous impetigo
or herpes or other
rarer causes
Comments Often both Super infected
with Candida
Anyway

Diagnosing and treating variant and more severe forms of napkin dermatitis
Most erosive nappy rash will just be severe contact irritant dermatitis
with or without seborrhoeic dermatitis, psoriasis or other primary skin
diseases. However, some will be genital herpes or bullous impetigo or other
skin diseases needing the attention of a doctor. Severe erosive napkin
dermatitis sometimes can be part of a symptom complex of child neglect or
primary carer stress, and these issues will need to be addressed by a more
experienced practitioner.

References
1. Atkin, Spraker, Aly, et al. Pediatr Dermatol Jul–Aug 2001.
2. Jordan, et al. Pediatr Dermatol 1986; 3:198–207.

Other references:
• Therapeutic Guidelines Dermatology.
• Royal Melbourne Children’s Hospital Paediatric Handbook.
• Adelaide Women’s and Children’s Hospital Paediatric Handbook.
• Hospital Paediatrics.
• Practical Paediatrics.
• Colour Guide to Paediatrics.
• Colour Guide to Dermatology.
• Irritant Napkin Dermatitis: Aust Fam Phys April 1999; 28(4):385–6.
 Paediatric Chronic Suppurative
Lung Disease

Author: Assoc Prof AB Chang (Flinders University NTCS, Alice Springs Hospital)

Topic reviewers: Robyn Dixson (RAN, Yirrkala Clinic); Angela Peermen (RAN,
Oenpelli Clinic); Mt Leibig Clinic staff; Kaz Knudsen (RAN, WA); Dy Kelaart
(RAN, Yuendumu clinic); Borroloola Clinic staff; Dr Ian Dumbrell (Port Keats)

Introduction
The true prevalence of chronic suppurative lung disease (CSLD) and other
respiratory illness in Indigenous children is unknown. There is however
little doubt that the burden of CSLD is disproportionately high in remote
and rural Indigenous communities. In Central Australia the prevalence of
high resolution computed tomography (HRCT) proven bronchiectasis in
children (<15 years) is at least 4.2 per 1000 children (denominator based
on ABS statistics for 2000 and includes population of the Anangu
Pitjantjatjara Lands). This far exceeds the prevalence of children with
cystic fibrosis in non-Indigenous Australian centres, yet there is no
concerted program or resources to manage these children who succumb to
premature death from their lung disease and have significant morbidity in
childhood and adulthood. Many children remain undiagnosed and there is wide
variation in the management of those identified with CSLD, varying from a
minimalist approach (no treatment) to intensive physiotherapy and
antibiotics. Reasons for the minimal approach include the perception that
‘nothing can be done’, and the lack of resources, both in the community and
hospital levels, not dissimilar to community attitudes for cystic fibrosis
several decades ago. The value of early recognition and
intervention/management of these disease processes for the regression
(where possible), and prevention and/or slowing down, of the advancement of
the disease process is increasingly recognised in asthma, chronic lung
infections and chronic obstructive airway disease (COAD).1,2,3,4,5 Based on this
principle, national and international programs currently exist for other
respiratory diseases such as asthma, chronic airflow limitation, cystic
fibrosis and non-respiratory diseases such as diabetes and chronic heart
disease.
In late August 2001, a workshop to discuss the issues around CSLD in
remote Indigenous children was attended by adult and paediatric respiratory
physicians, general physicians and paediatricians, researchers, and public
health physicians from around Australia and New Zealand. The management
approach outlined in this article was reached by consensus of the group.

Literature review and discussion

Why children with CSLD are different from adults
The respiratory system, like any other system, undergoes a process of
maturation in infancy and childhood. While external features, such as
walking and talking, are obviously developing, the developmental process of
internal features, such as control of the respiratory system, respiratory
muscles, thoracic cage and glandular development of the respiratory tree
are often forgotten by adult-focused practitioners. Insults to the
respiratory system at a young age may impair lung growth and lung
potential.6 Interventions at an early age before permanent irreversible
changes take place are increasingly recognised in disease processes such as
asthma.1
Another aspect of paediatric respiratory disease is the influence of
prenatal factors and, when insults to the system occur, growth potential
can be lost.6 In the respiratory system, it has been well documented that
lower respiratory infections (LRTI) in children can lead to later
respiratory morbidity, chronic lung disease and lung function
abnormalities.7–12 In adenovirus and many viral acute lower respiratory
infections (ALRI), the young child has increased risk of developing lung
function abnormality.8,13 Management should arguably be intensive in children
as it is now increasingly appreciated that inflammatory disease processes
may impair lung growth in addition to accelerated respiratory function
decline in later years.3,14,15

Principles/goals of management
CLSD has been termed an ‘orphan disease’16 because of its perceived low
frequency, neglected in research and treatment because of a lack of
commercial interest. In the absence of adequate data, the cystic fibrosis
(CF) approach (the commonest cause of chronic suppurative lung disease in
non-Indigenous children) is utilised. With intensive and improved
management in CF, the median life expectancy for an Australian child with
CF is now in the mid forties, a far cry from the situation three or four
decades ago when children succumbed in their first decade of life. The
outcomes of this approach have been documented by the Danish group.17 CF and
CSLD share common respiratory manifestations as CF is a variety of CSLD. In
contrast, the presumed initial insult in children with CSLD usually occurs
in infancy or early childhood.
The main general management points for children with CSLD are similar to
that of the respiratory management of a child with CF; directed against
infections, secretions, airway obstruction, and complications (e.g.,
hemoptysis, hypoxemia, growth failure, cor pulmonale). In addition,
specific management is aetiology specific e.g., the use of pooled
immunoglobulin for immunodeficiency. Treatment is aimed at reducing
morbidity from exacerbations and complications of CSLD, and reducing lung
inflammation by reducing the bacterial load. Management should arguably be
intensive in children as it is now increasingly appreciated that
inflammatory disease processes may impair lung growth in addition to
accelerated respiratory function decline in later years.3,14,15 In adults,
accelerated lung function decline have been found in patients with asthma18,
COAD with mucous hypersecretion19, smoking20, and coronary heart disease.18 In
CSLD, the presence of features of asthma is a known bad prognostic factor.21

Management of CSLD in children

Diagnosis
CSLD should be considered where children have one or more of the following
symptoms and signs: chronic moist or productive cough, exertional dyspnoea,
symptoms of reactive airways disease (RAD), growth failure, recurrent chest
infections, pulmonary hypertension, chronic hypoxaemia, clubbing, and
hyperinflation. CSLD should be differentiated from radiologically defined
bronchiectasis. Pathologically, bronchiectasis is defined as an abnormal
and permanent dilatation of the subsegmental airways.16 Radiologically, the
characteristic finding in bronchiectasis is the presence of ‘signet ring’
where a dilated bronchi is greater than the diameter of the accompanying
blood vessel in cross-section.22,23 However, the absence of this
characteristic finding does not exclude the presence of bronchiectasis.
Children with suspicious features of CSLD should be referred for evaluation
and a management plan.

Assessment
The primary aim is to search for familial and treatable causes and, second,
to define disease severity which impacts on treatment intensity. Pastuer
and colleagues recently reported the aetiological causes of bronchiectasis
in 150 newly diagnosed adults with bronchiectasis and identified one or
more causes in 47%.24 They concluded that patients with bronchiectasis
deserve thorough investigations.24 In the Alice Springs series,’ other major
contributing factor’ was identified in 12.2% children (IgG subclass
deficiency, congenital lesion, severe aspiration, TB). In addition,
bronchoscopy in 16 of those who had localised changes revealed localised
bronchomalacia in the corresponding lobe in six children. Reactive airway
disease manifested clinically by recurrent wheeze is sometimes present with
underlying CSLD and bronchiolitis obliterans.25 This should be treated on
its own merits. Children referred for assessment usually undergo (a) high
resolution CT scan of the chest (b) a series of blood tests (c) pulmonary
function test if over six years (d) bronchoscopy if localised changes are
present and (e) sputum evaluation.

Antibiotics and other medications

Based on Cole’s model for the pathophysiology of bronchiectasis26 and using
the childhood CF approach, intensive management of children with CSLD is
advocated. Exacerbations may require intermittent hospitalisation with
intravenous antibiotics and intensive physiotherapy and other airway
clearance methods (exercise and nebulised therapy). The Danish model of CF
utilises a three-monthly ‘chest tune-up’ regimen17 where children are
hospitalised for the above treatment regimen, irrespective of whether an
exacerbation is concurrently present. However, all exacerbations are
intensively managed either as an outpatient, ‘hospital-in the home’, or as
an in-patient. The hospital-in-the-home model is impractical in remote
Indigenous communities. Outpatient management may also be impractical in
some situations. Thus, children with moderate or severe CSLD are likely to
require hospitalisation. Brief antibiotic intervention has been shown to
significantly improve inflammatory profile in the airways27,28 and
27,28
systematically , as well as improve quality of life measures.28,29 A 12
month trial in adults with non-CF pseudomonas colonised bronchiectasis
showed a reduced number of hospitalisations for those on the continuous
treatment when compared to those in the symptomatic treatment arm.30 Another
12 month trial using a randomised controlled design showed that the
symptoms of cough expectoration, haemoptysis and general disability were
significantly less in the those treated with tetracycline than to those
treated with oral penicillin or placebo.31 Long-term intervention trials are
unavailable. The use of sputum colour has recently been shown to be a good
reflection of neutrophilic airway inflammation.32 Using a nine-point (0–8)
colour chart ranging from clear (water colour) to yellow to dark green,
Stockley and colleagues showed that ‘sputum colour graded visually relates
to the activity of the underlying markers of bronchial inflammation and
concluded that simple visual analysis of sputum provides guidance
concerning underlying inflammation and its damaging potential’.32 Sputum
bacteriology is associated with quality of life in adults with non-CF
bronchiectasis.29 Using quality of life instruments, Wilson and colleagues
showed that patients infected with pseudomonas had significantly worse
scores than those infected with Haemophilus and the non-chronic infected
groups.29
The use of maintenance antibiotics may be suitable in selected
situations where frequent exacerbations occur.33 However, its use may be
limited by practical factors. In adults regular use of macrolides and
trimethoprim have shown to be beneficial in reducing pulmonary
inflammation, infective exacerbations and improving lung function.33,34 This
has not been evaluated in children.35 The recommendation for the choice of
antibiotics should be guided by sputum bacteriology, severity of disease
and patient factors such as allergy, tolerability and medication
compliance. For example, an older child would best tolerate roxithromycin
on a daily basis but a young child with moderate bronchiectasis would be
best on amoxycillin-clavulanic acid on a twice-daily regime rather than
amoxicillin on a tds regimen. The high dose regimen is recommended. Current
data from sputum in Central Australian children with bronchiectasis
indicate that the first choice (if feasible) should be amoxil, as most have
microbes that are sensitive to amoxil. For practical reasons amoxycillin-
clavulanic acid may be preferable. Roxithromycin may be considered in those
with less severe bronchiectasis. Discussion of patient factors with local
community health staff is encouraged.
The use of inhaled corticosteroids for children with bronchiectasis has
not been evaluated. In adults, such studies were only of 4–6 weeks
duration, with a trend to improve lung function.36 Kolbe and colleagues
concluded in their recent Cochrane review that there is insufficient
evidence to provide clear guidelines to guide practice.36 When inhaled
steroids are used consideration to once daily, rather twice daily, dosing
may be appropriate in settings where adherence to treatment regimens may be
a concern.

Physiotherapy
Chest physiotherapy in children is a specialised area as physiotherapy
techniques differ for infants and children in comparison to adults.37
Techniques such as ‘bubble PEP’ commonly used in children are not used in
adults. Chest physiotherapy to improve mucociliary clearance is a standard
treatment regimen in children with CF and has been shown in a meta-analysis
to significantly improve sputum clearance.37 Cochrane and colleagues showed
that physiotherapy can reduce airways obstruction and sputum has a
detrimental effect on pulmonary function.38 In line with adults with
bronchiectasis and sputum producing COAD39, we advocate the use of daily
physiotherapy in children with CSLD, using the CF model. There are many
forms of physiotherapy and these different methods have not been evaluated
in children with CSLD. Reviews on physiotherapy are available
elsewhere.40,41,42
Postural drainage was standard therapy for CSLD in the past. Recent data
has shown the use of this may indeed increase lung dysfunction related to
increased gastro-oesophageal reflux and possible aspiration.43,44 In CF, this
manoeuvre is no longer used in many paediatric centres.
Nutrition
Good nutrition (both macro and micro) is highly important, not only for
reduction of acute respiratory infections in children45,46,47 but is also
related to improved lung function in children with CSLD.48 The effect of
nutrition in the developing lung (children) is more significant than that
on the developed (adult) lung. Aggressive nutritional support is one of the
mainstays of the current management of CF.48 Some children will be on
caloric supplements.

Minimisation of further lung injury

The impact of both active and passive environmental tobacco smoke (ETS) is
highly significant in all situations throughout life and in utero. Rates of
smoking amongst Aboriginal males in NT is higher than the Australian
average (59% vs 54% respectively).18 Whilst the prevalence of smoking in the
mainstream Australian community is declining, that of Indigenous
communities is increasing (personal communication), reflecting the same
pattern as in developing countries.49 Reviews on ETS and its effects on the
developing lung and accelerated lung decline are available elsewhere.50–53
Ezzati and Kammen have recently demonstrated an exposure response effect of
increased exposure to indoor biomass combustion on ALRI, and called for
public health initiatives to reduce average exposure to below 2000µg/m3.54
In addition to public health factors, there is little doubt that
immunisation is fundamental in preventing the development of respiratory
infections, one of the presumed leading cause of CSLD in Indigenous
children. Currently the 23 valent polysaccharide pneumococcal (Pneumovax
23) vaccine is recommended for children >18months and the 7-valent
conjugate pneumococcal vaccine (Prevaner) is expected to reduce the
incidence of pneumonia by at least 30%.55 There is some evidence that the
response of Indigenous children to vaccination can be sub-optimal56 and
repeated immunisation may be required in selected individuals. There is
recent evidence that polysaccharide pneumococcal (Pneumovax) immunisation
of targeted groups only is suboptimal.57 Booster pertussis and annual
influenza vaccination should also be considered.

Follow-up
The aim of regular review is to optimise potential lung growth in children,
prevent premature respiratory decline (where possible) and optimise quality
of life. Indigenous children in remote communities should not be denied the
recommended follow up for children with any form of CSLD. In the CF model,
a three-monthly review is recommended: lung function (for children aged
over six years), assessment and management of pulmonary decline and
infective exacerbations (sputum and cough changes, exertional dyspnoea),
complications of CSLD (pulmonary hypertension, chronic hypoxaemia, poor
growth, sleep disturbance, RAD, haemoptysis) and a review of contributory
factors (e.g. gastro-oesophageal reflux, asthma, environmental smoke
exposure). In our experience of remote Indigenous children, cough is often
under-reported and it is often necessary to exhibit the cough to gain an
appreciation of the nature of the child’s cough. Practitioners need to be
cognisant of these factors and, in addition to a three monthly medical
review, we advocate a minimum half-yearly review by a respiratory
physician. Ideally an intensive team approach with incorporation of allied
health expertise (nursing, physiotherapy, dietitian), as this model has
been shown to improve health outcomes for different diseases.17,58 The
 recommended frequency of medical and specialist review for children with
CSLD is based on the experience in Central Australia where significant co-
morbidities and underlying cilia disease were frequently found. Specialist
programs have shown the greatest impact in the care of children with
bronchiectasis from cystic fibrosis and cilia dyskinesia patients in other
centres.59,60

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treated cystic fibrosis patients: results of aggressive treatment. Pediatr Pulmonol
1996; 21:153–8.
 Sexual Assault and Abuse of
Children

Author: Nettie Flaherty

Topic Reviewers: Judith Hummerston (RAN, Willowra); Yuendumu clinic team; Dr

Peter Tait; Dr Tim Hannah (Timber Creek); Dr Ian Dumbrell (Port Keats)

Introduction
Child sexual abuse may be defined as any sexual act/threat that exposes a
child to, or involves a child in, sexual processes beyond his or her
understanding or contrary to accepted community standards. It is the use of
a child for sexual gratification by an adult or significantly older young
person.1 This broad definition acknowledges that the sexual abuse of
children involves a range of behaviours, including those commonly referred
to as sexual assault or rape, for example, anal and/or vaginal penetration
using a finger, penis or other object. It also refers to behaviours such as
exposing a child to, or involving a child in, pornography; fondling and/or
masturbation of a child; having the child fondle, touch or masturbate the
abuser; and coercing a child to engage in sexual acts with other children.
Understanding this broader definition is important for two reasons.
Firstly, sexual assault conjures up images of ‘stranger danger’, though in
the vast majority of cases children are sexually assaulted by someone they
know, who is in a trusted relationship to them, or to whom they are
related.2,3,4 In shifting the focus from the family, or the immediate
social network, as the site of abuse attention is also diverted from the
dynamics of child sexual abuse, thus compromising the health professional’s
ability to respond sensitively to the child’s situation. Child sexual abuse
is characterised by issues of secrecy, conflicted loyalties and power
amongst people who stand in close relationship to each other. Following
discovery of child sexual abuse there are a myriad of vested interests
involved in pressuring the child (the least powerful member of the family)
to retract, and the non-offending members of the family to disbelieve the
child’s allegations.5
Secondly, in perceiving sexual abuse as including a continuum of behaviours
that typically progress from less- to increasingly-invasive activity,
health practitioners are alerted to those signs and behaviours that may be
indicative of abuse, and the possibility of early identification and
intervention.

Indicators of sexual abuse

When a child has been sexually assaulted (as in rape) they are often
suffering injury and will be brought to the clinic. That they have been
injured because of a sexual assault will often be conveyed to the health
team.
In the absence of any physical evidence it is important to consider
those signs that are suggestive of sexual abuse. Sexual abuse should be
suspected when a child is brought to the clinic with any of the following:
 • Bruises, bleeding or other evidence of physical trauma in the
genital area
• Foreign objects in the genital or rectal openings
• Sexually transmitted diseases
• Pregnancy in a younger girl who refuses to reveal any information
about the father and/or complete denial of the pregnancy by the child
and her family
• Itching, inflammation or infection in urethral, vaginal or rectal
areas
• Trauma to breasts, buttocks or thighs6

A number of behavioural indicators are signs that a child is experiencing

significant stress, including:
• Regressive behaviour in younger children
• Sudden fears or phobias
• Running away from home
• Noticeable personality changes
• Changes in school performance
• Suicidal thoughts or attempts, or self-harming behaviours
• Withdrawal from peers
• Extreme mistrust6

Some behaviours are more directly related to the possibility of sexual

abuse, including:

• Drawings of an explicit sexual nature

• Age-inappropriate sexual play
• Bizarre, sophisticated or unusual sexual behaviour or knowledge
• Overtly seductive behaviour
• partial or full disclosure6
In some communities children are often allowed to watch videos of their
choosing without parental or other adult supervision or guidance. These may
include age-inappropriate sexually explicit material. Some remote
practitioners suggest that exposure to such material makes drawing any
conclusions based on age-inappropriate sexual play or advanced sexual
knowledge fraught. Others argue that exposing young children to such
material is itself abuse, and may at times be a part of a ‘grooming
process’, leading to more explicitly abusive behaviours. (See below ‘Stages
of sexual abuse’.) It is important not to assume that children displaying
unusual sexual behaviour or knowledge are doing so only as a consequence of
exposure to sexually explicit videos, and therefore to discount the
possibility of abuse. It may also be helpful to discuss the issue of access
by children to sexually explicit material with your local child protection
office.

Sexual abuse and other types of abuse

There is growing evidence to suggest that different types of violence occur
simultaneously within families.7,8 Two Australian studies in the early 1990s
examined the possibility of a relationship between child sexual abuse and
domestic violence. Using data from a hospital-based ‘child abuse tracking
study’ Goddard and Hiller9 reported that 40% of identified sexual abuse
cases and 55% of identified physical abuse cases were occurring in families
where domestic violence was also occurring. Tominson tracked suspected
child abuse and neglect cases within a Victorian regional child protection
network.10 This study indicated that domestic violence was a factor in a
sizeable proportion of both child sexual and physical abuse cases. Tominson
found that 19.4% of child sexual abuse cases also involved the child being
physically abused.
Such studies suggest that a violent coercive environment may be almost
as likely for sexual abuse cases as for physical abuse, particularly for
the more severe cases of physical and sexual abuse. Therefore, health
practitioners working with families where domestic violence is a feature
should consider whether behavioural indicators of stress in a child may be
a sign that other abuse is occurring to the child, including the
possibility of sexual abuse.

Sexual abuse in indigenous communities

Accurate data on the rate of sexual abuse of children is not available. In
many communities, including the Indigenous community, dialogue about the
issue of sexual abuse of children is just beginning to be heard by the
wider society. The Aboriginal and Torres Strait islander Women’s Task Force
on Violence revealed widespread concern amongst many Aboriginal people at
the level of sexual abuse of children:11
Throughout the consultations there were calls from both men and women to
expose the severity and serious long-term effects of sexual abuse for
victims, particularly children, who reportedly are increasingly being
sexually violated . . . Time and again the Task Force were told of young
girls becoming pregnant at an early age, some of whom had been sexually
abused repeatedly throughout their lives. Some, through such abuse, had
grown up with a distorted sense of what constitutes a loving, nurturing
and caring relationship . . . Whether by coercion or rape, the incidence
of sexual abuse of minors was indicated to be far more frequent than is
commonly acknowledged. This is an area that warrants urgent attention by
way of increased reporting of offences, appropriate interventions,
expanded education programs, and the employment of more sexual health
workers in all regions, but especially in rural and remote regions.

The clear message from the Task Force was that sexual abuse of children is
not acceptable to Aboriginal people, just as it is not acceptable in the
non-Indigenous community.
For many children whose wellbeing is the subject of a child abuse
notification, including those related to the possibility of child sexual
abuse, a picture of chronic neglect often emerges, characterised by very
poor growth and multiple admissions to hospital in infancy. The wellbeing
of such children is often well below the community norm and they have
commonly been considered to be ‘at risk’ in some way; yet there is no
single incident that may have previously brought the child to the attention
of child protection authorities. Often the trigger for notification is a
positive STI result. It is often unclear who the child’s primary carer is;
rarely the biological parents, often ‘many’ people. Alternatively the
‘named’ carer may be an elderly grandmother, perhaps sick and frail, and
receiving little or no help for many grandchildren. These children may, in
fact, be ‘growing themselves’ up. The extended family system of caring
does, when working well, provide a safety net for many children whose
parents are unable to parent effectively. For some children, however, the
lack of any stable identified carer, or having a carer who has overwhelming
demands placed upon them, leaves them at risk throughout their childhood to
neglect, abuse or exploitation. A positive STI in a child who is growing up
in this environment should always be viewed as strongly suggestive of
abuse.
Identifying and reporting suspicions of child sexual abuse creates
considerable anxiety among heath practitioners everywhere, and particularly
in remote communities. In the absence of a child’s disclosure — or
compelling physical evidence — primary health care staff express
uncertainty in their ability to identify signs that sexual abuse may be
occurring, and discomfort with asking questions about such a sensitive
issue which may generate conflict within the community and place clinic
staff in a vulnerable and potentially unsafe situation. It is vital that if
health practitioners suspect that a child may be being abused, but feel
uncertain about what they should do next, they consult with the local child
protection office for guidance. At a minimum this response attends to your
duty of care toward clients: it may also result in a child being protected
from further abuse.

Teenagers and sexual activity

An area which causes confusion for remote practitioners concerns teenage
sexual activity: a nine-year-old girl engaging in sexual activity causes
alarm, and indicates the need for concern for her general wellbeing, not
just the possibility of sexual abuse. She is clearly too young to legally
consent to sexual intercourse. Who is looking out for her? What are her
parents and other family members doing to guide, care and provide
supervision? Most practitioners would have little difficulty in identifying
this as a case where something is not right, and where notification needs
to occur. However, the question is often asked: at what age is sexual
activity/experimentation simply that and unlikely to be a marker for abuse?
It is important not to place overwhelming confidence in the age of your
client as being a protective factor for abuse: adult women are raped, and
their age does not protect them from this. Nonetheless, young people are
engaging in consensual peer-related sexual experimentation and activities
at younger ages than many realise, or necessarily approve of. Further, in
some communities, the age of marriage is comparatively young — fourteen and
fifteen year olds may be married and parents. Is this OK?
The interface between mainstream Australian law and accepted cultural
practices of minority groups is frequently marked by confusion and
ambiguity. Female circumcision (or genital mutilation), for example, is
specifically outlawed under the child protection legislation of every State
and Territory in Australia. The situation regarding many Indigenous
cultural practices is vague: the NT Criminal Code, for example, makes it an
offence for an adult to attempt to have sexual intercourse with a minor
(i.e. under 16). However, authorities in the Northern Territory and
elsewhere have, of necessity, taken a common sense interpretation of the
law: it would be rare for a nineteen-year-old to be charged with having
consensual sex with his fifteen-year-old girlfriend. The purpose of this
provision of the criminal code is to protect a vulnerable group from
exploitation, and to acknowledge the real power adults have over children
and young people. Even though a technical or literal interpretation of the
code would suggest an offence has occurred, where the circumstances
demonstrate that no such exploitation exists, such as in the example given,
charges are unlikely to be laid.
Child protection legislation generally defines ‘child’ as a person under
18. The purpose of this legislation is not to regulate sexual activity
among young people, nor to arbitrarily intervene in cultural practices that
affect young people, but rather to protect them from abuse and
exploitation. There is, and always will be, a ‘grey’ area at the border of
any accepted cultural practice, and what over time that culture continues
to find acceptable. It is important to remember there is considerable,
although not complete, agreement across cultures about what constitutes
child abuse and neglect. A fourteen-year-old may be ‘married’ and abused,
or not married and abused: there may be considerable disagreement across
cultures about whether a fourteen-year-old should be allowed to get
married, and surprising agreement about whether her partner’s behaviour
toward her is abusive. If you have concerns about a young person, even if
vague, it may be helpful to consult with your local child protection
office.

Stages of sexual abuse

Our understanding of the ‘progressive nature’ of sexual abuse tells us that
if we do nothing, not only will it not go away, it will most likely get
worse.6,12 The abuse may have begun with subtle behaviours at age six, and
progressed through a range of increasingly intrusive behaviours over a
number of years. It also helps us understand why children, when they tell
their story (and particularly under cross-examination) get muddled.
The following stages in the sexual abuse process have been described
but, like most stages in a process, do not necessarily unfold in such a
linear fashion for every child.13

Engagement or entrapment phase

The offender initiates the contact with the child or young person by
offering bribes or rewards, or special attention or affection. This stage
requires the offender to have access and opportunity, and for the offender
and the child to have some form of relationship: sometimes this stage is
the building to this relationship, and has been called the ‘grooming’
stage.

Sexual interaction stage

Once the child responds favourably to the special attention, some form of
sexual activity begins. This may begin as subtly as ‘accidentally’ looking
at the child undressing. However, it typically progresses toward more
obviously sexual behaviours, often involving penetration.

Secrecy stage
Once the sexual activity has begun secrecy must be maintained. This is
usually achieved by:
• Threatening that no-one will believe the child if they tell;
• Threatening that telling will mean something bad will happen to the
offender and it will be the child’s fault
• Threatening that the young person will be punished and will be removed
from the home
• Threatening that everyone will think the child/young person ‘asked for
it’ because they let it go on for so long
 • There may also be threats of, or actual, physical abuse to intimidate
the child.

Disclosure
Occurs when the secret is told, or discovered. Although all types of
disclosure results in a crisis for the child, and their protection must be
paramount, accidental disclosures (e.g. the discovery of a pregnancy) mean
the child is completely ill prepared for the disclosure.
When a child does disclose it is usually tentative and hesitant,
characterised by forgetting, minimising, distancing and discounting.14 The
response of the person listening to the disclosure will be communicating to
the child whether it is safe for them to continue.15 (See below ‘Appropriate
professional response to disclosure’.)

Suppression
If family members blame or punish the child, or dismiss their allegations,
the disclosure may be withdrawn. The child will then believe the offender’s
previous threats: this is most common where the abuse has occurred within
the family and the family do not believe the child. Some commentators
perceive retraction as a ‘normal’ part of the process.12 Whether this is
true or not, it is important to bear it in mind, so that if it occurs you
do not get ‘thrown’ when it occurs, and as a consequence decide not to
report the disclosure.

Reactions to the disclosure

Offenders generally react with alarm, and almost always deny the
allegation. After the child’s disclosure the offender can be expected to
exploit his power to control the child, other family members, and the
professionals involved. This may involve threats to harm.13,12
It is important to be mindful, when deciding which health worker or
community member to seek assistance or advice from, that there will be
people who have an interest in convincing the child to retract their
statement. Therefore, it is preferable to seek this advice from someone who
is not related to the alleged offender.
The non-offending parent is usually a mother.2,3,4,16 Many will react
immediately by expressing concern and responding protectively, but not all
will be able to maintain this stance throughout. Others may react with
disbelief and anger, particularly if she is dependent economically or
socially on the offender, or is fearful of retribution.
The vulnerability of the ‘non-offending parent’ is often underestimated.
When mothers do not respond ‘appropriately’, i.e. with a stance of belief
and support, they are often conceived of as somehow responsible for
creating the circumstances which have allowed the abuse to occur.5,17 There
is limited research available which considers the process of belief for
mothers. This shows that the ‘attainment of belief was inextricably linked
to the process of disclosure and discovery’, and even for those mothers who
were able to maintain a stance of belief, a period existed where they were
unconvinced that the sexual abuse of their child had occurred.5,17 All
mothers also experienced periods of ambivalence where they did not know
what to believe, and this ambivalence included both cognitive and emotional
aspects. Humphrey’s5 study over a six month period following disclosure
showed that mothers could move from belief to ambivalence to disbelief and
vice versa.
 Such movement suggests that the mother’s perception of the event is not
fixed and needs to be understood by practitioners who make judgements
about the mother’s position early in the assessment . . . The difficulties
in sustaining a stance of belief, protection and support, however, were
much greater for women who were attached or who had ambivalent feelings
towards the abuser who had been her partner prior to disclosure.

Thus, the safety of the child is a matter that requires ongoing assessment
and evaluation: the mother’s ability to provide protection and support for
her child is affected by her ability to attain and maintain belief. When
there is no collaborative physical evidence to support the child’s
disclosure, the non-offending parent is often left alone to defend the
child. Her subjective assessment of the validity of the child’s claim
becomes the arena for a power struggle between the abuser’s denial and the
child’s version.
This struggle is an uneven contest in which mothers reported that the
abuser and the forces which sustained him through his cultural, emotional,
economic and legal position had the upper hand.5

Appropriate professional response to disclosure of child sexual assault

It is important, if possible, to refrain from an overly emotional reaction
to a child’s disclosure of sexual abuse. In the absence of any injury that
needs attention, your role is to listen and provide support to the child,
and not to investigate the allegation. The best response is one where you:
• Show the child that you believe them
• Tell the child it is not their fault, whatever happened
• Say that adults sometimes do the wrong thing
• Tell the child this has happened to other children, not just them
• Tell the child they did the right thing by telling you
• Tell the child you will now try to stop it happening, and to do that
you have to tell the child protection agency.

Given one of the central issues in child sexual abuse is the betrayal of
trust, it is important you do not unintentionally demonstrate this by
making promises you cannot keep. One of these promises may be to reassure a
child you will not tell anyone: this is not a promise you can keep. The
risk to the child is high once they have disclosed, and considerable
pressure may be exerted to get the child to retract. Trying to confront the
perpetrator yourself, to ‘sort it out’, is not appropriate, and may
undermine subsequent police and/or statutory child protection
investigations. The end result may be a child who is at greater risk.
Do not push the child into telling you details of the abuse.
Interviewing children who have disclosed sexual abuse, in a manner that
attends to both therapeutic and evidentiary needs, is a specialist skill.
Repetitive questioning of the child is not only stressful for the child,
and may be experienced by the child as disbelief, it increases the
opportunity for the verbal evidence to be ‘contaminated’. Whilst the
successful prosecution of offenders is not the domain, or necessarily the
interest, of the health professional, it is important they do nothing to
obstruct this process. Even if criminal charges are not forthcoming, there
may need to be a Court hearing to arrange protection of the child. Further,
for some victims a successful prosecution, though unlikely, is part of the
healing process.
 If the child does want to talk, carefully document what was said, by the
child and by your self. In most health settings information is elicited
using focussed questions, and this type of question implies a desired
response. It is vitally important that you endeavour to keep focussed
questions to a minimum, because focussed questions carry with them, on a
continuum, a degree of risk regarding suggestibility. Focussed questions,
which draw information from recognition rather than recall memory, increase
inaccurate responses. This can be minimised by following a focussed
question by and open-ended question, thus placing the burden back on the
more accurate recall memory:18
In talking with the child it is important:
• Not to ask questions that contain the answer. For example, better to
ask ‘Where did it happen?’, rather than ‘Did it happen at your house?’
• Not to ask questions that contain a choice of answers. For example,
better to ask ‘How did you feel?’ rather than ‘Were you scared, or
angry or sad?’
• Not to name the suspected offender before the child has identified the
person. For example, better to ask ‘Who touched you?’ rather that ‘Did
your dad touch you?’

Prevalence
Boys and girls of all ages and from all cultural groups can be the victim
of sexual abuse. Most sexual abuse, like most sexual assault, goes
unreported.19 Child sexual abuse is characterised by secrecy: most ongoing
sexual abuse is rarely disclosed outside the immediate family. Reported or
investigated cases are the exception, not the norm.15,16 Sexual abuse is
often an area members of the public and professionals feel uncomfortable
about reporting because the allegation and the consequences, if proved, are
significant.
There are methodological problems with determining prevalence. These
include:
• Different definitions of sexual abuse across jurisdictions
• Questions of whether to include contact and non contact types of abuse
• Whether to use the victim’s subjective experience of an experience as
abusive, or whether to define abuse by things such as the age
difference between victim and offender
• Varying upper age limits on what constitutes a child.

Figures are frequently quoted estimating that one in every three to four
girls, and one in every seven to eight boys, have experienced some form of
sexual abuse by the time they are eighteen.16,20These figures have remained
relatively stable over the past decade or so, but they do include all forms
of behaviour that falls within the continuum of sexually abusive
behaviours.
It is not possible to have reliable data that sexual abuse has occurred,
even amongst those cases that are reported. One is usually faced with a
child’s disclosure that abuse has occurred, and an opposing adult statement
that it has not. It is rare for there to be witnesses, and unlikely to be
collaborative physical and/or medical evidence. In the NT in 1999–2000 11%
(42 children) of substantiated child abuse cases involved sexual abuse, in
Western Australia 27% (311 children) and in Queensland 6% (398 children).21
How many of these substantiated cases were what would commonly be referred
to as sexual assault is not known.

Do children make up stories of sexual abuse?

It is rare for children to make stories up about sexual abuse.3 In fact,
most sexual abuse of children and young people remains undisclosed and
unreported.3,12,16 Research has shown that, even where there is physical
evidence that suggests sexual abuse, disclosure does not always follow.
Lawson and Chaffin15 highlighted the difficulties that children, from age
three through to adolescence, had in disclosing sexual abuse. Over half of
the sample (57%) who were diagnosed with an STD did not disclose sexual
abuse. Sauzier 22 studied 156 children who had been referred to a program for
sexually abused children. Only 50% had disclosed abuse: the discovery of
abuse in the remaining children came about through the suspicions of
others. Two factors that decreased the likelihood of a child disclosing
abuse emerged in this study. Although aggression was equally likely to lead
to non-disclosure as to reporting immediately, threats and manipulation
inhibited disclosure. Children were also less likely to disclose when the
perpetrator was their father, or father figure.
After a review of the literature, Salter concluded that false reports by
children are rare and may occur in no more than 2% of cases.23 While it is
important to determine when a child is lying, and to ensure that we do not
support false allegations, the reality is that proving genuine disclosures
and protecting children from repeated abuse is the more pressing problem.3

How do protective workers decide whether sexual abuse has occurred or

not?
The protective worker’s decision of whether to substantiate sexual abuse is
based on gathering relevant data, followed by deciding what degree of
confidence could be applied to the decision as to whether sexual abuse has
occurred or not. Factors which assist the protective worker decide, in the
absence of physical evidence, whether abuse is more likely than not to have
occurred include:6,13,18,24
• The child’s statement, including such things as explicit detail,
word and sentence formation, a story that is told from the child’s
perspective, and the emotional and psychological responses of the child
• The content of the narrative, including the pattern of abuse, the
element of secrecy, coercion or threats
• Supporting features include the family history, such as other abusive
behaviours, substance abuse issues, and parental history of sexual
abuse
• The behaviour of the child during the time the abuse was happening
• The way the disclosure unfolded, who was told and why
• Consistency of the account in relation to different statements made by
the child to the core elements of the abuse, but not necessarily to the
peripheral aspects
• The child’s knowledge of sexual anatomy and function, and whether this
is developmentally and culturally congruent.

Perpetrators
Perpetrators of child sexual abuse constitute a markedly heterogenous
group.25,26 Wurtele and Miller-Perrin25 note that ‘the only common denominator
appears to be an offender’s lack of sensitivity to the child’s wishes and
needs, along with a willingness to exploit the child’s trust for the
abuser’s own gratification, profit or selfish purpose’.
At least 85% of perpetrators are known to the child, and they are most
commonly heterosexual men.16 In an Australian study16 the average age of
offenders against girls was about 30 years, and against boys about 22
years. (The average age of the onset of sexual abuse amongst the children
is about eight and a half years.)25
Of recent concern is the growing number of adolescent sexual offenders.4
Adolescents displaying the early signs of sexual offending tend to grow up
and commit sex offences until they are caught. Like adult offenders,
adolescents comprise a diverse group, with few broad characteristics.
Perhaps one of the most widely reported is a history of sexual abuse or
other maltreatment. While most male children who have been sexually abused
do not grow up to become offenders, widely divergent rates of prior abuse
have been reported in studies of male perpetrators. The victi-into-
victimiser has been estimated at variously between 30% and 70%.26
To date work with perpetrators and research studies has failed to typify
offenders by class, profession, family status, religion, ethnic group or
socioeconomic status.4 Neither has a psychological profile of a ‘typical
offender’ been able to be constructed. However, Finkelhor has proposed a
four-part model which identifies the conditions necessary for abuse to
occur:27
• A potential offender must have some motivation to sexually abuse a
child. They must feel some form of emotional congruence with the child,
sexual arousal with the child must be a potential source of
gratification, and alternative sources of gratification must be either
unavailable or less satisfying.
• Any internal inhibitions against acting on the motivation to engage in
sexual abuse must be overcome. For example, drugs or alcohol may be
used to lower inhibitions against offending. This may be combined with
the greater tolerance shown toward people who commit crimes whilst
under the influence of substances.
• Any external impediments to acting on the impulse must be overcome.
Inadequate care by a parent or guardian, maternal illness or absence,
or being the carer, can provide this opportunity.
• Avoidance or resistance on the part of the child must be overcome.
This may involve enticing an emotionally deprived child into accepting
inappropriate attention, or using overt coercion to achieve domination.

After abuse has occurred

The effects of childhood sexual abuse can extend well into adulthood,
particularly if the child did not receive appropriate help and support.
These effects include depression, withdrawal, anger, running away, self-
harm, substance abuse, sexual acting-out and suicide attempts.20 Other
reported effects include phobias, panic attacks, nightmares, sleep
disturbance, difficulty in establishing and maintaining relationships and
sexual difficulties.28,29
Although sexual abuse can have a long lasting psychological and emotional
impact, some people who are abused appear to suffer no serious trauma or
symptoms. Finkelhor20 reviewed the literature and concluded that between
one quarter and one third of sexually abused children have adequate
psychological and social resources to cope without experiencing serious
trauma or long lasting effects.
The effects of abuse are likely to be less serious if the abuse does not
involve force or violence, if there is no penetration, if it is of
relatively short duration, and if the abuser is not a father or father
figure.
Parental and social attitudes toward the child and their role in the abuse
are important determinants of the long-term effects of abuse. Prognosis is
best for those children who have been believed, who are not blamed, who
have family support, secure relationships, stable home environments and who
get appropriate counselling as needed.3,20,29
In order for families to support their child, it is important that they are
reassured that their child can lead a normal life, and that they can
recover.

References
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Bacon, 1989.
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The Free Press, 1984.
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Therapists Guide to Working with Adults, Children and their Families. New
Zealand: Oxford University Press, 1995.
4. Tominson AM. Update on Child Sexual Abuse Issues in Child Abuse and
Prevention. No5 Summer, 1995.
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18. Street H. Is it possible to establish the truth of a child’s
statement alleging sexual abuse? Adoption and Fostering 1996/7; 20(4):7–15.
19. Children’s Protection Society. Child Sexual Abuse Treatment Program:
Program Document. Victoria, Inc, 1993.
20. Finkelhor D. Early and long term effects of child sexual abuse: an
update. Professional Psychology: Research and Practice 1990; 21(5):325–30.
21. Johnstone H & Kelly S. Child Protection Australia 1999–00. Child
Welfare Series No 27, Australian Institute of Health and Welfare. Canberra:
AGPS, 2000.
22. Sauzier M. Disclosure of child sexual abuse: for better or for
worse. Psychiatric Clinics of North America 1989; 12:455.
23. Salter AC. Treating Child Sex Offenders and Victims. Newbury Park,
CA: Sage Publications, 1988.
24. Bradford R. Developing an objective approach to assessing
allegations of sexual abuse. Child Abuse Review 1994; 3:93–101.
25. Wurtele SK & Miller-Perrin CL. Preventing Child Sexual Abuse:
Sharing the responsibility. Lincoln: University of Nebraska Press, 1993.
26. Watkins B & Bentovim A. The sexual abuse of male children and
adolescents: a review of current research. Journal of Child Psychology and
Psychiatry 1992; 33:197–248.
27. Finkelhor D. Chapter 2 in Myers JEB (ed) The Backlash: Child
Protection Under Fire. Thousand Oaks, California: Sage Publications, 1994.
28. Browning DH & Boatman B. Incest: Children at risk. American Journal
of Psychicatry 1977; 134:69–72.
29. Mullen PE & Fleming J. Long-Term Effects of Child Sexual Abuse.
Issues in Child Abuse Prevention. No.9, Autumn. Australian Institute of
Family Studies, 1998.
 Urinary Problems in Children

Author: Dr Kieth Edwards (community paediatrician Darwin)

Topic Reviewers: Editorial committee

Rationale for changes to CARPA STM 3rd edition

Summary
Minimal changes include: heading; reallocation of the symptom section by
age to avoid repetition and to emphasise that one or more symptom may be
present; highlighting of the STI/sexual assault section.
The ‘Using a dipstick to look for UTI’ section was removed.
Amplification of the diagnosis protocol /flow chart and insertion of a
‘follow-up’ protocol/flow chart to strengthen surveillance for UTI in
children at risk. Changes to follow-up section include omission of
‘Children less than five years old’ section and ‘Children over five years’
section as covered in flow chart. Also, summary box deleted for same
reason. Replaced by prophylaxis box.
1. Heading change:
‘Urine Problems in infants and children (3 months to 12 years)
(Sick babies less than 3 months see page 86)’
Sick neonates may have multiple sites of infection and need urgent
treatment and different antibiotics and should be considered to have
‘neonatal sepsis’ rather than a UTI.
2 Paragraph headed: ‘Urine problems in children include: . . .’ and
‘urinary system’ removed, as ‘kidney disease’ is enough.
3. Paragraph headed ‘Urinary Tract Infection’. Symptom lists by age
were rationalised to avoid repetition and to emphasise that infant/child
may only have one of the symptoms. STD/sexual assault sentence
highlighted due to increased importance.
4. Paragraph headed ‘When you use the dipstick to look for a UTI, take
care’. This paragraph deleted as the issues are dealt with in the
protocol. Also to wait for the result of the M,C&S is potentially
harmful.
5. Diagnosis-treatment flow chart/protocol. Amplified to show steps more
clearly and to emphasise not sending M,C&S sample if dipstick test is
normal. Also, the changes recommend treating immediately for UTI if
nitrites and leucocytes are present as there is evidence that delay in
treatment increases the risk of renal damage. The treatment for UTI is
also changed based on NT urine pathogen sensitivities, Australian and
international evidence based recommendations. The current single daily
dose of Augmentin for three days is likely to be inadequate and increase
the failure/recurrence, and hence renal damage rate. Augmentin still best
first-line drug, with Co-trimoxazole recommended as second-line in
infants older than six months who are not sick. The protocol also
emphasises that infants less than six months, those with D+V or not
improving should be given IM gentamicin and referred immediately. The old
protocol does not make this emphasis.
6. Insertion of a follow-up flow chart/protocol. This is needed to
emphasise the need for surveillance (rechecking dipstick) in children who
 have had a definite or possible UTI and the importance of arranging renal
investigations and checking that they have been done. Also, the
importance of considering prophylactic antibiotic for all children with
renal abnormalities below five years of age and some above five years.

[Editor: The previous table of ‘normal BP in children’ has been replaced

with a guide for what should be thought of as high BP in children, as this
is what it is to be used for. The table is derived from a chart used in the
Adelaide Women’s and Children’s Hospital. (Blood pressure in school
children measured under standard conditions. Jureidini, et al. Med J Aust
1988; 149:132–34.]

Current understanding of UTIs in Aboriginal children

• Renal tract structural abnormalities predispose to UTI e.g., pelvo-
ureteric junction (PUJ) obstruction, vesico-ureteric reflux, urethral
valves, bladder diverticulum
• Stone formation within the renal tract also predisposes to
infection, and renal stones are common in Aboriginal children
• UTI is common in young Aboriginal children
• Chronic renal disease is common in adult Aboriginals, and it is
likely that renal damage begins in childhood
• Surgical correction of vesico-ureteric reflux is no more effective
than prophylactic antibiotics in preventing recurrent UTIs and long-term
outcome
• Renal scarring occurs most frequently in young children and infants
• Some children have chronic UTIs which are asymptomatic and not
diagnosed
• Asymptomatic haematuria is common in Aboriginal children
• Micturating cysto-urethrogram (MCUG) is a distressing invasive
procedure for most children. It detects vesico-ureteric reflux and
bladder abnormalities
• Renal ultrasound is a non-invasive well-tolerated investigation
which can detect most cases of renal scarring, but not all. It can also
detect severe vesico-ureteric reflux when dilatation of the ureter is
present.
• DMSA renal scan detects renal scarring more reliably than
ultrasound. It is semi-invasive as IV access is required
• Compliance is poor with prophylactic antibiotics in Aboriginal
children
• Third edition CARPA antibiotic regimen for UTIs is likely to result
in inadequate treatment of UTIs, particularly in young infants. Single
‘double dose’ oral treatment with Augmentin for three days only may have
these problems:
– Young infant more likely to spit/vomit dose
– 29% of infections in children under five in NT have complete or
partial resistance to Augmentin
– Improved outcome five to 21% with seven- to 10-day course

• ‘Clean’ urine specimen collection problematic at the community

health centre level (only ‘bag’ specimen possible, delay in obtaining M,C
& S result)
Changes recommended
In view of the potential poor renal prognosis in Aboriginal children,
diagnosis and treatment for possible UTIs needs to be improved. In view of
the initial uncertainty in diagnosis whilst awaiting M,C&S results the
trend should be to over treat rather than miss episodes of UTI. In
addition, those children who have had a proven UTI should be investigated
properly and kept on prophylactic antibiotics if indicated. Children who
have had a UTI should always have urinalysis checked when they are sick.

Evidence reviews: What are the effects of treatment of acute UTI

in children?
Placebo controlled trials of antibiotics for symptomatic acute UTI in
children are considered unethical. We found little evidence on the effects
of giving early empirical treatment versus awaiting the results of
microscopy or culture. Five retrospective studies found that delayed
treatment may be associated with increased rates of renal scarring, but we
found inconclusive evidence on the effects of shorter delays. Two
randomised controlled trials (RCTs) have found higher cure rate
(eradication of causative organism) with antibiotic treatment for seven
days or longer versus shorter courses. One RCT found no significant
evidence of a difference between oral and intravenous antibiotics for acute
treatment in children under the age of two years with an uncomplicated
first UTI.

Benefits versus placebo

We found no RCTs.

Immediate empirical versus delayed treatment

We found no RCTs comparing immediate empirical treatment versus treatment
delayed while microscopy or culture results are awaited. Five retrospective
observational studies found increased rates of scarring in children in whom
diagnosis was delayed between four days (in acute UTI) to seven years (when
a child presented with chronic non-specific symptoms).1
We found one RCT that compared oral cefixime for 14 days (double dose on
day one) versus intravenous cefotaxime for three days plus oral cefixime
for 11 days for UTI in children under two years (see below). It found no
evidence that children treated 24 hours after the onset of fever were at
greater risk of renal scarring than children presenting within 24 hours
(9/99 [9%] of children presenting before 24 hours developed scarring vs
19/159 [12%] of children presenting later; RR 1.3, 95% CI 0.6 to 2.7; P =
0.29). However, this incidental analysis was done retrospectively.2

Long versus short courses

We found one systematic review (search date not stated, 14 RCTs) comparing
short course (single dose to four days) versus longer courses (seven to 10
days) of a range of antibiotics.3 It found two RCTs that were adequately
powered to find an effect. One RCT (49 children) compared amoxicillin
single dose versus 10 day regimen, and the other RCT compared cefadroxil
one day versus 10 day regimen.4,5 Both RCTs found that longer courses cured
(eradication of causative organism on four days’ follow-up culture)
significantly more children (results from the higher quality RCT4: AR of
failure to cure 14/38 (37%) with short course vs 2/27 (8%) with long
course; ARI short vs long course 29%; RR 4.6; no 95% CI provided; P <0.01).
The remaining 12 RCTs found no significant difference between long versus
short courses but were too small to rule out a clinically important
difference (see comment below). We found no RCTs comparing five day courses
of antibiotics with other regimens.

Oral versus intravenous antibiotics

We found one RCT (309 children, age under two years, fever >38.2?C, first
UTI confirmed from catheter specimen), which compared oral cefixime for 14
days (double dose on day one) versus intravenous cefotaxime for three days
plus 11 days of oral cefixime.2 It found no significant difference between
treatments in mean duration of fever (24.7 h with oral treatment vs 23.9 h
with IV; P = 0.76), re-infection rate (132/153 (86.3%) with oral treatment
vs 134/153 (87.6%) with IV treatment; P = 0.28), incidence of renal
scarring (intention to treat analysis: 15/153 (10%) with oral treatment (21
children not scanned and counted as having no scarring) vs 11/153 (7%) with
IV treatment (13 children not scanned); P = 0.21), and mean extent of
scarring (8% of renal parenchyma with oral treatment vs 9% with IV
treatment).

Harms
Long versus short courses: The studies did not report comparative harms
for long versus short courses of antibiotics nor for immediate versus
delayed treatment.

Oral versus intravenous antibiotics: One RCT found weak evidence from a
post hoc subgroup analysis in children with grade III–IV reflux that
renal scarring at six months may be more common with oral versus
intravenous treatment (new renal scarring within six months: 8/24 (33%)
after oral antibiotics vs 1/22 (5%) after IV antibiotics; ARI 29%, 95% CI
8% to 49%; NNH 3, 95% CI 2 to 13).2

Comment
Versus placebo: Placebo controlled trials would be considered unethical
because there is a strong consensus that antibiotics are likely to be
beneficial. The improved response seen with longer versus shorter courses
of antibiotics is indirect evidence that antibiotics are likely to be more
effective than no treatment.

Long versus short courses: The systematic review comparing long versus
short courses of antibiotics rigorously evaluated the methods of the
included studies. It found that few studies accounted for confounding
factors such as age, sex, and previous UTI. Those that considered these did
so by selecting one subgroup only and not by stratifying children according
to these factors. This limits the ability to generalise about the results.
The 12 trials that found no evidence of a difference between long and short
courses were too small to exclude a clinically important effect.

Oral versus intravenous antibiotics: The trial comparing oral versus

intravenous antibiotics excluded three of 309 children because
investigators considered that the severity of symptoms in these children
warranted intravenous treatment.2
 Which children benefit from diagnostic imaging?
We found no evidence of benefit from routine diagnostic imaging of all
children with a first UTI. We found indirect evidence suggesting that
subgroups at increased risk of morbidity may benefit from investigation.

Benefits
We found no RCTs. One systematic review (search date 1994, 63 descriptive
studies) found no direct evidence that routine diagnostic imaging in
children with UTI was effective.1 The quality of studies was generally poor,
and none included clinically important long-term outcome measures.

Harms
The studies reported no evidence of harms. Potential harms include those
relating to radiation, invasive procedures and allergic reactions to
contrast media.

Comment
Subgroups of children at high risk of morbidity, including those with
vesicoureteric reflux, may benefit from early investigation.1 However, it
may be difficult to identify such children clinically.6 One prospective
study found that the highest rates of renal scarring after pyelonephritis
occurred between one and five years of age.7 A further study found that
presentation with pyelonephritic symptoms in children of all ages is
associated with high rates of renal abnormalities (abnormal initial scans
in 34/65 (52%) children).8

References
1. Dick PT, Feldman W. Routine diagnostic imaging for childhood urinary tract
infections: a systematic overview. J Pediatr 1996; 128:15–22. Search date 1994;
primary sources Medline, Current Contents, and hand searches of article
bibliographies.
2. Hoberman A, Wald ER, Hickey RW, et al. Oral versus initial intravenous therapy
for urinary tract infections in young febrile children. Pediatrics 1999; 104:79–86.
3. Moffatt M, Embree J, Grimm P, Law B. Short-course antibiotic therapy for urinary
tract infections in children: a methodological review of the literature. Am J Dis
Child 1988; 142:57–61. Search date and primary sources not stated.
4. Avner ED, Ingelfinger JR, Herrin JT, et al. Single-dose amoxicillin therapy of
uncomplicated pediatric urinary tract infections. J Pediatr 1983; 102:623–7.
5. McCracken GH, Ginsburg CM, Namasonthi V, et al. Evaluation of short-term
antibiotic therapy in children with uncomplicated urinary tract infection. Pediatrics
1981; 67:796–801.
6. Smellie JM, Normand ICS, Katz G. Children with urinary infection: a comparison of
those with and those without vesicoureteric reflux. Kidney Int 1981; 20:717–22.
7. Benador D, Benador N, Slozman D, Mermillod B, Girardin E. Are younger patients at
higher risk of renal sequelae after pyelonephritis? Lancet 1997; 349:17–19.
8. Rosenberg AR, Rossleigh MA, Brydon MP, Bass SJ, Leighton DM, Farnsworth RH.
Evaluation of acute urinary tract infection in children by dimercaptosuccinic acid
scintography: a prospective study. J Urol 1992; 148:1746–9.
Alcohol: Acute problems and
withdrawal syndrome
Author: Dr Moira Sim
Topic Reviewers: Dr Peter Tait; Dr Steven Skov; Dr Dan Ewald; Vivien (RAN, Amata
Clinic); Kaz Knudsen (RAN, WA); Dave Corstorpan (RAN, Nyirripi Clinic); Jane Kollner
(RAN, Ampilatwatja); Teresa Bowmen (RAN, Papunya)
Harmful effects of alcohol
Harmful effects of alcohol include problems related to the following:
Regular use Cardiovascular
Gastrointestinal
Central Nervous System
Metabolic & nutritional
Pregnancy
Intoxication Increased risk of accidents
Increased risk of violence
Dependence Family breakdown Financial crises
Lost work days
Crime
Hypertension
Arrhythmias
Cardiomyopathy
Gastrointestinal bleeding
Peptic ulcers
Fatty liver
Hepatitis and cirrhosis
Headache
Insomnia
Reduced coordination
Mood (depression &
anxiety) and personality
changes
Memory loss
Wernicke encephalopathy
(opthalmoplegia, ataxia &
confusion) Korsakoff’s
psychosis (loss of memory
and confabulation while
other cognitive function
is relatively intact)
Peripheral neuropathy
Impotence
Hyperuricaemia & gout
Thiamine deficiency
(Wernicke Korsakoff)
Folate and B12 deficiency
Birth defects (foetal
alcohol syndrome)
Assessment
Key issues to consider in assessment are as follows:

Drug history Amount, frequency and circumstances of alcohol use

All drugs used (licit and illicit): look for polydrug use
Treatment history Previous periods of abstinence
Previous experience of withdrawal and complications
Helpful and hindering factors in previous treatment
Dependence A maladaptive pattern of substance use leading to significant
impairment with ? 3 of the following occurring at any time over a 12
month period (DSM IV):
•tolerance
•withdrawal
•substance taken in larger amounts/periods than was intended
•persistent use despite desire and efforts to cut down or control
•a great deal of time spent in obtaining, using and recovering from
effects of substance
•important activities reduced because of substance use
•substance use continues despite knowledge harm caused
Other Medical Liver damage
Problems Poor nutrition
Neurological impairment
Other general medical problems (all cause morbidity higher in alcohol
use)
Psychiatric problems Depression and anxiety are common
Psychosis
Psychosocial issues Supports
Barriers
Goals and expectations in treatment
Physical effects of Evidence of withdrawal (see below) or intoxication (alcohol on
alcohol use breath, ataxia, slurred speech, sedation, hypotension, disinhibition)
Evidence of disease associated with alcohol: jaundice, Cushingoid
appearance, red eyes, prominent facial capillaries, spider naevi,
palmar erythema, Dupuytren’s contracture, hepatomegaly, cardiomegaly,
hypertension, peripheral neuritis
Withdrawal
The alcohol withdrawal syndrome is more likely to occur following cessation of at
least eight standard drinks of alcohol daily for at least several months. It
consists of autonomic and CNS hyperactivity.
1 standard drink = 10 g alcohol = 1 glass (120 ml) wine = 1 midi (285 ml) beer = 2
midis light beer = 1 glass (60 ml) port = 1 nip (30 ml) spirits.
Symptoms of withdrawal
Cardiovascular Tachycardia and hypertension

Respiratory Tachypnoea

Gastrointestinal Nausea, vomiting and diarrhoea

Central nervous system Agitation & anxiety

Tremor
Insomnia and nightmares
Depression
Hypersensitivity to stimulation & seizures
Confusion, disorientation & hallucinations

Skin Perspiration

[Editor: A mild fever can be part of the alcohol withdrawal syndrome, but always
check for other cause of fever.]
Withdrawal scales can be useful in the assessment of the degree of withdrawal. The
two most commonly used scales in Australia are the CIWA-Ar (Sullivan JT et al
1989. Br J of Addiction 84: 1353–1157) and the AWS (Novak, H (ed.) 1989. Nurse
Education and Nursing Management of Alcohol and other drugs. CEIDA: Rozelle NSW).
The former has 10 features to score and has been better validated in research, but
the AWS (which has seven features to score) is briefer and somewhat easier to use.
The current score recommended in this book is based on the AWS.

Detoxification
Arriving at the point of choosing to cease or reduce a drug is not easy and
although many people may make this decision, multiple attempts are required before
a sustained change is achieved. It is important therefore to be responsive to the
‘window of opportunity’ when a person presents wanting to reduce and or cease
alcohol use.
Detoxification is only the beginning of a treatment plan. Many people relapse
following initial detoxification. It is important to use the opportunity of
detoxification to discuss longer-term goals and plans for providing support and
preventing relapse.
In most cases detoxification from alcohol happens without any formal care from
health care professionals. However, in the case of moderate to severe alcohol
withdrawal, there is a risk of severe complications.
During detoxification the aim should be to support, improve comfort and to
avoid complications. The most important complications are delirium tremens,
Wernicke’s encephalopathy and seizures.
Withdrawal treatment regimen
Supportive care
Aim Action
Minimising Physical comforts: quiet, calm, clean, warm conditions,
discomfort baths
Monitoring and Monitoring for signs of severe withdrawal and complications
reducing such as delirium tremens
complications
Encouragement of Counselling is not appropriate during acute withdrawal but
engagement in consistent encouragement of later follow up is worthwhile.
longer
term treatment

Medication
Aim
Prevent complications (eg. delirium tremens, Wernicke’s encephalopathy, seizures),
treat symptoms, increase comfort during withdrawal.

Medications used
Sedative drugs reduce CNS hyperexcitability and reduce the risk of complications
such as delirium tremens and seizures. The drug of choice is Diazepam.
Sedation is generally contraindicated if:
• An underlying cause of delirium or confusion cannot be reasonably excluded
(e.g. subdural haematoma)
• Significant intoxication still present
• Blood alcohol level currently > 0.15%
Medications used

Sedation Diazepam: Two possible regimens

(Doses modified accordingto weight, Regimen 1
age, withdrawal symptoms and response) 10–20 mg every two hrs orally
max 60–120 mg in the first 24
hrs
usually minimal sedation
required after first 24 hrs,
medication usually can be
ceased before day four.
Regimen 2 (vary according to
individual needs)
Day 1–2: 10 mg qid with PRN 10
mg for individual variation
Day 3: 10 mg qid
Day 4: 5 mg bd
may taper over two more days.
NB. If previous history of seizures
ensure there has been 40–80 mg of
diazepam given on the first day.
Thiamine 100 mg IM daily for five days,* then
daily oral 100 mg and multivitamins
Other medications which may be The following may be used according to
required symptoms/signsantipsychotics
(haloperidol 5–10 mg oral or 2–10 mg
IM is preferred has it has the least
effect on lowering the seizure
threshold, however be aware of the
risk of seizures, hypotension and
dystonic reactions) [Editor:
Resperidone is also a good choice] NB.
The drug of choice for hallucinations
is diazepam. Haloperidol is used only
if there is limited response to
diazepam. [Editor: Get advice]
Anticonvulsants (carbamezepine or
phenytoin may be required if
withdrawal seizures are refractory to
diazepam
Analgesics (paracetamol)
Antiemetic (metoclopramide or
prochloperazine)
Antidiarrhoeal
Medication for dyspepsia (H2
antagonist [Editor: Or proton pump
inhibitor])
* The evidence does not support the use of oral thiamine since absorption is questionable
(Australian Medicines Handbook 2000).
[Editor: The withdrawal treatment schedule in the fourth edition CARPA STM
protocol empahsises the importance of other factors, such as past history of
complicated alcohol withdrawal, and current illness, such as infection.
Accordingly, the recommended doses of diazepam are given for different clinical
scenarios with and without the risk factors for bad outcomes.
There are a number of diazepam regimens in use in specialist centres in
Australia. They are similar in that they all use ‘solid doses’ of diazepam. We
know of no comparative trials of different diazepam regimens in Aboriginal people.
The differences between the dosing schedules and withdrawal scoring systems is
probably less important than how carefully they are used and how well the person
is monitored.
Other medications, such as metoclopramide for nausea and vomiting are
mentioned, however diazepam is the main treatment and treatment of first choice.
Gastrointestinal symptoms are usually due to the central nervous system reaction
to the withdrawal of alcohol, and largely respond to diazepam. The balance of
symptoms in alcohol withdrawal can vary, and in some instances CNS sedation with
diazepam will occur before gastrointestinal symptoms are adequately controlled,
and additional treatment is needed.
Alcohol is an irritant to the gastric mucosa and can cause acute gastritis.
This is likely to start during the drinking rather than after it has stopped when
withdrawal is prone to start.]

Monitoring for complications

It is important to monitor for complications, being particularly aware of:
• Early signs of delirium tremens
• Seizures
• Over sedation, especially in high risk groups (respiratory disease, hepatic
disease, polydrug users, co-existing medical problems).

Alcohol withdrawal scales used at regular intervals are helpful in monitoring for
complications.

Delirium tremens
Delirium tremens usually occurs two to five days after alcohol cessation or
substantial reduction, but occasionally can occur up to seven days later. While it
usually lasts three days, it can continue on for up to two weeks.
The features of delirium tremens can be remembered using the following
(pneumonic ‘CASE’):

Confusion Confusion, disorientation, delusions (paranoid) and visual, auditory or

tactile hallucinations,
Agitation Extreme agitation, hyperactivity, gross tremor
Seizures Generalised, onset day 1–4 after the last drink
Exaggerated features Autonomic instability (pulse, BP and temperature fluctuations), fluid
balance and electrolytes of withdrawal disturbance, exaggerated response
to stimuli.
Risk factors for delirium tremens
The risk of developing delirium tremens increases if:
• There is a history of previous severe withdrawal reactions
• Withdrawal is severe
• There is concurrent illness such as infection or uncontrolled diabetes.
Mild confusion and disorientation may occur during simple withdrawal, but if
persistent can signal the beginning of delirium tremens. It is important to
consider other differential causes such as Wernicke’s encephalopathy and subdural
haemorrhage.
Hallucinations that occur in DTs are persistent and very distressing. They need
to be differentiated from the following:
• Mild and transient hallucinations of a visual or tactile nature which may
occur at anytime during detoxification.
• Alcoholic hallucinosis that occurs in the presence of a clear sensorium (no
delirium), typically being auditory and derogatory in content. These do not
generally occur during withdrawal.

Differential diagnoses of delirium tremens include all other causes of confusion

including sepsis, hypoglycaemia and other metabolic disturbances, hypoxia, head
injury, Wernicke’s encephalopathy, hepatic encephalopathy and the effects of other
drugs.

The management of delirium tremens

Complications include dehydration, hypotension, arrhythmias, cardiovascular
collapse, renal failure and pneumonia. Delirium tremens is a medical emergency and
is associated with a high mortality rate. Mortality is substantially reduced with
adequate IV hydration, sedation and treatment of complications.

Seizures
Seizures occur in 5% of cases of withdrawal. They usually occur in the first two
days and are generalised and not recurrent. Single episodes of generalised
seizures are not associated with adverse outcome. Seizures are usually easily
controlled by adequate doses of benzodiazepines. Anticonvulsant drugs should only
be considered if seizures are not responsive to benzodiazepines. Status
epilepticus can be treated with intravenous diazepam in standard doses.

Wernicke’s encephalopathy
Wernicke’s encephalopathy is defined by the triad of confusion, nystagmus
with/without opthalmoplegia, and ataxia. However, occurrence of each of the
symptoms/signs of the whole triad is uncommon. Peripheral neuropathy is also
present in 80% of cases. It can be difficult to diagnose since some of these signs
can occur as part of intoxication.
It was common before the introduction of thiamine supplementation of food but
is relatively uncommon now. It is prevented by the use of parentral thiamine.
There is no evidence to support the use of oral thiamine during acute withdrawal
since gastrointestinal absorption can be impaired. Thiamine should be administered
prior to giving glucose (including sweet drinks and food) since a carbohydrate
load in the presence of thiamine deficiency may precipitate Wernicke’s
encephalopathy.

Relapse prevention
Counselling
Counseling during detoxification alone is unlikely to result in sustained effect.
It is important to make arrangements for follow-up. Individual and group sessions
can be offered.
Underlying mental illness
Some people may use alcohol as a form of self-medication for anxiety or
depression. Alcohol use itself may cause an apparent depressive affect. The
presence of depression is best assessed again after detoxification and treated
appropriately.
Pharmacotherapy
The drugs shown on the following page are used to facilitate relapse prevention.

Medications used for relapse prevention in alcohol dependence

Drugs Naltrexone Acamprosate Disulfuram

Recommendation First-line First-line Second-line

Mechanism of action Antagonism of Regulates transmission Aldehyde

opiate receptor along GABA dehydrogenase
neurones(probably inhibitor
through glutamate
neurons)
Reaction with No aversive reaction No aversive reaction Aversive reaction,
alcohol Prevents pleasant No alteration of CNS even with a small
‘high’ effect of effect of alcohol or amount(including
alcohol Sedation and withdrawal symptoms alcohol in cooking or
adverse psychomotor skin products) can be
effects still occur dangerous (flushing,
sweating,
palpitations, nausea
and vomiting,
headache, dyspnoea,
chest pain,
hypotension,
arrhythmias,
cardiovascular
collapse,
convulsions)

Clear evidence of Yes Yes No

reduction in craving

Clear evidence of Yes Yes Some evidence of

reduction in decreased intake but
alcohol intake compliance is a
limiting factor

Clear evidence of Yes Yes Some evidence of

increased abstinence increased abstinence
but compliance is a
limiting factor

Evidence of No Yes No
effect post-drug
therapy
Contra-indications Opiate dependence Renal Allergy to disulfiram
Chronic pain impairment(excreted or thiuram
requiring treatment unchanged in the derivatives (some
with opiates Hepatic kidney) Pregnancy pesticides, rubber
failure or active (ADEC B2) Lactation products) Ischaemic
hepatitis (ALT >3x (no data in humans) heart disease Severe
normal) myocardial disease
Renal impairment Psychosis Severe
Pregnancy (ADEC B3) hepatic or renal
Pregnancy (ADEC B2) disease Lactation
Lactation (safety not (safety not
established) established)

Drug interactions Opioids (antagonism None with diazepam, Isoniazid (increased

of action) disulfiram or toxic reactions)
Disulfram imipramine Phenytoin (increased
(combination may phenytoin levels)
result in increased Metronidazole
hepatotoxicity) (increased toxic
reactions) Naltrexone
(potential
hepatotoxicity from
combination, no
benefit shown of
combination) Warfarin
(increased
anticoagulant effect)

Adverse effects Nausea* Diarrhoea* Drowsiness*

Headache* Dizziness Nausea & vomiting Drowsiness* Headache*
Anxiety Abdominal pain Fatigue*
Fatigue Rash and pruritis Metallic or garlic
Insomnia Somnolence Rarely libido taste disturbance
Rarely hepatotoxicity changes and bullous Rarely jaundice,
skin reactions peripheral
neuropathy,
psychosis, confusion,
optic neuritis, blood
(*common) dyscrasias, rash

Preparation before Commence after acute Commence after acute Ensure potential
commencing treatment alcohol alcohol severity of reaction
withdrawal but withdrawal but with alcohol is
presence of alcohol presence of alcohol is understood
is not a not a contraindication
Ensure no alcohol has
contraindication
been consumed in the
Ensure not dependent
previous 24 hrs and
on opiates
advise that alcohol
should not be
consumed for 7 days
after cessation of
treatment

Dose 50 mg daily (can >60 kg 2 tabs tds, <60 Initially 100 mg

commence on 25 mg for kg 2 mane, 1 noon & 1 daily for 1–2 wks,
2–3 days to reduce nocte maintenance 200 mg,
incidence of side max 300 mg daily
effects)
 Alcohol: Information and brief
intervention

Author: Dr Moira Sim

Topic Reviewers: Kaz Knudsen (RAN, WA); Vivien (RAN, Amata), Jane Kollner (RAN,
Ampilatwatja); Dave Corstorpan (RAN, Nyirripi); Teresa Bowmen (RAN, Papunya)

Drinking in Indigenous communities

From the earliest days of European colonisation there have been stereotypes of
Indigenous Australians and the manner in which they consume alcohol. However,
throughout most of Australia Indigenous Australians learned about alcohol and the
behaviour associated with it from Europeans. Much of those stereotypes occurred in
frontier settings or during times of prohibition which established and encouraged
drinking patterns that were both furtive and harmful.6 Throughout most of Australia
it is only over the last four decades that Indigenous people have had unrestricted
access to alcohol, and they now drink in a wide variety of ways and environments.
Just as for non-Indigenous populations alcohol consumption is more common among
men, who also consume larger amounts than women. For both sexes heavier
consumption, particularly binge drinking, is more common among younger drinkers.6
Similarly, the social and health costs tend to be greater among those who drink
heavily, and thus whose families are also affected. However, there are also
differences between Indigenous and non-Indigenous consumption patterns.
From about the fourth decade of age on almost a third of Indigenous men are
more likely to attempt to give up alcohol, with the most common reason being
health related.
This and other research tells us that Indigenous people who drink, particularly
young drinkers, are more likely to do so heavily and to experience behavioural
consequences.3 Older drinkers are more likely to have related medical problems.
Older drinkers are also more likely to give up drinking, often because of concern
about their health, frequently after contact with a health professional.3
Addressing the needs of the younger drinking population demands careful attention
to acute health complaints and vigilance for undeclared problems, and addressing
any alcohol problems with a harm-reduction focus.
Health professionals can provide accurate information regarding alcohol use in
a way that is non-judgemental and supports an open clinic door. Older drinkers may
be more open to considering their drinking choices. Regardless, best clinical care
should include taking advantage of clinical opportunities to encourage patients to
reflect on their alcohol use. This is the basis of brief intervention. For
practitioners working in Indigenous settings, clinical care will be only one part
of a wider response to alcohol problems.

Brief intervention for alcohol

How practitioners raise the issue of alcohol consumption with Indigenous clients
will have much to do with personal style and opportunity. In raising the issue of
alcohol and personalising the link to that patient’s medical condition the
practitioners are providing a minimal brief intervention. A successful brief
intervention may simply mean raising the issue of alcohol, linking it to a medical
problem, providing relevant information in a manner that respects the patient’s
capacity to consider their situation and make decisions. Critically, it requires
keeping the door open and making the patient feel welcome.
Examples
John is a 42-year-old man with high blood pressure who comes in because of
abdominal pain. His pain is thought to be due to a peptic ulcer. John drinks one
bottle of spirits every day. In treating this pain the effect of alcohol on both
the abdominal pain and the high blood pressure could be raised. If the
practitioner is aware that other people in John’s family have had strokes, then
pointing out that high blood pressure causes strokes may have a meaningful impact
on him. The practitioner could then offer to help him to cut down drinking if he
wants to do that. John may not be ready to make changes at the time but this
intervention may turn out to be the single event, or one of a number of events,
that motivates him to make a change. If it does not, by raising the issue with
John in a non-judgemental way, the practitioner has left a door open, which lets
John know that he can be approached for help when he is ready.
Mavis is a 50-year-old woman who is brought in because she has fallen and hit
her head while intoxicated with alcohol. While tending to the injury, an
assessment for other harms as a result of alcohol reveals an enlarged liver. Using
the opportunity to point out that alcohol has ‘made the liver sick’, and that
stopping alcohol will give the liver a chance to get better, may help to motivate
behaviour change. The negative impact of other injuries could also be discussed.
A brief intervention may involve offering advice but should never be
judgemental and disempowering. Some people may change their behaviour soon after
as a result of an intervention, but in other cases it might take longer. People
may sometimes need many attempts before successful and sustained behavioural
change takes place. Alcohol and other drug use occurs because its effect is in
some way positive for the person using it. For example, it may help the person
escape from problems, reduce anxiety or cope with depression. While alcohol and
other drug use also has negative effects which are not wanted by the person, the
positive effects are often difficult to let go of. People therefore need
understanding and support in their struggle with the drug and its effects.
Motivational interviewing is a technique that can help the person to assess
their own behaviour and desire to change. This may be helpful in making decisions
with alcohol and other drug use. Brief motivational interviewing involves asking
the person about his/her own positive and negative experiences of the drug,
reflecting this back at the person so as to help the person clarify the situation.
Support can then be offered according to the needs identified. The specific
counselling approach of anything other than a brief motivational interview is both
outside the scope of this paper and the time available in most clinical
situations, with the exception of those in a drug and alcohol service.
For further reading to supplement this background to the topic please refer to
the reference list which follows.

References
1. Brady M. Giving away the grog. Canberra: Australian Institute of Aboriginal & Torres
Strait Islander Studies, 1995.
2. Brady M. The grog book: Strengthening Indigenous community action on alcohol. Canberra:
Commonwealth Department of Health and Family Services, 1998.
3. Brady M, Hunter E. Brief notivational interviewing flip chart. Canberra: Commonwealth
Department of Health & Aged Care, 2001.
4. Hunter E, Brady M & Hall W. Community report on services relating to alcohol in
Indigenous communities. Canberra: Report for the Office of Aboriginal & Torres Strait
Islander Health, 1999.
5. Hunter E, Brady M & Hall W. National recommendations for the clinical management of
alcohol-related problems in Indigenous primary care settings. Canberra: Report for the
Office of Aboriginal and Torres Strait Islander Health, 1999.
6. Hunter E, Brown J, Minniecon D. National implementation of the national recommendations
for the clinical management of alcohol-related problems in Indigenous primary care settings.
Canberra: Video and presentation for the Office of Aboriginal and Torres Strait Islander
Health, 2001.
7. Hunter E. Aboriginal health and history: power and prejudice in remote Australia.
Melbourne: Cambridge University Press, 1993.
 Anxiety
Author: Pamina Mitter (MBBS, Intercalated BSc, MRCPsych.)

Topic Reviewers: Kaz Knudsen (RAN, WA); Vivien (RAN, Amata); Jane Kollner (RAN,
Ampilatwatja); Teresa Bowmen (RAN, Papunya)

What is anxiety?
In Western populations it has been shown that perhaps between 17–24% of people
could be suffering from neurotic symptoms. The national survey of Mental Health of
Australians (1999) found that a little less than one in five Australian adults
(17.7%) had an anxiety, affective or substance misuse disorder in the past year.
Anxiety disorders were the most common.1 They affected just under one in ten adults
(9.7%). Of these, 7.1% were men and 12% were female. A least 40% of people with
anxiety disorders will have one other mental illness.
Post traumatic stress disorder was the most common of the anxiety disorders
(3.3%). Obsessive-compulsive disorder was the least common with only 0.4%
reporting symptoms consistent with this disorder. The anxiety disorders —
especially panic disorder, agoraphobia and post traumatic stress disorder — are
more common in females. The anxiety disorders are prevalent in people aged 18 to
54. Their prevalence only begins to decline after the age of 55 years.
Generally, most people with a mental illness respond well to good supportive
family relationships, work/ productivity, belonging/connectivity, spirituality,
and beliefs about the past, present, and future.2

Different anxiety disorders3

Specific phobia
This is characterised by a persistent and irrational fear and avoidance of a
particular object or situation.

Panic disorder
Individuals experience recurrent and unexpected panic attacks which are followed
by a persistent concern about having another panic attack or concern about the
implications of the panic attack (e.g. that they are going to die or have a heart
attack).

Agoraphobia (with or without panic attacks)

Individuals are anxious about being in a situation from which escape maybe
difficult or embarrassing, or in which help may not be easily available should
panic-like symptoms occur. The anxiety leads to avoidance of certain situations,
e.g. going out alone into crowded places.

Social phobia
Individuals are anxious about being in social situations in case they do something
embarrassing or look anxious. They often avoid others.
Generalised anxiety disorder
Individuals have persistent, generalised and excessive feelings of anxiety about a
number of events or activities. This tends to predominate the clinical picture.

Obsessive–compulsive disorder
Individuals experience unpleasant and intrusive obsess-ional thoughts that are
difficult to control, e.g. concern about dirt or about harm coming to their
family. This can be associated with carrying out rituals or compulsions regularly,
e.g. checking and hand washing excessively.

Acute stress reaction

Following a traumatic event individuals experience a short-term (days) reaction
that may involve disorientation, anxiety, amnesia, agitation and withdrawal.

Post-traumatic stress reaction

Individuals experience long-lasting anxiety about memories of a previous traumatic
event and may have nightmares, flashbacks and avoidance of cues that act as
reminders of the traumatic event.

Adjustment disorder
Individuals experience a short-lived period of distress and emotional disturbance
following a significant life change or stress.
Cross-cultural issues
In all mental illnesses it is useful to think in terms of biological,
psychological and social factors affecting the individual and possibly
contributing to mental illness.
In remote communities it is also particularly useful to consider the cultural
and social factors, as these provide the framework through which anxiety reveals
itself. These may contribute toward or provide help for anxiety disorders. For
instance, if someone has broken traditional law or feels that they have been
cursed they may experience anxiety, which may be entirely appropriate from the
community’s point of view.
On the whole it is less useful to try to divide problems into those that were
‘real’ biological illnesses or cultural phenomena. It is more helpful to try to
work with the client in a way that manages the person using the best available
resources. Cultural factors play a part in mental illness all over the world but
should not be seen to minimise the significance of the disorder. There is no
evidence to show that anxiety disorders should be more or less common amongst
different cultures, but they may manifest themselves differently. Often Aboriginal
families are very pragmatic and accept medication, seek help from a traditional
healer for the psychological and spiritual side, and will mobilise family for
social supports.4

Diagnosis of anxiety
In Aboriginal clients anxiety is one of the most difficult emotions to detect and
to understand its expression in words. There has been some work that shows how
non-Aboriginal clinicians can underestimate anxiety and emotional distress in
Aboriginal people.5 Nonetheless, there has been some linguistic research that
shows that Aboriginal languages reveal a surprising array of phrases relating to
anxiety and related somatic phenomena.6
A complication in making the diagnosis is that often the client will be anxious
about having to come to talk about their problems and may appear shy and worried,
when in fact this is not their usual behaviour. Conversely, many people who really
have these disorders will never come to you to seek help and their families may
have compensated for their problems and let them lead a sheltered life, e.g.
tolerated their obsessions or avoidance of panic inducing situations.7
Amongst Aboriginal people it will often be much more appropriate for people to
seek help from traditional healers for anxiety than from the health service. If
people come to seek help it maybe after other strategies have not worked.8
Somatisation (feeling physical symptoms from a psychological state) is
frequently seen in Aboriginal people as a manifestation of anxiety and distress.
Thus, anxiety as well as depression always needs to be considered when people
recurrently present with undiagnosable pains and symptoms.9

Differential diagnosis of anxiety disorders

Appropriate anxiety
In Aboriginal communities people experience a high rate of significant life
events. Fear of disease may be due to recent bereavements or experience of crime
or domestic violence. This may be appropriate and need reassurance and problem-
solving strategies.

Physical
Thyrotoxicosis, general ill-health, e.g. anaemia, poorly controlled diabetes,
hypertension etc may cause or complicate anxiety.

Psychiatric
Depression, early psychosis or early dementia may also be present.

Substance abuse
Excess caffeine, alcohol, petrol/ solvent sniffing, Kava, Marijuana and other
illicit drugs may confuse the diagnosis and management. These issues should be
simultaneously addressed.

Management
As discussed in the chapter on depression, the use of family and community members
to diagnose and manage mental illness is essential.4 For more traditional community
members the use of a traditional healer and an understanding of the cultural
background may be helpful. Beware though, a culturally appropriate explanation may
be given — but a treatable psychiatric condition may also be present. The advice
of a specialist mental health worker or psychiatrist should always be sought in
difficult cases, even if only via the telephone. It is extremely important to
exclude physical conditions before diagnosing a psychiatric one.4

Psychological therapies
Psychological therapies for anxiety disorders are the ideal first line treatment
in many countries. However, this involves using trained staff who have good
communication skills and language, and a well-motivated patient with reasonable
literacy skills. There is good evidence that cognitive behavioural therapy (CBT)
is an effective treatment in developed countries. CBT tries to enable the client
to link their behaviour, emotions, and physical symptoms to their thoughts. It
helps demonstrate how all these are interlinked and, by use of diaries and
homework (or alternative tools in remote Aboriginal communities), it aims to help
the client challenge their set patterns of negative thoughts, emotions and
behaviour, and hopefully decrease their symptoms.
Obviously, access to these treatments is limited in rural and remote
communities and may not always be workable in a very different cultural context.
Thus, I have described below easy relaxation and breathing exercises and explained
a little about a behavioural treatment of graded exposure which may be more
useable out bush.
After this I shall discuss possible drug treatments of these conditions, which
may need to be first-line in remote practice.

Suggested management strategies for anxiety disorders

All medication advice is based on the Prescribing Guidelines in the Australian
Medicines Handbook.10 Please also see the chapter on depression for further
information about mental illness and medication.

Specific phobia
Medications are not recommended except in one-off circumstances, e.g. the use of
benzodiazepines for extreme flying phobia.

Panic/agoraphobia
Educate the patient about anxiety and reassure them that they are not physically
ill.
Advise breathing and relaxation training initially. When they are confident
with these techniques plan a supported graded exposure to feared places/objects.
(As long as this is not contrary to cultural beliefs and taboos.)
Avoid using drugs or alcohol to reduce anxiety as this will worsen the problem
in the long run.

Slow breathing exercise

To be practised regularly and at the first sign of anxiety and overbreathing.
Overbreathing can make you feel short of breath, tingling in the toes and hands,
like yawning a lot, anxious and around the mouth (hyperventilation syndrome).
1. Hold your breath and count to five (do not take a deep breath).
2. When you get to five, breathe out and say the word “relax” to yourself in a
calm, soothing manner.
3. Breathe in and out slowly through your nose in a six-second cycle, i.e.
breathe in for three seconds and out for three seconds. Say the word “relax”
to yourself every time you breathe out.
4. At the end of each minute, i.e. after 10 breaths, hold your breath again for
five seconds and then continue breathing using the six-second cycle.
5. Continue breathing in this way until all the symptoms of overbreathing have
gone.

Relaxation exercise
For each muscle group in the body, tense the muscles for 7–10 seconds then relax
for about 10 seconds. Only tense your muscles moderately, starting from the
muscles in your feet, then your calves, then your thighs etc. until you have
tensed and then relaxed your whole body. Then lie still for a few minutes. This
needs to be practised twice a day for eight weeks to be really effective.
Principles of graded exposure
1. Use relaxation and breathing exercises before and whilst having exposure to
the feared stimulus.
2. Help the person identify any exaggerated fears that occur in the feared
situation and decide what is more likely to happen.
3. Remind them that anxiety rises initially when confronting a situation but it
also falls with in a few minutes. Only by remaining in the situation will
they learn that there is nothing to fear.
4. Plan a series of steps to build confidence in feared situations:
i. Identify the first small step towards overcoming the feared situation
ii. Practise this step until it no longer provokes anxiety
 iii. Move onto a more difficult step and repeat the practice
iv. Continue this process until the person can manage the feared
situation

Do not use drugs or alcohol to cope with the feared situation.

Medication
An SSRI is the first-line pharmacological treatment for panic disorder. An SSRI is
a selective serotonin reuptake inhibitor and is a class of antidepressant. There
are no trials comparing different SSRIs, which are all probably equally effective.
Doses are: paroxetine starting dose 10 mg (gradually increasing up to 40 mg);
fluvoxamine (25–200 mg); citalopram (10–40 mg); sertraline (25–150 mg); or
fluoxetine (10–60 mg). The onset of action may not appear for up to six weeks, and
the full response up to twelve weeks.
Note:
1. Up to 40% of patients with panic disorder experience an ‘activation syndrome’
of agitation on starting an SSRI. This can be minimised by education, using
half or even quarter the starting dose used for depression and gradually
increasing the dose. Fluoxetine might have a greater association with an
activation syndrome and so is not usually recommended for panic disorder.
2. About 40% of patients relapse on discontinuation of the SSRI, and so
treatment is usually continued for a minimum of 12 months. Once in remission
the dose can be reduced slowly.
3. Discontinuation syndromes may occur, especially with shorter acting SSRIs,
e.g. paroxetine. Once in remission the dose should be tapered slowly (about
25% every two months). These syndromes can cause dizziness, electric shock
sensations, anxiety and agitation, insomnia, flu-like symptoms and mood
swings.

Use of benzodiazepines in panic disorder

These drugs tend to be associated with improvement within the first week, but
tolerance usually limits their use over the longer term. They are sometimes used
when an SSRI is first started, but their use should be limited to a few weeks.
They will cause a withdrawal syndrome if used longer term, and if their use can be
avoided this is preferable. If they have to be used a planned discontinuation and
a tapering of the drug within six weeks is needed. Short acting drugs like
alprazolam can cause severe rebound anxiety and should be avoided.
Benzodiazepines should not be used for patients with a history of alcohol or
drug abuse. This is because of two main reasons. Firstly, those with a problem of
alcohol or drug dependence are at higher risk of becoming dependant on
benzodiazepines. Also the benzodiazepines potentiate the sedating effect of
alcohol and some other drugs like barbiturates.12 Taking alcohol and
benzodiazepines together can increase the risk of fatal respiratory depression.13

Social phobia
For clients with a severe social phobia, or have this combined with depression, a
SSRI is recommended. Those with social phobia do not usually experience an
activation syndrome and can start on a normal starting dose of the drug.
Dose: paroxetine (20 mg gradually increased to 50 mg); fluvoxamine (50–150 mg);
sertraline (50–150 mg); citalopram (20–50 mg); fluoxetine (20–60 mg).
Note:
1. The starting dose is used for 2–4 weeks and then increased if necessary.
2. The onset of action is within six weeks, but full response may take up to 12
weeks.
 3. 40% relapse on discontinuation, so a treatment is usually continued for at
least 12 months. Once in remission the dose can be reduced slowly.

Generalised anxiety disorders

Use an SSRI or venlafaxine, start at low dose in a similar manner to panic
disorder treatment.
Try to avoid the use of benzodiazepines, but if needed use for less than four
weeks and use one with a long half-life, e.g. diazepam.

Obsessive-compulsive disorder
An SSRI is the first choice medication.
Dose: fluoxetine starting at 20 mg and gradually increasing up to 80mg;
paroxetine (20–60 mg); sertraline (50–200 mg); citalopram 20–60 mg). All SSRIs are
probably equally effective, but choice depends on side effect profile. Gradually
increase the dose to maximum tolerated within eight weeks of start of treatment.
The patient needs to stay on this maximum dose for at least 12 weeks to see if it
works. Maintenance on the drug should continue for a year, but the dose can be
reduced by up to half the original dose once the patient is better.
The drug should be tapered and stopped slowly to avoid relapse and
discontinuation symptoms.

Acute stress reaction

Supportive counselling involving family and community supports is usually
effective.
The use of formal debriefing is not clear, and giving non-specific support may
be more appropriate.11
Advise against the use of alcohol or drugs to relieve symptoms.

Post-traumatic stress disorder

Refer for specialist psychological therapies if severe; consult with local mental
health services on possible referral options.
Treat as for panic disorder initially with an SSRI or venlafaxine.
Avoid the use of benzodiazepines.

References
1.
Andrews G, Hall W, Teesson M, Henderson S. The mental health of Australians. Canberra;
Commonwealth Department of Health and Aged Care, Mental Health Branch, April 1999.
2
. Curtis L. Personal recovery in psychiatric disorders. In: Central Australian Rural
Practitioners Association (CARPA), Standard Treatment Manual. Alice Springs: CARPA, 2002.
3 Not used.
4
. Sheldon M. Psychiatric assessment in remote aboriginal communities of central Australia.
FRANZCP: Alice Springs, 1997. Dissertation. www.ams.org.au/mark_sheldon/index.htm
5
. Morices R. Know your speech, community. No 1: fear and anxiety. The Aboriginal Health
Worker 1977a; 1(1):4–9.
6
. Morices R. Know your speech, community. No. 4 - serious mental illness. The Aboriginal
Health Worker 1977d; 1(4):10–15.
7
. Hunter E. Aboriginal mental health awareness: an overview part four, mental state
examination. Aboriginal and Islander Health Worker Journal 1993; 17(3):14–20.
8
. Dunlop S. All that rama rama mob, Aboriginal disturbed behaviour in central Australia (2
volumes). Alice Springs: Central Australian Aboriginal Congress, 1988.
9
. Reser J. Aboriginal mental health: conflicting cultural perspectives. In: Reid JT, Trompf
P. editors. The health of Aboriginal Australia. Marrickville, NSW: Harcourt, Brace
Jovanovich, 1991.
10
. Australian Medicines Handbook. Adelaide: AMH, 2001.
11. Mendelson G. ed. Australian Forensic Psychiatric Bulletin 2001; 20:25–7.
12. Weatherman R, Crobb DW. Alcohol and medication interactions. Alcohol Res Health 1999;
23(1):40–54.
13. British National Formulary, 2002.
 Cannabis: Effects and risks

Author: Dr Moira Sim

Topic Reviewers: Mental health editorial sub-committee

The following summary is largely drawn from ‘The Health and Psychological
Consequences of Cannabis Use’, National Drug Strategy Monograph Series No.25.
1998.

Effects
Acute effects of cannabis include:
• Psychological impairment (anxiety, panic) especially in naive users
• Cognitive impairment (attention, memory) while intoxicated
• Psychomotor impairment (increased risk if driving, operating machinery)
• Increased risk of psychotic symptoms in vulnerable (personal or family history
of psychosis)
• Increased risk of low birth weight babies if used in pregnancy.

Chronic effects of cannabis are less certain. The probable effects include:
• Respiratory disease (with smoking) e.g. chronic bronchitis
• Cannabis dependence syndrome (inability to abstain or control use)
• Subtle cognitive impairment (especially attention and memory) which may
persist after cannabis use is ceased.

The possible effects include:

• Increased risk of cancers in the aerodigestive tract e.g. oral, pharynx,
oesophagus
• Increased risk of leukaemia following exposure in utero
• Impaired educational/occupational achievement (association present but causal
link not clear)
• Birth defects following exposure in utero.

High-risk groups
These include: (i) adolescents, (ii) women of child-bearing age and (iii) those
with pre-existing disease.
(i) Adolescents: Association with poor school performance, causal link not
established. In theory cognitive effects of cannabis could impair educational
achievement. Early initiation of cannabis use increases the risk of progression to
heavy cannabis use and dependence.
(ii) Women of childbearing age: Cannabis use in pregnancy may increase the risk of
low birth weight babies and birth defects. Cannabis is generally considered to be
contraindicated in breastfeeding as it passes into breast milk; long-term effects
of exposure are unknown.
(iii) Pre-existing disease: People with the following diseases may be at increased
risk of exacerbation if cannabis is used:
• Cardiovascular disease (cannabis can cause mild physiological changes
characteristic of stress on the cardiovascular system)
• Respiratory disease
 • Schizophrenia (an association between cannabis and schizophrenia has been
identified, but a causal link has not been clearly established. It is prudent
to discourage those with an increased risk of psychosis from using cannabis)
• Dependence on other drugs (greater risk of developing dependence on cannabis).

Dependence

The existence of a cannabis withdrawal syndrome has been an area of debate.

However, there are now clear indications from research that some cannabis users
will become dependent and some will experience withdrawal symptoms upon cessation
of cannabis use.1

Withdrawal symptoms experienced include anxiety, irritability, restlessness, sleep

disturbance, sweating, rhinorrhea, diarrhoea, hiccoughs and anorexia.

[Editor: There is growing evidence supporting cannabis having a causal role in a

range of mental health problems (at least a dose response association between
cannabis use and later depression and psychosis symptoms or illness, corrected for
other drug use and prior mental health symptoms). This is summarised in an
editorial in the BMJ (JM Rey & CC Tennant. Cannabis and mental health. BMJ 2002;
325:1183–4.)]

References
1. From L Gowing et al. Evidence Supporting Treatment: The effectiveness of
interventions for illicit drug users. Australian National Council on Drugs,
2001. ANCD research paper No 3 (website www.ancd.org.au).
 Dementia

Author: Penny Abbington (specialist aged care nurse, Alice Springs)

Topic Reviewer: Dr Peter Tait

Definition
Dementia is a term used to refer to a group of symptoms that are the result of
deterioration in intellectual functions — such as memory, language, and planning —
and that is severe enough to hinder everyday activities and relationships.

Presentation
It is usually the carer or a family member who notices the changes and who then
reports this to a friend, the doctor or the clinic. They will usually report that
the changes have occurred over time. These changes are usually gradual and
imperceptible at first.
Families will often compensate and will say things like ‘grandma is getting
forgetful’ or ‘ it’s just old age’, but as the disease progresses the
deterioration in function becomes increasingly obvious and more difficult to
manage. The person with the dementia often does not have an awareness of their
memory loss and impairment and subsequent deterioration.

Early stages
• Forget things that happened recently; forget names of family; forget what they
want to buy from the shop
• Take longer to do things, forget how to dress, cook or do other things they
used to do easily
• Wander around aimlessly not knowing where they want to go, or where they are
or why they are there
• Don’t sleep much at night any more, or wake up and wander around
• They say the same things over and over, or ask the same question again and
again
• May talk about things that they shouldn’t, or talk about people who they
shouldn’t mention
• May accuse people of stealing things that they have mislaid or lost, or things
they only thought they had
• May have some problems with incontinence

Middle stages
• Memory getting worse, forgetting many things, even their children’s names, or
how many children they have
• Confusion gets worse, with them forgetting who they are or where they are or
what they’re doing there
• They may need lots of help now: to dress, undress, shower, go to the toilet,
prepare food, eat food and drink water
• Increasing bouts of incontinence, including faeces, to becoming totally
incontinent
• They may become emotional, get angry for no reason, or get upset and cry
• They may swear or say things that they culturally should not say or do
• They may talk a lot about when they were little and confuse those around them
for their mother or brother or father
 • They may just sit all day and do nothing, or they may get agitated and pace up
and down or wander away
• They may shout out words that make no sense at all
• They may forget all language they learnt as an adult and go back to the
language of their childhood

End stages
• Memory gets lots worse, remembering almost nothing at all about who they are
or who family are
• They may find it difficult to talk, and when they do it may not make any sense
at all
• They will need full assistance for all aspects of their health, hygiene and
nutrition
• May not be able to walk
• Will most likely be incontinent of urine and faeces
• They may just lie around not doing or saying anything

Causes
The three commonest causes of dementia are Alzheimer’s disease, multi-infarct (or
vascular) dementia and alcohol. The effects of these causes are by and large
irreversible. Alzheimer’s, in particular, gets worse over time.
There are also a number of other causes, some of which, if diagnosed and
treated, are reversible. These reversible causes of dementia are: depression,
central nervous system tumours, infections, organ failure, hypothyroidism, Vitamin
B12 and folate deficiency, and medication or drug use. In order to eliminate the
possibility of a reversible pattern of dementia a good picture needs to be painted
of the person.
A thorough history needs to be taken from someone who has known the person over a
period of time in order to get a complete picture of the progress of the disease.
The doctor, nurse or health worker needs to ask about all the following things:
D drugs: what medications is the person taking, alcohol and other drug usage
E emotion: history of mental illness, mood swings or being depressed for a while
M metabolic/endocrine diabetes, thyroid function
E ears and eyes (senses) deterioration or loss of hearing and sight.
N nutrition: causing vitamin deficiency
T tumour/trauma
I infection: UTIs, pneumonia, etc.
A atheroschlerosis/polyarteritis: inflammation and hardening of the arteries
leading to poor blood flow to the brain

Then a cognitive assessment needs to be done to look at whether there has been any
alterations to and deterioration in the way a person functions cognitively.

Cognitive assessment
The Mini Mental State Examination (MMSE)1 can be used to assess cognitive function.
It tests for orientation, registration, memory, language, construction, and
ideomotor praxis. A score out of 30 is obtained, and a score less than 24
indicates significant cognitive impairment.
However, this test has major limitations for someone who does not have English
as a first language, is unable to read, has impaired speech, sight or hearing, or
has a non-English cultural background. Furthermore, it does not assess frontal
lobe functioning. Nevertheless, it is a quick and useful way of assessing
cognitive function. It is widely available.
 Alternatively, one can ask or observe the following to assess cognitive
function:

• Functioning: is the person able to perform independently their activities of

daily living?
• Conscious state: are they alert, or are they drowsy? Does their conscious state
fluctuate during the course of the day? Are they awake at night and asleep
during the day?
• Attention and concentration: do they have difficulty attending to the interview?
• Orientation: can they tell the day and date, where they are?
• Memory: test short-term and long-term where possible, e.g. do they remember
things that happened recently, such as a hunting trip or when pension day is?
Can they tell you where they live, the names of their family? Do they remember
the way to the shop or to a relative’s place?
• Language: some old people go back to language used in early years and may forget
other language; can they name common objects e.g. shirt, collar, buttons, nose,
nostril, watch, pen, etc.; can they write a sentence? Read? Repeat a phrase
(such as ‘No ifs, ands or buts’). Comprehend commands?
• Arithmetic: ask them about change from buying something, use cards to count with
etc.
• Praxis: ask them to stand ‘like a boxer’, ask them to put on a jumper, ask them
to copy a diagram of two intersecting boomerangs.
• Agnosia: ask them to show you their thumb, index finger, ring finger; draw a
number on the palm of their hand and ask them which number it is.
• Reasoning: ability to plan and understand consequences e.g. how to prepare a
meal.
• Judgement: what they would do if bitten by a snake?
• Emotions: any history of emotional change, such as depression, irritability,
agitation, anxiety, or aggression.
• Thought and perception: sometimes hallucinations and delusions are present.
If the carer or person giving information tends to answer yes to the majority of
these questions, then the chances are that the person may have dementia.

Investigations
If a dementia is suspected it is important to do investigations to see if there
are any reversible/treatable causes of the dementia. Table 1 overleaf gives a list
of tests that should be undertaken.

Differential Diagnosis
Depression and delirium can often mimic dementia. Table 2 overleaf highlights some
of the differences.

Management
The main management issue in dementia is determining the special needs of the
patient and deciding whether the family or community are able to provide for these
needs. The types of care that a person with dementia may need might be: bathing
and showering, toileting, dressing or undressing, cooking or eating food,
communication, laundry, home help, gardening, firewood, taking medicines, social
activities, ceremony.
Often, the family have been coping with the care of the patient for a long time
but are now finding it more difficult to cope because the dementia has progressed.
In such situations, a Community Aged Care Package funded by the Commonwealth
Department of Health and Ageing can help a person with dementia to stay at home
and in their community. Such packages pay money for specific services needed by
the dementia patient.
 To apply for such a package, the patient needs to be assessed by the Aged Care
Assessment Team. Their phone numbers (prefix 08) are:

Alice Springs Urban 8951 6735

Remote 8951 7842
Tennant Creek 8962 4201
Katherine 8973 8503
Darwin Region 8922 7392
East Arnhem 8987 2860

The Aged Care Assessment Team can also organise respite for the dementia patient
to give them or their carer a rest. This helps the person to stay in the community
longer as the carer does not get too tired. Sometimes, the carer may be suffering
from depression because of the stress of looking after somebody with dementia. In
such cases, the carer will also need treatment.
In more advanced cases of dementia, where the sufferer requires 24 hour care,
the only option is placement in a hostel or nursing home. Once again, the Aged
Care Assessment Team will need to be contacted to organise this.
There are now drugs that are available to help delay the progression of
Alzheimer’s disease. They come from the class of medication known as
Acetylcholinesterase Inhibitors. Three drugs of this class are currently available
under the Pharmaceutical Benefits Scheme (PBS). They are: Donepezil (Aricept),
Rivastigmine (Exelon), and Galantamine (Reminyl). To be eligible for the drug
under the PBS, the patient needs a score of at least 10 on the MMSE.
Sometimes, the dementia sufferer will also be depressed, anxious, agitated,
aggressive, or psychotic with delusions and hallucinations. In these situations,
treatment with an antidepressant (e.g. Sertraline) or an antipsychotic (e.g.
Olanzapine) may be necessary. Before doing this, it is important to rule out
physical (e.g. pain, infection), communication (e.g. frustration at being
misunderstood), or task-related (expecting them to do things beyond their ability)
causes.

Table 1: Tests to determine possible cause(s) of dementia

Procedure Potential findings

Full blood count Infection, anaemia, myeloproliferative

disease
ESR Infection, tumour, autoimmune disease
Urea and electrolytes Dehydration, renal failure, hypokalaemia
hyponatraemia. Fasting blood glucose
Hypoglycaemia, diabetes
Calcium and phosphorous Parathyroid disorders, renal disease,
malignancy
Liver function tests Alcoholism, drug toxicity, liver disease
Thyroid function test Myxoedema, thyrotoxicosis
Vitamin B12 and folate Deficiency states
Serologic tests Neurosyphilis, AIDS
ECG Arrhythmias, evidence of ischaemia
Chest X-ray Infection, carcinoma, granuloma,
cardiomyopathy, other respiratory
diseases leading to cerebral anoxia
CT scan brain with/without contrast Diffuse or focal atrophy, infarcts,
haemorrhage, tumour, hydrocephalus
 Table 2: Clinical features of dementia, delerium and depression

Dementia Delirium Depression

1. Onset Insidious Acute Gradual
2. Duration Months/years Hours/days/??weeks Weeks or months
3. Course Stable & Fluctuates — worse Usually worse in
progressive(unless at night. Lucid morning, improves
vascular dementia— periods. as day goes on
usually stepwise)
4. Alertness Usually normal Fluctuates Normal
5. Orientation May be normal — Always impaired Usually normal
usually impaired Time
for time and place Place
Person
6. Memory Impaired recent & Recent impaired Recent may be
sometimes remote impaired
memory Remote intact
7. Thoughts Slowed Often paranoid & Usually slowed,
Reduced interests grandiose,? bizarre preoccupied by sad
Perseverate ideas topics, and hopeless
Delusions are ? paranoid thoughts
common
8. Perception ? normal Visual & auditory 20% have mood
hallucinations congruent auditory
common. hallucinations
Delusions are
common.
9. Emotions Shallow, apathetic, Irritable Flat, unresponsive
labile Aggressive or sad& fearful.
Fearful May be irritable.
10. Sleep Often disturbed. Nocturnal confusion Early morning
Nocturnal waking
wandering common.
Nocturnal
confusion.
11. Other features Other physical ? past history of
disease may not be mood disorder
obvious
Source: Dementia Services Development Centre, Dementia Touches Everyone: a Guide
for Trainers and Trainees in General Practice. University of Stirling, Scotland.
Minor modifications made to original table.

Other issues that need to be considered over the course of the dementia
• Psychological: addressing issues of loss, grief
• Family concerns about genetic vulnerability
• Physiotherapy: help with walking
• Occupational therapy: memory aids, ramps, wheel chairs, showering aids,
special eating utensils
• Continence: help for bedwetting
• Legal: power of attorney, guardianship and administration order, will
• Driver’s licence: cancellation if driving considered to be dangerous
Reference
1. Folstein MF, Folstein SE, McHugh PR. ‘Mini-Mental State’: A practical method for grading
the cognitive state of patients for the clinician. Journal of Psychiatric Research 1975;
12:189–98.
 Depression

Author: Dr Pamina Mitter (MBBS, INTERCAL BSC, MRCPSYCH)

Topic Reviewers: Dr Marcus Tabart; Kaz Knudsen (RAN, WA); Vivien (RAN, Amata); Jane
Kollner (RAN, Ampilatwatja); Teresa Bowmen (RAN, Papunya)

What is depression?
Depression is a mood state characterised by significantly lowered mood and a loss
of interest or pleasure in activities that are normally enjoyable. Such depressed
mood is a common experience in the general population. However, a major depressive
episode can be distinguished from this ‘normal’ depression by its severity,
persistence, duration, and the presence of characteristic symptoms (see later).

Common presentation
• Markedly depressed mood
• Loss of interest or enjoyment
• Reduced self-esteem and self-confidence
• Feelings of guilt and worthlessness
• Bleak and pessimistic views of the future
• Ideas or acts of self-harm or suicide
• Disturbed sleep
• Decreased libido
• Reduced energy leading to fatigue and diminished activity
• Reduced concentration and attention.
The depressed mood is relatively constant from one day to the next, although mood
may vary somewhat during the course of the day. Often the mood gets better as the
day progresses. Depression can also be accompanied by biological features (see
somatic syndrome).

Atypical presentation
Mood is reactive and brightens during positive events.
Two or more of the following are present:

i. Increased weight gain

ii. Excessive sleepiness
iii. Heavy, leaden feelings in the arms or legs, often lasting for many hours
iv. The individual has a lifelong trait of being particularly sensitive to
perceived interpersonal rejection.
Atypical presentation tends to be associated with younger age of onset of
depressive disorder and are more common in women.

Diagnosis
According to the World Health Organisation’s International Classification of
Diseases tenth edition (ICD-10), a diagnosis of major depressive episode requires
the following criteria to be met:
• The presence of a minimum number of symptoms
• Symptoms must be present for at least two weeks, unless the symptoms are
particularly severe or of rapid onset
• The individual has not experienced a manic or hypomanic episode
 • The episode is not due to psychoactive substance abuse or any organic mental
disorder.

For a diagnosis of depression according to ICD-10 at least two of these three must
be present:1
1. Depressed mood
2. Loss of interest or pleasure in normally pleasurable activities
3. Decreased energy or increasingly more easily fatigued.

Additional symptom(s) from the following list should be present to give a total of
at least four:
1. Loss of confidence or self-esteem
2. Unreasonable feelings of self-reproach or excessive and inappropriate guilt
3. Recurrent thoughts of death or suicide, or any suicidal behaviour
4. Complaints or evidence of decreased ability to think or concentrate (for
example indecisiveness)
5. Change in psychomotor activity, with agitation or retardation (noticed by
self or others)

6. Sleep disturbance
7. Change in appetite and weight gain or loss.

Somatic syndrome
To meet criteria for depression with a biological (somatic) syndrome four of the
following must be present:
• Marked loss in interest or pleasure in activities that are normally
pleasurable
• Lack of emotional responsiveness
• Waking in the morning two hours or more before the usual time
• Depression worse in the morning
• Marked psychomotor retardation or agitation as observed by other people
• Marked loss of appetite
• Weight loss (at least 5% in the last month)
• Marked loss of libido.

The severity of the disorder can be classified as mild, moderate or severe

depending on the number and severity of the symptoms.
In severe depression there is marked impairment of occupational and social
functioning, and most of the features of depression. Somatic features are likely
to be present and there may be some psychotic features. Psychotic features can be
hallucinations or delusions. Hallucinations are things that a person can hear,
see, taste, smell or touch that are not really present. Delusions are firmly held
false beliefs, e.g. that the person is being persecuted by aliens.

Prevalence in the Aboriginal population

The National Survey of Mental Health and Wellbeing (1995) found that in the 12
months prior to the survey 5.8% of the adult population had one or more depressive
disorders either major depression or dysthymia.2
The prevalence figures for children (4–12 years) and adolescents (13–17 years)
who may suffer from anxiety and/or depression are 3.5% and 6.8% respectively.3
Unfortunately, there is no comprehensive data describing the extent or nature of
psychological problems or mental disorders in Aboriginal or Torres Strait people.
The lack of data collection is problematic due to inappropriate measuring tools
and diagnostic instruments, and what Reser describes as ‘conflicting cultural
perspective of mental illness’.4 The National Survey of Mental Health and
Wellbeing also did not include this population group in the survey.2 However, work
done by McKendrick, Hunter and Kyaw suggests that rates of mental disorder are
high amongst Aboriginal people, but no higher than in the non-Aboriginal
community.5,6,7 According to Windsor the effects of spiritual disruption,
environmental insult, ideological conflict, political and sociological
disadvantage, physical ill health and an array of transient fixers and medical
staff have all contributed to the damage of mental health.8
The most recent figures available for the Northern Territory (except for the
Katherine region) are from an informal survey done for the CARPA STM to find out
what sorts of mental health issues health professional were dealing with at the
clinic level.9
Common concerns among health staff were family violence, psychotic illness,
suicide and self-harm, substance misuse problems, aggressive persons and
depression.
The CARPA survey figures for depression were higher: 20%, compared to 5.8%
noted in the National Survey of Mental Health and Wellbeing for the non-Aboriginal
community.2,9 The CARPA survey took a broad definition of depression and asked if
depression was due to chronic illness, cultural reasons, post-natal disorders,
women’s issues (such as miscarriages, domestic violence, sexual assault),
bereavement and other.9 The survey also did not differentiate between major or
mild depression. To conclude, there is no accurate data on the prevalence of
mental illness in the Northern Territory, but it is clear from existing literature
(in particular ‘Ways Forward’) that it does exist and can be debilitating if
appropriate care is not provided.10
Depression is under-treated because of:
• Low rates of diagnosis
• Patients’ attitudes
• Inadequate antidepressant prescribing.

The goals of treatment are to:

• Remove symptoms
• Restore patient functioning
• Prevent relapse.

Use of antidepressant medication

Worldwide depressive illness is a growing burden economically and on quality of
life. Current projections indicate that depression will rank only second to
ischaemic heart disease by 2020.11 Depression is a chronic and recurrent disease
with morbidity analogous to diabetes or hypertension.12
The use of antidepressants in treatment of depression has benefits and pitfalls
in all populations, how-ever, in remote areas there are additional difficulties
that need to be considered. Medication is more easily available than psychological
therapies in the remote areas and so will have a central role in any management
strategy. Nonetheless, taking the time to listen to someone’s problems can be very
useful, even if practitioners have no formal psychiatric training.

Types of antidepressants
SSRI (selective serotonin reuptake inhibitors): These are the newer
antidepressants. They tend to have fewer side effects (except for some
gastrointestinal disturbances) than the older drugs and they are relatively safer
if taken in overdose. The SSRIs have almost rendered the TCAs obsolete.
TCA (tricyclic antidepressants): These tend to have more side effects (like dry
mouth and constipation) and are toxic in overdose.
SNRIs (selective noradrenaline reuptake inhibitors) like Venlafaxine are also
available, and there are a range of other antidepressants with different side
effects and properties.
 The choice is based on efficacy, safety, tolerability, real world efficacy and
economic value.
There is very little evidence to show that any antidepressant is generally more
effective than another, but for an individual patient one drug may suit or work
better than another. It is reasonable to base choice on the medications that have
fewest side effects and are safest in overdose. These tend to be the newer and
more expensive drugs but, as patients are more likely to take these and improve,
it is worth using them as first-line. In the UK patients are seven times as likely
to take an adequate course of SSRIs than TCAs.13 Usually an SSRI would be suitable
as a safe first choice.

Reasonable treatment strategy for first-line treatment of depression

First choice: Sertraline 50 mg (an SSRI). This has less interactions with other
drugs and is less agitating, but reduce the dose in severe liver disease.
(First-line treatment is with SSRIs, though if need further treatment because
of poor response or too many side effects then consult with Mental Health Team,
and they may recommend other drugs such as TCAs or SNRIs.)
Clinical trials of antidepressants suggest an efficacy rate approaching 80%,
but in standard primary care only about 25% of patients have an adequate dose and
duration of treatment.12 This figure is likely to be lower in remote communities
where communication and follow-up is often less than perfect.
There is general agreement between guidelines from the British Association for
Psychopharmacology, WHO and Royal College of Psychiatrists guidelines.14
Given that a frequent problem is that too low a dose is used, the treatment
needs to start at a low dose and build to a high dose over a few weeks, titrated
against side effects, and to continue the dose for sufficient time to be
effective.
It is necessary to continue the effective dose for at least 4–6 months beyond
initial symptom resolution (or longer for subsequent episodes). Depression is
usually characterised by repeated relapses or recurrences, and continuation
studies show that up to half of patients will relapse if treatment is stopped
before this time.
Standard Effective Daily Doses: Sertraline 50 mg, citalopram 20 mg, venlafaxine
150 mg.

Maintenance therapy
In the 1980s there were several studies including, in the USA, The National
Institute of Mental Health Collaborative Program of the Psychobiology of
Depression. In this study, 400 patients were followed up for 15 years. One in
eight remained well. 80% had at least one recurrence, and 6% remained chronically
depressed throughout.15
Patients who are at high risk of relapse (that is, a return of symptoms that
meet the criteria for a major depression prior to the end of the index episode)
are those who: have a more chronic course; more than three past episodes; severe
index episode; family history; co-morbid anxiety or substance abuse; co-morbid
medical illness; poor social support; and ongoing psychosocial stressors.12.16
There is good evidence that for these patients long-term maintenance on
treatment would be beneficial. Though there are some unresolved issues about how
long this maintenance treatment should be, the best available evidence suggests 4–
5 years.16,17

Withdrawal of medication
Antidepressant medications do not have an addictive potential, but a withdrawal
syndrome has been described in some patients who suddenly stop their medication.
This is particularly described for the SSRI and SNRI groups. Therefore, it is
recommended that medication is gradually decreased over a two to four week period.
Some drugs, which stay in the body for a short time, have a higher risk than
others that are slow to be removed. Thus, paroxetine causes withdrawal symptoms
much more commonly than fluoxetine. Please check current drug information about
withdrawal syndrome for patients before starting.

Local considerations
Diagnosis
Many aspects of diagnosing mental illness are more complex when one is unfamiliar
with the local culture. Often a useful marker is other people’s perception of a
change in appearance or behaviour, for example acting in a culturally
inappropriate manner. After a bereavement it is culturally acceptable for some
Aboriginal people to make ‘sorry cuts’, but cutting at other times may be a sign
of mental health problems.
Shyness towards strangers can be extreme, especially in those less exposed to
Western culture. This can make interactions extremely frustrating and the
temptation for health workers to jump to the wrong conclusion must be anticipated.
The client may also wish not to appear rude and so try to please the health worker
with their answers. Thus, information from a third person is very important.
People may not be able to verbalise their mood as depression. Often ‘worries’
or ‘cranky mood’ can be useful ways to understand low mood and irritability. Also,
some people who persistently attend the clinic with non-specific physical problems
may actually be depressed.
Beware that seemingly odd beliefs and hallucinations (especially visual) may
not be pathological. However, persistent auditory hallucinations are likely to
need treatment.
As a result of multiple social stressors (like multiple bereavements,
unemployment, separation from family, substance misuse) people in remote
Aboriginal communities have many risk factors for developing depression. It is
important to keep a high index of suspicion when considering this as a diagnosis.18
‘Compliance’ with treatment and
management plans
Involving other community members and family as much as possible is often the most
important method of ensuring compliance. Good communication, understanding manner
and explaining things also helps. However, never assume compliance. Patients all
over the world often don’t want to be embarrassed by admitting they are not taking
their medication. Often clients do not communicate much or trust you until they
have met you on several occasions and understood your background and ‘story’. A
useful strategy is to talk in the third person about someone who had depression
and how they got better with medication.
Overall, in my experience, when people were ill they were keen to get help and
felt that Western medicine may have some special beneficial properties.19

Lack of monitoring
Because of the erratic nature of follow up and treatment out bush it is preferable
to have a simple treatment plan. Start low and rapidly build to a good dose, and
make sure they understand that it takes 2–4 weeks to have effect and they may be
bothered by side effects initially.

No response to treatment
If the client does not respond it may be useful to consider the possible reasons:
• Are they taking the drug?
• At the right dose?
• If not, why not? Is it because of side effects or forgetfulness: could someone
help administer the drug daily?
• Are they taking drugs or alcohol that may counteract any antidepressant?
 • Do they need a trial of an alternative medication (i.e. true therapeutic
failure)? If you think the latter is the case, seek psychiatric consultation.

Family and community input

The family are usually the main carers in remote communities and often act as
nurses, occupational therapists, rehabilitation officers and give emotional and
practical support. They are an invaluable resource in treating mental illness. It
is important that the correct family member becomes involved, as there is a system
within the family to determine who takes responsibility for that individual. Work
with the family to identify who best to do this. And who can be responsible for
the care when the primary carer has to go away.

Use of traditional healers

In remote communities traditional healers are often consulted before medical
advice is sought. Aboriginal people sometimes hold beliefs that they are ill or
hear voices as a result of a curse. In this context it can be very useful to seek
help from traditional healers and also to use medication. The two approaches are
not mutually exclusive and you may be regarded as more acceptable if you are
flexible with working with the local cultural beliefs.18

Complex patient groups

Women: pregnant or breastfeeding
If possible withdraw all drugs in the first trimester. If pregnancy is planned try
to withdraw drugs slowly beforehand. If an antidepressant is required SSRIs have
been found to have low teratogenicity and so are relatively safe to use in
pregnancy.20 As with all medications with pregnancy and breastfeeding, the risks of
medication needs to be weighed against the benefits and discussed with the woman.
Very few studies have been carried out about breast-feeding and
antidepressants. All antidepressants pass into the breast milk but usually in
small amounts. There have been some cases of neonatal discontinuation syndromes
with SSRIs, though SSRIs are safe and there is growing clinical support to
continue SSRIs if indicated post partum.20

Postnatal depression
This occurs in 10–15% of all women.21 Depression in the mother can effect the long-
term development of the infant if untreated. One quarter of these will need
medication. If women have had previous episodes of depression they may be at
higher risk, and it may be worth considering prophylactic antidepressants after
delivery.

Men: impotence
There is a higher risk with paroxetine and sertraline, but can be problem with all
SSRIs.

Children (<15 years old)

There is no clear evidence that antidepressants are effective in this age group.
However, it is extremely important to try to sort out the cause of stress for the
child. If a child seems to be suffering from depression, talk to the mental health
team about treatment options.

Elderly
The elderly have an increased sensitivity to medication and as one ages drugs get
removed from the body more slowly. Thus, it is best to try to minimise
medications.
 ‘Golden rule’: start low, go slow and monitor effects frequently.
Avoid drugs that put elderly at risk of falls, e.g. by lowering blood pressure
or making them sedated, e.g. benzodiazepines.

Medical co-morbidity
Medical ill-health increases the risk of depressive illness. Seek medical advice
about medication use and take care with interactions with other drugs. Sertraline
and Citalopram have relatively few drug interactions.
Diabetes: Do not use fluoxetine as there is a risk of hypoglycaemia.
Hepatic impairment: All antidepressants are cleared by the liver. SSRIs may be
used with caution at a half dose for severe hepatic impairment.20
Drug interactions in people on medications for chronic diseases are possible,
but prescribing information needs to be checked.

Psychiatric co-morbidity: anxiety

Often depression can be associated with anxiety, and starting treatment with an
SSRI can initially make this worse. Although the use of benzodiazepines can be
given for acute agitation and distress it is extremely important to use
benzodiazepines for less than two weeks and avoid their use completely if
possible.22

Substance abuse
Alcohol and substance misuse (e.g. petrol sniffing and marijuana use) can affect
diagnosis and treatment of mental illness. Substances can directly cause low mood
and hallucinations, but also some clients use substances to try to cure themselves
of mental health problems. In those with alcohol dependence 80% of people with
depression recover within a few weeks of abstinence without the need for
antidepressant medication.23
In the real world abstinence may be difficult but, if someone continues to
drink alcohol, it is unlikely that the antidepressant can work effectively.
Pointing out the impact that alcohol is having in their lives may be the only step
possible.

High suicide risk

Starting antidepressants can be a high-risk time as a patient may have more energy
but still feel suicidal, and thus act on this. The family may need to be more
vigilant, and potentially toxic drugs should be avoided. Liaison with the
specialist team would be advisable when making management decisions (even if over
the telephone only).

Self-care/colleague care
It is important to be aware of one’s own and one’s colleague’s mental health.
Working in remote health care is challenging and one can feel professionally
isolated. As a result the risk of mental stress and developing depression is
increased. As well as personal distress depression may affect one’s ability to
cope with the job or lead to leaving the post. Being aware of the risks is
important and it is a sign of strength to be able to accept help and advice, e.g.
from the Bush Crisis Line. Remember that when you are treating colleagues, relate
to them as patients rather than other professionals.

References
1. World health Organisation. ICD-10 Classification of Mental and Behavioural Disorders:
clinical descriptions and diagnostic guidelines. Geneva: WHO, 1992.
2. Dept of Health and Aged Care. The national survey of mental health and wellbeing;
national mental health strategy. Canberra: Commonwealth Dept of Health and Aged Care, 1995.
3. Sawyer MG. The mental health of young people. Canberra: Commonwealth of Australia, 2000.
4. Reser J. Aboriginal mental health: conflicting cultural perspectives. In: Reid JT, Tromp
P. The health of Aboriginal Australia. NSW: Harcourt Brace Jovanovich, 1991.
6 McKendrick J, Cutter T, Mackenzie A, Chiu E. The pattern of psychological morbidity in a
Victorian urban Aboriginal general practice population. ANZ J Psychiatry 1992; 26(1):40–7.
5. Hunter E. Aboriginal health and history: power and prejudice in remote Australia.
Cambridge: Camdridge University Press, 1993.
6. Kyaw O. Mental health problems among Aborigines. Mental Health Australia 1993; 5:30–6.
7. Windsor G. Toward community psychiatry in central Australia: the experience of the
initial trainee. Alice Springs: NT Mental Health Services, 1996; 29.
8. Remtulla N, Warchivker I. CARPA needs you: survey of mental health needs in the Northern
Territory. Alice Springs: Centre for Remote Health, 2001. Unpublished.
9. Swan P. Raphael B. Ways forward: National consultancy report on Aboriginal and Torres
Strait Islander Mental Health. Part 1 and 2. Canberra: AGPS, 1995.
10. Murray CJL, Lopez AD, editors. The global burden of disease. Cambridge: Harvard
University Press, 1995.
11. Moncrieff J, Wessely S, Hardy R. Active placebos versus antidepressants for depression.
Cochrane review. In Cochrane Library 2001; Issue 4.
12. Dunn RL, Donoghue JM, Ozminkowski RJ, et al. Longitudinal patterns of antidepressant
prescribing in primary care in the United Kingdom: a comparison to treatment guidelines. J
Psychopharmacology 1999; 13:136–43.
13. Psychopharmacology guidelines for treating depressive illness with antidepressants. J
Psychopharmacology 1993; 7:19–23.
14. Keller M. The long-term treatment of depression. J Clinical Psychiatry 1999; 60:17.
15. Forshall S, Nutt DJ. Maintenance pharmacotherapy of unipolar depression. Psychiatric
Bulletin 1999; 23:370–3.
16. Hirschfeld RM. Clinical importance of long-term antidepressant treatment. British Journal
of Psychiatry 2001; 179(42):4.
17. Sheldon M. Psychiatric assessment in remote aboriginal communities of Central Australia.
FRANZCP: Alice Springs, 1997. Dissertation.
www.ams.org.au/mark_sheldon/ index.htm
18. CARPA standard treatment manual. Alice Springs: Central Australian Rural Practitioners
Association, 2002; 4th edition.
19. Australian Medicines Handbook. Adelaide: AMH, 2002.
20. Byrne G, Raphael B. Post-partum depression. Current Therapeutics 1995 Aug; 51–7.
21. Furukawa TA, Streiner DL, Young LT. Antidepressant and benzodiazepine for major
depression; Cochrane review. In Cochrane Library 2001; Issue 4.
22. Davidson KM. Diagnosis of depression in alcohol dependence: changes in prevalence with
drinking status. Brit J Psychiatry 1995; 166:199–204.
 Family Violence

Author: Helen van Roekel

Reviewers: Monica Ostigh (RAN, Jabiru); Kaz Knudsen (RAN, WA); Vivien (RAN, Amata);
Jane Kollner (RAN, Ampilatwatja); Teresa Bowmen (RAN, Papunya)

What is family violence?

Family violence is behaviour by one family member that causes physical, sexual and
or emotional damage to others in the family, including causing them to live in
fear by threatening to harm people, pets or property. Family violence is most
commonly perpetrated by one partner towards another and/or by an adult towards a
child or children. Other forms include elder abuse or sibling abuse. Whether the
violence is physical, sexual or emotional it has long-term health effects.
The overwhelming majority of cases of violence against women involve a male
perpetrator and his wife or de facto. It is estimated that violence occurs in as
many as one in four relationships. Violence against women in Aboriginal
communities is reported to be far greater than in many other populations.1
A high proportion of female homicide victims are killed by their spouse or de
facto, approximately 30% Australia-wide, approximately 50% in the NT.2

When to suspect abuse (behavioural indicators)

• Injuries that are difficult to account for as accidental
• The patient may seem evasive, embarrassed or ashamed of the injuries
• Injuries are on areas of the body normally covered by clothing
• There has been a substantial delay between the time of the injury and
presentation for treatment
• An accompanying partner or family member wants to speak for the patient, and
insists on staying close by
• There is repeated use of emergency services
• Her medical history reveals many ‘accidents’ with injuries of suspicious
injuries
• She has vague complaints or pain without physiological cause
• There may have been suicide gestures or attempts
• Alcohol or drug abuse seems to be occurring, or frequent use of tranquillisers
• She presents with symptoms of anxiety or depression.

Types of violence
Mostly, we think of physical abuse, but there is usually a pattern of controlling
behaviours occurring. Most commonly, the emotional abuse being experienced is the
most devastating, eroding self-esteem and strength needed to resist the abuse.

Types of behaviours that may be experienced could include:

Physical abuse: punches, burns, choking, blows to stomach during pregnancy,
threats with weapons, assaults with weapons, eye gouges, twisting limbs,
destroying possessions, smashing furniture or crockery, hurting or killing family
pets.
Sexual abuse: demanding sex, rape, demanding sexual practices she doesn’t agree
with, forcing her to have sex in front of the children, using tactics or language
to humiliate her.
Social abuse: controlling what she wears, who she sees and where she goes,
preventing her from seeing her own family and friends, smothering (i.e. constantly
checking up on her with surprise phone calls and visits), accusations that she is
sleeping with other men, verbally degrading her in front of other people,
demanding she spend all her spare time with him.
Psychological abuse: mind games, threats to kill her, her children or her family,
threats of suicide, or have the children taken away by welfare, verbal abuse, put
downs, mind games, insults, ‘silent treatment’, unpredictable angry outbursts.
Financial abuse: controlling how much money she has, ensuring she never has
enough to pay bills and provide food, not allowing her to have savings, taking
money from her (especially on pension day) and spending it on himself.

Cycle of violence
Violent relationships are rarely bad all of the time, which makes the situation
highly confusing for women. Often, there is a series of violent and dangerous
times, with periods in between where the violent partner can be caring and loving.
Frequently, but not always, the pattern looks something like this:
Build-up stage: The violent partner slowly begins to put down and threaten his
partner.
Explosion: There is an incident of violence or threats, and the woman may try to
escape from her partner.
Buy-back stage: The violent partner begs forgiveness, or threatens her into
returning to him. He may minimise or deny the violence at this stage, or appear to
be truly sorry.
Pursuit stage: If the woman doesn’t return, he will pursue her. This may include
stalking, threats to kill her or the children, or threats to kill himself. Most
murders of victims occur at this stage.
Honeymoon stage: If she returns to him, he tries hard to treat her well, and
be a loving partner, he may cease consuming alcohol for a time, and try to be
a good father.
The cycle starts again, and there is usually a repeat of the violence. Over
time, the cycle tends to happen over a shorter time frame (days or weeks rather
than months), and gets more violent.

Why women stay or keep returning to violent relationships

• Threats of violence, often carried out (most murders occur as women are trying
to leave, or just after they have left the relationship)
• Religious reasons (‘Til death do us part’, ‘for better or for worse’)
• Family pressures to stay in the relationship
• His promises to change, or get counselling
• His threats to kill himself if she leaves him
• She wants to keep the family together, for children to know their father
• She believes that she can’t live without him, that she is incapable of
surviving on her own (a result of chronic emotional abuse, reduced self-
esteem)
• She has no or little family support, and is socially isolated
• She doesn’t know where to go for help
• She may still love her partner and want to stay with him, she just wants the
violence to stop.
Additional issues for Aboriginal women
As stated above, violence and murder is reported to be far more frequent for
Aboriginal than non-Aboriginal women, although domestic violence does occur in all
communities. For a health worker in a remote setting there are often no easy
solutions to stop the violence.
Aboriginal women report that they prefer the term ‘family violence’ to
‘domestic violence’, because this term takes into account the additional family
factors that can occur for women with extended family intervention.3 Often, other
family members may get involved, including some who will continue to abuse or
threaten the woman, even if her partner is no longer doing so. However, some women
are able to negotiate with sympathetic family members in order for them to put
pressure on her partner to stop his violence. These family ties can improve the
situation in some cases.
Women often report a great fear of payback or retaliation from family members
should her partner kill himself because she left him, or as punishment for him
being jailed or reported to police.
Aboriginal women are most often not able to leave their community and family
in order to move away from their violent partner. They also would not be able to
move to a new anonymous location where he could not find her again. The mere
remoteness of many communities makes it even more difficult for many women to seek
additional services or outside assistance.
Many women report that their partners are never violent unless they have been
drinking. While alcohol is not an excuse for violent behaviour, alcohol
consumption can make matters worse. However, much of the violence that does occur
in the Northern Territory does not involve alcohol or drug use.2

Pregnancy
Pregnancy is no protection against domestic violence; in fact, it often is the
trigger that starts domestic violence in a relationship.
Women in violent relationships are:
• Twice as likely to miscarry
• More likely to be prescribed medication through their pregnancy
• More likely to experience asthma and epilepsy and
• More likely to abuse drugs, alcohol and minor tranquillisers.4

As a practitioner be attentive to injuries on women’s abdominal and genital areas,

because these are often the areas targeted on pregnant women.

Children’s issues
Exposure to domestic violence has a profound and long-term effect on children.
Recent research indicates that children between 0–4 yrs show measurable
neurological delays in brain development when witnessing violence, and the
psychological effects are the same as if they had directly experienced the
violence themselves.5 This is the age where we normally assume children don’t know
what is happening. In fact, infants show clear disturbances in response to spousal
violence from at least six weeks of age.6
Child witnesses of domestic violence are found to develop post-traumatic stress
disorder symptoms in the same way as child victims of war or natural disasters.
That is, they are more likely to have dreams and recurring memories related to the
event, show hyper-vigilance, sleep disturbances, psychosomatic disorders,
withdrawal and anxiety, and have a lower level of cognitive performance.
Other behavioural indicators can include:
• Nervousness and anxiety
• Withdrawn behaviour
 • Adjustment problems, few interests and poor school performance
• Enuresis (bed wetting)
• Psychosomatic illnesses (asthma, stomach aches, headaches etc.)
• Excessive cruelty to animals
• Aggressive behaviour and language
• Pseudo-maturity
• Boys imitating aggressive behaviours, bullying/ abusing their mothers.

Also be aware of mandatory notification requirements. If you believe that their

home environment is adversely harming a child including psychological harm from
exposure to violence, you are required by law to report the matter to Family and
Children’s Services.

Practical strategies
Principles of working with victims of violence
Listen to the victim and show her you believe her:
• Be non-judgemental and respect her decisions, even if you don’t agree with
them
• Be aware of your own feelings, and remain calm
• Tell her she is not responsible for the violence
• Ask clear, direct, sensitive questions
• Provide accurate information, including the forms violence can take (physical,
emotional, sexual, financial, social), and the cycle of violence
• Ensure that she has the opportunity to make decisions about events, which
affect her life (i.e. whether to report to police, tell family or friends)
• Explore and dispel myths: it’s not her fault, she’s not the only one, she
can’t stop his violence, and it does affect her children.

Raising the issue

It’s easy to focus on treating the injury, and feel awkward about raising the
topic with victims of violence. But women are unlikely to raise the subject
themselves, and often do respond well to direct, clear, open questions. The
following ‘openers’ can help this process:
• That’s a really serious injury, how did it happen? It looks like someone hurt
you. Did someone hit/kick/burn you?
• Does your partner ever make you feel frightened?
• You seem scared of your partner. Has she/he ever hurt you?
• Have you ever been in a relationship where you have been hit, punched, kicked
or hurt in any way? Are you in a relationship like that now?
• Does your partner ever call you names or put you down?
• Does you partner ever force you to do things you don’t want to do? Has he ever
forced you to have sex when you didn’t want to?
• Are you ever afraid for your safety, or your children’s safety?
• Because abuse and violence are so common, I ask many female clients about it
routinely.
• You mentioned that your partner uses alcohol/drugs. How does he act when he is
drinking/on drugs?
• Has anyone ever forced you to do sexual things when you didn’t want to?
• Has your partner ever threatened to hurt you or your children?
• Does your partner accuse you of sleeping with other men, and watch you all the
time?7
Protective behaviours
Women may acknowledge the violence, but they may not be willing to immediately
leave their partners. While this may feel extremely frustrating, there is still a
course of action that you can recommend.
Talk to her about developing a plan of action to get her away from the violence
when she can see that it is about to happen again. Ask her to think about things
such as:
• Warning signs when she knows her partner is likely to get violent again
• Spare change, clothes, emergency supplies she can keep hidden in case she
needs to leave in a hurry
• A close personal friend or extended family member she can disclose to, who she
may be able to run to at any time
• A plan of action for children to run to a friend or neighbour’s house when
fighting is occurring.

By encouraging her to plan she can possibly safely escape the violence next time
it starts again. It is also worth discussing these plans even if the woman wants
to leave her husband. Often, women do return to violent partners as a part of the
violence cycle; at least with the plan they will have this information the next
time they need to leave.

Restraining orders
The domestic violence legislation in the NT covers a range of relationships,
including spouses, extended family through to great-great-grandparents, neighbours
and people who have shared a residence.
Restraining orders can be obtained when a person is likely to suffer violence,
threats and damage to their property or provocative behaviour at the hands of
their spouse or relative.
A ‘Section 4’ restraining order is a standard restraining order where the
client is required to make a signed statement outlining the abuse, and the matter
is brought before a magistrate within a few days or weeks, depending on when court
is sitting in the area. The order needs to be served on the offender before the
restraining order is active. These can be obtained if the danger to the woman is
not immediate.
Alternatively, a ‘Section 6’ order can be taken out more quickly, if the danger
is imminent and the victim has no safe place to go. In these instances, police can
contact a magistrate by phone and the order can be in place within a much shorter
time. However, the order still needs to be served on the defendant (that is, given
to the perpetrator) before the order is active.
Both types of orders can also be used if the patient is unconscious, with an
assumption of consent. Only police and magistrates can make the decision to take
out a Section 6 order, but any police officer has the authority to do it.
Restraining orders can allow for some contact between the parties if desired.
For example, it may be possible to allow the couple to live together, but he will
be breeching the restraining order if he consumes alcohol. Such orders are rare,
and have shown some problems, but could be considered in certain situations.
Assistance with obtaining restraining orders can be obtained from the Domestic
Violence Police Unit (8951 8888), and the Domestic Violence Legal Service (8952
1391), both in Alice Springs.

Self-care for workers

Frequently, perpetrators of violence are only violent towards their partners, not
other people. However, workers should never assume this to be the case, and should
always consider their own safety in situations of contact with victims of
violence.
Debriefing: Dealing with victims of violence can often be distressing and
frustrating. Make sure you have access to support people you can talk over the
incident with, including supervisors that may be located elsewhere.
Safety: Take whatever measures you can to ensure that you will be safe within
the community. Talk over the matter with other health staff, or police if
necessary. Take extra precautions, including not leaving the clinic alone at
night, and having backup support through the day where possible.

Dealing with perpetrators of violence

Dealing with a perpetrator, or someone you know has been violent, can be very
difficult, particularly if he attempts to talk to you about what his partner may
have said to you.
• Don’t reveal any information about her disclosure: this may make things much
worse for her. Remember that her disclosure is confidential information.
• Don’t ever minimise what he has done, or agree with excuses he may give for
the violence. The violence is his responsibility.
• Don’t assume that, because he has expressed remorse, he won’t do it again, and
it is safe for her to return to him.

If he is expressing a desire to see his children who have left with their mother
advise him to contact the Family Court Counselling service in Alice Springs, or
equivalent. The service in Alice Springs covers many remote areas of Central
Australia.
If you are at all concerned about your safety, or that of other workers, talk
to police or other staff about how you can keep safe, or who else can see this man
if he approaches the clinic.
Unfortunately, there are currently no intervention services for men who have
been violent, except if they have been jailed. A program is run in the Alice
Springs and Darwin jails for perpetrators of violence and rape. Alternatively,
some private psychologists outside of jail have engaged in this work.

Additional information
Hunter S. Domestic violence during Pregnancy. Office of Women’s Policy. Occasional
Paper no. 17. NT Government Domestic Violence Strategy, 1998.
Responding to Domestic Violence: A guide for GPs. Video produced by Office of the
Status of Women, Department of the Prime Minister and Cabinet, 1995.
Memmott P, Stacey R, Chambers C, Keys C. Violence in Indigenous Communities.
University of Queensland, 2001.
Catherine House, 86 Hartley St, Alice Springs. Phone (08) 8953 5914 during working
hours. Collection of resources and information relating to a variety of domestic
violence/family violence issues. An information folder is available for purchase.

Websites
www.ncp.gov.au
Website for National Crime Prevention, includes several papers and research
projects re: Aboriginal communities and Domestic Violence.
www.aic.gov.au
Website for the Australian Institute of Criminology, featuring many discussion
papers on child abuse, domestic violence and related topics.
www.austdvclearinghouse.unsw.edu.au
Australian Domestic Violence Clearing House: articles and information on
Domestic Violence projects and research from around Australia

Other services (Central Australia)

NPY Women’s Council: provide domestic violence support services in the NPY
language regions in SA, NT and WA. (08) 8950 5420
CAAFLU: Central Australian Aboriginal Family Legal Unit, based in Alice Springs,
providing legal support and information to Ntaria, Papunya, Yuendumu, Tennant
Creek and Alice Springs. (08) 8953 6355 or 1800 088 884
Alice Springs Women’s Shelter: emergency accommodation and case management support
for women and children escaping violence. (08) 8952 6075
Domestic Violence Legal Service: legal support with restraining orders and crimes
compensation, based in Alice Springs. (08) 8952 1391
Domestic Violence Police Unit: Police unit in Alice Springs with a focus on
restraining order applications and Family Violence matters. (08) 8951 8888
Central Australian Aboriginal Congress Social and Emotional Wellbeing Team:
counselling and support team, part of Aboriginal medical service. (08) 8951 4444

[Editor: These agencies are likely to be able to put you in touch with local
agencies in other areas.]

References
1.
Bolger A. Aboriginal women and violence. Australian National University North Australia
Research Unit, 1991.
2.
McCallum S. Data collection project report 1999. NT Government Domestic Violence
Strategy. Occasional paper no 35; 2000.
3.
Cummings E, Katona M. Aboriginal family violence. NT Government Domestic Violence
Strategy. Occasional paper no. 12; 1997.
4.
Stratigos S. Domestic violence screening and pregnancy. Paper presented at ‘The Way
Forward’ Children and Domestic Violence Forum, Partnerships Against Domestic Violence, 2000.
5.
Perry B. ABC Radio National. 2000.
6.
McIntosh J. Thought in the face of violence: a child’s need. Paper presented at ‘The Way
Forward’ children, young people and domestic violence proceedings, Carlton Crest Hotel,
Melbourne. Partnerships Against Domestic Violence. Canberra: Office of the Status of Women,
April 2000.
7.
Territory Health Services. Manual for Domestic Violence Intervention. Darwin: THS, 1995.
Grief and Loss

Author: Dr Ofra Fried

Topic Reviewers: Kaz Knudsen (RAN, WA); Vivien (RAN, Amata); Jane Kollner (RAN,
Ampilatwatja);
Teresa Bowman (RAN, Papunya)

I opened this protocol by drawing attention to the cross-cultural issues in

bereavement care because CARPA is used in regions of northern and Central
Australia which have diverse populations, including many different Aboriginal
language groups. In many cases service providers are of a different cultural
background to clients.1 Dealing appropriately with bereavement, grief and loss
requires some understanding of cultural differences.2,3,4 Because of the variety of
cultural responses it is inappropriate to be too prescriptive, and the best advice
is generally to refer to local knowledge.1,5,6,7 The particular cultural issues that
arise in many Aboriginal communities and were mentioned in the protocol (e.g. not
mentioning the name of the dead, vacating the place where a person has died) are
broadly relevant across Aboriginal Australia.6,8,9,10,11 This information may be
particularly useful for non-Aboriginal workers new to Aboriginal community work.
A significant loss of a child or partner will cause detrimental effects
physically, mentally or both in about a third of those most directly affected.12
Such losses in the short term increase the risk of death from heart disease13 and
suicide.12 About 25% of widows and widowers experience major depression and
anxiety disorders during the first year after the loss.12
The best way to help non-specialist care workers is to emphasise the range of
normal grief responses, and advise how to support those who are experiencing
normal grief. This helps the grieving person do the work of grief and reduces the
harm of an inappropriate intervention. Normal grief responses can include
presentations with physical health problems, inability to fulfil normal life
functions, and what even appears to be suicidal ideation (‘I wish I was dead’).14
Visual and auditory hallucinations about the deceased, the so-called
‘hallucinations of widowhood’ are reported in about half of recently bereaved
widows.15 These hallucinations can be distinguished from the hallucinations of
psychosis by the circumstances in which they arise (appear at times of sleepiness
or relaxation, i.e. hypnagogic hallucinations) and their transience — they
disappear as soon as the person awakes.12 Bereavement studies in Western societies
have described a series of stages of normal grief reaction, including the
anticipatory grief that may occur prior to an expected death.16,17 They have also
described the responses of shock (including disbelief, denial, anger), acute
mourning (searching and yearning, disorganisation, despair) and healing
(acceptance, resolving the loss, reorganisation of life) that occur after a
loss.17,18 Mourning practices are culturally specific.4 Examples include the
wailing characteristic of Aboriginal mourners and the practice of making ‘sorry
cuts’. Aboriginal people tend to be more open in their mourning compared with many
European Australians.15
Bereavement experts trained in a Western modality recommend the benefits of
therapeutic listening, which includes history telling, and asking specific
questions about the deceased, their death, and the relationship between them and
the person grieving.14,17 They generally recommend mentioning the dead person’s
name and making frequent eye contact with the bereaved. This type of bereavement
counselling may be intrusive in some cultural circumstances, including in many
Aboriginal communities.23 Western models of grief therapy should be adapted to
meet Aboriginal cultural needs as well as being responsive to individual
experiences of loss.19 Health workers from outside the cultural group of the
bereaved need to vary their responses in a culturally specific manner20 and to
seek local guidance about culturally appropriate behaviours.21
It was necessary to discuss the many sorts of losses that can result in and
aggravate the grief response.15 This makes it easier to understand how a given
death or loss affects an individual, enables identification of an abnormal grief
response, and facilitates early specialist referral or intervention.14 There is
some evidence that Aboriginal Australians suffer a high burden of accumulated
losses (including those of culture, power, land, and hope), which may compound the
grief response.19,22,15 Aboriginal families also suffer more premature illness and
mortality compared with non-Aboriginal families.19 Some factors that increase the
difficulty of a given bereavement relate to the life experience and personality of
the person who is grieving, others to the person who has died, and the manner of
their death.
The issue of blame may arise after a death, and ‘payback’ (revenge) may follow
the death of an Aboriginal person, particularly when the death was sudden,
unexpected or violent.15 Many concerns about the death and the care a person
received during their last illness arise from poor mutual understanding.
Aboriginal informants have emphasised the importance of ‘hearing the right
story’6, therefore there is value in giving information and in frank and open
discussion of any concerns. Weeramanthri has recommended a ‘post death conference’
some weeks after a death to reassure the family that everything possible was done
for their relative and to build trust.23 Non-Aboriginal staff need to be aware of
differences in causal attribution between Western medical and traditional
Aboriginal belief systems7, and recognise the need for the bereaved to establish a
‘social’ as well as a medical cause of death.9
How is the practitioner going to deal with this? On request, find out
information and arrange a meeting with family to discuss any issues, but please
note you may not have all the answers.
In general, grief associated with the death of an Aboriginal person is handled
through the family network, but it is important to recognise when outside help is
needed.23 An Aboriginal health worker (AHW) is more likely to know when there is a
problem requiring referral.15 There is little evidence that pharmacological
management is helpful, but specialist support is available from a wide range of
psychological and spiritual counsellors.14 Because of the cultural differences a
counsellor from the grieving person’s own language and cultural background may be
most appropriate. In most cases sleep patterns will return to normal. Occasionally
medication can be useful. If asked it is reasonable to offer a brief course
(maximum three or four nights) of sleeping tablets to help the person if they are
not getting enough rest. Antidepressant medications are not indicated for acute
grief.
I concluded the protocol by talking about the feelings of the health care
worker because they are rarely acknowledged, yet are very important to both the
worker and the patients they try to help.1 AHWs are particularly vulnerable to
stress following a death because they may have been related to the deceased, or
cared for them, and may be the subject of blame.23 A worker’s ability to deal with
others’ grief and loss depends on how well they have been able to resolve their
own. Additionally, stress and burnout amongst health care workers could be reduced
if their own human experiences and feelings were acknowledged.
People react very differently to losses, depending upon their cultural
background, personality, how they tend to handle stresses, previous experiences of
a death or loss, and personal and social support.
• A range of emotion is common; ask if there is anything you can do.
 Some deaths are harder to cope with, particularly if it was sudden or
unexpected, the person had a difficult illness before they died, the family are
worried about the care they got before they died, or the person who died was a
child or young person.
• People grieving after such a death are more likely to have problems
• Be patient, and listen well to their concerns
• Offer to get any information the family wants about the person’s illness and
care, then share it with them
• Be open to helping the family seek explanations for the death including
finding the autopsy and coronial results.

Do’s and don’ts of getting involved in sorry business

Do: explain the conflicts, i.e. provide care, help as asked unless dangerous.
Don’t interfere in the sorry process, especially payback and the violent sorry
grief.

References
1. Fried O. Cross cultural issues in the medical management and nursing care of terminally
ill Aboriginal people in central Australia. Alice Springs, Northern Territory: University of
Sydney, 2000. Masters Thesis.
2. Ata AW. Bereavement and health in Australia: gender, psychological, religious and cross-
cultural issues. Melbourne: David Lovell Publishing, 1994.
3. Eisenbruch M. Cultural aspects of bereavement: II Ethnic and cultural variations in the
development of bereavement practices. Culture, Medicine and Psychiatry 1984; 8:315–47.
4. Irish DP, Lundquist KF, Nelson VJ, eds. Ethnic variations in dying, death and grief:
diversity in universality. Washington DC: Taylor & Francis, 1993.
5. McGrath CL. Issues affecting the provision of palliative care services to remote
Aboriginal communities in the Northern Territory, Aust J Rural Health 2000; 8:47–51.
6. Wake D, Martin K, Dineen J. Yarlpuru: on sorrow. Talking to the families of dying
Aboriginal people. Australian Nursing Journal 1999; 6(9):16–18.
7. Weeramanthri T. Practice guidelines for health professionals dealing with death in the
Northern Territory Aboriginal population. Mortality 1998; 3(2):161–72.
8. Blackwell N. Oxford textbook of palliative medicine; cultural issues in Indigenous
Australian peoples. Oxford: Oxford University Press, 1998.
9. Sansom B. The camp at Wallaby Cross: Aboriginal fringe dwellers in Darwin. Canberra:
Australian Institute of Aboriginal Studies, 1980.
10. Maddock K. The Australian Aborigines: a portrait of their society. London: Allen Lane,
The Penguin Press, 1972.
11. Meggitt MJ. Desert people: A study of the Walpiri Aborigines of central Australia. North
Ryde: Angus & Robertson, 1962.
12. Murray Parkes C. Bereavement in adult life. BMJ 1998; 316:856–9.
13. Rogers MP, et al. On the health consequences of bereavement. N Engl J Med 1988;
319(8):510–11.
14. McKissock MA, McKissock DR. Bereavement: a ‘natural disaster’. Medical Journal of
Australia 1991; 154(20):677–81.
15. Hunter E. Aboriginal mental health awareness; an overview. Part seven; death, loss, dying
and grieving. Aboriginal and Islander Health Worker Journal 1993; 17(6):21–7.
16. Costello J. The emotional cost of palliative care. European Journal of Palliative Care
1996; 3(4):171–4.
17. Wheeler SR. Helping families cope with death and dying. Nursing 1996 July; 26–30.
18. Cooley M. Bereavement care: a role for nurses. Cancer Nursing 1992; 15(2):125–9.
19. Swan P. Grief and health: the Indigenous legacy. Grief Matters 1998; 1(2):9–11.
20. Prior D. Palliative care in marginalised communities. Progress in Palliative Care 1999;
7(3):109–15.
21. Fried O. Providing palliative care for Aboriginal patients. Australian Family Physician
2000; 29(11):1035–8.
22. McKendrick J. Thorpe M. The legacy of colonisation: trauma, loss and psychological
distress amongst Aboriginal people. Grief Matters 1998 Sept; 4–8.
23. Weeramanthri T. Practice guidelines for health professionals dealing with the death of a
Northern Territory Aboriginal person. Menzies School of Health Research Occasional Papers,
1996.
 Kava

Author: Allan Clough (MSHR)

Topic Reviewers: Prof Bart Currie (MSHR); Deb Beaver (RAN, Bagot Clinic); Helen
Collinson (RAN, Adelaide River)

About kava
Kava (Piper methysticum Forst. f. ‘intoxicating pepper’) is known in different
parts of the world by different names such as ‘kawa pfeffer’ or ‘rauschpfeffer’
(German), ‘kawa’ (French), ‘yaqona’ (Fiji), ‘kawa’ or ‘kava kava’ (Polynesia),
‘sakau’ (Micronesia), ‘wati’ and ‘tigwa’ (New Guinea), for example.1,2

What is kava?
Kava is both a plant and a beverage made from the rootstock of the plant.
‘Kava’ the plant is really a sterile group of cultivars of the wild Piper
wichmannii from New Guinea, the Solomon Islands and Vanuatu. It is an achievement
in plant breeding of rural, tropical gardeners who searched for and domesticated
it in northern Vanuatu about 2500–3000 years ago. Ni-Vanuatu and other Pacific
peoples continue to refine it today. From Vanuatu it went into the Pacific with
the forerunners of the modern Polynesians.1 Today, the plant and the beverage are
both pivotal to the economy, society and ritual traditions3 of several Pacific
island societies and nations.
‘Kava’ the beverage is widely consumed for its conscious-altering, hypnotic and
muscle-relaxant properties. It is a soporific brew with anxiolytic and mild
anaesthetic, sedative and analgesic effects.2

Kava in the natural therapies industry

Using materials imported from Pacific countries, kava is manufactured into
preparations of dried root, tablets or liquid extract for internal and external
use or as an ingredient in ointments and creams, and marketed with a plethora of
trade names. Kava-based products have recently been promoted as natural
alternatives to anti-anxiety drugs and sleeping pills in Europe, North America and
Australia.1,4 You can even buy kava and related products, now referred to as a
‘world drug’, over the Internet.

Kava’s key constituents

‘Kava pyrones’ are fat-soluble pyrones also known as ‘kava lactones’. There are
six main ones: kavain, dihydrokavain, methysticin, dihydromethysticin, yangonin
and desmethoxy-yangonin.2 Total lactone content of dried kava powder may be 10–15%
(average 12.5%) of dry weight, depending on the ecological conditions of plant
growth and the plant parts used to manufacture the powder. In fresh kava, lactone
content is around 2–3% of total weight.1
Mood-altering qualities
Mood-altering effects of kava have been variously described. They begin with
numbness in the mouth and throat that soon progresses to the limbs with an overall
sense of relaxation and wellbeing. With higher doses loss of motor control and
sleep induction occurs.11 These effects were thought to be superior to those of
alcohol by the people who decided to bring kava into their communities in Arnhem
Land after visits to Fiji in the early 1980s.12 Kava was regarded as a possible
challenge to the violence and social disruption associated with alcohol in remote
communities.13

Other effects
Sedative and hypnotic activity occurs, an effect that is greater with kava resin
(comprising the full suite of lactones) rather than with any one of the lactones
in isolation.2
Kava lactones act to alter neuronal excitation by direct interaction with
voltage-dependent ion channels and also enhance the binding capacity of GABA-A
receptor binding sites in some parts of the brain.14
Sleep may be promoted by actions on the limbic system through modulation of
emotional processes; deep sleep phase is lengthened with shorter wakeful phases.10
Anxiolytic activity without sedation.15 Relaxation of skeletal muscle and
anticonvulsant activity2 Local anaesthetic and analgesic.2
Potentiates acute effects of alcohol and possibly other drugs active on the
central nervous system.16
A dry, scaly skin rash (kava dermopathy) is a well-known effect of excessive
and chronic use but which regresses if kava intake is ceased or reduced, possibly
related to disruptions in lipid metabolism in kava users.17
Adverse economic effects in small communities.5

Overdose
There is no evidence available of overdose but, with prolonged use, the
characteristic skin rash may occur. Toxicity is low; LD50 for a standardised kava
extract administered orally in rats was 16 g/kg and in mice 1.8 g/kg. Kava did not
produce physiological tolerance in mice after seven weeks of daily exposure to
minimally effective doses.10

Other possible effects

Heavy doses of alcohol potentiate kava’s hypnotic, sedative and toxic effects.16 In
the United States recently an otherwise healthy man suffered reversible coma after
taking benzodiazepine in combination with the recommended dose of a natural
therapy that contained kava.18 One isolated case of ‘fitting’ (featuring choreiform
movements) with prolonged and heavy use has been reported in eastern Arnhem Land.19
Unpublished data suggest that similar unusual episodes have occurred in Arnhem
Land communities associated with heavy kava consumption. These have led to
presentations to the community clinic, but which did not require hospital
admission.
It has been suggested that those driving vehicles and machinery, and pregnant
or lactating women, should not use kava, but there have been no systematic studies
carried out.

Kava’s legal status in Australia

The Commonwealth Therapeutic Goods Administration monitors the importation of kava
into Australia, and importers require a licence to do so. In one state, Western
Australia, the sale and supply of kava was restricted in 1988 under S.22 of the WA
Poisons Act, but allows Pacific Islanders and others to seek permission from the
relevant minister to possess kava for traditional purposes.5
 Considerable effort has been made in the NT to manage the supply and
consumption of kava in Top End Aboriginal communities. With bipartisan support,
the NT Government has tried twice. The first legislative attempt was in 1990 under
provisions of the Consumer Protection Act5, the second in 1998 under the Kava
Management Act.6 The explicit objectives of the more recent legislation include
harm minimisation and to encourage ‘responsible’ kava use under a licensing system
to be implemented in late 2001 or early in 2002. The new system was not in place
at the time of writing (December 2001). A fundamental requirement of the proposed
system is that the supply of kava must be in accordance with a licence, and
possession and consumption of kava will be permitted only in designated licensed
areas.7

Traditional views of its use and effects

Kava’s ceremonial and religious role in Pacific Island societies is well known.
Over more than 50 years of research students of these societies have described
kava being used in rituals to enable contact with supernatural beings.
Kava has been widely used for medicinal purposes in the Pacific.4,9 And it has
also been used in Western herbal medicine since the nineteenth century,
recommended for treatment of a variety of ailments, mainly employing its mild
analgesic properties.10 Kava is not used for medicinal purposes by Arnhem Land
Aboriginal people.

Two cross-sectional studies in Arnhem Land Aboriginal populations

Two cross-sectional surveys of health effects of kava use in Arnhem Land have been
conducted. In one community in eastern Arnhem Land a study was conducted in March
2000, and its results have been submitted for publication. After adjusting for
alcohol use and sex, kava users more frequently showed dermopathy characteristic
of heavy use, skin disorders (tinea and sores) and a lower body mass index. They
had increased levels of liver enzymes (GGT and ALP) and blood lymphocytes were
decreased. No evidence of proteinuria was found. Kava users and non-users were
functionally equivalent on neurocognitive tests. Liver enzymes return to normal
upon ceasing or reducing consumption, as was found in previous studies.20
Results of an earlier pilot survey in 1987, also conducted in an eastern Arnhem
Land community21, had suggested similar health burdens for kava users. ‘Heavy’ kava
use was associated with scaly skin and ‘very heavy’ users were more likely to be
underweight and to have signs of liver damage (elevated GGT). Kava users showed
changes in their blood, suggesting possible increased risk of infections
(decreased lymphocytes) and kidney disease (proteinuria and haematuria) as well as
changed responses to simple neurological tests.21
The result of reversible changes in liver enzymes in Aboriginal populations
stands in contrast to a recent case of fulminant liver failure reported in Europe
that was associated with use of an extract of kava over a few months for anxiety
treatment.22 While there is currently no evidence for long-term liver damage in
regular kava users in Arnhem Land, this requires further assessment over longer
periods, particularly in heavy users.

Case-control studies
Studies of the risk amongst kava users of ischaemic heart disease (IHD) and
pneumonia in eastern Arnhem Land have been conducted, and their results are being
prepared for publication. A tendency (not statistically significant) for an
association with IHD amongst kava users and an association with multiple
admissions for IHD, as well as a tendency for an association with pneumonia,
suggests that kava’s effects should continue to be monitored closely. However, we
cannot confidently assert that kava consumption alone is a risk factor for IHD or
pneumonia in this population.

Other studies
Kava is recognised as a risk factor for melioidosis in the Top End of the NT.23
Kava has also been implicated in sudden cardiac deaths, particularly amongst
Aboriginal sportsmen.24 Kava’s diuretic properties would make it plausible that
those with established IHD, in particular, would be at higher risk of cardiac
events if they performed heavy exercise while dehydrated. Also, it is plausible
that people with abnormal cardiac output or effective mechanical performance,
especially with heavy exercise, may be at higher risk of arrhythmia or abnormal
atrioventricular function given kava’s well-known muscle-relaxing effects.

Kava drinking in Arnhem Land

The beverage has been (since 1982) enthusiastically consumed by some local
residents in a number of Aboriginal communities in Arnhem Land, and it continues
to be used today despite legislation.8 The name ‘kava’ is used in Arnhem Land, but
local people also know the Fijian name ‘yaqona’ and the grades of Fijian kava
‘waka’ and ‘lewena’ that are derived from the lower and upper rootstock of the
plant respectively. Kava, the plant, is not grown by Arnhem Land Aboriginal
people.
The preferred method of drinking kava in Arnhem Land is an infusion of dried
powdered kava in water, preferably chilled. Kava’s psychoactive components, the
kava lactones, are mostly suspended in the infusion with smaller amounts in
solution. Cups of, usually, about 100 ml are taken. The effectiveness of lactone
extraction in a brew of kava with water is not standard. It is subject to social-
contextual as well as physical variations in the mixture. The efficiency of
extraction of these active constituents in infusions of kava powder in water is
around 80%. Aboriginal people in Arnhem Land tend to consume kava at a steady
tempo, consuming on average 37 g of kava powder containing around 3800 mg of kava
lactones in 670 ml of water in an hour. Heaviest kava users have been known to
consume as much as 900 g of kava powder, equivalent to perhaps 93 000 mg of
lactones in a week.8

Prevalence of kava use in Arnhem Land

The large numbers of people spending significant amounts of time drinking kava has
attracted official scrutiny since the early years of kava use in Arnhem Land.
Recent estimates of the crude prevalence in kava-using communities in the region
in 1994–97 were 53% (67% males and 35% females) amongst people over the age of 15
years (Clough, A et al.25, paper submitted for review). A prevalence of current
(within the previous month) kava use in 2000 in one community of around 33% (44%
males and 10% females) is lower than these earlier estimates and suggests a
possible decline in the prevalence of kava use since the Kava Management Act 1998.
More recent data is not available to be conclusive about these changes.
Earlier studies carried out in 1985 and 198726 found that more (71%) males than
females (20%) in the same age group across Arnhem Land drank kava. Studies in
single communities showed that at about the same time from 56% to 66% of the
population were using it.8 Various studies have consistently reported a greater
proportion of males (from 53% to 71%) than females (from 6% to 51%) using kava.26
In 1992, in eastern Arnhem Land again, 66% of males and 33% of females were kava
users.5
Heaviest kava users are described as djadaw’ marama in the Gumatj dialect in
eastern Arnhem Land; that is, they are known to drink kava for 24 hours from one
day to the next, through the night and up to the next morning. Amongst kava users
during 1994–97, 52% of them had a history of drinking in this manner, a common
style of usage (Clough, A, unpublished data).

Economic impacts
In the late 1980s kava could be purchased from suppliers in Sydney at $12.50/kg.
The end price to the Arnhem Land consumer in 1990–91 was $100/kg, a profit rate of
800%. Recently, prices to consumers have varied up to around $270/kg in the
illegal trade with a purchase price in Sydney of $34/kg, a similar profit rate of
around 700%. It has been shown that communities may spend almost one-fifth of
available cash resources on kava. Around half of the gross profits from kava sales
in Arnhem Land communities leave the community, with the rest redistributed or re-
focused locally.

How much kava is too much kava?

From a community point of view, until Aboriginal people themselves decide to stop
drinking kava, there is little doubt that it will continue to be used in Arnhem
Land. The available data suggest that kava’s more serious health effects emerge
when kava is used at an average level of more than around 400 g/week. If more than
half the males and 20–40% of the females in a community are using it, and if 20%
of the available cash in a community is used to purchase it, effects on community
functioning are likely.

Relating current knowledge to the protocol

As can be seen from the information above, there is not a great deal of evidence
about the precise nature of the health impacts of kava use. In particular the
benefit of interventions is unclear. Consequently, the protocol is largely based
on a common sense interpretation of the available information as described above.

Practitioners should:
• do a full examination, including skin. This is included to alert
clinicians to the probably higher risk these people have for other conditions,
such as malnutrition and pneumonia, plus drawing attention to the skin
conditions that heavy kava users appear to be predisposed to, including
secondary skin infection
• consider full blood examination and liver function tests. The
significance of the raised liver enzymes and low lymphocytes are not clear but
may signify a health impact via nutrition or toxic effects. Demonstrating
altered pathology results to someone interested in the health effects of kava on
their body may influence their intake.
• ask about numbers of bags of kava usually consumed and the numbers of
people with whom it is shared. This may be important with the planned kava
regulation legislation and getting an understanding of the place the drug has in
the person’s life. More than 400 g per week is likely to lead to health
problems.

Advice for kava drinkers

• Annual check-ups. The evidence for this is weak. The recommendation is
based on the indication that kava users may turn out to be at higher risk for a
number of conditions, such as ischaemic heart disease, serious infectious
disease and skin infections. There is no evidence to guide how often these
check-ups should be. Annual check-ups are routinely recommended for adults as a
‘well person check’. Kava users may be prone to being missed in opportunistic
health checks due to the predominance of men drinking kava. Pneumovax and Fluvax
 will be particularly important in this group of people, probably at increased
risk of malnutrition and pneumonia.
• Think about amount of money leaving the community that could be spent
otherwise. This is based on the Top End studies that found that a large
proportion of one community’s money was leaving the community.
• People with heart disease or who are pregnant should reduce or stop
drinking kava. This is based on the Top End studies described above and a
general concern about possible poor impact on pregnancy, especially via poor
nutrition.
• Kava users may have extra chances of serious infections. This is based
on the Top End studies described above.
• Kava drinkers should avoid drinking in 24-hour sessions. This pattern of
drinking is associated with very heavy consumption rates and health problems.
• Using kava with alcohol or benzodiazepines and possibly other drugs
makes the bad effects of all the drugs worse. Kava potentiates the sedative
effect of benzodiazepines and alcohol.
Skin and liver problems usually return to normal in about a month after stopping
drinking kava. Underweight people tend to regain lost weight.

References
1. Lebot V, Merlin M, Lindstrom L. Kava, the Pacific Elixir: The definitive guide to its
ethnobotany, history and chemistry. Rochester, Vermont: Healing Arts Press, 1997; 2nd ed.
2. Singh Y. Kava: An overview. J Ethnopharmacology 1992; 37:13–45.
3. Turner J. ‘The water of life’: Kava ritual and the logic of sacrifice. Ethnology 1986;
25:203–14.
4. Kilham C. Kava: medicine hunting in paradise. Rochester Vermont: Park Street Press, 1996.
5. d’Abbs P. A review of kava control measures in the Northern Territory. Darwin: Menzies
School of Health Research; 1993 April. Report No: 3/95.
6. d’Abbs P, Burns CB. Draft report on inquiry into the issue of kava regulation. Darwin:
Menzies School of Health Research, 1997.
7. Northern Territory of Australia. Kava licensing matters. Department of Industries and
Business, Racing, Gaming and Licensing Division; 2001.
http://www.nt.gov.au/dib/ licensing/html/kava.shtml
8. Clough AR, Burns CB, Mununggurr N. Kava in Arnhem Land: a review of consumption and its
social correlates. Drug Alcohol Rev 2000; 19(3):319–28.
9. Katz R. The straight path: a story of healing and transformation in Fiji. Reading:
Addison-Wesley, 1993.
10. Mills S, Bone K. Kava (Piper methysticum Forst. f.). In: Mills S, Bone K, editors.
Principles and practice of phytotherapy: modern herbal medicine. Edinburgh: Churchill
Livingstone, 2000.
11. Prescott J, Jamieson D, Emdur N, Duffield P. Acute effects of kava on measures of
cognitive performance, physiological function and mood. Drug and Alcohol Rev 1993; 12:49–58.
12. Dunlop I. We believe it, we know it’s true [video]. Lindfield, NSW: Film Australia, 1996.
13. Cawte J. Kava: A challenge to alcohol. Aboriginal Health Worker 1986; 10(1):12–24.
14. Cairney S, Maruff P, Clough AR. The neurobehavioural effects of kava. Aust NZ J
Psychiatry [forthcoming].
15. Pittler MH, Ernst E. Efficacy of kava extract for treating anxiety: systematic review and
meta-analysis. J Clin Psychopharmacol 2000; 20:84–9.
16. Foo H, Lemon J. Acute effects of kava, alone or in combination with alcohol, on
subjective measures of impairment and intoxication and on cognitive performance. Drug and
Alcohol Rev 1997; 16:147–55.
17. Ruze P. Kava-induced dermopathy: a niacin deficiency? Lancet 1990; 335:1442–5.
18. Almeida JC, Grimsley EW. Coma from the health food store: interaction between kava and
alprazolam. Ann Intern Medicine 1996; 125(11):940–1.
19. Spillane P, Fisher D, Currie B. Neurological manifestations of kava intoxication
[letter]. Med J Aust 1997; 167:172–3.
20. Riley M, Mathews J. Heavy kava use by Aboriginal Australians. In: Prescott J, McCall G,
editors. Kava: Use and abuse in Australia and the South Pacific. University of New South
Wales: National Drug and Alcohol Research Centre, 1988; 26–8.
21. Mathews J, Riley M, Fejo L, Munoz E, Milns N, Gardner I, et al. Effects of the heavy
usage of kava on physical health: summary of a pilot survey in an Aboriginal community. Med
J Aust 1988; 148:548–55.
22. Escher M, Desmeules J, Giostra E, Mentha G. Hepatitis associated with Kava, a herbal
remedy for anxiety. Br Med J 2001 Jan 20; 322:139.
23. Currie BJ, Fisher DA, Howard DM, Burrow JNC, Selvanayagam S, Snelling P, et al. The
epidemiology of melioidosis in Australia and Papua New Guinea. Acta Tropica 2000; 74:121–7.
24. Young M, Fricker P, Thomson N, Lee K. Sudden death due to ischaemic heart disease in
young Aboriginal sportsmen in the Northern Territory, 1982–1986. Med J Aust 1999; 170:425–8.
25. Clough AR, Burns CB, Guyula T, Yunupingu M. Diversity of substance use in eastern Arnhem
Land (Australia): patterns and recent changes [paper submitted for review] 2001.
26. Alexander K. Kava in the North: a study of kava in Arnhem Land Aboriginal Communities.
Monograph. Darwin: Australian National University North Australia Research Unit, 1985.
 Mental Health:
Selected overarching issues

Author: Marcus Tabart (Psychiatrist, Alice Srpings)

[Editor: The following chapter is divided into three parts. ‘Part 1: Changes to
anti-psychotic medication in the CARPA STM’ was written by Marcus Tabart, a
psychiatrist in Alice Springs. ‘Part 2: Personal recovery in psychiatric
disorders’ was written by Laurie Curtis, Clinical Assoc Prof at the Trinity
College of Vermont, Burlington, Vermont, USA and was reviewed by Marcus Tabart and
the CARPA mental health editorial subcommittee. ‘Part 3: Some ideas on the
psychology of cultural relationships’ was written by Craig San Roque, a
psychologist practicing in Alice Springs.]

Part 1: Changes to anti-psychotic medication in the CARPA STM

Emergency treatment
The Therapeutic Guidelines: Psychotropic Version 4 and the bulk of contemporary
Psychiatric Literature now emphasise the harmful extrapyramidal side effects
(EPSE) that occur with the use of traditional high potency antipsychotic
medications such as haloperidol and trifluperazine (stelazine).1
Not only are these side effects (e.g. akathisia, dystonic reactions and
Parkinsonian stiffness) unpleasant, they can reduce the likelihood of future
treatment adherence. Another unwelcome side effect of antipsychotic medication is
Tardive Dyskinesia (TD). This is a disfiguring irreversible involuntary movement
disorder affecting oro-buccal-lingual musculature in particular, though the
abnormal movements are not necessarily confined to this musculature alone. The
incidence of this disorder due to exposure to traditional antipsychotic
medications is 5% after one year increasing up to an incidence of 25% with five
years exposure. If the patient is over 65 years the annual incidence of TD is a
staggering 26%. The incidence with atypical antipsychotic medication (e.g.
risperidone, olanzapine, quetiapine and clozapine) is in the vicinity of only 1%
per year.1
We know the clinical course of the majority of people with psychotic spectrum
disorders is one of exacerbations and remissions, and medication adherence is a
crucial determinant of recovery.
Droperidol is an effective agent to provide rapid and safe onset of sedation in
the setting of a psychiatric emergency when behavioural control needs to occur
quickly. It is a low potency antipsychotic, and as such is less likely to cause
EPSE than haloperidol.2 In the emergency setting, with an acutely behaviourally,
agitated and disturbed person (whether it be due to psychosis, mania, or
excitation states caused by drugs or an acute brain syndrome), the use of
droperidol is the current best practice. We are proposing to use droperidol
instead of haloperidol in the fourth edition of the CARPA STM for this group of
people.1
Droperidol produces marked tranquillisation and sedation. The onset of action
is from three to ten minutes following intramuscular or intravenous
administration. With haloperidol, by comparison, the onset of action via the
intramuscular route is about twenty minutes. The full effect may not be apparent
for thirty minutes. The duration of the sedative effect is between 2–4 hours. The
usual dose is between 5–10 mg IMI.3
Droperidol is rapidly absorbed by the intramuscular route. This is the
preferred route of administration. Its elimination half-life is about two hours.
It is safe to repeat the dose within 30 minutes of the initial dose if the desired
sedative effect has not been satisfactorily achieved. Though the incidence of EPSE
is much lower with droperidol than haloperidol one would also give benztropine
with the initial dose of droperidol.1
The current literature is sparse about the effects of combining droperidol with
midazolam. One can say that on most occasions, droperidol alone should be
sufficient; combination with a benzodiazepine — whether via the oral or parenteral
route — will potentiate the sedative effects of droperidol; and the combination is
most probably safe. The Royal Melbourne Hospital is currently conducting a trial
using such combination therapy (pers. comm., Pharmalab, the manufacturer of
Droperidol).

Maintenance treatment
It is recommended that Risperidone is made available to all remote clinics and for
it to be the antipsychotic medication of choice for the management of psychotic
disorders.
Risperidone can be used to the following circumstances:
i. In the acute setting where a person is psychotic and agitated but is able
to have a tablet and does not require evacuation;
ii. For longer term use in those people with a psychotic illness such as
schizophrenia or delusional disorders.4

Risperidone is well absorbed after oral administration, reaching peak plasma

concentrations in one to two hours. The elimination half-life is 24 hours and so
it can be given as a once-daily dose. The dose for best efficacy and tolerability
is 2–6 mg/day (average 4.5 mg/day). Rather than to raise the dose above these
levels in agitated patients, partial responders, or acutely ill patients, one
should consider instead augmentation with a benzo-diazepine such as diazepam.
Amongst Risperidone’s advantages are:
i. It is an atypical antipsychotic and has less propensity for EPSE so is
better tolerated by people
ii. Probably has a reduced incidence of Tardive Dyskinesia compared with
haloperidol
iii. Has better efficacy with negative symptoms in schizophrenia than
haloperidol
iv. Possibly reduces cognitive and affective symptoms in schizophrenia more
efficaciously than haloperidol
v. Less weight gain than with other antipsychotic medication
vi. Well accepted for treatment of agitation and aggression in elderly dementia
patients
vii. Well-accepted treatment for treatment in bi-polar disorders
viii. A depot preparation will be available towards the end of 2002.4
ix. Risperidone is significantly cheaper than Olanzapine yet both have similar
effectiveness.5

[Editor: In recent years, droperidol has been reported to cause prolongation of

the QT interval.a,b,c,d Discussion with a number of psychiatrists including Josh
Geffen (Senior Lecturer, Dept of Psychiatry, University of Queensland) lead to the
view that:
QT interval issue is dose dependent so one dose of 10–15 mg droperidol is
unlikely to cause QT prolongation. The balance between risk of harm from
 medication and risk of not treating was judged to lie with using a single dose of
droperidol.

(The review by Glassman summarises the risk as ‘Although sudden unexpected death
occurs almost twice as often in populations treated with antipsychotics as in
normal populations, there are still only 10–15 such events in 10 000 person-years
of observation’.b)
We have recommended to leave out extra doses of droperidol and instead use
further doses of midazolam, although noting some more risks of respiratory
depression with this agent.
An IM preparation of olanzapine is becoming available within 12 months; this
will be the preferred IM antipsychotic to use in the emergency situation. However
as it is not yet available, it is not mentioned in the STM.
a. Raftos J, MBBS FACEM. Treating the acutely psychotic patient. Australian Family
Physician Sept 2002; 31(9): 813.
b. Glassman AH, Bigger JT Jr. Antipsychotic drugs: prolonged QTc interval, torsade de
pointes, and sudden death. Am J Psychiatry 2001 Nov; 158(11):1774–82.
c. McAllister, HR, et al. Rapid Tranquilisation: Time for a reappraisal of options for
parenteral therapy. Brit J Psychiatry June 2002; 179:485–9.
d. Reilly JG, et al. QTc-interval abnormalities and psychotropic drug therapy in
psychiatric patients. Lancet 2000; 355:1048–52 (NB the QT prolongation with
droperidol was obtained from patients on the oral droperidol for a minimum of two
weeks).]

References
1.
Therapeutic Guidelines: Psychotropics. version 4. Victoria: Therapeutic Guidelines Ltd,
2000.
2.
Chambers RA, Druss BG. Droperidol: efficacy and side effects in psychiatric emergencies.
J Clin Psych 1999; 60(10):664–7.
3.
MIMS Annual. 2001.
4.
Stahl SM. Psychopharmacology of antispsychotics. UK: Martin Dunitz, 1999.
5.
Emmerson B, Estensen A, Powell J, et al. Strategies to manage inpatient drug costs.
Australasian Psychiatry 2001; 9(3):249–52.

Part 2: Personal recovery in psychiatric disorders

Contrary to popular beliefs, worldwide research suggests that many, if not most,
individuals diagnosed with serious mental disorders (e.g. schizophrenia, bi-poplar
disorder) can and do recover.
Recovery may mean that a person becomes symptom-free or it may mean that the
person may have symptoms that do not impede their living full and productive
lives. In its essence the process of recovery means that an individual is not
dominated, internally or externally, by illness or disability, even if symptoms
are still present.

This picture illustrates this change.

Me It

IT Recovery ME

This is not a quick or easy process for most people. It is common for individuals
to get stuck, sometimes for years, on the left side, where they view the world
through the illness and the world sees the illness, not the person. It becomes a
self-fulfilling process.
Serious mental illness affects almost every aspect of an individual’s life, as
well of his/her family and often his/her community. The process of personal
recovery also involves careful attention to both internal and external elements of
a person’s life: home; work/productivity; social/interpersonal;
belonging/connectivity; spirituality; beliefs about the past, present, and future;
as well as physical health and psychiatric symptomatology.
Appropriately prescribed psychiatric medication is an exceptionally helpful
tool for many people. However, it is not the only important tool.
Recovery-oriented mental health treatment helps an individual to gain the
knowledge, skills, and tools to help him/herself to minimize or manage distressing
symptoms and to meet the challenges of day-to-day living.
Recovery-oriented mental health services are ‘do with’ rather than ‘do to’
services. The individual person, often with his/her family, must be full partners
in the treatment process and are the prime agents of change. This involves
including the individual/family in all assessment, treatment, support, and
decision-making procedures.
Factors that help to stimulate and support personal recovery from psychiatric
disorder can be divided into ‘internal’ and ‘external’ conditions.

Internal conditions
• Hope: Belief that positive changes can happen and that life is worth living;
focus on strengths, allies, and capacity for change.
• Belonging/connection: Feeling a part of something larger than one’s self; being
accepted by others; having respectful, trusting, and reciprocal relationships.
• Meaning/purpose: Finding place and purpose within a community and culture. For
some this means work and earning an income, for others this may mean being able to
connect with the spiritual world, or fulfill valued social roles.
• Empowerment: Exercising autonomy and self-governance; accepting responsibility
outcomes of personal decisions and actions; courage and risk-taking.
• Healing: Defining self as apart from the illness; recognising strengths as well
as limitations; developing knowledge and effective strategies for self-care and
symptom relief; greater ‘wholeness’ and balance.

External conditions
• Valued social roles: Fulfilling and being honoured for ‘everyday’ roles and
contributions to community as a parent, worker, friend, healer, care-taker, elder,
son/ daughter, artist, tenant, participant in ceremony, and so forth.
• Human rights: Acknowledgement of human rights and the damaging impact of social
and economic marginalisation; respect for personal rights and dignity.
• Opportunity and access: Reduction of stigma; increased opportunities and access
to needed resources (includes basic resources such as shelter and food, as well as
healthcare and other services).
• Effective mental health treatment and services: An orientation to a ‘positive
culture of healing’ as the core element of professional services; positive and
respectful staff attitudes; access to appropriate medication, physical healthcare
and crisis response resources; proactive attention to recovery education and
planning, crisis prevention; integrated substance abuse and trauma-informed
services.
• Support: Friends, family, other consumers, professionals all constitute a web of
support that provides help, problem-solving, reassurance, feedback, and positive
expectation.

What you can do

As a person
 • Self-check your personal beliefs about the long-term course of psychiatric
disorders and the process of recovery
• Communicate the expectation of recovery and success, be a ‘holder of hope’ for
others
• Use culturally respectful terms and person-first language (e.g. say ‘persons
with schizophrenia’, rather than ‘the schizophrenics’); use terms that
highlight valued social roles rather than patient, client, service recipient
roles
• Spend more time listening than talking.

In relationship building
• Be a partner or ally for the individual/family, rather than expert
• See people as people, not patients; engage on a person-to-person level with
each person and family member
• Allow for alternate ways of seeing or defining the problems, as well as the
solutions (e.g. avoid defining the situation or symptoms from solely a medical
model or western view-point).

In assessment and care planning

• See individuals as intricately woven into their families, community and
culture. These carry meaning, even if the ties appear to be severed or
unraveled
• Encourage and provide space for people to ‘tell their story.’ Listen for
meaning in metaphors, perceptions about the causes of problems, previous
attempts to cope or problem-solve, strengths and dreams, patterns of symptoms
or triggers, community connections, natural supports and resources, how the
person gains or loses respect in his/her family or community.
• Ask about domestic violence, substance use, and childhood emotional, physical
or sexual abuse. These forms of violence can have lasting impacts that can
mimic psychiatric disorders.
• Help individuals identify personal dreams and desired life changes.
Collaboratively explore various paths for achieving these outcomes.
• Develop care plans that can be fulfilled by the individual and
carers/community. Use mental health resources as a back-up resource.

In care and treatment

• You cannot make someone recover. You can provide information, tools,
encouragement and support to aide each person in this process. You can also
inadvertently impede the process
• Listen when people tell what has been helpful/not helpful. Integrate this
input into planning.
• Take a broad definition of ‘therapeutic’. There are many pathways to
healing.
• Provide knowledge and information about mental illness, recovery, self-
management approaches, community resources, and so forth.
• Use approaches that validate the individual as ‘expert’ on their own lives.
You are an assistant or ally to their process of personal recovery.
• Engage the individual in any decisions about medication. Avoid medication
protocols that disrupt valued functions (e.g. hearing the voices of ancestors)
or meaningful roles (e.g. sexual functioning).
• Medications are a means to an end, not the end in and of themselves. Focus
on the positive life outcomes that come from use of effective medications,
rather than the horrors of non-compliance.
• Expect the process of recovery to include crises, setbacks, and new
beginnings. It is a spiraling rather than a linear process.
• Collaboratively develop proactive relapse prevention and wellness plans.
In the community
• Avoid removing an individual from their community or personal supports,
particularly for an extended period of time. Help individuals retain personal
connections during ‘away’ periods (e.g. during hospitalisation).
• Help each individual construct a personal support network within his or her
family, allies/friends, and traditional healers. Professionals may be an
element of the support network, but should never dominate it.
• Work to identify positive ‘models of recovery’ that help to demonstrate
that ‘people make it’.
• Help individuals find or re-establish valued roles and positions within a
community or culture.
• Help individuals find ways to be givers not just receivers. There are many
ways people do this in personally meaningful ways: e.g. reciprocal
relationships, peer support, volunteer activity, advocacy work, story telling
to help inform others.

Bibliography
Anthony W. Recovery from mental illness: the guiding vision of the mental health service
system in the 1990s. Psychosocial Rehabilitation J 1993; 16(4):11–23.
Curtis LC. Moving beyond disability: recovery from psychiatric disorders. One person’s
perspective. In Towson MD. The capstone. The Council on Quality and Leadership in Supports
for People with Disabilities, 2000; 17(2):8–9.
Curtis LC. Practice guidance for recovery-oriented behavioral healthcare for adults with
serious mental illnesses. In Towson MD. Personal outcome measures in consumer-directed
behavioral health. The Council on Quality and Leadership for Persons with Disabilities,
2000; 25–42.
Deegan P. Recovery: the lived experience of rehabilitation. Psychosocial Rehabilitation J
1988; 11(4):11–19.
Estroff SE. Self, identity, and subjective experiences of schizophrenia; in search of the
subject. Schizophrenia Bulletin 1989; 15(2):189–96.
Harding CM, Zubin J, Strauss JS. Chronicity in schizophrenia revisited. Brit J Psychiatry
1992; 161:27–37.
Jacobson N, Curtis LC. Recovery as policy and practice: how states are implementing the
concept. Psychosocial Rehabilitation J 2000; 23(4):333–41.
Jacobson N. Experiencing recovery: dimensional analysis of recovery narratives. Psychosocial
Rehabilitation J 2001; 24(3):248–56.
Ridgway P. Re-storying psychiatric disability; learning from first person recovery
narratives. Psychosocial Rehabilitation J 2001; 24(4):335–43.

Part 3: Some ideas on the psychology of cultural relationships. ‘Black

and White and the things between us’
[Editor: This paper does not offer an explanation for a particular protocol or
clinical action, but is included as it may help remote practitioners gain some
useful insight into their own experience as a practitioner, and hence be
sustaining. In the authors words:
In short, taking care of one’s patients and taking care of oneself may involve
becoming more professionally aware of how projection and transference operate as
subliminal communications.]

. . . therapy must remain an obstinate attempt of . . . people to recover the

wholeness of being human through the relationship between them. (RD Laing1)

Introduction
This paper can be linked to the subject of self-care [Editor: for practitioners].
It reveals another aspect of the self-care picture and introduces an idea on how
relationships between people of different cultures can be thought about, drawing
on the experience of psychotherapy.
It suggests that more attention be given toward understanding the psychological
nature of experience in remote area Indigenous life. Also, that the mental health
of Aboriginal people and of non-Aboriginal health professionals might be supported
and understood better if key workers and administrators made the effort to become
systematically aware of the way mental life actually operates.
The dynamic relationship between Black and White people is shot through with
partially unconscious desires, expectations and communications, as well as
subliminal attempts to change each other’s bodies, beliefs, behaviours and uses.
The demands made upon a person by self, family, work, administrative and
political agendas are entangled, complex and sometimes dehumanising. Managing this
often unconscious dynamic is confusing and emotionally exhausting and may
contribute to the particular kind of ‘burnout’ and dissatisfaction experienced in
remote-area work.
However, I also suggest that effort to analyse inter-cultural, psychological
transactions would be worth proper attention. This might include a study of the
mental operations of transference and projection as it applies to what happens
between people of different cultures, especially in Aboriginal country. This is an
entirely new field.

Part 1
Intercultural ‘static electricity’
Therapeutic workers of all kinds often find that, because they get so close to the
feelings, bodies, injuries and events of many traumatised people, they pick up
emotionally charged ‘static electricity’ from their patients and the working
environment. Absorbing the emotions associated with exposure to trauma is probably
a part of being human. Our capacities for sympathy and empathy are brought into
play. It is commonly understood that de-briefing, good supervision and a well
managed support team can help to ‘wash out the static’ and maintain a high
standard of therapeutic effectiveness and humanity.
If we take the psychiatrist RD Laing’s point about honouring and working
therapeutically within the relationship, we have to remind him that therapeutic
work within intercultural relationships has a very special twist to it. Especially
when it is happening in and on Australian Indigenous country.1
In remote-area work the ‘emotional static’ we pick up has a special twist to it
because of the way life is lived in ‘remote areas’ and because of the different
ways people of White and Black cultures work upon each other, psychologically.
The difficulties of work in those regions and the difficulty of putting good
supervision or psychological support into place may mean that the work becomes
hard to bear. One’s therapeutic capacity becomes dulled, or hard to manage, normal
defences against pain and confusion may become exaggerated or distorted.
Psychologically justified paranoid defences of dissociation and dehumanisation may
take over as an individual struggles to survive a (psychic) inter-cultural
situation which may be only barely understood, despite the endless hours of
repetitive dinner table or camp fire gossip about ‘us’ and ‘ them’.
Some of the ‘static electricity’ generated between persons is generated by the
clash of peoples, a clash that has taken place historically in Australia, and is
still taking place. This clash or abrasion is not always straight out physical
assault or conflict. It may have an elusive, sideways, understated, easily
deniable quality to it which may have something to do with the way Indigenous
people manage conflict, combined with the way those of an Anglo-Australian
mentality have managed the bureaucratic takeover of the continent.
It is not my job here to carry out a political/historical analysis. The problem
for us as professional health workers, however, is that the psychological
consequences of that historical conflict and the misunderstandings of the
relationships of conquest may come to a head in our own work spaces: in hospital
waiting rooms, accident and emergency wards, remote area clinics, drug and alcohol
settings, police vehicles, court rooms. I am speaking not only about family
conflicts and violence displayed in public spaces, but also about a much more
subtle, almost subliminal tension, which is generated by and between persons when
they meet in such spaces, apparently to help each other and be helped. Sometimes
the slow procedural boredom of the institutional settings makes the deep inner
story of Australian life seem dull and of no consequence. But out bush the drama,
tragedy and tension is stark and visible, but sometimes the very drama of it makes
it hard to think. There are many things, which happen between us, which are
difficult to think about and difficult to speak about.
I ask you to consider if it is worth spending time to think carefully about
such matters as the difference in the psychological make up of people raised in
such unique ways as the Indigenous Australian and the settled/immigrant Australian
(no matter what the countries of origin may be). We do have different origins and
purposes and yet we have become uneasily entwined. We are expected to safeguard
each other’s health and wellbeing, and yet the evidence or experience suggests
that the health of Indigenous people is barely improving and the health of many of
the non-Indigenous workers suffers. What is going on? What are we doing to each
other? Could it have anything to do with our difficulty in recognising, feeling
and working with the differences?
If we think of a typical bunch of people who might find themselves in treatment
or at work in a typical bush clinic then we may have a mixed bag of concepts of
sickness and cure, cause and effect. The nature of the ‘healing contract’ may be
interestingly different. Indeed the very basis of the sense of self may be
different. So too, the sense of family identity, morality, ethics, spirituality
and the role of the country in the formation of the mind. Indeed, the sense of the
location of the mind and the boundaries of the mind may be quite different.
Our languages, for instance, are very different in structure, history and uses
and thus the way our thoughts are put together can’t help but be different. The
metaphors and images in which our languages are based are different and thus the
pictures in the mind, which words help create, will be different for people who
have been born into such different language beds as, say, the Warlpiri and the
English. If language is about communication, and the mutual understanding of
language is uncertain, then the communications will be vague, uncertain and
simplified. We might get by with talk about objects and so called concrete
realities, but talk about feelings, ideas, meanings, causes, and depths of human
experience . . . what then?
I suggest that the varieties of the difference between Black and White (or ‘us
people’ and ‘you other people’) ought to be understood and appreciated more fully
and systematically than most of us have so far managed. Appreciating similarity
and unity has its value, so has recognition of uniqueness and difference.
I am introducing the idea here that stress, trauma and burnout in remote-area
practice may be partly caused by our failed attempts to handle the differences
between us. Managing inter cultural relationship is about self awareness and self-
care as much as it is about taking care of others. Self-care manuals may show you
how to handle and even get rid of the ‘static electricity’ from your system. (By
‘static’ I mean, the worry, the somatic symptoms, the exhaustion, the confusion,
and the aftermath of ‘flight and fight’ reactions experienced when working in a
threatening, culturally strange environments.) This subject is well covered in the
CRANA sponsored booklet, ‘Stress: On surviving burnout in remote areas’.2 Essential
reading. By the way, I have yet to come across a manual, written by Aboriginal
people, with a title something like ‘Burnout: On surviving White people in our own
country.’

Intercultural transference and projection

If we were to take the matter one step further than the (valuable) stress
prevention manuals we might want to draw upon the insights of those two famous
psychological explorers, Sigmund Freud and Carl Gustav Jung. The key subject for
us is their psychoanalytic work on transference/counter transference and
projection. This is a complex subject, and I will not be able to do it justice
here, but I can place before you a few ideas, as a kick-off.
When I suggest that a kind of psychological static electricity gets generated
between people who work in cross-cultural settings I am talking about eruptions of
love, hate, envy, fear, contempt, confusion, shame, anxiety, grief. Suchlike deep
emotions are stirred up between persons, whether the relationship is a
professional one or a personal one. These emotions generate bodily reactions, they
set off behaviours and they start up psychological images, stories and scenarios
in mind and ‘heart’.
‘Transference’ means ‘carrying something over from one place or one time or one
person to another’. It has technically complex meanings in psychology, but
basically ‘transference’ is about the way emotional reactions, images and ideas
behave as we shift them about between ourselves.
‘Projection’ is the way we send mental and emotional images and messages to
each other. Traditional sorcerers/witchdoctors know about projection and use it to
affect people ‘magically’. The ‘electric tension’ in a relationship is created as
we shift about and send between us bundles of emotionally charged ideas, images,
feelings and reactions.
When transference and projection kick in, so too do memories, fantasies, false
stories, unreasonable expectations, imagined wrongs, paranoia . . . Most family
feuds and vengeance cycles are kept going through psychological procedures like
this. People may not stop to sort out the truth but keep piling more and more
emotional fuel on the fire, shifting blame, fantasy and fear around from person to
person until no one person can think or act for themselves. This happens in
Aboriginal communities and between families, and it happens in government
organisations.
Freud and Jung’s idea about the transference and projection transactions that
get going between people (and organisations) is that dangerous business starts
when we don’t really know for ourselves what we are doing and thinking. When the
reactions are unconscious to us, ourselves. When we don’t know our own mind and do
not stop to think.
My paper is about starting up the idea that we might just be able to learn how
to process the particular kind of reactions that get stirred up in remote-area
work settings. To do this we might be able to learn from Freud’s mob.
The psychological ‘static electricity’, or the transference projections that
you may pick up, may come to you as odd feelings, visceral or bodily reactions,
strange ideas and images, sudden emotional charges, dream fragments, late night
thoughts and intuitions. These reactions may be seen as eccentric aberrations or
signs of ‘nervous breakdown’, ‘bush fever’. But these reactions can all be decoded
and identified. Some may be transference communications between one’s
client/patients and oneself; some may be subliminal dream-like intuitions about a
situation in the community. Some may be about deep shifts in one’s own psyche. In
short, transference and projection process can be used as a diagnostic tool and as
a self-educative process.
However, the skill in collecting and decoding elements of intercultural
transference and projection is a genuine skill and it does have to be worked upon.
Special practice has to be developed to decode and interpret transference
processes between people in normal therapeutic relationships, in protected
consulting rooms, or in-group process. But imagine how difficult it is when the
relationship is between a ‘doctor’ and a ‘patient’ of different cultural and
epistemological backgrounds. Some remote-area workers manage this difference
amazingly well and we could learn from them. Such people may have the skill and
experience to be seated in the camp of the pragmatic health scientists and at the
same time be seated in the venerable camp of the pragmatic spiritual animists. You
could perhaps name a few Aboriginal and non-Aboriginal people who are good at this
‘two-way thinking’, being able to sit in both camps at the same time.
In summary, I suggest that much of the heartache, misunderstanding and stress
generated between Aboriginal and non-Aboriginal workers has to do with our mutual
naivety and mutual inability to process what is being communicated between the two
camps. Few health services have taken the beneficial step of implementing
psychologically attentive work incident discussion as a self-reflective way of
relieving stress and decoding intercultural process. Most such interventions are
after-the-fact, as post trauma debriefing, and are not carried on as a
professional development opportunity. This may be because ‘stress’ is seen as an
aberration to quickly recover from, rather than as indication of something to
learn from.

Part 2
Reciprocity of psychic life

. . . Any technique concerned with the other without the self, with the behaviour
to the exclusion of experience, with the relationship to the neglect of the
persons in the relation, with the individuals to the exclusion of their
relationship, and most of all, with an object-to-be-changed rather than a person-
to-be-accepted, simply perpetuates the disease it purports to cure. (RD Laing.1)

This little sermon from RD Laing, an experienced and revolutionary

psychotherapist, affirms the values of attending to people as fully human even
while they are being treated scientifically. In his writings he also introduces
the idea of reciprocity of psychic life; that we catch things from each other as
persons; even if we think we are protecting ourselves and remaining professionally
detached while treating people as patients or as ‘objects’ to be cured.
Laing, like Freud and Jung before him, discovered that being a part of the
therapeutic profession lays one open to influence from one’s patients and the
situations or conditions in which they live. Working in primary health care
definitely means being personally immersed in the conditions of one’s patients
because primary health care workers and front line public health workers are
living in the very situations that are making their patients sick or distressed.
Being part of the mix of life and death on a remote Aboriginal community lays
the psyche open to influence in very specific ways. The influences can be
creative, instructive, confusing, destructive, exhausting and life changing . . .
all at once. Decoding and understanding what goes on in the day-to-day situations
in intercultural therapeutic transactions could be part of routine professional
debriefing. It usually happens, unfortunately, that making sense of our experience
together is often sidelined into backbiting gossip cycles and understanding is, in
this way, diminished and degenerated.
Psychoanalysts developed the notion of ‘transference’ and ‘counter
transference’ as a way of explaining the peculiar ideas, sensations, feelings and
images that occur to patient and therapist when they are in each other’s presence.
They developed this process into a therapeutic tool. They make a systematic study
of interpersonal projection by noting carefully their own reactions while in the
presence of the other (the so-called patient). This observation includes giving
careful attention not only to the patient’s signs, symptoms and reactions but also
to the therapist’s own bodily sensations, images, feelings, ideas and the
afterthoughts that arise spontaneously when in the presence of the other person,
the so-called patient. This observation includes noting, for instance, the varied
sensations of love, hate, fear, uncertainty, unknowingness and misunderstanding
which occur when with the patient. These sensory clues may be seen as signs of the
patient’s psychological problem as well as signs of the cultural or environmental
conditions in which the patient and the therapist are situated. One has to think a
bit like a detective.
I want to open up this idea and invite you too to learn to be observant of the
range of ideas, feelings, impulses, desires and actions which come to you when you
are immersed in the presence of persons of another culture. DW Winnicott, an
English paediatrician and psychoanalyst, became fascinated with what he called the
‘area of overlap’ between a mother and child. He called this space of sense and
feeling between a parent and child a ‘potential space’, because there is so much
potential there and so much could happen in it. Others, like the Australian
psychiatrist Russell Meares, are tuned in to what psychologists call the
‘intersubjective space’. Those of us who work in the overlapping
intersubjective/potential space between people of Aboriginal background and those
of mostly European or Asian background may have something to learn from Winnicott,
Meares and company. We may have something to teach them also. I am inviting people
of Aboriginal and non-Aboriginal descent to seriously look into this matter of
what goes on, psychologically, between us, while we work.

Some technicalities: The movies in our heads

As we have already noticed, transference is about ‘psychological stuff’ that gets
passed from one person to another. Sometimes we feel and see and understand this
‘stuff’ with no trouble. Mothers are often very good at reading their kid’s
transference, without even noticing how clever they are when reading their child’s
secret signals, hungers, and cries. Lots of psychological ‘stuff’ gets passed back
and forward between husbands, wives and family. Sometimes, however, it is very
hard to decode this psychological stuff and we react to it without understanding
it and get into trouble.
Transference operates partly through projection. Projection can be understood
as a way in which our ‘internal’ mental/ emotional movies are projected upon the
screen of other persons, places and situations ‘outside’ us. This capacity for
projection is a part of being human. It is a form of communicating. Things are OK
when people can check their scripts against each other’s version, but sometimes
people can’t see that they are reacting to their own movie and they don’t do a
reality check. They react to their own projected movie as though it was reality
and not created by them. It’s easy to see other people doing this. Not so easy to
catch oneself. One of the ways to see how projection works is to track cycles of
blame and revenge.
Different cultural groups have different basic ‘cultural movie scripts’ that
are created by some mysterious process of cultural consensus. These are the
creation myths or primary cultural ideologies. Swallowing cultural ideologies is
part of the deal of being part of group life. It is these ideologies which we
communicate subliminally and use as patterns to shape our personal transactions
with each other.
Transference and projection can be a very useful part of creative human
relationship. But some transference projections, which are unconscious and given
no chance to be thought about, can cause deep harm. Intense destructive
unconscious projection turned on another person can create madness. Between Black
and White, transference and unconscious projections can create a state of madness.
If the projections are tracked, by doing work on what is happening, the
intercultural madnesses to which we subject each other might just have a chance of
being lightened, loosened and cured.

Five senses, a brain and three psychological capacities

There have been a hundred years of psychoanalysis. We can’t squeeze everything
learned about the human mind into these pages, but the following few points might
help your thinking on this subject.
We have five senses: sight, hearing, touch/sensation, smell and taste.
As we turn our senses upon the world our brain does things with these sense
impressions. The brain works by transforming senses into brain messages and
gathers them together to make meanings. It is the capacity to make meaning out of
the impressions that come through our skin, eyes, ears, nose and mouth that is so
amazing about humans.
We have three incredibly useful capacities that help us to make meaning out of
sense data.
One is the capacity for psychological integration of experience. The ability to
collect bits of information and put it together and then do mental work on those
collected bits so that it makes sense. Some of this seems to happen spontaneously
but some of this mental work has to be done by thinking and by doing psychological
work. (i.e. W Bion’s alpha function, philosophers and scientists are good at this)
The second capacity is our ability to transform experiences or change the
shapes of things in our minds. This capacity is related to symbolic process and
thinking. Artists are good at this.
The third capacity is our ability to communicate.
When these three capacities are in action they are influenced by members of the
‘family’ of primal emotions. Love, hate, envy, sorrow, grief, contempt, disgust,
anger, fear, rage.
Mixed in with all this mental and emotional activity is purpose, intention or
desire.
When taken together, the combining of sense impressions, the brain’s
transformative actions, emotions, intention and desire, and communication, gives
us our basic psychological motor. The basic parts are simple but what they do when
they combine is very very complex.

Communication transference
Transference projections might have several main ‘intentions’. I am selecting two
for the purposes of this paper. The first is the effort at communication.
When this form of projection/transference is operating interculturally, it is
about how persons from one culture are trying to pass something to persons from
the other culture. These ‘I’m trying to tell you something’ procedures might be
straight out or indirect, ironic, polite or confused. The communication may not
even be particularly conscious. The people involved may not know how to put it to
each other or the other may not understand or know how to listen and receive.
Ralph Fold’s honestly observed book, Crossed Purposes (UNSW Press 2001) is full
of examples of cross-purpose communications between Pintupi and European
Australians. His stories are worth studying for this reason.
When something cannot be communicated and understood between humans, then other
ways have to be found. Misunderstanding and the fact that the message does not get
across means that people get more and more dissatisfied with each other, perhaps
passive or aggressive actions are taken and desperate measures of emotional or
physical violence ensue. Taking care of oneself in intercultural work means
learning how to attend to and decode culturally formed communications and also how
to process the emotional impact of failure.

Metamorphosis transference
These procedures are about (psychological) effort to change someone’s shape.
When people get into a relationship a dynamic often comes into play whereby one
or the other is trying to change the other. In intercultural work you may not be
too clear about what the other is trying to change you into but you may feel some
pressure to take on a shape with which you may or not be happy. Distress arises
when you have to resist and defend against having your shape changed or protect
the shape of yourself, your psyche or your identity from being pushed into ways
which you are not happy about.
Again, Ralph Fold describes this process with clarity. He uses examples from a
Western Desert community of some revealing philosophical and practical tussles
about, for instance, what ‘being the boss’ means to the White administrator and to
the Pintupi. He describes pressures upon himself (as a supposed ‘ boss’), from
Pintupi men to behave in the manner of a ‘boss’, as they see it. The Pintupi
version of the boss’s job is to provide for everyone, not restrict use of
resources and finances, but arrange for the sharing of them among the appropriate
people. He describes the impact upon himself of pressure to make him into a
specific kin/skin relative and therefore fulfil the obligations which go with it.
He describes the pressure upon Pintupi to change the shape of family life and
tribal priorities to satisfy the desires of various, varying, consecutive often
contradictory administrators, agents, advisers and health workers. The subliminal
shape-changing pressure generated by administration has buried within it
philosophical, religious and psychological manipulations. It is, in a sense, a
propaganda war between the Pintupi and the Europeans that Fold’s book describes.
Ideological conflict between Black and White is not fought on any grand
battlefield. There is no declared war in Australia. It‘s just that the
psychological conflict rolls on in an understated, somewhat messy way in the
background, all the time, like some low-grade chronic illness.
You will be familiar with the desperate and perplexing psychological resistance
battles that turn around the use of money, or a vehicle, a sewerage system, food,
a water source, a piece of country or an injury to a body. And, of course, sex. In
the process we try to push each other into shapes which make sense in our own
cultural patterns and images. We tend to feel quite justified in doing this.
Internal disturbance and aggravation occurs as one or the other resists.
In short, taking care of one’s patients and taking care of oneself may involve
becoming more professionally aware of how projection and transference operate as
subliminal communications. And how projection of implicit patterns and
transference of unthought out passions operate to force changes in each other’s
shapes. Physically and mentally we may be trying to invest persons of another
culture with our own patterns; and be trying to get them to fit our own possibly
unconscious purposes and desires. They will be doing the same to you.
Stress and distress arises between humans when they misunderstand each other’s
communication or when people feel themselves being changed into shapes and shoved
into patterns which are alien to them as persons and contrary to implicit cultural
desires. Black does it to White and White does it to Black. Some of it is planned,
as in a war. Some of it is unconscious.
Drunkenness and intoxication add a further dimension of disorder.

Three other things to worry about

Efforts at communications and shape changing (metamorphosis) can be coloured by
three main types of desire: creative desire, destructive desire and preservative
desire.
You may have noticed how such and such a person in the community has the
persistent/consistent desire to make something new or useful out of other people.
This might present as the desire to serve, to love, to cure, to educate, to help,
to save; or to learn from. Many of the communications from that person serve that
purpose. This creative shape-changing effort can end well, or badly. It may lie
behind much health service/missionary effort.
The desire to change another may actually contain in it an (unconscious?)
desire to destroy, break down or dispose of the other. The shape-changing effort
and the subliminal communications are intended to ruin, dissolve, disperse or
otherwise destroy body, mind or integrity.
 The desire for preservation, containment or holding may come across in many
ways as a desire to be held, taken care of, or to take care of others. It may have
in it the wish to hold something steady and constant. It may, for instance, be
about culture preservation. Usually this is thought of as a good thing, preserving
the life of one’s people, culture and country. In work within the Indigenous world
this desire may pervade many actions and reactions between Black and White. The
communications will be about it, as will efforts to prevent, resist or outwit the
non-Indigenous ‘shape changers’.
Creation, destruction and preservation seem to be archetypal processes in life.
The combination of these three patterns plays out in interesting and mysterious
ways, especially in the bush.

Conclusion and a wish that this subject could be developed

You might never have the slightest chance, in a busy bush clinic, to sit around
the table and do a reflective analysis on all this stuff. Who has time for that?
But you never know, maybe one day some health administration will set up the
conditions where staff can systematically learn from the intercultural experience
and develop the capacity to analyse our situations. Why? Well, perhaps to develop
some compassion and patient tolerance for each other’s bungled efforts at
communication.
Psychoanalysts have learned that therapists must analyse their own
preconceptions and partly unconscious expectations, otherwise they unwittingly
impose false solutions and false cure upon their patients. Part of the stress of
working in remote areas and on Aboriginal country is brought about by confusions
in communication, in expectation, in projection. There may be profound differences
between the psyches of persons raised in European, Asian and Indigenous Australian
cultures, but these differences may be worked with in a conscious and systematic
manner by health professionals. It is surely a part of the ethics of the practice.
Our mutual interventions in each other’s lives cure and also destroy. Bearing
the pain and humour of this complexity and contradiction may be a test of maturity
as human beings. As Laing suggests, we could become ‘obstinate in our attempt to
recover the wholeness of being humans in relationship’ . . . and not perpetuate
the disease which we purport to cure.

Key references
Fold R. Crossed Purposes. Australia, UNSW Press, 2001.
San Roque C. On Cultural Transference. University Western Sydney, 1999. Unpub PhD. Contact:
roq@ozemail.com.au

1. Laing RD. The Politics of Experience. England: Penguin, 1990.

2. Kelly K. Stress; On surviving burnout in remote areas. Alice Springs: CRANA, 1999.
 Petrol Sniffing

Authors: Part 1: Craig San Roque (Psychologist, Intjartnama Aboriginal Corporation

Petrol Sniffing Project, previously Petrol Link Up); Marcus Tabart.
Parts 2 and 3: Craig San Roque
Topic Reviewers: Parts 1 and 2: Dr Rob Parker; Monica Ostigh (RAN, Jabiru); Kaz Knudsen
(RAN, WA); Vivien (RAN, Amata); Jane Kollner (RAN, Ampilatwatja); Teresa Bowmen (RAN,
Papunya).
Part 3: Dr Rob Parker.

Part 1: Clinical aspects

Origins
In Australia prior to World War II there was no evidence of petrol sniffing. It
had been reported as a practice among children and adolescents in the USA as early
as 1934.1
Brady reported the first documented use of petrol amongst Top End Aboriginals
in 1950 at two sawmills, whilst in Central Australia the practice seemed to have
begun in the 1940s. Brady was unable to find any evidence that US Army personnel
introduced the practice.2

Prevalence and pattern of use

The prevalence of petrol sniffing amongst young Aboriginal people should be seen
in a wider context of adolescent mental health problems, adolescent risk-taking
and experimentation, and the widespread volatile substance abuse amongst some
sections of the general population.
The Victorian Parliamentary Inquiry into Inhalation of Volatile Substances3 it
stated that:

‘Volatile substance abuse (VSA) occurs in association with a number of

different substances, each of which require a range of categorically different
interventions:
• Average young people who experiment with VSA
• VSA associated with delinquent behaviour and low socioeconomic status
• VSA in urban and rural Aboriginal communities
• Petrol inhalation in remote Aboriginal communities
• VSA amongst disadvantaged and homeless adults
• Abuse of anaesthetic gases by professional groups
• Abuse of amyl and butyl nitrites by those in the gay communities.’

The Mental Health of Young People in Australia 2000 survey found that 9% of the
adolescent population had abused volatile substances in their life. It was further
found that those with substance abuse backgrounds were more likely to have mental
health problems.4
Rose observed, ‘[t]hose engaged in VSA reported significantly less family
support and lower self-esteem, and significantly more lifetime thoughts of suicide
and suicide attempts and lower perceived school ability as compared to non-users.
In clinical groups and those within the justice system, solvent users had higher
rates of emotional symptoms (mostly depressive) and abundance of adverse life
events, family dysfunction and higher rates of relatives who have attempted
suicide’.5
 There are many parallels between Aboriginal petrol sniffers and the widespread
increase in adolescent volatile substance abuse in urban communities, though there
are also important differences.
Some studies have found that Aboriginal youth are more likely to use petrol
more intensively and for longer periods of time than non-Aboriginal urban VSAs.3,6–9
Indeed, Brady and Torzillo found that 50% of teenagers who began sniffing as
10–14-year-olds were still sniffing at age 25–29.8 The greater majority of urban
VSAs, however, engage in no more than brief periods of experimentation, use
generally declines significantly by the age of 18 and often reflects a shift to
another substance of abuse.3
Petrol sniffing is thought to occur principally amongst remote Indigenous
communities throughout the world, though all this may mean is that we do not know
enough about VSA in urban communities.
The prevalence is hard to quantify. It is often a clandestine activity and
occurs at night. Brady (in 1992) reported that it was present in 56 out of 837
Aboriginal communities throughout Australia.2 Its usage tends to come and go in
communities; a chronic sniffer may collect recruits and then be moved on by the
community, imprisoned for delinquent behaviour or an intervention occurs and the
practice is temporarily extinguished.2,6,9 Mosey estimated that there were almost 200
users sniffing in Central Australia in 1997.9 The age of users is from 8–30 years,
though there are anecdotal reports of children as young as four inhaling petrol.
Males are more likely to sniff than females (3:1).
Overall, it appears that since 1994 there has been a reduction in intensity in
some areas, particularly Central Australia where it has been common, although it
is still common in some communities. This reduction has occurred at the same time
as its use has sprung up in other Aboriginal communities.6,9

Aetiology
There are many theories that attempt to explain the existence of this phenomenon.
Burns1 summarises some of these theories.
• As a feature of adolescent risk-taking and experimentation
• Peer group influences in a setting that often provides little in the way of
meaningful activity
• Rejection of and rebellion against significant role models
• Desire to be autonomous and seeking self-identity
• Pharmacological characteristics of the petrol itself. It has a rapid onset of
action inducing a sense of euphoria which encourages psychological dependence.
It is cheap and readily available
• Indigenous aspects of child rearing and patterns of personal autonomy within
Aboriginal culture may be relevant
• Recent history of colonisation, assimilation and cultural dislocation may be
conducive to the genesis and perpetuation of the problem
• Such a history of social, economic, educational disadvantage and disruption of
the ability of parents to exert control over children may have increased
susceptibility to use harmful drugs.

Brady noted that communities associated with the pastoral industry seemed to be
less likely to have petrol sniffing epidemics.2 Poverty as a factor has not been
adequately explored. It has been demonstrated that it is a factor in adolescent
substance abuse in urban areas.3,4

Clinical effects
Petrol is a mixture of c4–c12 hydrocarbons (including benzene, toluene, n-hexane)
and organic lead (tetraethyl lead). The hydrocarbons have both an anaesthetic and
narcotic effect whilst the lead also has intoxicant properties. Leaded petrol is
the preferred vehicle of abuse. Unleaded petrol only contains 0.013 g/L lead and
is made up of 70% volatile hydrocarbons, though both leaded and unleaded petrol
contain similar amounts of toluene (13%). Toluene is well known as a cause of
cognitive and neurological deficits.10,12
The adverse health effects of lead exposure are well established. In children
exposed to lead it has been found that the higher the lead level the greater the
deficit in IQ points.11
The volatile hydrocarbons are highly lipophilic and are rapidly absorbed,
distributed through the body and cross the blood–brain barrier. The half-life in
the body of the hydrocarbons is between 7–24 hours, whilst lead can persist in the
brain with a biological half-life of over 500 days.1
Fifteen to twenty inhalations of petrol will cause euphoria and an intoxication
much like alcohol. This acute intoxication will last for three to six hours.
Excitement, restlessness, elation, misperceptions, illusions, or even visual
hallucinations; a sense of invulnerability as if ‘fear dissolves’, disinhibition
and aggression (often), increased libido (so there is a higher level of STIs in
this group) and slurred speech and gait problems are features of acute
intoxication.
Prolonged inhalation or rapid inhalation of a highly concentrated vapour may
lead to violent excitement, ataxia, visual hallucinations (often of demons,
snakes, spirits), confusion and delirium; paranoia; loss of consciousness, coma,
seizures and death.
Sudden sniffing death has been recorded, but is rare and it is thought that the
volatile hydrocarbons cause cardiac sensitisation to catecholamines that are
released during physical exertion or stress.1,12,13

Petrol sniffing encephalopathy

Mostly occurs following acute intoxication in chronic users but it has been
reported to occur, more rarely, in the absence of chronic usage. Encephalopathy is
associated with nausea, vomiting, excitement, hallucinations, disorientation,
clouding of consciousness, seizures, cerebellar ataxia and occasionally other
psychotic symptoms.14
In Goodheart’s study of 25 patients with encephalopathy 20 were chronic users
and eight died. The deaths were attributed to sudden cardiac arrest or respiratory
failure due to aspiration pneumonia. Autopsies found neuronal loss in the cerebral
cortex, cerebellum, reticular formation, brainstem and in particular Ammon’s
Horn.13,14
This study also highlighted that in the survivors only one patient was
functionally independent at the time of discharge.14

The chronic sequelae of petrol sniffing

Includes neurobehavioural changes with lethargy, irritability, anorexia and weight
loss; movement disorders, cerebellar ataxia, peripheral neuropathy; myoclonus and
neurocognitive defects in the areas of attention, psychomotor speed; learning new
tasks, memory and visuospatial dysfunction.1,14
There has been some debate in the literature about the relative contribution of
lead and volatile hydrocarbons to the neurocognitive impairments seen in petrol
sniffers. A review of the literature would make these summary points:
1. Both lead and the hydrocarbons contribute additively to neural dysfunction
particularly in the cortex, cerebellum, and the brainstem areas.

2. The longer the exposure to these neurotoxins, the greater the damage
3. Both sniffers and ex-sniffers are more likely to have neurocognitive
deficits than non-sniffers. These deficits occur in those who have not
necessarily experienced episodes of acute encephalopathy and the severity of
abnormalities is reduced with abstinence.
 4. The range of impairment is mild, and reversible changes with cessation of
the sniffing to severe and irreversible encephalopathic states resembling
dementia that could be fatal.
5. The neurocognitive impairment is more severe in those sniffers who have had
episodes of acute encephalopathy.
6. As blood lead levels correlate with mortality14 unleaded petrol has been
introduced into some communities. These have seen a reduction in petrol
sniffing related hospital admissions.1,7
7. A longitudinal study is required to establish if there is any reversibility
in the neuro-toxic effects of petrol.13

Mortality and morbidity

There is still limited accurate data available about the actual number of petrol-
related deaths in Australia. There were 63 deaths reported in Australia between
1981–91, though due to problems with reporting it is likely that this figure is an
underestimate.1 Causes of death include septicemia, cardiac failure, pneumonia and
lead poisoning as well as burns and accidents.8
Again it is difficult to quantify morbidity but Burns found that petrol
sniffing accounted for 4% of all medical conditions in the Northern Territory, and
there were 133 admissions to Alice Springs Hospital between 1981–90.1

Other health effects

These effects are summarised in table 1. There is no evidence that petrol sniffing
per se is causative in the development of psychiatric illness, though it is
evident that a number of people with mental health illness may sniff petrol. Such
usage may precipitate relapses of their underlying illness.
Psychological dependence occurs though true physical dependence is uncommon.15

Social effects
Very briefly, the social impact on individuals who petrol sniff includes:
• decreased school attendance and hence performance
• alienation from family and community
• ostracisation
• involvement with the juvenile justice system (fortunately mandatory sentencing
is now repealed in the NT)
• promiscuity
• increased inter-family conflict
• social disruption
• reduced morale in communities
• flaunting of authority
• property damage.1,2,5,7
Table 1: Adapted from Roper 199816
Acute Prolonged Inhalation Chronic
Acute encephalopathy Neurological Neuropathy
hallucinations delirium ataxia
euphoria loss of consciousness tremor
delusions decreased respiratory nystagmus
dissociation from rate toxic encephalopathy
environment seizures

weightlessness hypoxia peripheral neuropathy

irritability coma Renal metabolic acidosis
Behavioural Sudden death Haematological disorders
emotional/sexual myeloid metaplasia
disinhibition

aggression aplastic anaemia

hyperactivity respiratory disorders
somatic emphysema
anorexia aspiration pneumonia
body pains malnutrition
headache and fatigue Skin infections
Neurological STD
motor incoordination
muscle weakness
slowed reflexes
Cardiac
Sudden death

Clinical management
Health clinics and hospitals are involved in the management of petrol sniffers in
acute illness, including the management of seizures, agitation, strange and
bizarre behaviour, violence, self-harm behaviour, and accidental injuries such as
burns. These are labour intensive tasks which can paralyse clinics for days at a
time.17
Apart from these acute presentations the general health of this group of
chronic sniffers is poor, often due to the indirect effects of their poor
nutrition. They are more prone to skin disease, sinus and upper respiratory
infections and the like. Fasting or an erratic dietary intake can increase the
absorption of lead, so attention to diet is important.2
There is no pharmacotherapy per se for petrol sniffer dependence unlike that
available for nicotine, alcohol or opiate addiction. The mainspring of care in the
acute crisis is protection of the airway and urgent evacuation to a facility with
ventilation capacity, especially if encephalopathy is suspected because of the
mortality associated with this condition. If sedation is needed for behavioural
‘dyscontrol’ use a mixture of benzodiazepines and/or antipsychotic medication (see
Psychiatric Emergencies protocol). Seizures should be managed as per the Fits
protocol.
In hospital attention to hydration, airways support, treatment of sepsis and
seizures, intensive nursing care and chelation therapy has been used for more
severe cases of encephalopathy and lead intoxication.
Chelation therapy
Chelating agents are chemical compounds which bind heavy metals such as lead. The
use of EDTA, BAL, Penicillamine and Succimer in encephalopathic petrol sniffers
assumes that tetraethyl lead is the chief neurotoxic agent in leaded petrol. It is
known that both lead and the hydrocarbons contribute to this toxicity.
Evidence for the use of chelating agents in petrol sniffing remains
inconclusive. In Goodheart’s group chelation lowered lead levels by mobilising
inorganic lead within the blood. A reduction in blood lead levels and neurological
improvement has followed chelation therapy.1,13,14,18
Chelation therapy has not been uniformly used in those hospitals likely to
admit petrol sniffers as there has been disagreement as to its effectiveness and
safety.2 In this author’s experience chelation therapy is very uncommon in Alice
Springs. This year a baby of a chronic petrol sniffer received chelation therapy
due to elevated lead levels. Obviously, its effectiveness will be determined in
years to come in terms of whether the baby achieves a normal
psychological/neurological development (personal communication Dr. Wheaton,
Paediatrician, ASH).
While in Darwin Dr. Burrow (Staff Neurologist) described an aggressive
management approach that includes oral succimer or EDTA/BAL if unable to tolerate
the oral route. He has found that this group had better outcomes than those who
had not been chelated. It is also evident that the need for this treatment has
declined over the past few years. This may be related to the introduction of
unleaded petrol in many of the Top End communities (personal communication1,12,13).
Chelation therapy can have serious side effects, including nephrotoxicity,
hepatotoxicity and skin reactions. D’Abbs 2000 and Brady 1992 summarise the other
concerns with chelation;
1. If exposure to lead continues whilst on penicillamine this may lead to
increased lead absorption. Often sniffers return to the practice after
discharge from hospital.
2. The literature is equivocal about its effectiveness with organic lead
toxicity (i.e. petrol sniffing) compared with the evidence for use with
inorganic lead toxicity.
3. In some animal studies using EDTA, although levels in the blood, bone and
liver may decrease, the levels in the brain may increase by as much as 100%.
4. It is not known how effective chelation is in removing lead from the brain.
5. There have been no controlled trials to establish its effectiveness.

Despite these cautions the consensus view seems to be that the role of chelation,
although limited, may be beneficial in the short term at least.
All agree that primary and secondary intervention strategies have the most
potential to reduce petrol sniffing morbidity and mortality.7

Rehabilitation
Rehabilitation is an area generally neglected by the literature. There is
inadequate data as to the numbers of sniffers with significant disablement. Mosey
(in 1997) reported 59 severely disabled people in the Central Australia region,
although she recognised that this figure is likely to be an underestimate. Several
of this group required twenty-four hour institutional care, and one cost the
Northern Territory $100 000 per annum for their care.9
However, the majority of the burden of care for this group rests with the
families who often labour without much support. Most out-station programs are not
designed for the severely disabled sniffer, nor are they able to cope with the
severely behaviourally disturbed person.
There remains considerable debate about what an effective model of
rehabilitation looks like and where it should be.7,9 NT Government policy has
favoured the out-station rehabilitation programs, such as those found at Mt. Theo
and Injartnama (though support is often financially tenuous) rather than urban
based programs.
Although:
1. Not all remote communities or urban centres have access to out-station
programs.
2. Carers are often exhausted and sometimes request respite options in urban
areas where there are more health, educational, recreational and other
facilities available.
3. Out-stations often are very isolated and have limited access to health,
education facilities or allied health professionals such as physiotherapists
or counsellors.
4. Research is required to evaluate the effectiveness of such programs.7,9
These out-station programs are popular as they provide respite, an opportunity to
dry out, are culturally appropriate and the young are often involved in meaningful
activity.
D’Abbs commented of the utility of urban residential programs: ‘the limited
outcome data available suggests that such a use of resources may be less effective
than a program based on recreation, community development and individual and
family counselling’.7

[Editor: Part 2 of Petrol Sniffing goes into more detail of approaches to

rehabilitation and recovery after petrol sniffing induced brain injury (or any
other brain injury).]

Interventions
Any successful intervention must address concurrently three characteristics.
1. The pharmacological properties of ‘the drug’.
2. ‘The set’ or particular attributes of people using the drug.
3. ‘The setting’ or the socio-cultural-political-ecological environment in
which the usage takes place.19

Without such attention interventions may suffer from being ad hoc, crisis-reactive
and discontinuous. These inconsistencies have been a feature of historical
approaches to this problem.7,9
A summary of interventions is in table 2.

For an excellent summary of the range and efficacy of interventions used, d’Abbs
and Maclean’s 2000 review is highly recommended.
A summary of the salient points of interventions includes:
1. Any intervention is better than none.9
2. For success there needs to be a whole-of-community participation in the
devising and implementation of any program and a variety of interventions are
required that look to the ‘drug, the set and the setting’.7
3. d’Abbs believes that the outlook is brighter than a decade ago, possibly
due to the introduction of avgas, unleaded petrol and out-station
detoxification and rehabilitation programs.
4. Any programs developed need to be supported by the wider community,
including whole-of-government, to ensure consistency, encourage sensitive
evaluation and the provision of technical support and advice. A coordinated
approach is mandatory.7,8,9
5. Programs need to reduce the number of adolescents taking up the practice,
minimise the exposure to those who use, and provide care to those who are
disabled.8
 6. ‘The most effective long-term strategies against petrol sniffing are likely
to be those which broadly improve the health and wellbeing of young
Aboriginal people, their families and communities’.7

Brady agrees that success is not likely to come from drug-related interventions
alone but a more holistic approach: ‘People abandon their drug use when it begins
to interfere with too many other valued aspects of their lives. If there are no
other valued aspects to life then there is simply no compulsion to abstain.’2

Table 2: Some petrol sniffing interventions (adapted from d’Abbs 2000)

Level of intervention Intervention strategy
Primary: prevent emergence/spread Education
Restricting availability of
petrol
Adding deterrents to petrol
Recreational programs and
activities
Movement to out-stations
Initiations and other
ceremonies
Outlawing petrol sniffing

Secondary: reduce/halt further progress Individual and family

counselling
Skills training
Legal punishment and other
statutory sanctions
Night patrol
Community development
Harm-reduction including the
use of unleaded petrol and
avgas

Tertiary: treatment of users Hospital treatment

Rehabilitation

References
1. Burns CP. An End of Petrol Sniffing. PHD Thesis University of Sydney, 1996.
2. Brady M. Heavy Metal: The Social Meaning of Petrol Sniffing in Australia. Canberra:
Aboriginal Studies Press, 1992.
3. Parliament of Victoria Drugs and Crime Prevention Committee. Inquiry into the Inhalation
of Volatile Substances. Jan 2002.
4. Sawyer MG, et al. The Mental Health of Young People in Australia: The Child and
Adolescent Component of the National Survey of Mental Health and Wellbeing. Commonwealth of
Australia, October 2000.
5. Rose J. VSA: Background Paper for the WA Working Party on Solvent Abuse. WA Government,
2001.
6. Burns C, et al. Patterns of Petrol sniffing and other drug use in young men from an
Australian Aboriginal Community in Arnhem Land. Drug and Alcohol Review 1995 a; 12(2):159–
69.
7. d‘Abbs P, Maclean S. Petrol Sniffing in Aboriginal Communities: A Review of
Interventions. Co-operative Research Centre for Aboriginal and Tropical Health, 2000.
8. Brady M, Torzillo P. Petrol Sniffing Down the Track. MJA 1994; 160:176–7.
9. Mosey A. Report on Petrol Sniffing in Central Australia. Central Australian Alcohol and
Other Drug Services, 1997.
10. Ron M. Volatile Substance Abuse: A Review of Possible Long Term Neurological,
Intellectual and Psychiatric Sequelae. British Journal of Psychiatry 1986; 148:235–46.
11. Cicuttini FM, et al. The Public Health Problem of Environmental Lead Exposure. MJA 1994;
160:173–4.
12. Maruff P, et al. Neurological and Cognitive Abnormalities associated with Chronic Petrol
Sniffing. Brain 1998; 12:1903–17.
13. Cairney S, et al. The Neurobehavioural consequences of Petrol (gasoline) sniffing.
Neuroscience and Biobehavioural Reviews 2002; 26:81–9.
14. Goodheart RS, et al. Petrol Sniffers Encephalopathy. MJA 1994; 160:178–81.
15. Macgregor M. A synopsis of Inhalant Solvent Abuse from a Central Australian Perspective.
Territory Health Services, 1997.
16. Roper SJ. Petrol Sniffing and Preventive Interventions on the Anangu Pitjantjatjarra
Lands. Master of Science Thesis, 1998. Copy held at Central Australian Alcohol and Other
Drugs Services, Alice Springs.
17. Brightwell K. Petrol Sniffing in Central Australia. Medical Elective Project, June 2000 .
18. Burns CB, et al. The Efficacy of Chelation Therapy and Factors Influencing Mortality in
Lead Intoxicated Petrol Sniffers. Aust NZ J Med 1995; 25:197–203.
19. Zinberg NE. Drug, Set and Setting: the Basis for Controlled Intoxicant Use. New
Haven:Yale University Press, 1984.

Part 2: Dealing with brain damage after petrol sniffing

The bush mechanics of cognitive skills recovery: some suggestions

We are thinking about how to develop or rehabilitate cognitive skills of people
affected by petrol sniffing or other similar forms of acquired brain damage. The
suggestions here are for remote-area workers on the understanding that help for
people in that condition will probably be sporadic and unsupervised, and efforts
at rehabilitation will probably be carried through outside the institutionalised
health service and away from consistent professionalised help. We are talking
about bush work.
For the effects of volatile substances on the brain and nervous system, see
part one above.
The suggestions given here are really about a set of principles. They are
offered based upon the position that the human being, especially young human
beings, have remarkable powers of recovery.
When faced with the problem of making up recovery strategies to encourage the
rehabilitation of cognitive capacities there are, of course, the basic diagnostic
questions to be asked about the person, their history, situation, as well as
considering carefully the people and environment where the rehabilitation
procedures would have to be carried through.

The person
This is normal diagnosis and prognosis assessment.
• History of the problem and the person.
• Characteristics and the nature of the disabling process.
• The seriousness and chance of recovery.
• The strength of the person’s will, purpose and capacity to make effort.

The setting
What actions can be taken to stimulate cognitive development may depend upon the
setting of the life situation, e.g. in a community or in some form of supported
care. This includes consideration of the family group situation, how the family
handles the person and whether all rehabilitation has to be handled by
professional input or whether family members can be engaged in carrying out
stimulating activities. This has to be realistically assessed. There is no point
in making well-meaning suggestions that cannot be followed through. There are
factors operating in most remote-area communities which make it difficult to care
for disabled people. These factors need to be assessed realistically.

Where to begin
Imaginative therapists give attention to how the local situation can be used for
the benefit of the patient by making use of the opportunities around. I remember a
creative physio who helped her ex-petrol sniffing patient to recover the use of
muscles by getting him to crawl and then walk through the resistance of deep sand
of a desert creek bed. She took advantage of local conditions. Such therapists are
attentive to how cognitive skills are normally developed in children and young
people in the specific remote-area environments, culture and language group in
which they work. The story will be different, for instance, if the injured person
has been brought up in, and still lives in, a Top End fishing environment, a
central desert settlement or a town camp. Culture and environment help shape the
mind and help shape the way specific mental capacities and abilities develop.
After assessing the chances of recovery and what might be ‘normal’ strategies
in a hospital-supported treatment, one might have to consider what will work in an
Indigenous bush setting and what opportunities there are to make use of. This may
take imagination, patience, and courage by the practitioner, as well as
adaptability.
As a rule of thumb framework to help devise such strategies the following
principles may help.
1. Cognitive capacities are about our abilities to take in information and
impressions through the five senses. Use all five senses.
2. The brain normally works swiftly to put together these impressions, to make
order, sense and meaning for specific human purposes. Develop exercises which
challenge the brain’s capacity to find and make order, sense and meaning in
simple systematic stages where a purpose, desire and even a survival need are
felt by the patient.
3. Different cultural groups, in order to survive in different environments,
have developed the senses in unique or specialised ways and have unique,
specialised and agreed ways of considering what order, sense and meaning are.
Be aware of and make accurate use of culturally specific challenges based on
local survival techniques and culturally supported skills.
4. The concept of Multiple Intelligences is useful. Cognitive skills might
regenerate through stimulating exercises across all five senses and across
the spectrum of a variety of intelligences which involve skills in handling
relationships, kinaesthetic and sensory skills, skills with numbers,
language, pattern-making, arts, thinking, logic, improvisation and humour.
Cognitive development therefore can take place and be stimulated in many
modalities of intelligence. Remember bush mechanics.

You can work out a kind of grid framework for developing exercises in any setting.
The patients, family or friends may be prepared to carry them on once the
principles are grasped, understood and practised.
The four-sided framework can be set out on paper, or the ground if working in
camp, and worked through with family or carers.
1. Set out the five senses. The brain works with these five modalities of
perception.
2. Mark out a variety of multiple intelligences (see note below), which you
are happy or able to work with. In a systematic way set about devising
exercises or challenges in those modalities which will stimulate the patient
and the carers and make sense to them.
3. Note what the environment and cultural habits/practices have to offer, both
positive and negative.
Select a series of basic activities (from the list below), which are likely to
stimulate cognitive capacities through work in any of the five senses and across a
variety of intelligence modalities. The selection of modes of intelligence to work
with will depend upon what the patient is capable of, or known to be capable of,
and what is appropriate and available in that cultural group. These matters have
to be thought about in order to make the exercises relevant and sustainable.
I have used the word ‘things’ here. ‘Things’ can be any actual or mental
objects which can be used, moved around, played with, sorted, joined, recognised,
remembered etc., and include words, sounds, music, smells, colours, stones, paint,
body parts and people as well as internal ‘things’ such as memories, experiences,
dream fragments, stories, feelings and thoughts.
The complexity of the things and the complexity of the exercises with them
depend upon the degree of damage in the patient and the degree of complexity that
the patient and their family can deal with.

4. Basic activities which help the brain do work include variations of:
• Recognising and identifying things
• Sorting things
• Linking things
• Putting things together and into places
• Pattern making and pattern recognition
• Remembering things
• Tracking things
• Puzzle solving
• Jokes
• Play
• Dexterity/hand/body/eye coordinations
• Rhythm/dancing/singing
• Cultural story, pattern/image making, music etc.
• Family relationship mapping (who is who and where)
• Country/geographical mapping and memory (who comes from where
and who has been where)
• Animal observation, recognition and mimick- ing.
• What else?

These are some suggestions to stimulate your own problem solving capacities.
Specialist colleagues who work in speech therapy, physiotherapy, etc., will have
developed repertoires of techniques which you might call upon to adapt. The
suggestions here are made to help anyone whose work might bring them into contact
with people whose cognitive abilities may have been affected by sniffing and where
no specialists are available.
(The concept of multiple intelligences (Gardiner) is that all people have a
general intelligence, but that special capacities may develop in different
directions for special purposes. People may have aptitudes with which they are
born, such as musical, mathematical or verbal ‘intelligence’. Some people are
blessed with sensory motor or kinaesthetic physical abilities, which might come
out as a skill in football or gymnastics or performance. Different cultural groups
may set priorities or favour the development of certain ‘intelligences’. Sometimes
gender differences and socially constructed gender expectations may come into play
here. In remote-area Aboriginal society the notion of multiple intelligences is
very significant because the priorities of what is considered intelligent in the
dominant, mostly European urban-based society and educations system may mean that
Aboriginal favoured intelligences are downplayed. Someone working to restore
cognitive abilities may wish to check these matters out.)

Part 3: Surviving psychic pain

Social matters, the context of the problem and a summary of local and personal
experience
[Editor: This section gives a more personal account from Craig San Roque, who has
many years of experience working with petrol sniffers. It goes over some ground
covered in the other parts of this topic and may help practitioners make sense of
their role in the broader petrol-sniffing scene.]
 Mt. Theo’s success [with sniffers] has not been about changing any individual,
but changing what’s cool and groovy.1

Introduction
This background paper is not intended as a review or analysis of the clinical
treatment of patients suffering from the misuse of volatile substances. Rather, it
looks at social matters, the context of the problem and a summary of local and
personal experience. It offers some guidance to the practitioner new to the area
so that he/she may get a handle on the complex and elusive behaviour of
‘sniffers’. This paper is about attitude, it recognises the distress which the
practice causes to people who have to deal with it. There are, as yet, no easy
steps toward alleviating what some see as a collective existential trauma but,
maybe, getting some help with attitude and history will save the practitioner a
few headaches. This paper is written by someone who has spent more than ten years
directly involved with the problem in Central Australia. It is unashamedly
subjective and attentive to the feelings which sniffing stirs in many persons,
Indigenous and non-Indigenous.

Meeting the problem

Psychic pain
Petrol sniffing makes people very upset. It is painful to see, painful to have to
put up with. For health professionals who have an instinctive response to relieve
pain and to care for people it is particularly frustrating — and even bewildering
— to be helpless, unable to do much to intervene in the cycle, let alone stop it.
Sniffing volatile substances is now part of the harsh reality of life in the
bush, just as drug use is part of city life, but coming upon it for the first time
can be a shock. Faced with sniffers’ apparently senseless, self-destructive
behaviour you may become puzzled, afraid, angry and hungry for explanation. There
may be no satisfying explanation and no satisfying solution. If you are such a
person, meeting sniffers for the first time, you may despair at working partners
and family members who seem to have given up trying to change sniffers’ behaviour.
You may wonder if you too could live with sniffers as though they were shadows.
You may hear hard, cynical comments about ‘useless families’ and ‘dysfunctional
communities’. You may feel a peculiar kind of psychic pain when in the presence of
sniffers. You may discover that demonised sniffers are actually quite sweet, naïve
and just bit lost — when not intoxicated. You may wonder what all the fuss is
about.

A sniffing syndrome?
All such reactions are a part of the ‘sniffing syndrome’. By ‘sniffing syndrome’ I
mean here not the pattern of symptoms of a disease but that there is a pattern of
behaviours and reactions, thoughts and feelings which seem to go with the
sniffing. The characteristic pattern can be seen operating among sniffers, among
their families, among workers and is also seen in the characteristic way in which
the media and community, state and federal governments and agencies react to and
respond to ‘ the problem’.
Describing and analysing the social/cultural aspects of the sniffing pattern is
a subject in itself, too big for this paper, but some parts of the pattern of the
syndrome include the following:
• repetitive cycles of emotions of frustration and despair and anger
• passive acceptance of terrorist-like behaviour
• paralysis of thought and action
• rejecting or demonising sniffers
 • passing the buck, blame and scapegoating of ‘family’ and hard working
individuals or (unsupported) programs for ‘not doing anything’
• bewildering funding requirements and requests for yet more reports.

(Fortunately the Commonwealth health service agencies involved seem, in 2001–02,

to be moving towards establishing a comprehensive policy framework as evidenced in
the Youth Wellbeing projects terms of reference, as evidenced in the Central
Australian Youth Link Up project’s terms of reference).
It is worth noting, in a professional manner, the way the social aspect of the
‘sniffing syndrome’ works at a macro level, as well as noting your own micro
reactions and changes in perception and attitude. Noting the shifts in the
psychological effect of sniffers’ behaviours upon yourself, the work team and the
mood of the community groups are all part of the diagnostic process. These
observations may help in the development of a local holistic response to a
haunting, elusive problem.

Noting history
Over the past twenty years or so there have been many people, Aboriginal and non-
Aboriginal, throughout Australia, who have literally given blood, sweat and tears
to help sniffers. They deal with the peculiar aura of anarchic depression which
sniffers evoke and carry around as though it were some kind of genie, which comes
out of the can.
Unfortunately, and frequently, the experiences of past workers, the way they
have described the problem and their contributions are forgotten or blindly
criticised or diminished by the new wave of enthusiastic politicians or
professionals. This forgetting of what has come before is part of the problem.
There is something about the petrol sniffing which attacks links in thought; it is
as though gaps are made in human beings’ capacity to think. The failure of both
Aboriginal and non-Aboriginal people to think through the problem is a problem in
itself. Maybe it is the failure to know how to think about it which seems to lead
to repetitive paralysis of concerted action.
Despite this there are systematically worked out and documented patterns of
response, which have been developed. For instance, the work by: the Healthy
Aboriginal Life Team (HALT) in the late 1980s until 1991; Petrol Link Up2;
Intjartnama/San Roque during 1996–99 Western Line project; Yuendumu project
throughout the 1990s; NPY Women’s Council project 1999–2002; and the South
Australian Aboriginal Drug and Alcohol Council.3 The d’Abbs, Maclean 2000 Review,
the Mosey and MacFarland and Roper reports and the substantial consistent work of
Maggie Brady all indicate patterns of response.4–8
Andrew Spencer Japaljarri, who could now be named as a grandfather of sniffing
theory, during his work with the petrol sniffing intervention team HALT, pointed
out strategies again and again in conversations and in concept paintings in the
HALT posters. In 1993 he summarised his ideas for action in his definitive
painting ‘Thinking About Young People’ (now in the custody of Intjartnama).
Unfortunately, most of HALT’s reflective work on the problem of ‘how to think
about sniffers’ was brushed aside when the Menzies’ evaluation of HALT found fault
with and reported criticism of some of their actions and outcomes. This criticism
and the way it was taken up and led to the abandonment, not resurrection, of the
HALT efforts is a typical instance of the ‘sniffing syndrome’ in action. The baby
went out with the bathwater. However, the inspirational groundbreaking work of
HALT (Spencer, Franks and Lowe) remains as a guiding spirit for many.9
Top End writers and communities (such as Maningrida) and in other regions must
have similar collections of material. It is not possible here to summarise and
review Australia-wide projects. However, d’Abbs and Maclean provide leads.4 But
for all the reports and recommendations there is still a mood that nothing much
has happened to shift the problem.
An encouraging note of despair
It is a strange experience to walk into the world of petrol sniffing. To some it
is like stepping into a black hole where nothing makes sense and every positive
effort disappears; to others its is a bewildering labyrinth of grief, lost
opportunities and lost ideas. I am reminded of the French existentialist novel The
Plague by Albert Camus.10 This is a bleak account of an epidemic which devastates a
remote North African desert town. The doctor and the mayor are discussing the
problem of disposing of so many accumulated bodies. They take some comfort in
having found a solution, if not to the plague, at least to the burial and the
paperwork problem.
Dr. Rieux comments: ‘Yes, and though the burials (go on and) are much the same,
we keep careful records of them. That, you will agree, is Progress.’
At the risk of drawing out the pessimism, but hoping that ‘forewarned is fore-
armed’, it has to be underlined that with the ‘petrol plague’ there is not much
sight of progress, we cannot even pride ourselves that records are carefully kept.
The burials go on. The plague has the upper hand. Thus, advice to those entering
the sniffer system is often as simple as this:
Study the history; keep expectations measured and low; resist being paralysed;
take note of the patterns; write incidents and stories down; keep calm and steady
when in the presence of sniffers; do not become isolated; link up with other
agencies; advocate positive youth activity groups; insist that thoughtful planning
be used, not emotional action and reaction; mind your own psychic pain; and hold
on to a sense of humour.

Sniffing: What is it?

The section below will help get you started. (For a fuller story and leads to
other work see the reference lists in d’Abbs, Maclean Review, the ADAC SA manual,
the Petrol Link Up Report 1995.4,2)

The stuff
Volatile substances common and accessible in bush regions include super and
unleaded petrol, solvents, spirit-based glues (especially in tyre repair kits),
spirit-based paints, polyurethene, paint spray cans and other aerosols. These are
often mixed as chemical cocktails with household cleaners and any other chemical,
which might appeal to an inventive mind. Word always passes around.11
Volatile substances, when inhaled and used as a drug, change perception,
emotion and sensation, in this sense they can be classified as mind and mood
altering drugs.
The special ingredients in petrol and glues which affect the human brain are
the additives which are intended to make them do their job better. They are not so
useful for the human.
The chemical additives include the hydrocarbons, especially tolulene and
benzene. The hydrocarbons affect the brain chemistry. Some research has been done
on how the hydrocarbons, fluorocarbons, methanol, methylene chloride, etc. deal
with the brain biochemistry and what the effect and damage is. Useful papers by
Ron and Maruff, give a lead into this subject.12,13 However, the psycho-
pharmacology and the nature of the hydrocarbon/neurochemistry reaction is still
rule of thumb business. Or, if there are specialist researches, this information
has not been translated into a form which is useable in relationship with people
who live in remote-area Indigenous Australia. The Petrol Link Up’s ‘Brain Story’
is an attempt to set out a format for such efforts.2
Hydrocarbon/human chemistry reactions do not in themselves seem to be
addictive. You can say that sniffers become obsessed with sniffing and dependent
on the cult or life style, and will work ingeniously to get their stuff, but it
does not seem to be true chemical dependency. Consequently, the withdrawal dynamic
— as found with nicotine, opiates or alcohol — does not apply, so one cannot make
comparisons or infer that petrol dependency follows the usual drug withdrawal or
overdose patterns. However, one may as well think of petrol sniffing as an
addiction because of the persistent reliance by core sniffers on having it around
them. People have to keep sniffing to keep high, which is why one sees cans
carried permanently as a necklace, ready and available.
In the bush it is mostly the vehicle fuels, the workshop and garage glues and
paints, which are easy to get. Despite the use of diesel and the successful
promotion and introduction of AVGAS/COMGAS as the preferred remote area fuel
(intended to reduce access to the sniffable stuff), ingenious youth bleed local
vehicles, look out for tourist vehicles, seek out other likely substances and
experiment with volatile mixtures. ‘Petrol runners’ exist along with the ‘grog
runners’ and ‘dope dealers’, and even close ‘family’ will sell petrol to sniffers
or be blackmailed to supply them.
Leaded (or ‘super’) and unleaded petrol both contain the volatile substances,
the hydrocarbons. Leaded petrol contains lead, of course, which has a
characteristic way of damaging the human brain. Lead is toxic (poisonous), but it
is not the lead which makes the ‘high’, although some kids seem to think so. It is
probably the hydocarbon content, but the lead as well as the hydrocarbons change
and damage the brain’s delicate system.
Research work has been done at both Alice Springs and Darwin hospitals on lead
chelation therapy (i.e. to clean the lead out of the body system). This research
may be available through Burns and Currie’s useful papers and the hospital
libraries.13 See also Brady, and Brady, Torzillo.14,15
Leaded petrol is phasing out (2001). How the new lead-replacement fuel will
affect sniffers is open to question.
In general diesel and AVGAS (aviation fuel) are not volatile enough to produce
the sniffer’s high, but sometimes mixtures are made or kids will experiment and
add plastics or polystyrene-based matter to provoke a reaction. It is not clear if
the perceived ‘high’ is a placebo effect or if there is a genuine mind altering
reaction. Either way sniffing such mixtures is still dangerous.
There has been a lot of work on the popular drugs, opiates, amphetamines,
cannabis, alcohol etc., but not on the volatile substances. Despite media
publicity over many years the politicised concerns, the rhetoric and some good
foundation material there seems little interest in supporting and updating
Australia-specific research that might help set up a systematic and informed
procedure for the analysis of volatile substance composition, its effects on the
human body systems, the social and cultural systems, the Indigenous perspective
and the assessment, intervention and treatment of Indigenous children and youths
who are affected by the petrochemical repertoire.

The effect
The hydrocarbons are said to ‘melt’ the fatty tissue, the myelin sheath that
protects our neurones, (rather like the insulating plastic on electric cables).
Under the impact of the hydrocarbons the neural networks gradually degenerate. The
degeneration is gradual, progressive.3 It is not clear if the degeneration of the
nerve material itself has a psychological or altered state effect on perception
and sensation or if it is mostly the hydrocarbon chemistry bonding with the brain
biochemistry which produces the sought-after euphoria and altered states.
Petrol sniffing does produce a characteristic pattern of reaction. The
reactions are also a result of how long and how often and how persistently a
person will be inhaling fumes. Sniffers describe changes in their perception of
hunger, heat, cold, space, time, movement and the relation between so-called inner
and outer realities. Sensory, visual and auditory hallucinations are described.
Sniffers might become uninhibited, emotionally tender and friendly like a puppy,
lose sense of personal boundaries, lose sense of social or cultural restriction.
 At some point the negative social effect sets in and consistent sniffers begin
to move into the ‘camp of the outsiders’. They may become exiled. They may ignore
normal kinship relationships, threaten and offend immediate family, especially
women and elders, break sexual and social conventions, become anarchic,
psychopathic, paranoid and disturbingly dangerous. The personal negative effects
can be simply described as neurological degeneration with consequent psychological
degeneration. There is a continuum of this degeneration, it may continue over many
years of sniffing, slowly getting worse. On the other hand some chronic sniffers
recover, not everyone ends up on death row and threats of ‘damnation’ are not
always fulfilled. If only the picture were so simple.
Persons in the grip of what could be called a ‘temporary petrol sniffing
derangement’ may appear to be psychotic. This is a dangerous state and should be
treated as such. When in this state persons may act in a berserk manner.
Unpredictable violence is likely. There are many recorded incidents of the sudden
use of weapons, setting alight by petrol dousing, accidents and self-harm. The
state may pass and the person returns to a normal, even contrite, child or youth
again. This change of personality can be bewildering to family. (The change also
helps family to excuse their behaviour). In general it is advisable to treat
confrontations with a deranged sniffer with all the caution and backup needed in
critical incident management.

The psychology
While there has been observational and anecdotal work done on behaviour, behaviour
management and the community reactions to sniffers which clinic staff may find
helpful, the psychological, spiritual and mental aspects are hardly mentioned in
the literature even though many Indigenous people speak about sniffing and the
experience of sniffers in these terms.
The taboo about speaking about the spiritual and subjective aspects of mental
life in the bush is loosening up, however, and there are a few psychologically
minded practitioners who do not limit themselves to the constructs of a
mainstreamed organic psychiatric framework.
A study of the imagery used by Indigenous people when painting and talking
about sniffers will reveal astute psychological observations and family system
explanations (e.g. The paintings of Marlene Nampijimpa Ross’s ‘Lonely Boy Story’
canvas; Bertha Nakamarra Dixon and Kumanjai Minutjukur’s work for HALT in Anangu
Way reveals such complexity of analysis once one learns to read the paintings).
The question of the psychological state of sniffers, both as a pre-existing
condition and as a drug induced condition, needs serious research and attention by
both Indigenous and non-Indigenous thinkers and practitioners.
In some troublesome and troubled individuals there may be pre-existing
psychological or sociopathic states which become amplified by the sniffing
effects. Bush clinic workers may have to become alert to look at sniffers who are
in trouble from several angles at once.
NPY Women’s Council have been supporting a traditional healer’s project and
some very interesting issues have been raised by some ngangkaris re the treatment
of sniffing. The Intjartnama and Yuendumu projects have also contributed here.
However, reviews of petrol sniffing projects, even in 2002, seem to ignore the
psychological, phenomenological and epidemiological dimensions as well as ignore
and fail to consolidate the astute observations made by Indigenous people in their
own terms. There is a kind of sidelining which occurs. This deserves more
appropriately conducted investigations, especially since the Indigenous view is
not adequately represented in mainstream literature or research.

A bit about imagery

The petrol sniffing scenes in the film Yolngu Boy are a good enough depiction of
the states, behaviours and background dilemmas of a boy in the grip of petrol. The
way the film shows his inner imagery and delusions shows the way things are. You
might be interested to hear about an unexpected result of that film. There are
rumour stories told by sniffers about the boy (the actor) in the film who has
apparently come back from the dead after he passes away in the film. The boy dies
in a (suicidal?) fall while under the influence of petrol. You see the boy’s death
in the film, but later people have seen him (the actor) walking around. This
‘proves’ that sniffing doesn’t kill you. It proves that sniffers can come back to
life . . . like Jesus . . .
If you get a chance to listen to sniffers talk it is worth noticing what they
say about the images and the symbols. There was a time in one community when each
sniffer ‘painted up’ their cans. In another some sniffers painted themselves up
with black ash. Sniffers draw, talk about and remember specific images while under
the influence which are similar to those experienced by persons in the grip of
paranoid states. They speak of voices, companion spirits, devils and monkeys,
distorted animal spirits who communicate with them or instruct them to do this or
do that.
The sniffer stops being the agent of his/her own action and passes
responsibility over to another. Some sniffers can be sensitive to the feeling of
being attacked and may act as though possessed by destructive hero figures whose
job it is to attack, destroy and take others to death. This imagery gets mixed up
with American film demons, sexual pornography and traditional Indigenous
supernatural forces. (e.g, mamus, kadaicha, ‘Rambo’ and obscene language and body
parts mixed up together).

Take care
Knowing that sniffers can get into disturbed, dangerous and delusional states,
workers and family of sniffers tend to be very careful around them. This partly
explains the apparent passivity about stopping sniffers. Some horrific deaths have
been inflicted by people who have attacked others when in the grip of drug-induced
persecutory fears and delusion. I mention this not to inflame fears or demonise
sniffers but to underline that watchful caution is always needed, since the
internal experience of sniffers while intoxicated may be quite unpredictable.
Another caution is that the term ‘sniffing’ is often used loosely. It is not
clear how much alcohol, amphetamines, cannabis etc. may have also been taken.
Adult drinkers may use petrol as an alternative or supplement drug. Sniffers are
not only ‘the kids’. One may be dealing with hardened poly drug users whose pre-
existing mental states, self control and obedience to social control may be in a
permanently disordered condition.
It seems that the volatile substances/hydrocarbon effect stimulates dream-like
and nightmare-like states. The inner states are often ignored in favour of
immediate symptom treatment or social behavioural control.
It is my suggestion that the inner altered states are sought after for a
purpose. The search for the altered state will not cease unless the sniffer is
removed from the source and the group and is distracted or satisfied by some other
activity or internally satisfying experience. This satisfaction may be as simple
as a good meal, attentive love, physical excitement and challenging risk. There
may have to be deeper solutions. The so-called deeper solutions may well have to
address spiritual crisis, but one also has to be careful of idealising or
romanticising the spiritual and cultural solutions.
In general it can be said that sniffers need to be taken care of and care needs
to be taken with them. However, the behavioural stance taken by most sniffers when
intoxicated means that it is almost impossible to take care of them and to attempt
to do so may be frustrating and dangerous, unless one is extremely skilful. The
skill can be acquired. And so can weapons; and not even the most experienced
worker is invincible when a sniffer has a weapon in their hands and unpredictable
imagery in their minds.
The big picture
In short, habitual sniffers may experience bodily and mental hallucinations,
primal fears, feelings of invincibility and contempt for normal respect, love and
care for self and others. Despite the presentation of being powerful many sniffers
are in fact in a delicate or vulnerable physical and mental state. Some are
aggressive and some are quiet, passive and fade away into an internal or
introverted world.
The ‘sniffing syndrome’, as seen in the individual person, includes a combined
multifaceted picture. Elements of this picture include, depression, lethargy, loss
of appetite, changes in body and timing rhythms, sleeplessness, agitation,
emotional lability, euphoric states, sexual promiscuity (with a suggestion of
enhanced sexual pleasures or liberation) potential sociopathic brutality, and
psychotic like states, even if temporary, along with outlaw gang behaviour.
Behaviours may depend on age, maturity of sexual stage and the conventions of the
sniffer cohort and gender group.
Mild, occasional or children sniffers might seem playful or innocuous, and
their behaviour is sometimes tolerated as experimentation or as keeping them out
of ‘the family’s way’. But most thoughtful and observant Indigenous people agree
that sniffing is not ‘cute’ and not ‘cool’.
All in all, sniffing is not a pleasant activity to be around. It is a form of
intoxication which tends toward the anti-culture, the rejection of humanity and
the morbid seduction of death. The psychic atmosphere of the habitual sniffer is
mostly disturbing and has a deadening or vacuous impact upon the social
environment. The places where sniffers hang out are recognisable by the trashed
and necromantic ambience.
There are many unanswered questions. What, for instance, is the degree of the
petrochemical effect on the brain/psyche, and how much is the behaviour a display
reaction to the conditions of life in a settlement? As we have already suggested a
proper and useable study of Indigenous Australian sniffer’s psychological and
biological states is long overdue.
Some researchers suggest that the children of marginalised, supressed,
Indigenous or poor minorities tend, worldwide, to be the habitual users of petrol
and volatile substances as a drug.16 This may simply be a matter of cost and ease
of availability but there may be other issues.
The essentials of the clinical picture and immediate treatment of the sniffer
as an individual ‘patient’ are presented in the CARPA STM section on sniffing.
Prevention and treatment programs which deal with sniffing as a family, community
and cultural matter are usefully summarised in D’Abbs & Maclean, 2000 and ADAC
SA.4,3
It is beyond the scope of this paper to review and update the situation
nationally: the interested reader may have to investigate the situation in one’s
own area. In Central Australia there are projects with seasoned experience in
dealing with sniffing as mentioned above. They include Petrol Link Up (til 1995).2
A contact point may be through the Northern Territory Government’s Alcohol and
Other Drugs services. Out-station projects include Intjartnama, near Hermannsburg,
and Mt Theo, out of Yuendumu. Aboriginal agencies include NPY Women’s Council,
Tangentyere Youth projects and Central Australian Aboriginal Congress Youth
Services and Waltja Tjutangu Palypai. The Remote Area Night Patrols have gathered
a wealth of on-the-ground experience. In Central Australia there is a support
network, CAISAN, which acts as a forum for many sniffing-related projects. Forming
such a network is part of dealing with the matter. This group has exchanged
information, initiated projects, supported colleagues, welcomed and informed
newcomers, kept a corporate memory together and persisted. CAISAN lobbied
resolutely for the Youth Link Up Service which, based at Tangentyere, began
operation in 2002 and may provide a welcome contact, advocacy and integrating
function.

The causes
‘Sad Boys are Sniffing’
(Quote taken from a HALT poster)

Why do kids sniff?

Some day, maybe, someone will get the chance to put together a full research-based
study on the causes, carefully listening to the young people as well as to their
friends, family and elders and written in language(s) and presentable to
Aboriginal groups in their own terminology. Until that document comes we have to
be content with the various ideas that circulate in popular discussion.
Some ideas are as follows.
• Some people find cause in history, poverty, boredom, alcoholic carelessness,
neglect and family breakdown.
• Others suggest that it is a mental problem because Aboriginal and non-
Aboriginal people can’t quite get their minds around what it is all about.
• Some emphasise that sniffing is a symptom of cultural despair, a part of the
history of dispossession and a symptom of the tangled side of the mutually
destructive Black/White relationship. Sniffing behaviour, therefore, might be
seen as a dramatic acting out by groups of young people of a story about this
generation’s grief, worry and depression about their situation. No one person
is writing the script, but it’s the same story in variations all the way from
Redfern to Wilcannia, to Alice to Derby.
• Some say the sniffers are part of the emergence of a protest movement of young
Black Australia. The revolt is against the elders and tradition. It is also an
attack on White culture and property. Anger, envy, contempt or protest? Maybe
it’s just about not having enough food, love and action.
• Others point out that the sniffing gang, roving day and night, is simply what
you will find anywhere in the world, from western Sydney to Los Angeles,
‘Guns, drugs, sex, rock and roll’ are part of the image conscious adolescent
romance of life and death. Others suggest the night-time, roving, whistling
hunter bands of young men is a continuation of the old time young male
initiatory group behaviour. Changed a bit though. There is a mirroring of the
Americans and a continuation of custom, mixed up.
• Some point out that there has to be more understanding about Aboriginal child-
raising methods. There are customary reasons why people don’t say ‘no’ which
is linked to the time and manner in which boys pass over to becoming men and
then have to deal with power, passion, autonomy and responsibility. Some boys
make it through to a cultural maturity and some mistake petrol-power and grog-
power for the real thing. These matters may be difficult to talk about tact
and sensitivity is involved.
• Others say that sniffers are just kids without direction and discipline. It is
their parent’s fault, or it’s the kids copying what they see their parents do,
wasting their lives on being drunk. But some parents blame the Whites for
bringing grog and petrol in the first place. The circle of blame goes round
and round like a strange kind of wrong way payback.
• Others say that all the fancy explanations don’t matter a damn, it doesn’t
matter what the causes might be, kids will sniff just because they want to.
And many sniffers don’t really care what anyone else says. They say ‘ It’s my
body and I’ll do what I like.’ End of story.
Causes are there to be found and addressed by family, community and government.
The cause of petrol sniffing is to be found not only in the sniffers’ camp and the
sniffer’s problems. It is also to be found in the unique way in which Aboriginal
minds work, and in the unique way others’ minds work and react. We misunderstand,
misinterpret and miscommunicate with each other constantly. Also, unfortunately,
our government departments — while expressing a wish to help — often,
inadvertently muddle the problem. Workers in the field often lose heart or become
resentful when they have to become dependent upon or deal with government agencies
which change policy, change direction, change staff, change position and shift
goal posts. The non–government or Aboriginal organisations are not necessarily any
different, since they reflect the way the dominant government procedures operate
and what is expected of them. Community-based players usually feel like they are
on the bottom of the pecking order and that no-one supports them and no-one
listens. The ones at the bottom are the ones dealing with the sniffers daily and
nightly. That might indeed be you and the quietly distraught grandmother of a
sniffer who sits in front of you in the clinic.

Solutions
Analysing causes might be a first step in trying to get your mind around a heart-
rending problem. You will have seen that sniffing is not just a medical or
clinical problem about respiratory failure or ‘fitting’ or malnutrition or thought
disorder or neurological damage. The petrol-affected patient is there as sign and
symptom of complex social, communal and psychological matters. Furthermore, the
anarchic behaviour of sniffers reacts in a usually disturbing and disintegrating
way upon the family groups and living environments. Everyone eventually gets
affected and infected: the school staff, the police, the storekeepers, etc. Thus,
not only is a sniffer a sign or symptom, he or she is an active agent for
increasing stress and turmoil and depression in a family system which may already
be under pressure. Sniffers might enact and dramatise the problem of young people
in trouble with their culture, their future and their direction, but it is rare
for a sniffer to help to become part of the solution.
Understanding the complex causality and knowing the history may lead to
inventing unique and specific strategic solutions for your area. However, as a
helpful starter, the ADCA SA manual gives a useful and comprehensive survey of the
kinds of solutions which most Aboriginal groups are likely to want to try. The
thoughtful d’Abbs & MacLean report surveys already tested solutions.4 There are
many and they are put together in different ways, although there is a basic
pattern which is usually about removing or stopping access to the petrol,
introducing activities, attending to family matters and setting up projects.
As a simplification all solutions are composed out of a mix of six elements:
people, ideas, resources, action imagination, containment.
The sixth element is all-important; it means that a Holding System or Container
has to be carefully put together in a way that works well enough in that specific
community or location. The holding or containing system puts all the other bits
together and links people, ideas, resources, action and imagination.
Many petrol prevention projects fall apart because the central container does
not hold or is not held by its supporting or funding agencies or the buck keeps
being passed to ‘someone else’. Nothing holds together and sniffing keeps slipping
in through the gaps in the net. The container might be an elder’s council, a youth
council, an action group, a government agency or a strong individual. Sometimes
people expect a health clinic and its connections to be an integral part of the
preventative and possible treatment solution. The question clinic staff have to
work through is what role the clinic may have in stimulating or partially holding
the containment process until something coherent can be up and running.
Unfortunately agencies or individuals often go it alone, so a first step in any
solution strategy is to form intercultural partnerships, links and support
networks. Out of such a matrix, a sustainable solution might just be found and
carried through.
 The evasion and resistance to forming such a link-up may come from surprising
quarters, so part of a solution strategy includes being aware of the strengths and
shapes that resistance will take from within a community, an organisation or a
support agency. Some workers say that working hands-on with sniffers is fairly
easy compared to the really serious stress, which comes from dealing with the
inconsistent demands of bureaucracies, Aboriginal power politics and family
dynamics. They speak especially about the stress involved in negotiating between
often incompatible perceptions, requirements and fantasies about the problem.
Burn-out of sniffing projects is directly related to this and to the absence of
structural support for sniffing prevention projects.
At Intjartnama we talk about this problem metaphorically, as though there were
a petrol spirit/ mamu which itself works to break down solutions because the mamu
wants to keep the sniffers sniffing. The mamu is always up to tricks; the mamu is
quite quick to travel to Canberra and make mischief there if it thinks someone is
beginning to really support sniffing prevention. The mamu is equally able to get
someone to stand up at an Aboriginal community meeting, make wonderful speeches in
favour of stopping sniffing and then go and sell petrol to a neighbour’s kids.
Its worth restating that the use of intoxicating substances may never be
stopped. Too much is invested in it. Chasing intoxication has been a part of the
life and death of most cultures of the world from ancient times. Some cultures
have developed social and ceremonial control of intoxicants. For others, drug-
making and using has become a serious part of economic survival. Chasing grog and
drugs (petrol) is a serious pastime within Aboriginal society, just as it is in
mainstream Australia.
You may want to inquire within your local family or cultural group if there are
any internally-generated ways of intoxication control which allows for moderate
use. There may be people, ideas, stories, experiences and traditional dreamings
which can indicate a pattern or an approach, which can help local people adapt
their attitudes to intoxication and instruct the young. Sometimes the Christian
story helps. But if there are no ideas of control within the local culture then
people may have to rely on external ‘whitefellah’ controls, the police, the law
and external restrictions. With petrol sniffing this is very hard. It may be
generations before Indigenous groups set up internal control for alcohol and drug
use. Perhaps only bitter experience is the key.
People like being in altered states. Maybe all you can do is keep young people
away from the substances which are most dangerous for them and find alternative
ways of getting into the altered state.

A meditation
Finally there is a philosophical question to meditate upon which might help one to
think about and think around the experience of living with sniffers.
The question is simply this:
What is it that makes us human?
What is it that makes us Anangu, Yanangu, Yappa, Rilla, or Yolngu ?
What is it that makes us who we are?

We all live in mobs, bound by connections and mutual obligations. And each mob may
have its answer to this question.
There is something about the way sniffers behave that makes us upset because
sniffers seem to break the rules of being human. They break the rules of being
anangu, yanangu yappa, rilla or yolngu
The mind of the sniffer seems to slip away from the things that bind us
together as humans. They seem to slip away from mutual obligation. They seem to
slip away from the connections. We may love the person who sniffs or pity the sad
and lonely, the angry boys and girls, but what makes people so upset is the way
they slip away and it is so very hard to bring them back.
Did they slip away or were they let go?
If only there were a way to keep these young people human, to keep them anangu,
yanangu, yappa, rilla, yolngu.
Thinking about this causes pain. It is a pain which we seem to have to bear and
live with.

Further reading
See endnotes for references mentioned above.
There are three available and essential sources of information and references
published in Australia with remote-area workers in mind. Look into these three
because they have done most of the hunting and gathering of useful and up-to-date
material.
All references in the text of this paper can be found there.
1. Cooperative Research Centre for Aboriginal and Tropical Health PO Box 41096
Casuarina NT. http:www.crc.org.au.4
2. The Petrol Link Up Report.2
3. Aboriginal Drug and Alcohol Council of SA Inc. publication. This package
also includes the D’Abbs and Maclean Review and an A4 reproduction of Petrol
Link Up’s ‘Brain Story’ flip chart.

This excellent and accessible package is well organised, clearly and visually
presented, is full of positive ideas and experiences, contacts and leads. Every
Aboriginal-oriented clinic or care agency should have one. Contact:
ADAC.SA
53 King William St
Kent Town SA 5153
Phone (08) 8362 0395

In addition:
Intjartnama Out-station near Hermannsburg has a range of material, teaching
stories and painted canvasses distilling their experience in caring for sniffers
and developing practical interventions for their area. They also act as custodian
for paintings and graphic material developed by Petrol Link Up.
Contact intjartnama@octa4.net.au, but these out-stations are not equipped to be
distribution agencies.
Mt Theo Out-station project similarly has unpublished reports and summarised
experience of more than ten years effort in the Yuendumu, Warlpiri region. Try as
contact mttheo@bigpond.com
NPY Women’s Council Youth projects are developing much experience in their
region, and in collaboration with Intjartnama have material on the use of out-
station/homeland/detox and community strategy development. ‘The Never Give Up
News’ is a newsletter specifically designed to report on petrol sniffing projects
and activities. Get it. Contact NPY in Alice Springs.
Useful media reports include Paul Toohey’s series in the Australian over 2001–
02.

Some representative articles and reviews include:

Understanding Inhalant uses. A summary of Information. On the web has a
comprehensive 10 page listing of relevant articles etc. www.tcada.state.tx.us/
research/inhalants/reference.html

Social and historical:

Nurcombe, Bianchi, Money, Cawte. A hunger for stimuli; the psychosocial background
of petrol inhalation. Brit J Med Psychology 1970; 43:367–374 (Australian
material).
 Carlini EA et al. The use of solvents . . . among children and adolescents from
a low socio-economic background: a study in Sao Paulo Brazil. Int J Addictions,
1988; 23(1):1145–56.

Psycho-neurological:
Rischbieth, Thompson, Hamilton-Bruce, Purdie, Peters. Acute encephalopathy
following petrol sniffing in two aboriginal patients. Clinical and Experimental
Neurology 1987;23:191–4 (Australian material)
Unfortunately, and despite consistent pleas from front-line workers, there has
been very little Australia-specific research into the effects of petrol sniffing
on the brain and body and psychology of Aboriginal youth and family systems. An
up-to-date study on the toxology, epidemiology, long-term effects, degenerative
process and the treatment of volatile substance use does not appear to be
available, so practitioners are advised to be cautious and not assume that the
story is complete or known. For all the care we have taken, the CARPA STM cannot
present the definitive picture. We would welcome information and advice.

References
1.
Stojanovski A. Yuendumu petrol sniffing project. In SMH Insight, 10/12/2001.
2.
Shaw G, San Roque C & Armstrong W. The petrol link up report. National Drug Strategy.
Canberra: Australian Government Publishing Service, 1995.
3.
Biven A. ed. Aboriginal Drug and Alcohol Council of SA - Makin’ tracks: project and
manual. Brain story flip chart. South Australia: ADAC, 2000.
4.
D’Abbs P, MaClean S. Petrol-sniffing in Aboriginal communities. A review of
interventions. Darwin: Co-operative Research Centre for Aboriginal and Tropical Health,
2000. http:www.crc.org.au
5.
Mosey A. Report on petrol-sniffing in central Australia alcohol and other drugs program.
Alice Springs: Territory Health Services, 1997; Unpublished report.
6.
MacFarland B. A project report on petrol sniffing in central Australia. Alice Springs;
Territory Health Services in co-operation with Tangentyere Council, 1999; Unpublished
Report.
7.
Roper S. Petrol sniffing and preventive interventions on the Anangu Piyjantjatjarra
lands. South Australia: Flinders University, 1998. Thesis.
8.
Brady M. Heavy Metal. Canberra: Aboriginal Studies Press, AIATSIS, 1992.
9.
Spencer JA, Franks C, Lowe HJ. Andrew Spencer Japaljarri: Artist and Counsellor. In:
Thompson L (editor). Aboriginal Voices: Contemporary Aboriginal artists, writers and
performers. Brookvale, NSW: Simon & Schuster, 1990.
10.
Camus A. The plague. Penguin, 1977; 144.
11.
http:www.inhalants.org/chemical.html
12.
Ron M. Volatile substance abuse; a review of possible long-term neurological,
intellectual and psychiatric sequelae. Brit J Psychiatry 1986; 148:235–46.
13.
Maruff P, Burns CB, Tyler P, Currie BN, Currie J. Neurological and cognitive
abnormalities associated with chronic petrol sniffing. Brain 1998; 121:1903–17.
14.
Brady M. Lead toxicity and nutritional factors: some implications for petrol sniffing.
Australian Health Information Bulletin 1989; 12:15–18.
15.
Brady M. Torzillo P. An overview of the prevalence of petrol sniffing and related
mortality. In: The Drug offensive; workshop on lead and hydrocarbon toxicity from chronic
petrol inhalation. Canberra; Australian Government Publishing Service, 1995.
16.
Carlini EA. The use of solvents and other drugs among children and adolescents from low
socio- economic background: a study in Sao Paulo, Brazil. International J Addictions 1988a;
23(911):1145– 56.
 Psychiatric Emergencies Legal
Advice

Authors: Dr Peter Tait; Terry Barker (Section Head of the Mental Health Unit of Social
Emotional Wellness Branch of the NT DHCS)

Topic Reviewer: Dr Marcus Tabart

A psychiatric emergency is when a person is thinking or behaving in a very

disturbed way and there is risk of harm to themselves or others due to a mental
illness or mental disturbance.
Substance abuse in and of itself does not constitute a psychiatric emergency
and does not fall within the provision of the Mental Health and Related Services
Act NT 1998 (MHARS). A psychiatric emergency refers to a person who is suffering
from a mental illness or mental disturbance.

Sedating or restraining the person

A person cannot be sedated or restrained involuntarily outside of the provisions
of the MHARS. A Section 34 (‘Recommendation for Psychiatric Examination’) would
need to be authorised by an Approved Psychiatric Practitioner (APP) or DMO
(doctor) before sedation can take place. The DMO or APP can then authorise
medication to be given by a registered nurse, ambulance officer or Aboriginal
health worker. Form 35A (‘Notification and Report for Emergency Treatment
Administered without Approval of the Tribunal’) must be completed by the person
administering the treatment and a copy sent to:
• The person in charge of the approved treatment facility
• The person who prescribed the medication, and
• The tribunal.

If Section 34 is recommended a person must be sent to an approved treatment

facility for psychiatric assessment. Therefore, any mention of sedation should not
be made until the process of assessment and recommendation for psychiatric
examination is discussed.

Plan further care

Decide if the person needs hospital care; this may be voluntary or involuntary.

Voluntary admission
The person agrees to go for treatment. Arrange with the doctor.

Involuntary admission
In the NT a doctor can sign a Section 34, but one cannot be authorised by a member
of the police force. However, police may be involved in taking a person for
examination under this provision. Section 163 of MHARS authorises a member of the
police force to apprehend a person and take them to a medical practitioner, APP or
designated mental health practitioner (DMHP) for assessment.
This makes the patient ‘involuntary’ under the MHARS. It authorises staff to
restrain and sedate the patient and take them to hospital for examination.
Under the MHARS Act a person can only be sedated involuntarily in order to:
 • Prevent the person causing immediate harm to themselves or others
• Prevent behavior that is likely to cause harm to themself or others
• Prevent further physical or mental deterioration of the person
• Relieve acute symptomology.

As previously stated any treatment would need to be authorised by a a DMO or APP

and administered by a registered nurse, ambulance officer or Aboriginal health
worker. Form 35A must be completed by the person administering the treatment and a
copy sent to:
• The person in charge of the approved treatment facility
• The person who prescribed the medication, and
• The tribunal.

The following amendment to Section 34 protocol is provided as an example of

current approved procedures under the MHARS ACT for persons in remote communities
where access to a DMO or APP is limited. Additionally, clarification of RFDS and
Air Med proecedual guidelines would need to be established.

Authorisation by telephone
A ‘Recommendation for Psychiatric Examination’ (S35) or a document relating to the
treatment of a person, can only be approved if the approved person signing the
document has personally examined the person. Refer Section 160 (1). The Chief
Executive Officer has issued a direction that, in those infrequent circumstances
where it is not possible for an approved person to physically examine a person,
this assessment can be conducted by telephone where the following criteria are
met:
• The person is in a remote area where access to an authorised psychiatric
practitioner, medical practitioner or designated mental health practitioner is
not practically available; and
• The authorised psychiatric practitioner or the district medical officer has
conducted an assessment of the subject by telephone or other means that are
reasonable in the circumstances of the case and are satisfied on reasonable
grounds that:
• The subject is in need of treatment under the Act; and
• Any person making a request for assessment of the subject has a genuine
interest in, or a real and immediate concern for, the welfare of the subject.

This authorisation may only be provided by either an authorised psychiatric

practitioner or a district medical officer (doctor).
Where a request for assessment is made in a remote community and there is no
medical practitioner available, staff will consult by telephone with an APP or the
DMO. Where the DMO is consulted he/she will obtain advice from the APP if
required.
If, following assessment, the DMO is satisfied that the person requires care
and transfer for psychiatric assessment a recommendation for psychiatric
examination must be made on Form 34A (‘Recommendation for Psychiatric
Examination’) and sent to the approved treatment facility where the person is
being taken.
Depending on the person’s mental state the DMO may authorise emergency
treatment prior to the person being escorted to the approved treatment facility.
Where authorised this medication may be given by a registered nurse, ambulance
officer or Aboriginal health worker. Form 35A must be completed by the person
administering the treatment and a copy sent to:
• The person in charge of the approved treatment facility
• The person who prescribed the medication, and
 • The tribunal.

Before the person is transferred the DMO must notify both the appropriate APP and
staff at the approved treatment facility, to ensure they are prepared for the
admission and are fully briefed regarding the person’s clinical situation,
transport and treatment requirements.

Practice notes
The DMO should consult by telephone with the on-call APP to discuss the case,
request advice if necessary and inform of any actions taken.
Psychosis

Author: Dr Andrew W Frukacz

Topic Reviewer: Dr Guy Windsor (psychiatrist)

Introduction
Psychosis is defined as a major mental disorder of organic or emotional origin in
which a person’s ability to think, respond emotionally, remember, communicate,
interpret reality, and behave appropriately is sufficiently impaired so as to
interfere grossly with their capacity to meet the ordinary demands of life.1
Patients with psychosis present with hallucinations, delusions, disturbance in
mood and thought disorder. Psychotic disorders are not uncommon with various
epidemiological studies showing that between 0.5–1% of the population suffer from
a psychotic disorder at any one time.2 It is important to diagnose and treat
psychotic disorders because they can be frightening for the patient and their
relatives as well as leading to considerable disability and suicide. The National
Survey of Mental Health and Wellbeing (1999) found that between 4–7 persons per
1000 adults resident in urban areas are in contact with mental health services
during any given month because of symptoms of a psychotic disorder. The lifetime
prevalence of schizophrenia is about 1%.
Between 5–15% of patients suffering from a psychosis will commit suicide.3
Patients with psychosis have greater mortality and morbidity. Finally, psychosis
is associated with significant disability with regard to social and occupational
functioning. There is evidence that delays in the detection and treatment of
psychotic conditions can lead to reduced responsiveness to treatment and more
severe residual symptoms.4
Psychosis is not a condition itself but rather a final common pathway for a
number of different conditions that include organic or physical conditions, drug
and alcohol abuse, mood disorders and schizophreniform disorders.

Diagnosis
One needs to consider the possibility of a psychotic illness in anyone who is
experiencing a change in behaviour. Psychosis can occur at any age but is most
common in late adolescence and early adulthood. It is becoming more apparent that
health practitioners need to be watchful for early signs or symptoms of psychosis.
These are signs and symptoms that are not specific; in other words they can occur
in any number of conditions. However, they are often seen in the early phase of
the condition and early diagnosis relies on picking up these features. This allows
the practitioner to institute early treatment for psychotic conditions, which has
been shown to reduce the morbidity associated with psychotic illness.5,6

Prodromal symptoms of psychosis

• Suspiciousness
• Depression
• Anxiety
• Irritability
• Restlessness
• Change in appetite
• Sense of alteration of self, others or the outside world
 • Social isolation or withdrawal
• Marked impairment in role functioning
• Markedly peculiar behaviour
• Marked impairment in personal hygiene
• Blunted, flat or inappropriate affect
• Digressive, vague or metaphoric speech
• Odd or bizarre ideation
• Unusual perceptual experiences
• Marked lack of initiative, interests or energy.

Many of these symptoms are non-specific, but incipient psychosis is suggested

by:
• Marked, unexplained and consistent changes in behaviour
• A pattern of increasing severity
• Clustering of symptoms
• Family history of psychosis
More specific features of psychosis can then be looked for. These include:
• Hallucinations. These are seeing, hearing or otherwise experiencing things
that are not really there. Hallucinations can occur in any modality, but in
schizophrenia they characteristically involve auditory hallucinations, whilst
in organic states visual hallucinations can occur.
• Disturbance in mood or feelings. This can involve depression or sadness or
expressing feelings that are out of context with what the patient is saying,
such as laughter when talking about someone hurting them.
• Thought disorder. In which the normal flow of thoughts is disrupted; this may
be mild, in which case the patient seems vague and difficult to understand, to
severe in which the patient’s speech is garbled and incoherent.
• Disturbance in behaviour. The patient may be mute and immobile (catatonic) or
may display other behavioural abnormalities, such as rocking to and fro, or
making unusual gestures such as hand movements.
• Delusions are false beliefs, such as that people want to hurt the patient or
that the patient has special powers or that the patient is being controlled in
some way.
• Withdrawal. Seen as not wanting to mix with people the patient previously was
mixing with, and not taking interest in things and not looking after
themselves as much.

When called to a patient with a possible psychotic illness it is imperative to

initially assess the safety of the patient and of the health practitioner.
Psychotic patients can act irrationally because of delusions or hallucinations.
One should approach such patients in a calm manner explaining that you have been
asked to see them because people have been worried about their health, and then
explain that you would like to talk to them about this. Sometimes it helps to
examine a psychotic patient with another health worker. One should not be
confrontational. One should attempt to create a calm and safe environment of low
stimulation for these patients.
If the patient is in danger of harming themselves or is threatening then it is
important to contact someone else. This may be the police or a family member or
community elder.
The first step in assessment is to determine whether there is a physical cause
for the psychosis. This is done on the basis of the mental status examination.

Individual mental state assessment

Appearance: Simply describe the patient’s physical presentation: clothing,
hygiene and cultural appropriateness.
Behaviour: Briefly describe the patient’s behavioural style, including agitation,
retardation, and any inappropriate or unusual behaviour.
Conversation: Describe both the content of conversation, perhaps with some
quotes, as well as the form, which includes the rate of conversation, as well as
the logic, or otherwise, of thought processes.
Affect and mood: Note the individual’s mood level, variability, range, intensity
and appropriateness.
Perceptual abnormalities: Note any psychotic symptoms or other perceptual
abnormalities, including hallucinations and delusions. These perceptual
abnormalities can occur in any of the five senses.
Cognition: Describe orientation, memory and attention, or ability to concentrate.
The ‘Mini Mental State Examination’ is an excellent brief cognitive assessment
that can be performed by most clinicians in three to five minutes.
Dangerousness: Comment on any suicidal or homicidal ideas, beliefs or feelings.
Insight: Assess the patient’s insight into his or her condition. This may be hard
to judge, but is particularly important because of the management implications of
poor treatment compliance.
Judgement: Assess the patient’s level of judgement, in particular regarding safety
issues.
Rapport: Briefly comment on how you believe the interaction was between
yourself and the patient, and in particular how the patient made you feel.

Certain features of the mental state suggest an organic cause. Fluctuating levels
of consciousness and impairment in concentration, attention and memory indicate a
need to rule out physical causes. Physical features, such as abnormal vital signs—
including fever and tachycardia, flushed appearance, rapid breathing and recent
head injury — would likewise indicate a need to explore for organic causes for the
psychosis.
If one suspects a physical cause for the psychosis one would need to
differentiate between:
1. Psychosis due to a medical condition
2. Psychosis due to alcohol and other drugs, such as inhalation of petrol
fumes
3. Psychosis due to withdrawal from drugs
4. Psychosis due to degenerative condition such as Alzheimer’s disease.

What to do
• When a patient with psychosis is referred to you obtain as much information
from any relatives or carers as possible
• When you are ready to assess the patient go with someone
• Sit with the patient in a quiet and calm environment. It may be important to
be in surroundings that are familiar to the patient. What we are trying to do
is to reduce the level of anxiety or fear in the patient
• Ask how the patient is feeling. Ask the patient what he thinks is going on
• Ask also about suicidal feelings or ideas. If the patient says they have been
having suicidal ideas or feelings it is important to assess this further
• Ask about what plans the patient has had about suicide
• Ask about how close the patient has come to carrying out any plan
• Ask about feelings of hopelessness: this is associated with increased risk
of suicide
• Ask about previous attempts: again, this is associated with increased risk

• Initially ask open-ended questions in an effort to obtain as much information

about the patient’s experience as you can. Then ask questions about specific
features of psychosis
 • Have you ever felt that people were talking about you behind your back?
• Have you ever heard people talking and then looked around and there was no-
one there?
• Have you ever had experiences that you found hard to make sense of or
understand?
• Have you ever found it hard to follow your train of thought?

• Ask about whether they have ever had any mental illness before. If they have,
ask about the symptoms and how it was treated. Ask about medications and
whether they have stopped taking medication that they should still be on
• Ask if they know of anyone in the family who has had trouble with mental
illness
• Ask if they drink and how much
• Ask if they use drugs or sniff petrol: ask how often and for how long
• Do a mental status examination and record your findings
• If possible do a physical examination: check especially for pallor,
breathlessness, fever and sweats, high or low pulse, high or low blood
pressure, pupil changes and neck stiffness, head injury, abnormal movements,
weakness and paralysis
• Blood tests should be arranged for electrolytes, creatinine, liver function
tests, thyroid function tests and full blood count and ESR, and STS
• Institute a treatment plan or discuss the treatment plan with a medical
practitioner or mental health worker. (Check with local health centres or
hospitals for details of these contacts)

Treatment 7,8

The first thing to decide is where to treat the patient. Patients should be
treated in the least restrictive setting that is safe for them and allows for
effective treatment. If the patient is a danger to themselves or others, or unable
to look after themselves and have no family or friends to look after them, or if
there are underlying medical conditions that require inpatient treatment, then
hospitalisation should be seriously considered.

Involuntary treatment: referral and sedation authorisation

If the patient is a danger to themselves or others and is not willing to accept
treatment then the provisions of Sections 34 and 35 of the NT Mental Health and
Related Services Act 1998 may need to be invoked to provide for involuntary
treatment. In the NT all doctors, health professionals (including ambulance
officers who have had the specific training), and police can do this.
Psychiatrists and District Medical Officers can invoke these provisions over the
phone. A Section 34 or Section 35 of the MHARS cannot be authorized by a member of
the police force. This is described in more detail in the Psychiatric Emergencies
Legal Advice chapter.

Involuntary treatment: restraint

Some patients may need to be restrained to prevent them being a danger to
themselves or others. If this becomes necessary then one person should be
coordinating the procedure. There should be one person assigned to each limb and
one person assigned to the head. The idea is that at the appropriate time the
restraint team approaches the patient calmly but firmly, grabbing the assigned
part of the body and placing the patient prone.
Some patients with psychosis can be treated with supportive care alone. This
involves being with someone who can ensure that the patient is safe, and eats and
drinks appropriately. This is particularly the case with psychosis due to drug and
alcohol intoxication or withdrawal.
 Where the psychosis is due to an underlying medical condition then this will
need to be treated. However, where symptoms do not resolve with supportive or
medical treatment specific treatment for the psychosis is required. This will
depend on the severity of the psychosis and the agitation of the person.
In all levels of agitation oral medication should be tried first, and the
intramuscular route used if this is not practical or fails. Intravenous use of
sedation and antipsychotics is not recommended because of the danger of
respiratory suppression and the difficulties of getting intravenous access in
agitated people.
(A relatively simple protocol for sedation of agitated/psychotic people is
given in the CARPA STM protocols.)
Remember that sedation is dangerous. Be prepared to manage the person’s airway
and ventilation. Don’t give benzodiazepines to children and give old people lower
doses.
Risperidone is preferred as the oral antipsychotic because it is less likely to
cause extrapyramidal side effects, such as muscle stiffness and spasms (appendix A
antipsychotic side effects). Similarly, droperidol is the intramuscular choice as
it is a low potency antipsychotic. Thus it is less likely to cause acute dystonic
reactions and, having the advantage of causing less respiratory depression, it
does not need benztropine as well.9,10,11
When sedation is achieved establish an IV line to maintain hydration and to
permit IV medication access if later required by the medical officer. If the
patient has been drinking heavily then intramuscular Thiamine 100 mg is required
to prevent Wernicke’s encephalopathy and lactic acidosis.
In the long term treatment will be determined by the underlying cause of the
psychosis. Treatment will usually involve a combination of medication and
psychological and social treatments.

Medications
Patients with psychotic conditions will usually require long-term treatment with
either antipsychotic medications or mood stabilisers. Where the patient is
suffering from a schizophreniform illness or delusional disorder antipsychotic
medication is indicated. It is best to use one of the newer antipsychotic
medications because of the better side effect profile compared to the older anti-
psychotic medications. In particular the newer antipsychotic medications produce
less extrapyramidal side effects and there is less likelihood of tardive
dyskinesia, which is a long-term side effect characterised by abnormal movements,
particularly around the mouth. The newer antipsychotic medications and their
dosages are:
• Risperidone 2–6 mg per day
• Olanzapine 5–20 mg per day
• Quetiapine 150–400 mg per day
• Clozapine 100–400 mg per day

Clozapine is only approved for treatment of psychotic conditions where the patient
has been resistant to treatment with two other anti-psychotic medications. This is
because it has been associated with agranulocytosis, which in some cases has been
fatal. For this reason patients need regular blood monitoring and need to be alert
for symptoms and signs of agranulocytosis such as fever, sore throat and ulcers.
Where compliance with oral medication is a problem depot medications can be
helpful. There are three more commonly used depot medications:
• Flupenthixol decanoate, 20–40 mg IMI fortnightly
• Zuclopenthixol decanoate, 200–400 mg IMI fortnightly
• Haloperidol decanoate, 50–150 mg IMI monthly
Mood stabilisers are used for the treatment of bipolar affective disorder and can
also be used to augment the effectiveness of the antipsychotic medications in the
schizophreniform disorders. There are three mood stabilizers:
• Lithium, 250–1000 mg per day (however lithium can be difficult to manage
when the person is mobile and/or not feasible to regularly monitor blood
levels)
• Sodium evaporate, 500–1500 mg per day (blood levels required regularly)
• Carbamazepine, 200–800 mg per day

The older antipsychotic medications can still be useful, especially where patients
do not tolerate the newer medications or find them ineffective.

Psychological treatments
Psychotic conditions can produce problems with motivation and impairment in social
functioning. These are best dealt with by psychological methods. Most patients
with chronic psychotic conditions should be seen on a regular basis by a mental
health worker, doctor or community nurse. The purpose of this is to:
• Build a rapport so that the patient can begin the process of trusting those
people in the health system who can best help him
• Monitor the mental state and the effectiveness of treatment (this will also
require an assessment of compliance)
• Provide education about the nature of the condition and of how treatment
works so as to enhance compliance
• Monitor for side effects and deal with them (this is especially important
for enhancing compliance)
• Help deal with issues of shame and ostracism about having a mental illness
• Encouragement to re-engage in usual activities
• Support to deal with drug and alcohol abuse.

The family of the patient may also need education and support. This should be
directed at helping them understand the nature of the illness and how to deal with
the behavioural problems associated with it.

Medical follow-up
Mental health clients have the same incidence rate of other health problems, i.e.
diabetes, hypertension, sexual health, as the rest of the population, but often
their behavioural and psychological concerns take prominence and other health
issues are not followed up.12 Mental health clients are also frequently on
medications that require regular blood tests and monitoring of side effects.

References
1. American Psychiatric Glossary. Washington DC:American Psychiatric Press Inc, 1998.
2. Kaplan & Saddock. Comprehensive Textbook of Psychiatry. 7th ed.
3. Kaplan & Saddock. Comprehensive Textbook of Psychiatry. 7th ed.
4. Copolov D. Psychoses: a primary care perspective. MJA Practice Essentials Mental Health.
Australasian Medical Publishing Company Limited, 1998.
5. McGorry PD, Jackson HJ. The Recognition and Management of Early Psychosis. A Preventative
Approach. United Kingdom: Cambridge University Press, 1999.
6. National Survey of Mental Health and Well Being report for people living with psychotic
illness; an Australian study 1997–98. Commonwealth Dept of Health and Aged Care.
7. Practice Guideline for the Treatment of Patients with Schizophrenia. American Psychiatric
Association, 1997.
8. Practice Guideline for the Treatment of Patients with Delirium. American Psychiatric
Association, 1999.
9. Kerwin RW. The New Atypical Antipsychotics. British J Psychiatry 1994; 164:141–8.
10. Therapeutic Guidelines: Psychotropic. Version 4. Therapeutic Guidelines LTD, Victoria,
2000.
11. Stahl SM. Psychopharmacology of Antipsychotics. UK: Martin Dunitz Publisher, 1999.
12. Lawrence D, Holman D & Jablensky A. Duty to care. Preventable Physical illness with
mental health. Perth: The University of Western Australia, 2002.
 Suicide

Author: Jane Vadiveloo BSc (Hons) MPsych (Forensic)

Topic Reviewers: Kaz Knudsen (RAN, WA); Vivien (RAN, Amata); Jane Kollner (RAN,
Ampilatwatja); Teresa Bowmen (RAN, Papunya)

Suicide affects many people across all ages and many cultures. Suicidal behavior
is not just the act of a person taking his or her own life. Suicide also includes
self-harm, attempting suicide and thinking about suicide.
Risk behavior is closely associated with suicidal behaviour and includes
behaviour that places a person’s life and health at risk e.g. fast and dangerous
driving, regular heavy drug use, unsafe sex with various partners.

Rates
Global situation
Suicide rates across the world have increased by 60% over the past 45 years, with
an increase in the numbers of youth suicides. Mental Disorders are associated with
more than 90% of all suicides although it is recognised that sociocultural factors
are involved and that suicide is more likely to occur in times of crisis.1

Australia
The pattern of suicide death rates for Australians across all ages has been
relatively constant since 1921, with an average annual rate of approximately 21
deaths per 100 000 for males, and 5.5 deaths per 100 000 for females.2 The age
pattern of suicide has changed over this time, however, with less middle-aged
people dying from suicide and an increase in the rate of young people and older
people dying from suicide. Suicide rates in young men tripled between 1960 and
1990 while the rates for young women doubled.

Gender
Males are five times more likely to die from suicide than females, though more
females attempt suicide and are hospitalised following suicide attempts. It is
estimated that for one completed suicide there are 50–100 attempts.3
Methods
In Australia the most common method of suicide attempt for both males and females
is drug overdose. However, more males die by hanging than any other form of
suicide, and more females die from drug overdose than other methods of suicide.4
Hanging is one of the most lethal forms of suicide i.e. it is easy to die from
hanging.
For Indigenous people hanging has become the most common method of suicide. The
increase in suicide by hanging in Indigenous communities can be related to the
struggle of Indigenous peoples at the political, community and individual level:
. . .the Aboriginal collective experience of two hundred years of incarceration,
capital punishment, and outback murders . . . makes all hanging deaths ‘custody’
deaths in that they relate to a bloody history of incarceration
institutionalisation, and eroded freedoms, and reflect relentless and oppressive
circumstance . . .5

Hunter, Reser, Baird and Reser provide an in-depth discussion about Indigenous
suicide.5 They discuss suicide in terms of cultural meaning and understanding,
media representation, symbolic representation and the influence of deaths in
custody. Amongst other things, they suggest that increased representation of
Indigenous peoples committing suicide by hanging has led to this method becoming
common within the Indigenous community.

Mental health and suicide

Although most people with a psychiatric disorder do not suicide, it is reported,
‘90% of suicides in all age groups are associated with psychiatric or addictive
disorders’.6 Depression is believed to be the most common associated factor linked
to suicide.3,6

Young people
National Action Plan for Suicide Prevention reports that up to one in ten young
people attempt suicide, and up to 50% of young people think about suicide (suicide
ideation).4
Australia has one of the highest rates of youth suicide in the world. Suicide
is one of the leading causes of death for young people. For young men aged 15–24
years it is the leading cause of death.3
At any time 1–3% of adolescents suffer from a major depressive disorder.7 Up to
24% of young people will have suffered at lease one episode of major depression by
the time they are 18 years of age. Self-report studies indicate that 77% of young
people reporting deliberate self-harm have a mental health problem.8

Indigenous Australia
The suicide rate amongst Aboriginal and Torres Strait Islander peoples is
approximately 40% greater than the national average.4
Suicide rates for young Indigenous people is approximately double that for non-
Indigenous young people.8
Rural and remote Australia
The rate of suicide in remote areas is almost twice the rate of urban areas.4 There
has been a four-fold increase in male youth suicide in rural areas in the past 25
years. For 15–19-year-old males the rates have increased by up to six-fold.9

Northern Territory
Northern Territory has a higher rate of suicide than the national average with 45
per 100 000 compared with a national average of 25 per 100 000 people. The rate of
suicide for young females in the NT is over three times the national average.
Table 1: Rates of suicide per 100 000 of 15–24 year olds (1998) Australian and the Northern Territory10

Males Females Total

Northern Territory 31 14 45
Australia 25 4 29

Table 3: Total number of adult suicides in Central Australia by age and cultural
background (figures from 1989–2001)
Years of age 26–29 30–39 40–49 50–59 60–69 70–79 TOTAL
Indigenous males 2 7 1 2 – – 12
Caucasian males 9 6 12 5 2 1 35
Indigenous females – – 1 – – – 1
Caucasian females – 1 – – – – 1
Asian female – – 1 – – – 1
Total 11 14 15 7 2 1 50

Table 4: Rates of suicide between Alice Springs, Tennant Creek and remote locations

1989 1990 1991 1992 1993 1994 1995 1996 1997 1998 1999 2000 2001 Total
A/S 5 1 1 2 3 2 3 2 7 9 5 8 4 52
Remote 1 1 1 1 0 1 4 2 1 3 3 4 1 23
T/C 0 1 1 0 0 0 2 0 0 2 2 1 1 10
Total 6 3 3 3 3 3 9 4 8 14 10 13 6 85

A/S = Alice Springs Remote = remote community T/C = Tennant Creek

The Central Australian region11
Young people
Between 1989 and 2001 there was a steady increase in the number of youth suicides
in the Central Australian region. Figures indicate that the pattern of suicide for
non-Indigenous young people was relatively constant, with an increase in 1997 and
1999. Over this period, 11 young men and two young women completed suicide. The
pattern of suicide for Indigenous young people changed dramatically over this
period. Between 1989 and 1992 there were no recorded suicides by young Indigenous
people. Between 1993 and 2001, 23 young Indigenous people completed a suicide, 18
of these were male (see figure 2).
While there was a decrease in the number of young people completing suicide in
2001, the increase of youth suicides over the past five years is considered by
health professionals in the Central Australian region as an ongoing crisis. In
response to this crisis, the Life Promotion Project was implemented in 1998 to
coordinate the response to suicide and suicide prevention in the region.12
Table 2 indicates that nearly all youth suicide was completed by young people
aged between 15 and 25 years. The highest risk group is young Indigenous men aged
between 20 and 25 years. Anecdotal reports suggest that children under the age of
10 have attempted suicide in the region.

Table 2: Total number of youth suicides in Central Australia by age and cultural
background (figures from 1989–2001)

10–14 yrs 15–19 yrs 20–25 yrs TOTAL

Indigenous male – 5 14 19
Caucasian male – 4 5 9
Indigenous female 1 2 1 4
Caucasian female – 2 1 3
Total 1 13 21 35

Adults
In contrast to young people, the pattern of adult suicide indicates a crisis in
the non-Indigenous male population. A total of 35 non-Indigenous men completed
suicide between 1989 and October 2001, with 25 of these suicides occurring since
1995. The rate of suicide in the remaining adult population remained relatively
consistent with some variations occurring in the adult Indigenous male population
(see figure 3).
Table 3 indicates that most adult suicides were completed by people aged between
25 and 50 years. The highest risk group is non-Indigenous men aged between 40 and
50 years.

Table 4 indicates that the rate of suicides between Alice Springs, Tennant Creek
and remote locations occurred at a ratio of 5:2:1, which is relatively consistent
with population levels for these three regions.10

A framework for prevention

Knowing, risk factors, possible signs and patterns of behaviour for a person
provides us with a prevention framework.
Suicidal people are normal people feeling a lot of stress and/or sadness. Many
people at some time in their life think about suicidal. Suicidal behaviour is more
likely when a person is finding it hard to cope with stressful things in their
life.

Risk Factors
Risk factors most commonly associated with suicide
 • Presence of a mental illness, particularly depression
• Previous suicide attempt/s
• In Central Australia, anecdotal evidence from clinicians indicates that
sexual abuse is a high risk factor, particularly for young women. The
monitoring of young people at risk and the coordinated response to completed
suicides by the Life Promotion Program indicates that sexual abuse as a high
risk factor for young women in Central Australia. As a clinician working with
people at risk for six years in Alice Springs, I have found that young women
with suicidal behaviour have often experienced sexual abuse.
Risk factors are factors that are commonly associated with suicide. They may
increase the likelihood of a person committing suicide, attempting suicide or
engaging in destructive behaviours. While many people who commit suicide have
experienced common risk factors, there are many people with these risk factors who
do not engage in suicidal behaviour. Risk factors may vary according to
population.6
People who present with suicidal behaviour often experience the following
factors8,6,13—17:

Mental Health
• Depression and other mood disorders
• Schizophrenia
• Conduct disorder
• Substance abuse disorders
• Low self-esteem

Previous suicidal behaviour

• Lethality: hanging is the one of the most lethal forms of suicide, overdose is
less lethal
• Number of attempts; risk increases as the attempts increase
• Suicide by a family member increases suicide risk by five-fold

Trauma and abuse

• Conflict, violence and other abuse; chronic exposure to violence
• Trauma: up to 75% of young people who report a history of sexual abuse also
report suicidal behaviour8

Loss or Change
• Death by suicide of family or friends
• Death or loss in friends or family
• Chronic illness or disability/physical illness
• Relationship loss
• Job loss
Family and life experiences
• Poor relationship with or between parents, including separation/divorce;
violence/abuse, parenting style/neglect, overprotection, and criticism
• Parents being in prison
• Placed in welfare as a child
• Children of Vietnam Veterans

Media
• There is a link between media reporting on suicides and an increase of
suicides after the reporting

Development, identity and environment

• Sexuality issues
• Choice of music (related to death)
• (Sense of) failure at work/school
 • Legal issues
• Incarceration

Social disadvantage
• Unemployment
• Limited educational opportunity
• Poverty
• Homelessness

Coping skills
• Vulnerability and low resilience
• Self destructive coping skills
• Limited support networks

Behaviours
• Drug use
• Risk behaviours
• Violence

There are community and political issues that affect suicidal behaviour by
creating social isolation, disadvantage and patterns of behaviour, which place
certain groups in the community at risk of suicide. These include:
• Social isolation due to community intolerance (mental illness, sexuality,
cultural background)
• Social isolation due to negative discourse by the community, media and
politicians e.g. about young people, Indigenous peoples, refugees
• Patterns of behaviour developed within a community e.g. hanging as a means of
suicide for Aboriginal people; hunger strikes by asylum seekers
• Laws and policies that increase the likelihood of social isolation, family
difficulties, and that limit social and economic opportunity e.g. mandatory
sentencing, removal of bilingual education, stolen generations.

Warning signs
Sometimes it is hard to tell that a person is suicidal. In most cases, however,
there are warning signs. Although they are sometimes subtle, people often give
clues and signs about their suicidal thoughts and intentions. As with the risk
factors, the following does not predict suicide. If we know the person, we should
be aware of major changes in behaviour and recent stresses which may make the
person more vulnerable.

Look out for the following

• Recent event (or build up) that may make it difficult for the person to cope,
such as recent (or anniversary of) loss/death, relationship breakdown
• Recent patterns of thoughts, feelings and behaviour (not just one off)
• The person is not behaving the way they usually do

To identify warning signs be aware of what people are saying, how they are
behaving and how they appear to be coping. Warning signs for suicidal behaviour
are similar to signs of depression. Be aware of the following.

Things people say and think

• Unhappy with self, life or preoccupied with death
• No sense of future, not able to cope, want it all to end

Changes in personality and behaviour

 • Sudden lift in spirits
• Irritability, restlessness
• Anger
• Sleeping and eating patterns change
• Withdrawal
• School or work performance deteriorates
• Crying and moodiness
• Alcohol or other drugs
• Numerous accidents
• Dangerous risky behaviour

Preparations for death

• Goodbyes
• Making will
• Statements that might imply not seeing that person again
• Giving things away
• Writing or drawing things about death or suicide

Signs of depression
• Feeling worthless, guilty
• Tired, not being able to concentrate or make decisions
• Not caring about self, not interested in things and not wanting to do anything
• Problems with sleep; too much or too little
• Withdrawn, restless, irritable

Working with someone at risk of suicide

Many people are scared about suicide, and don’t know what to do when someone talks
about suicide or is showing suicidal behaviour. It is common for people to respond
with panic, anger, or ignore the behaviour claiming that it is ‘attention
seeking’.
People who attempt or talk about suicide should not be dismissed as attention
seeking. All talk of suicide should be taken seriously. It is hard to tell how
serious a situation is until you sit down and talk to the person and make an
assessment of their needs.
There is no evidence that talking about suicide encourages it to happen. Many
people who have thoughts of suicide are scared of these thoughts and are scared of
dying. The step of suicide is often a desperate step when people cannot see a way
out of their situation. If you can talk about it without judgement and with care
it can help reduce the risk of it happening. Always remember to refer to someone
else if you don’t feel confident. Knowing when you need help, as a clinician, is
very important when dealing with people who are suicidal or have mental illness.

Assessment
Assessment for suicide begins with a standard mental status examination.18
Assessment then turns to presentation of risk factors, with particular focus on
previous suicide attempts, signs of depression, current life stress, and suicide
intent (thoughts and plans). Current stress commonly associated with suicidal
behaviour includes recent loss, relationship breakdown and sexual abuse. Table 5
provides a guideline for assessing risk of suicide.
When responding to someone who is suicidal you need to address their immediate
needs and their longer term needs. In the short term you need to assure the
person’s immediate safety. This may require supervision and monitoring or referral
to a mental health facility. It also involves access and referral to counseling
and treatment. Treatment may include both medical and psychiatric assessment.
 If you are dealing with a person in the longer term, the following provides
some steps you can follow:
• Define problem/s
• Define alternatives approaches
• Develop plans to deal with problems
• Establish a commitment, on both sides
• Set goals: steps that are achievable and can be celebrated
• Evaluate how the person is going
• Make plans for coping with future crisis
• Build support networks
• Monitor risk

Guidelines in approach
How you work with people who are suicidal is very important. The following are
guidelines which come from my own experience as a practitioner as well as the
workbooks, manuals and papers that are referenced during this paper.

Remember the barriers

• To deal with suicide a person must cross many barriers. Some of these are:
• Shame
• Reluctance to talk about suicide
• Keeping things private
• Fears of confidentiality and everyone in the community knowing their
business
• Not knowing where to go

Communication
• Dealing with suicide is a matter of trust. It is important that you are
interested, and respect the person’s situation
• Listen to what the young person has to say
• Don’t tell them what to do: explore with them their thoughts and feelings and
options
• Only promise what you can deliver
• Take the person seriously
• Give them power over their situation: focus on their strengths and support
them to make decisions
• Stand in their shoes
• Validate and value them: hear what they are not saying

Confidentiality
Duty of care means that you must do whatever you can to ensure that a person who
is suicidal is safe. This means you can never promise to keep a secret about
suicide, and you can never promise to keep everything confidential. It is best
that the person knows this from the beginning. Explain to the person that it is
about their wellbeing and safety. Where possible, make sure the person knows whom
you are telling, when and why. If you can get the approval of the person who is
suicidal, this can be very powerful.

Expression
Support the person to express their feelings and thoughts; make sure that the
environment is safe (i.e. private, few distractions) and that you feel confident
to deal with whatever may come up. There are people who want to die but don’t want
to take their own life, and there are others who want to die and intend to act on
these thoughts.
Consequential questioning and understanding permanence
Often people who are suicidal are self-focused, desperate and concentrated on
specific issues. They often lose sight of how their behaviour may impact on others
and what other options are available to them. By asking questions about a person’s
life, why they want to suicide and whether they understand the impact of suicide,
a clinician can shift the way the person is seeing the world. Suicide is usually
an option when a person can no longer cope with their feelings, or can see no way
out of a difficult situation. Once a person can see the difference between wanting
to die and wanting their feelings or situation to change, you can start problem
solving.
Table 5: Risk assessment for suicide15

Risk factors Low risk Moderate risk High risk

1. Personal Loss and Substantial with
difficulties experiences acute current
•Long-term stress Little resulting in stress
•Short-term stress moderate stress
response
2. Responses and Occasional Daily or more Constant thoughts
resources thoughts often thoughts Indirect
•Coping strategies Can express Some expression expressing
Suicidal thoughts thoughts and feelings
Expression of Some activities Losing touch with
feelings Stable interrupted reality
Other relationships, and Little change in Functioning
•Lifestyle and activities daily life disturbed
behaviour(Stability) Instability in
Networks available Some support some areas
•Networks and willing to network, but not High risk
Family, friends, support as much as person behaviours
work, clubs, support needs Resists help, no
services, other support or not
available
Difficulty with
peers, unstable
relationships etc.
3. Previous suicide Multiple low One of high or
attempt lethality medium
•Lethality None or one of low One medium lethality
•Number of attempts lethality lethality Several recent
Repeated threats attempts
4. Suicide plan
•Details Vague Specifics Planned
•Availability Not available Closely available Means ready now
•Time frame immediately Hours Immediate
•Lethality None Drugs/alcohol, car Hanging, gun,
Low (slash wrists, carbon monoxide
pills)
•Chance of
intervention Others present Other may be
mostly called on No-one around
5. Emotional state
(chronic/acute) Feels low/down Irritable, lonely, Extreme sense of
•Depression sad, worthlessness,
•hopelessness/despair decrease in energy anger, mood
and interest changes, despair
Resources and referral

Resource Contact
Life Promotion Program
Central Australia------------------------------------------- (08) 8952 3311
Top End------------------------------------------------------(08) 8999 4938

Mental Health Services

Central AustraliA--------------------------------------------(08) 8951 7710
Top End------------------------------------------------------(08) 8999 4988

Danila Dilba, Darwin -----------------------------------------------(08) 8936 1717

Congress Social and Emotional Well Being Centre, Alice Springs -----(08) 8951 4444

Wurli Wurlinjang, Katherine ----------------------------------------(08) 8971 0044

Anyingini Congress, Tennant Creek ----------------------------------(08) 8962 2385

Gove Hospital ------------------------------------------------------(08) 8987 0211

Darwin Hospital (will refer to Mental Health Services, Darwin)------(08) 8922 8888

Alice Springs Hospital (will refer to Mental Health Services, Alice Springs)
(08)8951 7777

Katherine Hospital -------------------------------------------------(08) 8973 9211

Tennant Creek Hospital (will refer to Mental Health Services – Tennant Creek)
(08)8952 4399

Alice Springs Youth Accommodation and Support Services, Alice Springs (08)89534200

Anglicare, Top End--------------------------------------------------(08) 8985 0000

Look at strengths and times of coping

Ask about times when the person did not want to die. These are times of coping and
strength and provide an evidence of a person’s ability. Also ask if there have
been times when they have wanted to suicide but didn’t. This is also a time of
coping. Investigate what resources and strategies they used.

Deal with the problem/s

• Make the problems manageable
• Break down all of the pressures that the person is feeling/under
• Separate them: write them down, put them in boxes etc.
• Address each one, starting with the ones that are most easily resolved
• Create a new picture — step by step — with the person
• Work on the strengths that you can identify in the persons life, internal and
external.

Reference material
Bell CC, Clarke DC. Adolescent suicide. Paediatrics Clinics of North America 1998;
45(2):365–80.
Hunter EM. Aboriginal suicides in custody: A view from the Kimberley. A & NZ J Psychiatry
1988a; 22:273–82.
Hunter EM. Aboriginal health and history: power and prejudice in remote Australia.
Melbourne: Cambridge University Press 1993.

References
1. WHO, 2001.
2. National Advisory Council for Youth Suicide Prevention. National action plan for suicide
prevention, consultation draft. Canberra: Commonwealth Department of Health and Aged Care,
1998.
3. Queensland Health. Keep yourself alive: Youth suicide prevention; information for
parents. Brisbane: Dept Health, 1997.
4. National Advisory Council on Youth Suicide Prevention. National action plan for suicide
prevention. Canberra: AusInfo, Dept of Health and Aged Care, 1998.
5. Hunter EM, Reser JP, Baird M, Reser P. An analysis of suicide in Indigenous communities
of far north Queensland. Cairns: James Cook University, University of Queensland, 1999; 34.
6. Graham A, Reser J, Scuderi C, Zubrick S, Smith M, Turley B. Suicide: An Australian
psychological society discussion paper, Australian Psychologist 2000; 35(1):1–28.
7. Yealamucka Health Service, Yamba community. Depression in young people, clinical practice
guidelines. National Health and Medical Research Council, Looking Glass Press, 1997.
8. Mental Health Branch, Commonwealth Dept of Health and Family Services. Youth suicide in
Australia, a background monograph. Canberra: AGPS, 1998.
9. Human Rights and Equal Opportunity Commission. Reports of the national inquiry into the
human rights of people with mental illness. Canberra: AGPS, 1993.
10. O’Kane A, Tsey K. Shifting the balance - services for people with mental illness in
central Australia. Alice Springs: Menzies School of Health Research, 1999.
11. The following figures are derived from NT Coroner’s records.
12. The Life Promotion Team is located in Alice Springs, see Referrals Table. They provide
planning, resources and training to organisations and individuals in the Central Australian
Regions.
13. Martin G, Clark S, Beckinsale P, Stacey K, Skene C. Keep yourself alive. Adelaide:
Foundation Studies, 1997.
14. Pawsy R, Krupinska O. Suicide and depression, In young people at risk: mental health and
homelessness issues. In Fully, Pawsey (eds). Victoria: Dept Child, Adolescent and Family
Psychiatry, Austin Hospital, 1994.
15. Queensland Health. Life Focus: a resource package for workers on the prevention of youth
suicide and self-harm. Woolloongabba: GOPRINT, 1999.
16. Shea CS. The practical art of suicide assessment: a guide for mental health professionals
and substance abuse counsellors. Brisbane: John Wiley & Sons Inc, 1999.
17. Shoalhaven Mental Health Services. Suicide is everybody’s business: lets take a closer
look. NSW: Dept Health, 1997.
18. See background document on Mental Status Examination.
 Asthma in Adults

Author: Dr Emma Kennedy (TEDGP)

Topic Reviewers: Theresa Yee (RAN, Oenpelli); Kaz Knudsen (RAN, WA);
Deb Beaver (RAN, Bagot Clinic); Jan Saunders (Education Manager,
Asthma NT)

The incidence of asthma is increasing worldwide. In Australia a number of

studies have revealed increasing prevalence in adults and children.1,2 There
is considerable regional variation in asthma rates.
The available information on the prevalence of asthma in adults of the
Aboriginal population suggest regional variation, however, there are some
conflicting results. Some studies report a lower prevalence of asthma in
rural Aboriginal adults than in non-Aboriginal adults.3 They suggest that
atopy and airway hyper-responsiveness are dependent on response to
environmental factors, possibly accounting for the difference. Bremner et
al. report a greater impairment of lung function in Aboriginal people in
rural Western Australia than the compared population of rural non-
Aboriginal people; this could be related to inherited characteristics or
the presence of disease, asthma, respiratory infections and other illness.4
In a paper on hospitalisation rates of people with respiratory disease in
WA5, Aboriginal people were admitted to hospital with asthma more
frequently than non-Aboriginal people.
Interestingly, people in non-metropolitan areas also had higher
admission rates for respiratory illness. This may account for some of this
increase, given a high proportion of Aboriginal people live in non-
metropolitan areas.
A diagnosis of asthma may be difficult to distinguish from respiratory
illness caused by infection as they cause similar symptoms. Aboriginal
people have a higher prevalence of other causes of respiratory illness,
especially those linked to cigarette smoking. (See Smoking section of this
manual.) At times the diagnosis of asthma is made incorrectly. Asthma
therapies will be less effective in this instance.6
Asthma affects children and adults. There is much similarity in
diagnosis and management, however, there are some important differences to
consider. In adults the diagnosis is often confused or combined with that
of chronic obstructive airways disease. Asthma is reversible airflow
obstruction, characterised by cough, wheeze, chest tightness and
breathlessness. It is episodic and caused by hyperresponsive airways,
muscle constriction and mucus production.
The diagnosis is best made with spirometry demonstrating reversibility
of the obstruction with salbutamol, a beta agonist, which relaxes smooth
muscle in the bronchioles. Often the diagnosis is attempted by using a peak
expiratory flow metre to estimate response to salbutamol. While this is a
compromise often made in remote areas, spirometry is the ideal diagnostic
aid and becoming less expensive and more available and portable.
 Asthma management guidelines are available and recently updated in
Australia outlining a six-step approach to optimise management.7 This
document refers to important areas for management of asthma in our context
and should be used with reference to the national guidelines.

Other important diagnoses to consider

• Exclude other causes of respiratory illness (Note that there will
often be co-morbidities in Aboriginal populations)
• Infections: more likely to have a temperature, unwell contacts, a
short history of illness
• Aspiration: acute history of cough and wheeze associated with
aspiration
• Heart failure: a history of heart problems, medications like frusemide
or angiotensin converting enzyme inhibitor (ACEi)
• ACEi medications can cause a dry irritating cough as a side effect
• Foreign body inhalation: symptoms associated with inhaling a foreign
body e.g. peanut
• Pneumothorax, spontaneous: a history of acute onset breathlessness,
with some pleuritic chest pain, commonest in young tall thin men
• Pneumothorax, traumatic: acute onset breathlessness and pleuritic
chest pain in association with trauma to the chest
• TB and malignancy may present with a long-standing cough and shortness
of breath

Taking a history
The important features of history identifying asthma are:
• Recent symptoms, particularly nocturnal cough and interference of the
symptoms with daily activities
• Previous asthma exacerbations, especially admissions to hospital and
intensive care units
• Medication use, frequency and doses
• Triggers i.e. dust, pollen, smoke, allergies
• Personal or family history of atopy in terms of hayfever, eczema and
allergy

Treatment is outlined well in the National Asthma Campaign guidelines.

Acute asthma
Presentations vary in severity from mild to severe.

Symptoms and signs

Mild: Some increase in cough and wheeze, particularly at night or after
exercise. This may occur in response to an upper respiratory tract
infection and responds to salbutamol.
Observation reveals slightly raised respiratory rate and expiratory
wheezes on listening to the chest. The person talks in sentences. Forced
expiratory volume (FEV1) and peak expiratory flow rate (PEFR) are >75%
predicted.
Moderate: The cough and wheeze occur throughout the day and night and the
symptoms restrict activities. There is some response to salbutamol,
however, this is temporary. Observation reveals increased respiratory rate,
use of accessory muscles to breathe and wheezes throughout the chest. The
person will speak in phrases and is obviously breathless at rest. FEV1 and
PEFR are between 50–75% predicted.

Severe: Anxious, increase in breathlessness and chest tightness, with a

feeling of being unable to inhale adequately, limited speaking and obvious
increased effort to breathe. May have central cyanosis, using all accessory
muscles of the chest to breathe and may have a silent chest on
auscultation. FEV1 and PEFR <50% predicted and oximetry <92% saturation.

Non-acute asthma
When reviewing asthma in someone who is not acutely unwell, it is important
to consider the following steps modified from the six-step asthma
management plan.9
Assess asthma severity
Assess overall severity when the patient is stable, not during an attack.

Achieve best lung function

Treat until best lung function attained, use lowest dose required to
maintain good control and function.
Maintain best lung function: avoid triggers
Identify and avoid triggers.

Maintain best lung function: use optimal medication

Ensure understanding of the use of medication and use the minimum number of
medications and doses necessary to prevent acute exacerbations.

Treatment of acute asthma8

(Note: slight context-specific variations from the National Asthma
Management guidelines)
Treatment Mild attack Moderate attack Severe and life
threatening attack
Oxygen No 6–15 l/m via mask
to keep oxygen
saturation >90%
Bronchodilator 4 puffs 4 puffs 5 mg salbutamol/2.5
e.g. Salbutamol concurrently via concurrently via ml saline every 15–
via nebuliser or spacer or5 mg spacer or2 x 5 mg 30 mins Ring DMO/GP
spacer salbutamol/2.5 ml salbutamol/2.5 ml re transfer
saline repeat 4- saline repeat 1–
hourly as 4-hourly as
necessary necessary
Ring DMO/GP
Consider transfer
Oral Consider Yes First give IV
corticosteroids hydrocortisone, oral
e.g. prednisolone later
Intravenous Not necessary 200mg stat 200 mg 6-hourly and
steroids e.g. needs DMO/GP review
hydrocortisone
Observations Regular Continuous Continuous
How to assess severity in non-acute asthma10
Symptoms Mild Moderate Severe
Wheeze, Occasional e.g. Most days Every day
tightness, with viral
cough, shortness infection or
of breath exercise
Symptoms at None <once/week >once/week
night
Symptoms on None <once/week >once/week
waking
Required No Usually not Usually
admission to
hospital in last
year
Previous life No Usually not May have a
threatening history
attack (ICU or
ventilator)
Bronchodilator <twice/week Most days >3–4 a day
use eg
salbutamol

FEV1 >80% 60–80% <60%

(%predicted) >90% recent best 80–90% best <80%
Morning peak
flow
In remote areas it is important to consider evacuation plans for people with
moderate/severe asthma.

Develop a plan for times the asthma is worse

Plan how to manage acute attacks and access medical care.
Education and regular review
Ensure understanding of the illness and its treatment.
Emphasise the need for regular review.
Review use of medication and inhaler technique at each visit.

Important: All people with asthma should have a ‘reliever’ medication e.g.
salbutamol, and know how to use it.

Diagnosis
Diagnosis is made on spirometry showing airway obstruction reversible with
salbutamol. The FEV1 increases by 15% or more in adults and children after
reliever (bronchodilator), provided that the baseline in adults is more
than 1.3 litres. Spirometry accurately assesses impairment in lung function
and demonstrates presence and reversibility of airway obstruction to the
patient. A diagnosis of asthma is supported if morning and night time
spirometry demonstrate >15% change. Peak expiratory flow rates (PEFR) are
not as reliable as spirometry as a diagnostic tool, however, in situations
where there is limited facility for spirometry, we use both, peak flows
(the peak expiratory flow increases by 15% after reliever, provided the
adult baseline is more than 300 litres/minute) and therapeutic trials, to
assist diagnosis and management in adult asthma. In this situation, using
the PEFR rather than the spirometer, it is most valuable when attention is
paid to achieving maximum effort for three results, before and after
bronchodilator. However, given the increasing portability of spirometry, it
may be possible to arrange spirometry in the remote setting in the future.
PEFR are helpful for early recognition of deterioration, when symptoms
are intermittent, asthma is unstable or treatment is being altered. They
are also useful for people who have symptoms but who have normal spirometry
with no significant reversibility.
For children or others unable to reliably use a spirometer or peak flow
metre, therapeutic trials may support the diagnosis.11
It is important to differentiate asthma from chronic obstructive
pulmonary disease; the treatment options overlap, however the response to
treatment may differ. It is common for someone with COPD to report they
have ‘asthma’, however there is less reversibility of their airway
obstruction and therefore less response to relievers. In practice the
prescription of reliever medication is often for airway responsiveness and
relief of symptoms regardless of the diagnosis.

Triggers
There is evidence that smoke inhalation exacerbates asthma.12 Moving camp
fires away from houses and reducing the cigarette smokers within range of
the person with asthma can reduce the number of asthma exacerbations, i.e.
smokers smoke outside dwellings. Recent research in the Top End showed
higher rates of hospital presentations with asthma during peak fire
season.13
Knowledge of the effect of triggers, i.e. awareness of pollen and dust
causing hayfever, on the pattern of asthma, will assist the person to
preempt and treat asthma early.

Education
‘Self-management education (training in management of asthma individualised
to the patient) involving a written action plan, self-monitoring (peak
expiratory flow measurement or symptom diaries) and regular medical review
leads to improvements in health outcomes and should be offered to adults
with asthma.’14 It is clear that adequate management of asthma in the primary
care setting makes a difference. Primary care is the ideal place to
establish the person’s concerns and clarify their knowledge, the importance
of monitoring their asthma at home, becoming familiar with the use of peak
flow metres and equipment used for treatment, and appropriate management of
asthma symptoms. All patients require an individualised regime to assist
them to control their asthma symptoms and tailor their use of medication.
There is a guide to assist health professionals to achieve this.15
Simply imparting information only, (limited asthma education) has
limited benefit in reducing the frequency of hospital admissions, doctor
visits or medication use but may play a role in improving patient’s
perceptions of their symptoms. For adults at high risk there is reduction
in emergency department visits.16 The pertinence of this must be emphasised
and health professionals in remote Northern Territory must consider the
most appropriate way to communicate culturally, assisting the population to
understand the relationship between symptoms and signs, triggers,
underlying pathology and management.
Treatment
The goals of treatment are: to minimise daily experience of symptoms; to
reduce the frequency of exacerbations by maintaining medication and by pre-
empting exacerbations and managing them promptly; and using the minimum
medication to achieve this.
There are three groups of medication and multiple options for delivery:
1. Relievers
beta2 agonist salbutamol (Asmol, Ventolin, Respolin), metered dose
inhaler (MDI) or nebules
Terbutaline (Bricanyl), turbuhaler or nebules
Ipratropium (Atrovent), MDI or nebules

2. Preventers
Steriods, beclamethasone (Qvar), MDI, autohaler
Budesonide (Pulmicort), turbuhaler, MDI
Fluticasone (Flixitide), autohaler
Prednisolone tablets and intravenous hydro-cortisone, short courses for
exacerbations
Sodium chromoglycate (Intal), MDI
Nedocromil sodium (Tilade), MDI
Leukotiene antagonists as oral medication
3. Symptom controllers
Long-acting beta2 agonist, Salmeterol (Serevent), MDI, accuhaler
eformoterol (Foradile), aeroliser and turbuhaler

Symptom controllers, such as long-acting beta2 agonists, salmeterol and

eformoterol, are commenced in patients with frequent nocturnal asthma
already receiving treatment with maximal doses of inhaled corticosteroids.
When added to inhaled steriods there is an associated improvement of lung
function and symptoms.17 These should be used after review by a medical
practitioner.
There are a number of issues pertinent to the remote setting in
Australia — availability of medication, simplicity of instruction to assist
management in emergencies, ease of delivery of medication to avoid
complications of malfunctioning equipment and access to medical advice and
management. For simplicity it is important to consider the first-line
medications in detail and recognise the potential for treatment with
alternatives, seeking medical advice as appropriate.

First-line medications
Relievers
Salbutamol and terbutaline, acute relief of symptoms via inhaler or
nebuliser.
Notes:
1. Spacer versus nebuliser: for acute asthma attacks, spacer devices used
with inhalers are as effective as nebulisers in delivering
medication.18 This is critical as nebulisers may malfunction or function
poorly and therefore deliver less medication. The advantage of a
nebuliser is the opportunity to use oxygen in the delivery of the
medication for severe asthma, however, oxygen can be delivered nasally
or intermittently via mask together with salbutamol via spacer.
2. There is some evidence to suggest, in mild intermittent asthma, using
salbutamol regularly rather than in response to symptoms is associated
 with deterioration in FEV1.19 Therefore it is important to instruct
appropriately.
3. There is some evidence in acute asthma management in hospitals that
treatment with continuous beta2 agonist seems to be associated with
greater improvement in FEV1, when compared with intermittent
treatment.20 (Note that there were no systematic reviews and the
studies are small)
4. Adding ipratropium (Atrovent) to salbutamol in treatment of severe
exacerbations can improve response21,22 however there is little
evidence for its use in less severe episodes.

Treatment of non-acute asthma (adapted from ref 23)

Severity Common features Maintenance therapy
Very mild Episodic Short-acting beta agonist e.g. Salbutamol
for use as necessary
Sodium cromoglycate for exercise induced
asthma
Mild Occasional Low dose inhaled corticosteroid regularly
symptoms (up to (e.g. 400 mcg/day beclomethasone or
2/wk) budesonide; 200 mcg/day fluticasone)
Exacerbations >6–8 Or use nedocromil sodium or sodium
weeks apart cromoglycate, but if control of symptoms
Normal FEV1 when not achieved use low dose corticosteroid
asymptomatic Short-acting beta agonist prn
Moderate Symptoms most days Inhaled corticosteroid (e.g. 750–1600
Exacerbations <6–8 mcg/day beclomethasone or budesonide;
weeks apart 400–750 mcg/day fluticasone)
affecting daytime Short-acting beta agonist prn (a long
activity and acting beta agonist could be added here
sleep; and lasting after review with DMO/GP)
several days Oral corticosteroid may be required in
acute exacerbation to reduce the chance
of deterioration
Severe Persistent High-dose corticosteroid (up to 2000
Limited activity mcg/day beclomethasone; 2400 mcg/day
level budesonide; 1000 mcg/day fluticasone)
Nocturnal symptoms Plus long-acting beta agonist
>1/wk Short-acting beta agonist prn
Frequent need for Consider addition of leukotriene receptor
emergency antagonist e.g. montelukast (Singulair)
treatment in discussion with DMO/GP
Oral corticosteroid when appropriate
Preventers
Corticosteroids — beclamethasone inhaler, budesonide, oral prednisolone and
intravenous hydrocortisone.
Sodium cromoglycate — effective in mild asthma as a regular dose, and
before exercise in exercise induced asthma.
Notes:
1. The choice of preventer depends on the severity of asthma and the
patient’s regular medications. (see table below re maintenance
treatment).
2. In maintenance therapy commence inhaled steroids if the symptoms of
asthma are occurring more frequently than twice/week.
3. Commence with inhalers using oral and intravenous steroids in acute
exacerbations and for short periods only.
4. In acute asthma, there is some evidence that systemic corticosteroids
taken early in the exacerbation reduce rates of hospital admission and
relapse.24 The initiation and duration of use of systemic steroids will
depend on the individual and the nature of the exacerbation. This may
mean a lower threshold for treatment in remote areas treating
proactively to prevent deterioration and the need for transfer.
5. Leukotriene antagonists added to use of beta2 agonists for mild-to-
moderate persistent asthma, reduce asthma symptoms and beta2 agonist
use. There is a systematic review showing no significant difference in
rate of exacerbations between leukotriene antagonists and inhaled
corticosteroids however corticosteroids significantly increased
quality of life, lung function and symptom control.25 At this stage use
of inhaled steroids is preferable for simplicity of asthma management
in remote settings and should be continued even if control is improved
with the addition of a leukotriene receptor antagonist.

The other medications listed are used in patients who have asthma less
optimally treated by first-line measures. These are likely to be less
familiar to staff and communities and require careful monitoring and
education in their use. The recent update on asthma management by the
National Asthma Campaign is a helpful resource to add to this document.

Issues for remote settings

1. Which device do I recommend?
A metered dose inhaler is more effective when used with a spacer. This
should be encouraged as much as possible, and particularly for severe
attacks. Medication is delivered effectively via a spacer and all clinics
should have one available for management of acute asthma.
Turbuhaler or accuhaler delivery of medication is more easily managed
than the coordination of a metered dose inhaler, unless the metered dose
inhaler is used with a spacer. Turbuhalers and accuhalers are much less
bulky to carry around and also give good medication delivery to the lungs
when used correctly. In the wet tropics, Turbuhalers tend to absorb too
much moisture and may not function well.
Regularly check the device is used correctly.

2. Do people become psychologically dependent on their puffers, over-use

the nebuliser or beta agonists?
This is a risk for any one with breathing difficulty, as the experience can
be very frightening. The more a person understands their symptoms and the
mechanism producing them the more they understand the treatment, therefore
using medication appropriately.

3. How many people are using the correct technique?

This is an issue managed optimally with good communication assisting people
to connect their symptoms with an understanding of how the lungs work and
the use of the medication and delivery devices.

4. Continuation of smoking despite the diagnosis of asthma?

This is a universal issue. Asthma can be a motivator to cease smoking. See
the smoking section for the importance of brief interventions etc.

5. In acute presentations of asthma, health professionals in remote

locations must consider the patient’s prognosis over the following 24
hours, acting to evacuate before deterioration. The assessment should be
made on the severity of the presentation, response to medication on
immediate treatment and the patient’s past history.

6. Primary health care is an ideal environment for optimal management of

asthma.
The contact with health professionals at community level can initiate and
support the education, prevention and treatment to maintain optimal health.

7. Maintenance of vaccination for pneumococcal and influenza vaccines is

important in prevention of infectious exacerbations/ complications of
asthma.
Specialist review and support is important for people with frequent
exacerbations and severe disease.

References
1. Ruffin R, Wilson D, Smith B, Southcott A & Adams R. Prevalence, morbidity and
management of adult asthma in South Australia. Immunology and Cell Biology 2001;
79:191–4.
2. Peat JK, van den Berg RH, Green WF, Mellis CM, Leeder SR, Woolcock AJ.
Changing prevalence of asthma in Australian children. British Medical Journal 1994;
308:1591–6.
3. Veale AJ, Peat JK, Tovey ER, Salome CM, Thompson JE, Woolcock AJ. Asthma and
atopy in four rural Australian Aboriginal communities. Medical Journal of Australia
1996; 165:192–6.
4. Bremner PR, de Klerk NH, Ryan GF, James AL, Musk M, Murray C, Le Souef P,
Young S, Spargo R, Musk W. Respiratory symptoms and lung function in Aborigines from
tropical Western Australia. Am Journal Respiratory and Critical Care Medicine 1998;
158:1724–9.
5. Williams P, Gracey M, Smith P. Hospitalisation of Aboriginal and non-
Aboriginal patients for respiratory tract diseases in Western Australia, 1988–1993.
International Journal of Epidemiology 1997; 26(4):797–805.
6. Peat JK, Veale A. Impact and aetiology of respiratory infections, asthma and
airway disease in Australian Aborigines. Journal of Paediatric Child Health 2001;
37:108–112.
7. Asthma Management Handbook. National Asthma Campaign 1998, Melbourne,
Australia.
8. ibid.
9. ibid.
10. ibid.
11. ibid.
12. Goldsmith CW & Kobzik L. Particulate air pollution and asthma: A review of
epidemiological and biological studies. Reviews on Environmental Health 1999;
14(3):121–34.
13. Johnston F 2002 Darwin, NT (personal communication).
14. Gibson PG, Coughlan J, Wilson AJ, Abramson M, Bauman A, Hensley MJ, Walters
EH. Self-management education and regular practitioner review for adults with asthma
(Cochrane Review). In: The Cochrane Library, Issue 3. Oxford: Update Software, 2001.
15. Asthma adherence a guide for health professionals. National Asthma Campaign
1999. Dept Health and Aged Care, Melbourne, Australia.
16. Gibson PG, Coughlan J, Wilson AJ, Hensley MJ, Abramson M, Bauman A, Walters
EH. Limited (information only) patient education programs for adults with asthma
(Cochrane Review). In: The Cochrane Library, Issue 3. Oxford: Update Software, 2001.
17. Shrewsbury S, Pyke S, Britton M. Meta-analysis of increased dose of inhaled
steroid or addition of salmeterol in symptomatic asthma (MIASMA). British Medical
Journal 2000; 320:1368–73.
18. Cates C. Holding chambers versus nebulisers for beta2 agonist treatment of
acute asthma. (Cochrane Review). In: The Cochrane Library, Issue 3, 2000.
19. Cates C, Fitzgerald M. Asthma. Clinical Evidence June 2001;
20. ibid.
21. Rodrigo G, Rodrigo C, Burschtin O. Ipratropium bromide in acute adult severe
asthma: a meta-analysis of randomised controlled trials. American Journal Medicine
1999; 107:363–70.
22. Rodrigo GJ & Rodrigo C. First line therapy for adult patients with acute
asthma receiving multiple dose protocol of ipratropium bromide plus albuterol in the
emergency department. American Journal Respiratory Critical Care Medicine 2000;
161:1862–68.
23. Asthma Management Handbook. National Asthma Campaign 1998 Melbourne,
Australia.
24. Cates C, Fitzgerald M. Asthma. Clinical Evidence June 2001.
25. ibid.
 Chronic Disease Management
in Health Centres

Editor: In August 2001 a group of experienced NT physicians, DMOs and

editorial committee members met to discuss the developments in chronic
disease management to be included in the fourth edition of the CARPA STM.
These editorial comments below are based on the views of this locally
relevant expert group.

Things we wish to promote through the CARPA STM

• The value of ‘keeping on trying’ in people with high absolute
cardiovascular risk, as they will have highest potential health gain.
This means that, though it may be tempting to give up trying to make
progress with managing chronic health conditions or health threats with
some individuals, if they are at high risk of suffering complications
of their condition the health service should continue to offer and
encourage a useful relationship with the person.
• Focus on positive things like stopping smoking rather than be overly
focussed on poor glycaemic control.
• Emphasise the benefit of once-a-day doses. (To the extent of removing
captopril from the formulary).
• Reminder that people can take all their medications at the one time of
the day e.g. night.
• Encourage a step-wise approach to the management and engagement of
people with chronic diseases, don’t try to do it all at once.
• Encourage making plans for follow-up, building relationships.
• Time management tips.
• Encourage training for staff on managing multiple agendas and tips
that help fit opportunistic health checks into other presenting issues.

Tips
Some people have developed useful ‘stories’ for talking about and
explaining chronic diseases. These might usefully be collected and offered
as part of staff training. For example, glycaemic or lipid control can be
discussed with many men as being like a carburettor in an engine. Smooth
running of the engine needs the right types of fuel (food), and a faulty
carburettor can be helped with medicines but can not be replaced with a new
one, etc. In time damage can build up in the engine (body) even though it
appears to be running well (asymptomatic).
• If it is hard to get people into town, try case-conferencing and care
planning by phone. Use specialists over the phone.
• Plan care and referrals so they need less specialist reviews in town
(e.g. copy of review pathology to specialists followed by phone
review).
• Try to make personalised care plans based on negotiation with the
patient and discussion of pros and cons of options.
• Save time by avoiding a stack of meaningless BP checks and BGL checks
(without putting the clients off).
 • The person is not the disease, depersonalise the disease. Avoid value
statements and words, e.g. good, bad, better. Better to use words like
helpful, protecting, risky, safer.

Useful chronic diseases resources

Chronic Diseases Network NT
One stop information shop on chronic diseases related topics. If you are
after a poster, policy, program, reference, or video and have not been able
to track it down give the network a call on (08) 8922 8280 and they will do
their best to meet your request.
Central Australian (NT Department of Health and Community Services)
chronic disease team at Health Development has a standardised chronic
disease resource kit that is currently being distributed to all health
centres.

The Australian Kidney Foundation (AKF) resources

• For Information from the AKF NT office contact Toni Kelly on (08) 8945
4047.
• For more information from the AKF WA office contact Jen O’Rielly on
(08) 9322 1354.
• The Kidneys: An excellent educational flip chart for Aboriginal
communities and health workers. Produced by the Australian Kidney
Foundation WA. Free!
• Fifth edition of Living with Kidney Failure, a book for patients going
onto dialysis. For more information contact the AKF NT.
• Water Works Your Kidneys, a lower primary teaching resource produced
by the AKF WA. For more information contact the AKF WA. Free!
• Kidney Disease: preparing for dialysis, a video for remote Aboriginal
people. This video is aimed at Indigenous clients preparing for
dialysis treatment and highlights the importance of dialysis and what
to expect in the city. Free from AKF WA.
• The AKF also has an extensive range of useful brochures or fact
sheets. These include ones on diet, diabetes and kidney stones.

Nightcliff Renal Unit

• The Nightcliff Renal Unit has developed excellent local resources,
including a video Kidney Problems: stories about choices, that provides
basic information about different choices in seven languages.
• The unit also has comprehensive training manuals for AHWs and RNs.
• For more information contact the Nightcliff Renal Unit on (08) 8948
9000

Healthy Skin flip chart and video

• Launched May 2001 at Galiwin’ku. This great A3 chart, ‘Healthy Skin
Story’, is an initiative that grew out of the need for educational
resource material to support community education and assist communities
to run ‘Healthy Skin’ programs.
• For more information contact Michelle Dowden, Galiwin’ku population
health nurse on (08) 8997 9031.
Scabies flip chart
• This flip chart is a pictorial presentation on the causes and
treatment of scabies.
• For more information contact Gabbi at the CRCATH on (08) 8922 7861.

The Heart Foundation

• The Heart Foundation has a great range of resources that include
Listen to your heart, Heart story and the Tobacco book.
• For more information contact the Heart Foundation on (08) 8981 1966.

Pongi Pongi (tobacco) book

• The Pongi Pongi (tobacco) kit is a kit of health promotion resources
about tobacco developed by Tiwi communities/Bagot community/NHF and
Menzies School of Health Research.
• For more information contact Rowena Kalikajaros on (08) 8981 1966.

Aboriginal Resource and Development Services Inc (ARDS)

• Telephone Darwin Office (08) 8982 3444, or visit their website at
www.ards.com.au
• ARDS have an extensive range of publications and information papers.
They have also recently released a scabies video in Aboriginal language
on the prevention and treatment of scabies. 30 minutes. Cost $33.00.

Asthma Foundation
• For information on the following resources contact the Asthma NT
office on (08) 8922 8827.
• Short wind poster and flip chart/educational resource.
• Healthy living: controlling your asthma video.
• Range of fact sheets and brochures.

Diabetes Australia NT
• DANT also has an extensive range of resources for consumers and
providers of chronic disease programs, such as healthy eating recipes.
• For more information ring them on (08) 8927 8488.
• Healthy Shopping Guide, $2.20
• Keeping Families Strong, One Tucker, One Family, an A3 flip chart for
health professionals.

OATSIH
• The Office of Aboriginal and Torres Strait Islander Health has a range
of useful publications, such as the National recommendations for the
clinical management of alcohol related problems in Indigenous primary
care settings.
• For information call (02) 6289 4967 or visit their website at
http://www.health.gov.au/oatsih/pubs.htm

Cooperative Research Centre for Aboriginal and Tropical Health (CRCATH)

• The CRCATH has an extensive range of occasional papers and research
reports such as: Indigenous Australians and Tobacco: A literature
review and Forgetting Compliance: Aboriginal Health and Medical
Culture.
• For more information visit the website at www.ath.crc.org.au or phone
(08) 8922 8841.
Menzies School of Health Research
• MSHR has a wide range of useful publications including: Environmental
Health Handbook and Rheumatic Fever Information Package.
• Ring (08) 8922 8624 or visit their website for a list of publications
at
www.menzies.edu.au/ocpapers/index.html

Arthritis and Osteoporosis NT

• This association regularly runs the Healthy Living Self-Management
course that assists people with chronic diseases to better manage their
condition. They also run leaders courses that train people to run the
courses. There are also useful information pamphlets.
• Call (08) 8948 5235 between 10.00am–2.00pm.

Australian Institute of Health and Welfare

• There are a number of excellent publications including Heart Stroke
and Vascular Diseases Australian Facts 2001.
• For more information call (02) 6244 1032 or visit
http://www.aihw.gov.au

The Bush Book

• The Public Health Bush Book has been written as a resource for people
who work with remote Aboriginal communities in the Northern Territory.
It has been written by people who have worked in, or with, remote
community health care teams over many years, and relates their
accumulated learning to published national and international evidence.
• To order, contact Health Promotion Policy and Program Development,
Health House, PO Box 40596, Casuarina 0811 or fax to (08) 8999 2420.

DHCS website
• DHCS website (http://www.nt.gov.au/dhcs/) has access to a huge range
of information, including the Bush Book, statistical reports, the
Health & Welfare of Territorians and the Chronicle.

Bush Telegraph
• The Bush Telegraph is a website that has comprehensive information
about NT communities and the types of services available.
• Visit it at
http://finke.nt.gov.au/BushT/Community.nsf

DHAC Mental Health Branch

• Resources brochures at
http://www.mentalhealth.gov.au

Centre for Disease Control (CDC)

• Recently released discussion paper on anaemia in Aboriginal children
and the new treatment of anaemia in Aboriginal children. Also have wide
range of information sheets on communicable diseases, and are revising
the scabies treatment protocol.
• For more information contact Darwin CDC on (08) 8922 8044.

Living With Alcohol and Tobacco Action Project

• LWA & TAP has a number of valuable resources that include: Choose
Yourself education kit, Cheers, and Taking Care of Business.
 • For more information call (08) 8922 8704.

HEATworks
• HEATworks has a range of pamphlets, magnets, badges, books, posters
and videos on chronic disease related topics, including diabetes, and
cardiovascular disease. They have pamphlets for desert mob and salt-
water mob.
• Call for more information.
Kimberley Aboriginal Medical Services Council Inc Health Promotion Unit
Ph: (08) 9193 6043
Fax: (08) 91922500
Email: heatworks@wn.com.au

Nganampa Health Council

• Nganampa has a variety of useful resources that include:
Videos on environmental health, child’s health, food and work
Audio cassettes (including The Shower Block song)
Posters on women’s health, learning to stay well
T-shirts
Reports and books
• Call Nganampa Health Council on (08) 8952 5300 or fax (08) 8952 2299.
 Chronic Lung Disease

Authors: Rosemary Lee (DHCS, Remote Health); Graeme Maguire (Menzies School of
Health Research)

Topic Reviewers: Kaz Knudsen (RAN, WA); Dave Corstorpan (RAN, Nyirripi Clinic);
Dr Penny Roberts-Thompson (Nguiu)

Background
Chronic obstructive pulmonary (lung) disease (COPD) is a major contributor
to global and local morbidity and mortality. At a global level COPD is
responsible for 4% of all deaths and over 80% of those due to respiratory
disease.1 In 1998 2.2 million people died as a direct result of COPD, a
number equivalent to the number of deaths due to HIV.1 COPD is, however, a
chronic disease from which those afflicted do not usually die immediately.
It is estimated that worldwide over 28 million people or 2.1% of the
world’s population suffer from COPD.1 A World Bank/World Health Organization
study estimated that COPD was the twelfth ranked burden of disease in 1990
and is expected to rise to fifth place by the year 2020. Thus, these deaths
mask the far greater problem posed by COPD, namely its influence on quality
of life, families and careers, economic productivity, and limited health
resources.
COPD is, however, an even greater cause of morbidity and mortality for
Indigenous Australians. A study of hospital admissions in Western Australia
between 1983 and 1991 revealed that age-standardised hospital admission
rates for COPD were 8.8 and 4.5 times greater for Aboriginal women and men
respectively compared with non-Aboriginal Western Australians.2 Similar
overrepresentation was seen in a Northern Territory (NT) study by Plant and
co-workers who showed that in 1988 age-standardised hospital admission
rates for COPD were 4.2 and 1.7 times greater for Aboriginal women and men.3
In addition, this over representation of respiratory morbidity, as
represented by hospitalisations, became more marked over the period from
1979 to 1988, especially for women. This same over-burden of poor
respiratory health was reflected in causes of mortality in Aboriginal
adults in the NT. A study by Cunningham and others of causes of death of
Aboriginal people in the NT between 1979 and 1991 showed that COPD
accounted for 10% of excess mortality for women (the greatest contributor
of any of the studied causes) and 7% of excess deaths for men (the third
most important cause after motor vehicle accidents and pneumonia-
influenza). Further, the standardised mortality ratio for COPD were 22.4
and 14.8 for Aboriginal women and men respectively compared with non-
Aboriginal Northern Territorians.4 A later review of Indigenous mortality in
the NT by Dempsey and Condon5 demonstrated that this health disparity had
persisted until 1997. Thus, COPD is a major cause of global morbidity and
mortality and is a significant factor in the hospitalisation of NT and WA
Aboriginal adults and the premature death of NT Aboriginal adults.
The pathophysiology of COPD has undergone extensive study since the
seminal work of Doll and Hall and the British Doctors Study, which
demonstrated the association between tobacco consumption and death from
COPD.6–10 This was followed by Fletchers’ later study that illustrated the
decline in lung function seen in 15% of tobacco smokers.11,12 The
demonstration of an association between tobacco smoking and COPD prompted
the Lung Health Study which showed that smoking cessation was effective in
reducing the decline in lung function seen in cigarette smokers with
airflow obstruction.13 Whilst tobacco consumption has been identified as the
major aetiologic factor in COPD there is increasing evidence that
environmental pollution14,15,16 (especially wood/biomass fires), abnormalities
in antiproteases (including α1-antitrypsin deficiency), infections in early
life17,18,19 and intrauterine growth impairment/low birth weight17,20 may all play
a variable role in the development of this condition.
There is continuing potential confusion relating to the management of
COPD in contrast to that of asthma. Asthma is predominantly a condition
associated with Type 1 hypersensitivity, eosinophilic inflammation, airway
smooth muscle hyperreactivity and hypertrophy, airway wall fibrosis,
mucosal oedema and mucous plugging. In contrast, COPD is predominantly
associated with an airway neutrophilia, mucosal oedema and a loss of airway
support with premature airway closure on expiration. It is therefore not
surprising that drugs which have been shown to be effective in asthma —
including short- and long-acting bronchodilators, inhaled steroids, and
leukotriene receptor antagonists — may not be similarly effective in COPD.
Nevertheless, health providers are often provided with ambiguous messages
particularly from pharmaceutical companies. These guidelines therefore aim
to illustrate where agents typically utilised in asthma may be helpful in
COPD whilst seeking to de-emphasise the importance of inhaled steroids and
newer agents.
These guidelines for the management of COPD aim to provide a framework
for the management of COPD and chronic lung disease, particularly for
Indigenous Australians. They have been drafted with the recognition that
delivery and access to health care in remote communities in Australia often
poses unique and challenging issues to health providers, patients, and
their carers. These guidelines do not aim to be a systematic review of all
potential therapeutic interventions for COPD. Rather, they attempt to use
evidence to most efficiently utilise limited health resources. Whilst we
have outlined what we believe is best practice we are cognisant that it may
not always be possible to provide everything that is suggested here.
Nevertheless, we believe that these guidelines in turn may be useful in
advocating for such resources when they are not available.
Finally, an important caveat is that guidelines such as this, whilst
seeking to be comprehensive, do not aim to present all knowledge pertaining
to COPD nor every possible therapeutic or preventive option. Thus,
individual patients may sometimes be managed in ways that do not reflect
what is outlined here. Such differences in clinical practice are legitimate
as long as they are based on evidence gleaned from clinical trials or
proven therapeutic response in individual patients.

Definition (including rationale for the inclusion of

bronchiectasis)
Chronic Obstructive Pulmonary Disease (COPD) is a slowly progressive airway
disease that produces a decline in lung function that is not fully
reversible. The loss of lung function (airflow limitation) is associated
with an abnormal inflammatory response of the lungs to noxious particles or
gases. The characteristic symptoms of COPD — cough, sputum production and
shortness of breath (dyspnea) on exertion — often precede the development
of COPD by many years, although not all individuals with cough and sputum
production develop COPD.
The diagnosis of COPD is based on the patient having a history of
exposure to risk factors and the presence of airflow limitation that is not
fully reversible with treatment, with or without the presence of symptoms,
such as chronic cough and sputum production. Whilst tobacco is the major
risk factor for development of disease 5% of people with COPD in the
developed world have no significant history of tobacco consumption. This
may be even higher in the developing world populations and in Indigenous
Australians. Thus, whilst a lack of a history of tobacco use should prompt
a search for another cause of airflow obstruction it should not exclude the
diagnosis.
The inclusion of bronchiectasis under the guise of COPD may surprise
some readers. In remote communities the differentiation between COPD and
bronchiectasis is often not possible and the evidence for any difference in
management is minimal. Certainly there are rare congenital causes of
bronchiectasis (e.g. cystic fibrosis and immune deficiencies) that may
warrant different management. Such patients should be identified by an
earlier onset of disease, especially in the setting of a limited history of
tobacco consumption, and should be referred for specialist attention.

Existing guidelines
Existing guidelines for the management of COPD include those developed by
the American21 and British Thoracic Societies.22 More recent initiatives have
been the Global COPD guidelines developed as an international collaboration
involving representatives from a broad range of countries, including
Australia, with the National Heart, Lung, and Blood Institute and the World
Health Organization23 and the first draft of the Australian COPD management
guidelines developed as an initiative of the Thoracic Society of Australia
and New Zealand.24 In general, these show a great deal of concordance and
the general outline employed by the British, GOLD and Australian guidelines
is utilised here.

Aims and principles of management

These are: (1) Assessment and monitoring of disease; (2) Reduction of risk
factors/secondary prevention; (3) Managing chronic disease/long-term
management; and (4) Managing acute exacerbations of chronic disease.

1. Assessment and monitoring of disease/grading of severity

COPD can be defined as mild, moderate or severe based on the degree of
airflow obstruction determined by spirometry. The grading of severity in
existing guidelines varies slightly, but all rely on the finding that
Forced Expiratory Volume in one second (FEV1) as a percentage of the
predicted value in a comparable well population – (see Spirometry, below)
and the ratio of this with the Forced Vital Capacity (FVC) are an indicator
of the risk of premature death, and correlate with functional impairment.25–30

Spirometry
Spirometry has three common uses in COPD. First, in diagnosing and grading
the severity of COPD, second in monitoring progression and third in
considering alternative diagnoses for airflow obstruction, particularly
asthma. The grading of severity is dependent on spirometry values. Values
of FEV1 are compared to ‘normal’ values of lung function obtained from a
‘healthy’ population controlling for age, gender and height. The ratio of
measured and predicted value is then calculated ([measured]/[predicted] x
100%). In the case of Aboriginal Australians in the NT the most
representative values are those of Veale et al.31 though other normal values
for Indigenous Australians in Far North Queensland32 and northern Western
Australia33 are available. These values were derived from populations of
Aboriginal Australians in the Centre of the NT and in Far North Queensland.
A similar study in the Top End of the NT34 demonstrated close concordance
with these results. For non-Indigenous Australians the values of Knudson35
or Gore36 are most commonly used, and values for Torres Strait Islanders are
likely to be most consistent with those derived from coastal residents of
PNG.37
An additional use of spirometry is to determine the rate of disease
progression (indicated by the average annual decline in FEV1) and thus to
predict subsequent morbidity. The average rate of decline in FEV1 with age
is approximately 20 ml/year.12 Cross-sectional studies in Indigenous31,34 and
non-Indigenous Australians35,36 demonstrate a presumed rate of decline. In the
setting of COPD this increases and is typically over 60 ml/year.12 Taking
into account acceptable intra-subject variability (<200 ml of FEV1[38]) it
can be seen that spirometry should be repeated every two years in order to
determine the rate of decline in those who are declining at a high rate and
therefore most at risk of rapidly progressing to more severe disease and
its associated morbidity.
The final benefit of spirometry is to identify individuals who have
significant reversibility/increase in FEV1 after the administration of
bronchodilator. Reversibility with bronchodilator is often used as a
defacto measure of airway hyperreactivity, and thus asthma. Although it is
not within the scope of this document to explore the complexities of this
association it is nevertheless important to note that this is not the case.
In reality asthma is a diagnosis made by a combination of symptoms,
variability in lung function over time and a response to anti-asthma
medication. Epidemiologic studies have utilised a definition of asthma as
symptoms and underlying airway hyperreactivity and a lack of significant
airway hyperreactivity (to histamine, methacholine or hypertonic saline)
can be used to eliminate a diagnosis of asthma. Nevertheless, many patients
with airway hyperreactivity will not have a clinical diagnosis of asthma
and it is traditional dogma that advanced airflow obstruction associated
with asthma may not be immediately reversible with bronchodilators. What
this means is that you cannot necessarily exclude asthma if there is a lack
of immediate reversibility with bronchodilators.
If spirometry is to be clinically useful it must be performed in a
consistent and validated manner using a properly calibrated spirometer with
strict adherence to protocols regarding reproducibility and patient
technique.38 In so doing individual patient results can be generalised to
previous studies of treatment or prognosis. Put another way, inaccurate and
unreliable spirometry is likely to be worse than no spirometry at all.
Adequate spirometry is achievable in a community setting. A cross-sectional
survey of respiratory health in a remote NT Aboriginal community
demonstrated that 93% of adult residents could perform adequate
spirometry.39
Peak expiratory flow rate (PEFR)
PEFR is an inferior method to diagnose COPD compared with spirometry. In
general, it cannot be recommended that Wright peak flow meters be used as a
diagnostic tool as they provide little information relating to patient
technique or effort. Further, although PEFR is correlated with FEV1, intra-
subject variability is greater even in the setting of close attention to
technique. As a result normal values for PEFR are broader for any given
gender, height and age. In a cross-sectional study of residents of a remote
Aboriginal community in the NT only 52% of the variability in FEV1 was
explained by PEFR, and in those without symptomatic respiratory disease
age, gender and height explained only 40% of the variance in PEFR compared
with 60% for FEV1.34
Nevertheless, in Aboriginal Australians a value of PEFR >400 l/min has a
negative predictive value for a low FEV1 (<80% predicted) of 94% (95% CI
91–97%) irrespective of age, height or gender.34 Thus, if spirometry were
not readily available a PEFR of >400 l/min would reasonably exclude the
diagnosis of COPD. Lower values would, however, require confirmatory
testing with spirometry to make or exclude a diagnosis of COPD.

2. & 3. Reduction of risk factors/ Managing chronic disease

Monitoring frequency
There is no proven optimal frequency of review. In general, the frequency
of review will be determined by health system resources, the severity of
disease, perceived patient knowledge of disease and treatment, whether
continuing to smoke, the number and complexity of interventions and the
presence of co-morbid conditions.
A general recommendation would be that those with mild/moderate disease
should be reviewed annually, and this could be timed with the annual
influenza vaccination. Review should occur more frequently, especially if
subjects have previously demonstrated a willingness to consider smoking
cessation.
Subjects with severe disease, who are on long-term oxygen therapy or who
are having therapeutic venesection, should be reviewed at least every six
months to reemphasise smoking cessation if continuing to smoke, to review
and address knowledge of and adherence to therapy and to monitor and
address environmental issues — including the impact of their respiratory
disease on self-caring and carers. If possible this group of patients
should also have their long-term care plan discussed annually as part of a
multidisciplinary review in association with local health providers,
physiotherapy, occupational therapy and a specialist physician.

Care plans
The development of care plans for all patients with chronic diseases as
part of multidisciplinary care involving patients and their carers should
be encouraged. These would be particularly of benefit for patients with
moderate or severe disease and for those with multiple additional chronic
medical problems. Such care plans should seek to address long-term
management, including monitoring frequency and an action plan for acute
exacerbations.

Investigations
Spirometry
See above
CXR
A single plain PA chest X-ray should be performed at diagnosis. Although
this may support a diagnosis of COPD/bronchiectasis (evidence of
hyperexpansion, emphysema or airway dilatation/thickening) it is
predominantly utilised to exclude conditions that may have similar clinical
presentations. These include chronic infections (e.g. tuberculosis) and
interstitial lung disease. Subsequent CXRs may be required if there is a
sudden change in symptoms (especially haemoptysis), loss of weight
(TB/malignancy), or chest pain (malignancy/pneumothorax) or if patients
present with an acute exacerbation with atypical features (haemoptysis,
chest pain). Patients who have a severe acute exacerbation necessitating
hospitalisation will usually have a CXR on admission, particularly to
exclude pneumonia. There is no current evidence or consensus to suggest
that screening CXRs or CT scans are useful for the early detection of lung
cancer in this setting or a population with a history of tobacco
consumption.

ECG
An ECG should be performed at diagnosis to provide a baseline for later
assessments and to specifically look for evidence of right ventricular
hypertropy/cor pulmonale. Further, an ECG may provide evidence to support
an alternative diagnosis including rheumatic/valvular heart disease or
cardiac failure related to ischaemic heart disease. Patients with any such
changes would require local doctor ± specialist review.

FBE/haemoglobin
In general, haemoglobin should be measured at first presentation. Anaemia
may contribute to unexplained shortness of breath and chronic lung disease
may be associated with polycythaemia, which may require treatment
(therapeutic venesection) or be indicative of significant hypoxia suitable
for long-term oxygen therapy. All haemoglobin concentrations greater than
16 g/dl should be confirmed with a full blood examination. Subjects with
moderate and severe disease should further have a repeat haemoglobin
estimation annually. (see therapeutic venesection and long-term oxygen
therapy below).

BMI
Being underweight is associated with chronic lung disease and is most
likely a sequale rather than a cause of this condition. This is also the
case for Indigenous Australians.40 Although good evidence to support
nutritional supplementation/dietician review in those with wasting is
lacking41 it is reasonable to monitor BMI and to consider education ±
nutritional supplementation if the BMI falls below 20 kg/m2. Nevertheless, a
recent systematic review of nine trials assessing the benefit of
nutritional supplementation in patients with COPD and low body weight
demonstrated no significant benefit on anthropometric measures, lung
function or exercise capacity.42

Pulse oximetry/oxygen saturation

Pulse oximetry, when available, can provide useful additional information
pertinent to the management of chronic lung disease. In long-term
management it can be a useful screening test to determine if further
assessment is required to consider suitability for long-term oxygen therapy
(LTOT) or a requirement for supplemental oxygen for air transport; and in
the setting of an acute exacerbation can allow the titration of
supplemental oxygen. Nevertheless, the limitations of pulse oximetry must
be appreciated to facilitate its rational and safe use.

(Figure not shown)

Figure 1. Oxygen dissociation curve comparing haemoglobin saturation and tissue
oxygen tension

It is perhaps most important to understand the association between

oximetry readings and the measure that it is taken to approximate, namely
tissue oxygenation. To do this it is necessary to be aware of the
relationship between oxygen saturation (SO2) and tissue oxygen partial
pressure (pO2). This relationship is summarised by the oxygen dissociation
curve (figure 1). Because the curve becomes relatively flat above an
arterial pO2 of 60 mmHg (corresponding to an approximate saturation of 90%),
pulse oximetry is relatively insensitive to changes in pO2 above this level.
Further, the position of the curve, and therefore the specific relationship
between PO2 and SO2, may change depending on factors such as temperature,
pH, and the erythrocyte concentration of 2,3-diphosphoglycerate (2,3-DPG).
Increasing temperature, falling pH (more acidic environments) and increased
levels of 2,3-DPG occur in metabolically active and hypoxic tissue, reduce
the affinity of oxygen for haemoglobin and encourage the dissociation of
oxygen from haemoglobin. This is reflected in shifting of the oxygen
dissociation curve to the right (2 in figure 1) and facilitates oxygen
delivery to metabolically active tissue. In contrast, falling temperature,
and increasing pH increase the affinity of haemoglobin for oxygen and
encourages the binding of oxygen as occurs in the pulmonary capillary (1 in
figure 1).
When perfusion of the skin is decreased, as may occur with a low cardiac
output, the oximeter signal may also be unreliable or even unobtainable.
Finally, other forms of haemoglobin, such as carboxyhaemoglobin (carbon
monoxide associated with haemoglobin) and methaemoglobin (a rare
abnormality in haemoglobin usually associated with a sensitivity to
sulphur-containing drugs) cannot be differentiated from oxygen-containing
haemoglobin (oxyhaemoglobin) using standard oximetry. In these rare cases
the result of the oximetry reading correlates even less accurately with the
tissue oxygen tension.
With these factors in mind it can be seen that in general an oximetry
reading over 94% is likely to reflect adequate tissue oxygen tension (i.e.
pO2 >60 mmHg) and usually obviates the need for further assessment for LTOT.
The requirement for supplemental oxygen for air transportation raises an
additional issue. Whilst the proportion of oxygen in the atmosphere (the
fractional inspired oxygen, FIO2) remains largely unchanged at the higher
altitudes encountered during air travel in unpressurised aircraft the
ambient pressure falls as altitude increases. The net effect of this is a
reduction in the partial pressure of inspired oxygen (pIO2) (pIO2 = FIO2 x
ambient pressure) and as a result tissue oxygenation. Even in commercial
pressurised aircraft the ambient pressure is typically maintained at 550
mmHg, or about 70% of that at sea level. In individuals without low tissue
oxygenation on the ground the resulting reduction in tissue oxygenation is
well tolerated without adverse effect. Individuals with low levels of
tissue oxygenation at ground level, as can occur in chronic lung disease
when stable and particularly during an exacerbation, may however become
dangerously hypoxic during air travel.
 These guidelines advocate the assessment of subjects with severe disease
in a centre where blood gases can be performed. We are, however, cognisant
that this may require air travel of people who may have significant
hypoxia. If oximetry is available a reading less than 94% is likely to
indicate a pO2 that is sufficiently low to warrant supplemental oxygen for
air transport. Issues relating to transport with oxygen must be addressed
in liaison with the clinician the patient is referred to and the commercial
carrier (if an RPT or charter service is used). It may also be possible to
utilise medical evacuation (RFDS and AirMed) flights and this should be
discussed with the relevant service.

Smoking cessation
The causative link between COPD and tobacco consumption has been well
established.6,8,9,10,12 As a result it is clear the most important primary
preventive initiative for COPD is to prevent people commencing smoking and
to stop those who do smoke before they develop COPD. Nevertheless, there
are a small group of people who develop COPD and who do not have a history
of tobacco consumption.43 The second role for smoking cessation is as
secondary prevention. The Lung Health Study demonstrated that in smokers
with COPD that smoking cessation was associated with a reduction in the
accelerated decline in FEV1.13 Although the success in converting smokers to
sustained quitters was reasonably low, it is likely the effect today is
even more than that demonstrated in this earlier study with the advent of
newer and more effective smoking cessation strategies.
A meta-analysis comparing low intensity counselling, high intensity
counselling and specific pharmacotherapy for smoking cessation in subjects
with COPD is currently in process and should provide further support and
more contemporary direction for specific smoking cessation strategies in
this population.44

Vaccination
Vaccination for Streptococcus pneumoniae and influenza is frequently
advocated for those with COPD and is recommended as part of the national
vaccination guidelines.44 Certainly acute exacerbations of COPD are a
significant cause of morbidity and mortality and these are associated with
both these agents. A recent meta-analysis of influenza vaccination reviewed
four studies in patients with COPD and five with patients belonging to
high-risk groups, of which a proportion also had COPD.46 Although the data
were limited it suggested that influenza vaccine in COPD decreased
exacerbations in the following year, although only in the three weeks after
the vaccination. The authors concluded that influenza vaccination was
associated with some early adverse effects, although these were not serious
and were outweighed by the long-term benefit of vaccination.
The evidence for a beneficial effect of poly-valent pneumococcal
vaccination for non-Indigenous patients with COPD is less persuasive.
Observational studies have demonstrated superior vaccine efficacy for
invasive disease in subjects with chronic diseases including chronic lung
disease.47 Nevertheless, a more recent meta-analysis of randomised-
controlled trials has concluded that there is evidence only to support
vaccination in reducing bacteremic pneumococcal pneumonia in low-risk
adults.48 A current protocol by the Cochrane Airways Group investigating the
role of pneumococcal vaccination in COPD will provide more up-to-date
information relating to this question.49 Nevertheless, in the Northern
Territory rates of invasive pneumococcal disease are high, and the current
recommendation is to provide the 23-valent vaccine to all Indigenous
Australians aged 15 years or greater irrespective of the presence of
chronic lung disease.50

Delivery system of inhalation therapy

In general, the choice of delivery system for inhalational therapy in
stable COPD is dependent on patient preference. No method of delivery — be
it pressurised metered dose inhaler (pMDI), dry powder inhaler or nebuliser
— appears to be superior.51 In general, dry powder inhalers, breath actuated
inhalers and spacers may be useful if patients have difficulty coordinating
inhalation with standard pMDIs. Spacers may be particularly useful if
inspiratory flows are low as occurs in severe disease and if local side-
effects due to propellants or inhaled steroids are encountered.

Bronchodilators
In general, bronchodilators and particularly ipratropium have been shown to
not alter the rate of decline in FEV1 in COPD.13 There is no evidence to
suggest this would be different for subjects with bronchiectasis.
Nevertheless, bronchodilators can result in a temporary increase in FEV1
that may, in those with severe disease, be clinically significant.13 As a
result we have suggested that whilst bronchodilators may be used in any
level of severity of chronic lung disease they may be particularly
beneficial in subjects with severe disease where the small average
improvement may become clinically significant. Both β2 agonists (e.g.
salbutamol) and anticholinergics (ipratropium bromide) can produce this
effect. Nevertheless, there is some evidence that their effect may be at
least partially additive52, and thus in severe disease the use of β2 agonists
(e.g. salbutamol) and anticholinergics may be beneficial

Long-acting β2 agonists
Like bronchodilators in general, long-acting β2 agonists are associated with
an improvement in lung function. In general, this improvement is small and
of minimal clinical significance. In a meta-analysis of four RCTs of
salmeterol the average improvement in FEV1 after 4–16 weeks of treatment
was 100ml.53 Such an improvement is of doubtful clinical significance and no
study demonstrated an improvement in functional performance as demonstrated
by an improvement in the six minute walk test. Nevertheless, one study did
demonstrate an improvement in QOL and a reduction in breathlessness. In
general, these finding would indicate that there is little role for long-
acting β2 agonists in the routine management of COPD. Nevertheless, in
patients with severe airflow obstruction — and particularly those with
evidence of reversibility but not sufficient to warrant the diagnosis of
asthma — a trial of salmeterol or eformoterol may be warranted.

Theophylline
Methylxanthines as exemplified by theophylline/ aminophylline are
associated with a fixed improvement in FEV1 similar to β2 agonists and
anticholinergics. Nevertheless, like these there is no evidence that they
alter the decline in FEV1 when used long-term. In general the use of oral
theophylline for maintenance therapy has been discouraged due to potential
toxicity, monitoring requirements and no evidence that they are superior in
improving FEV1 as compared to inhaled bronchodilators. The authors,
however, realise that oral bronchodilators may improve adherence to therapy
compared with inhalation preparations due to a combination of patient
preference and an inability to properly use inhaled bronchodilators, even
when supplemented with spacers or nebulisers. In this case theophylline use
may be warranted.
Determination of theophylline levels is recommended soon after
initiating therapy (within two weeks), before increasing the dose when a
patient fails to have an expected response and when an adverse reaction or
toxicity is suspected. Further levels should be monitored whenever drugs
known to alter theophylline elimination are introduced or withdrawn and
upon the addition of any new medication with an unknown effect on
theophylline elimination. (Theophylline clearance increased by:
carbamazepine; phenobarbital; phenytoin; rifampicin and tobacco consumption
and reduced by: allopurinol, oestrogen containing contraceptives;
fluoroquinolone antibiotics; macrolide antibiotics (though azithromycin
appears to have no effect); methotrexate; propranolol; thiabendazole;
ticlopidine and verapamil). In general, before the institution of
theophylline all current medications should be reviewed in relation to
their effect on theophylline clearance. If none of these events occur it is
generally recommended that levels be performed at least every six to 12
months in stable patients.54

Inhaled steroids
In general, the utility of inhaled steroids in the management of COPD may
be summarised by reviewing their effect on the rate of decline in lung
function/FEV1, initial effect on lung function, effect on acute
exacerbation frequency and effect on quality of life and its decline with
disease progression. Large multicentre randomised-controlled trials —
including the Lung Health Study, ISOLDE (Inhaled Steroids in Obstructive
Lung Disease in Europe) study55 and the EuroSCOP (European Respiratory
Society Study on Chronic Obstructive Pulmonary Disease) study56 — all failed
to demonstrate any reduction in the rate of decline in FEV1. Nevertheless,
a meta-analysis of three earlier studies 57 did demonstrate such a reduction
over two years of treatment with relatively high doses (generally 1 500 µg
of beclomethasone diproprionate) of inhaled steroids. Whilst most recent
studies and the specialist respiratory community in general conclude that
inhaled steroids do not alter the rate of decline in FEV1 a Cochrane review
currently being conducted may clarify this position.58
The above trials did, however, demonstrate an improvement in lung
function with the addition of inhaled steroids, but this was an initial
effect and, as noted above, was not associated with any difference in the
ultimate decline in lung function. The size of this effect was generally
small and ranged from 4055–98 ml.56 Although such a difference is likely to
be clinically insignificant an increase of 100 ml in FEV1 in those with
severe disease may result in a significant symptomatic improvement. In
light of this we have advocated the general use of inhaled steroid in those
subjects with severe/stage three disease.
The evidence for the use of inhaled steroids in bronchiectasis is less
substantial. A meta-analysis of trials in bronchiectasis was able to find
only two suitable randomised double-blind controlled trials of inhaled
steroid use in bronchiectasis and these were conducted for a maximum of six
weeks.59 Whilst such studies were too brief to determine any change in
decline in lung function there was a non-significant trend for improvement
in lung function measures. Certainly this would be consistent with the
findings in COPD and would support a similar recommendation for inhaled
steroid use in this sub-group of individuals with chronic lung disease.
 Inhaled steroids have, however, been shown in occasional studies to
reduce the frequency of exacerbations. In the ISOLDE study exacerbations,
defined as an increase in symptoms necessitating the prescription of oral
corticosteroids or antibiotics by a general practitioner, were less
frequent in those on inhaled steroids (fluticasone proprionate 1 000 µg/d —
a high dose comparable to approximately 2 000 µg of beclomethasone
diproprionate) (0.99/year) compared to those on placebo (1.32/year). This
represented a statistically significant reduction in exacerbation frequency
of 25%. A similarly designed study comparing fluticasone proprionate 500
µg/d with placebo over six months demonstrated no significant difference in
the number of exacerbation, but did show a significant reduction in the
number of moderate or severe exacerbations.60 In view of these findings we
have suggested that subjects with frequent acute exacerbations of chronic
lung disease (in this case we have chosen an arbitrary cut-off of three
exacerbations) may benefit from the addition of inhaled steroids. Whilst
data are lacking for Indigenous Australians our initial findings in a
prospective cohort study would suggest that exacerbations (defined as two
of increased sputum volume, change in sputum colour or increased dyspnoea)
are likely to be more frequent in Indigenous compared with non-Indigenous
population with chronic lung disease. Our initial estimates are that self-
reported acute exacerbations of COPD in Indigenous Australians in the Top
End of the NT occur on average once every two months.61
The final potential role for inhaled steroids that may be clinically
relevant is the effect on quality of life. No well-validated measure of
quality of life for Indigenous Australians is available and perceptions of
health, disease and function are likely to be different in this population.
Thus, caution should be used in generalising quality of life studies in
non-Indigenous populations to Indigenous Australians. Nevertheless, there
is evidence that inhaled steroids may at least be associated with an
initial improvement in quality of life and a reduced decline in this
measure over time in non-Indigenous developed world populations. Using the
disease-specific St George Respiratory Questionnaire (SGRQ), the ISOLDE
study demonstrated that inhaled steroids delayed a clinically significant
reduction in respiratory health status from 15 to 24 months.55 In turn the
SGRQ has been shown to be a better predictor of hospitalisation and death
within 12 months than FEV1.
At this time the high rate of subjects lost to follow-up (approximately
50% in each group), and the use of a quality of life questionnaire which is
not validated for Indigenous Australians makes it difficult to advocate the
routine use of inhaled steroids in the local practice setting based on a
rationale of improved quality of life. Nevertheless, this is an area that
requires further local investigation.

Oral steroids
Long term
There is no proven role for oral steroids in the long-term management of
stable COPD or bronchiectasis. Like inhaled steroid they may be associated
with a one-off increase in lung function even in stable disease but this
has not been shown to reduce the rate of decline in lung function in the
long term. Although a one-off improvement in lung function may be
clinically significant in patients with severe disease the side effects of
long-term systemic steroids would preclude their routine use. Nevertheless,
the authors realise it may occasionally be difficult to wean systemic
steroids in some patients as this can occasionally be associated with
further exacerbations of disease. In the minority of patients in whom this
occurs the use of high doses of inhaled steroids may occasionally allow the
weaning of systemic steroids, though no evidence from RCTs is available to
support this. If weaning of systemic steroids is not possible it is
important to consider alternative diagnoses, including asthma and
interstitial lung disease, and specialist review is warranted as well as
monitoring for adverse effects of long-term steroids (including diabetes,
hypertension and osteoporosis). The risk of reactivation of latent
tuberculosis in patients on long-term systemic steroids should be
considered. Appropriate investigations and consideration for isoniazid
prophylaxis should be discussed with the treating doctor (see section on
TB).

Oral steroid trial

A trial of oral steroids is occasionally advocated to determine which
subjects may benefit from longer term inhaled steroids.22 A recent large
randomised controlled trial of long-term fluticasone proprionate, however,
demonstrated that the improvement in FEV1 associated with prednisolone 0.6
mg/kg/day for 14 days did not correlate with the subsequent decline in FEV1
in those assigned to inhaled steroids. Although short courses of oral
corticosteroids are reasonably safe the use of steroid trials to plan
future inhaled steroid use is not advocated here.

Long-term oxygen therapy

Long-term oxygen therapy (LTOT) refers to the use of supplemental oxygen in
patients with significant hypoxia due to lung disease. In general the aim
is to increase the tissue oxygen partial pressure (pO2) to levels above 60
mmHg and to maintain these levels for at least 16 hours per day. In
appropriately selected patients LTOT is associated with increased survival.
People who benefit are those with lung disease and a paO2 <60 mmHg whilst
breathing room air. Several studies have supported the role of LTOT in
patients with chronic lung disease (in this COPD) and significant
hypoxaemia.62–64 In general LTOT has improved survival in such patients at
both two and five years. Of note the Nocturnal oxygen therapy trial (NOTT)62
and a study by Fletcher et al65 demonstrated no significant benefit from
supplemental oxygen at night for patients who had isolated nocturnal (only)
oxygen desaturation. A recent systematic review has also supported the role
of LTOT in patients with chronic lung disease and a paO2 <60 mmHg.66
The assessment for suitability for LTOT typically requires the
collection of an arterial blood gas (ABG) sample. As a result this requires
the referral of a patient to a centre where this can be performed (usually
a hospital). An oximetry reading that is <90% on room air would correlate
which such a low reading and would be a reasonable de facto measure.
Nonetheless many patients with oximetry readings between 90 and 94% may
still be appropriate for LTOT and should have ABGs performed. It is
important that assessment occurs when the patient is stable and not having
an acute exacerbation of their disease. ABGs performed whilst hospitalised
should therefore not be used to assess the suitability for LTOT but can be
useful in identifying those who require further assessment once stable.
Since it can take over two weeks to return to baseline lung function after
an acute exacerbation even ABGs on discharge from hospital can be
misleading.
Current smoking is an absolute contraindication for LTOT as smoking and
supplemental oxygen is an explosive combination and can be associated with
life threatening facial and airway burns. It is therefore important to
confirm that patients are not currently smoking before considering LTOT. If
there is any doubt abstinence can be determined by assessment with
urinary/serum/salivary cotinine.
Typically LTOT is delivered using nasal prongs at a rate of 2–4 l/min.
LTOT is usually delivered using an oxygen concentrator. This requires a
reliable power supply and in turn is associated with increased home
electricity costs. Backup cylinders of oxygen may be supplied if the
electricity supply is unreliable. Although these can be kept at home it is
often more convenient in remote communities for such cylinders to be stored
at the local health centre. To encourage mobility and maximise quality of
life it is possible to provide smaller cylinders for excursions outside the
home.
It is important to realise that LTOT has only shown to be of benefit if
used more than 12 hours per day, and particularly more than 16 hours. As
such LTOT supplied by an oxygen concentrator alone can restrict mobility.
It is important that patients on LTOT are encouraged to maintain their
mobility and mobile small cylinders can therefore be useful. The details of
delivery of LTOT should be discussed with the relevant respiratory nurse
(Darwin and Alice Springs).
Supplemental oxygen is also occasionally used if exercise capacity is
limited by hypoxia. The evidence for this is limited and the benefit of
supplemental oxygen in improving exercise capacity should be objectively
assessed before it is prescribed for this use. A planned systematic review
of supplemental oxygen for exercise alone is planned and should help
address this issue.67 It is, however, important to draw a distinction
between ambulatory oxygen as a method of improving adherence to LTOT, which
is of proven benefit, and its use only for exercise, which remains
controversial. Finally, supplemental oxygen is sometimes used in late stage
disease as palliation. Its use in this setting should be discussed with the
local palliative care service if available. In both cases it should be
remembered that current smoking is an absolute contraindication for its
use.

Therapeutic venesection
Long-standing tissue hypoxia due to severe chronic lung disease can be
associated with an increase in the total red cell mass (polycythaemia).
Whilst this can increase tissue oxygen delivery it can result in increased
blood viscosity, worsening pulmonary hypertension and an increased risk of
intravascular thrombosis, and particularly thrombotic stroke. The red cell
mass is reflected in the standard full blood count by an increase in the
haemoglobin and particularly the packed cell volume (PCV)/haematocrit
(HCT). The risk of intravascular thrombosis increases when the PCV rises
above 0.55 (i.e. 55% of the blood volume is made of cells, and particularly
by erythrocytes). If the PCV is above 0.55 it should prompt an assessment
for the suitability for LTOT if this has not been performed. If the
polycythaemia fails to respond to maximal medical treatment (including LTOT
if indicated) then regular slow therapeutic venesection may be indicated.
This should be discussed with the caring doctor/specialist as some patients
do not tolerate venesection well.

Mucolytics
Oral mucolytics include N-acetylcysteine (NAC), S-carboxymethylcysteine,
bromhexine, ambroxol, sobrerol, cithiolone, letosteine and iodinated
glycerol, N-isobutyrylcysteine (NIC), and myrtol. N-acetylcysteine (NAC) is
the most frequently used and studied agent. A systematic review of regular
mucolytics (for at least two months) in COPD demonstrated a significant
reduction in the frequency of exacerbations with their use.68 The summary
measure of effect of mucolytics was a small but significant reduction in
the number of exacerbations per month of 0.07. The average exacerbation
rate across these studies was 2.7 per year and extrapolated to a reduction
in exacerbations of 0.8/patient/year. There is insufficient data for
mucolytics in bronchiectasis specifically, nevertheless, it is likely a
similar effect would be seen in this condition.
Hypertonic agents (hypertonic saline 3–14% and mannitol) are also
frequently utilised in chronic respiratory disease. Unlike mucolytics these
agents do not attempt to solubilise sputum, making it less viscous and
easier to expectorate. Rather they attempt to correct the impaired
mucociliary clearance that is a characteristic of bronchiectasis and COPD.
Whilst hypertonic agents have been shown to improve markers of sputum
clearance69 controlled trials of their benefit in reducing exacerbation
frequency or improving lung function are lacking. Nevertheless, current
trials investigating such clinical efficacy of hypertonic saline are
currently in process and should address this question.

Prophylactic antibiotics
Patients with chronic lung disease and frequent acute exacerbation or
copious sputum production are occasionally prescribed long-term
antibiotics. Dosing regimens include continuous use of a single antibiotic
or rotating use of different antibiotics. Evidence to support such a
practice as a way of reducing exacerbation frequency or decline in lung
function or improving quality of life is confusing, with occasional studies
demonstrating benefit and many showing no effect. The use of long-term
antibiotics further raises questions of selecting for resistant bacteria in
such patients. Two systematic reviews are currently in process which may
help to address this area for both COPD70 and bronchiectasis71 and studies
addressing the efficacy of prophylactic antibiotics in Indigenous
Australians with chronic lung disease living in remote communities are
planned.

Physiotherapy
The role of physiotherapy in the management of chronic lung disease covers
a broad range of interventions. The role of physiotherapy, as part of a
multidisciplinary approach to rehabilitation, has been shown to improve
quality of life and mobility and will be explored below. Apart from
rehabilitation physiotherapy is also occasionally advocated to encourage
expectoration of sputum. Techniques utilised to achieve this, covered by
the broad-term bronchopulmonary hygiene physical therapy (BHPT), include
exhalation techniques, postural drainage and external percussion. BHPT is
labour intensive and can place additional demands on health providers,
patients and their families. Further, in some patients it is associated
with adverse side effects including hypoxia72 and a temporary reduction in
lung function.73 A systematic review of the use of BHPT in COPD and
bronchiectasis demonstrated no significant clinical benefit on lung
function or paO2 in either condition.74 Nevertheless, only seven trials with
a total of 129 subjects were deemed to be of sufficient methodological
quality for inclusion. This finding would nonetheless indicate that if
there is a beneficial effect of BHPT it is likely to be small and that
further study is required to determine this with particular emphasis on
quality of life and exacerbation frequency. The lack of conclusive benefit
from BHPT, the demands it places on patients and their carers and the risk
of adverse effect mean that we have not advocated the routine use of BHPT
in chronic lung disease.

Pulmonary rehabilitation
Unlike BHPT (see above) there is an increasing body of evidence from
randomised controlled trials to support the benefit of pulmonary
rehabilitation in chronic lung disease. Evaluated pulmonary rehabilitation
programs have utilised a multi-disciplinary approach in either an inpatient
or outpatient setting. Whilst pulmonary rehabilitation programs do not
appear to improve lung function they are associated with clinically
significant improvement in exercise capacity as measured by a six minute
walk test and maximal oxygen consumption, a measure of fitness.75 Outpatient
programs involving physiotherapy assessment, exercise training, dietary
assessment and advice and occupational therapy assessment are also
associated with a significant improvements in quality of life76, and these
improvement persist for at least 18 months77 and up to two years.78 Whilst
such programs are resource intense their immediate efficacy and persisting
clinically significant benefit would encourage the development and funding
of similar programs for patients with COPD in the NT.

Surgery
Surgical options in COPD include bullectomy, lung volume reduction surgery
(LVRS) and single or double lung transplantation. For bronchiectasis they
include resection of focally diseased lung and lung transplantation. Such
procedures are difficult to evaluate in the setting of a randomised
controlled trial. Whilst there is currently little evidence to support
long-term benefit for LVRS79 this is, however, currently being evaluated as
part of an RCT, the National Emphysema Treatment Trial. Nevertheless, it is
already apparent that such interventions can be associated with substantial
morbidity and mortality.80 In general these procedures (except focal
resection in bronchiectasis) are reserved for patients with advanced
disease. Nevertheless, patients with advanced disease, especially when this
is associated with an FEV1 <35% predicted, should be reviewed by a
specialist physician where the suitability for such procedures can be
determined.
The role of resection of focal bronchiectasis remains unclear and is
informed largely by case series with an absence of controlled trials.81 Many
patients with presumed focal disease are often found on further
investigation to have more generalised disease. If, however, bronchiectasis
is confirmed on high resolution CT (HRCT) to be confined to one or two
lobes it is reasonable to consider this option and to refer patients for
specialist review irrespective of lung function.

4. Managing acute exacerbations of chronic respiratory disease

Background
Despite the prevalence of COPD and the frequency of exacerbations resulting
in utilisation of increased medical resources there is no standard
definition of an acute exacerbation (AE). A proposed working definition
from the American Thoracic Society is a ‘sustained worsening of the
patient’s condition, from the stable state and beyond normal day to day
variations, that is acute in onset and necessitates a change in regular
medication in a patient with underlying COPD’.82 There are further
subclassifications of severity based on clinical need.
In the absence of a generally accepted definition, evaluation of the
published literature has been problematic. However, most definitions
include the three clinical findings of worsening dyspnoea, increased sputum
production and sputum purulence. Most patients receive most available
therapies and the presence of co-interventions has made analysis of any
single therapy more difficult. Further, the majority of research studies
are in an emergency department or in-patient setting while the majority of
episodes of acute exacerbation are treated on an outpatient basis.
Inhaled bronchodilators, corticosteroids, antibiotics and non-invasive
ventilatory support have all shown efficacy but methylxanthines, mucolytics
and chest physiotherapy do not appear of benefit. While oxygen is
frequently required, in an identifiable subgroup it increases the risk of
respiratory failure and needs to be utilized with caution.83

Bronchodilating agents
Short-acting beta agonist type (e.g. salbutamol) and anticholinergic (e.g.
ipratropium) inhaled bronchodilators appear to have comparable effects on
spirometry, and the combined use of them has not been clearly demonstrated
to confer advantage over larger doses of either alone. Patients receiving
ipratropium alone had the lowest rate of side effects. Again, conclusions
are limited by differences in inclusion and exclusion criteria and the
small numbers of trials.83
A meta analysis of eight RCTs failed to find evidence supporting any
delivery system conferring advantage over another, MDI use appearing
equally efficacious as nebuliser and response being dose dependent.83

Antibiotics
The role of antibiotics in acute exacerbations has been controversial.
While nine placebo controlled trials concluded there was significant
improvements in outcomes for those treated with antibiotics, six studies
were unable to find statistically significant differences. It would appear
the overall benefit is related to the severity of the exacerbation, and
antibiotics are recommended for all with increased dyspnoea, increased
sputum volume and the development of purulent sputum.84 While in one study
those treated with antibiotics had significantly lower relapse rates
(independent of the severity of their underlying disease or the severity of
the exacerbation85) in other studies those identified as most likely to
benefit were those with higher numbers of exacerbations per year and those
with comorbid illness (diabetes, asthma and CHD).83,86
There is little evidence for recommending the most appropriate duration
of treatment; trials typically ranged from 3–14 days.83
The agents used for the RCTs included amoxycillin, trimethoprim-
sulfamethoxazole and tetracycline.

Corticosteroid drugs
The pathological features of AE of COPD share with exacerbations of asthma,
as well as worsening of the inflammatory component of the disease during
exacerbations, provide rationale for the use of corticosteroids. In a
Cochrane review, use of systemic corticosteroids improved spirometry over
the first 72 hours and reduced relapse rates but there was no evidence that
their use reduced the likelihood of dying or decreased hospital stay.87 The
SCCOPE trial found FEV1 improvements with steroid use highest after the
first day of treatment, still statistically significant up to the third day
but no longer significant at two weeks. There appeared no advantage in an
eight-week course over a two-week course. Patients receiving steroids were
2.7 times more likely to have adverse reactions, and the recommendation was
for further research into the risk benefit ratio.83

Oxygen therapy
While oxygen therapy does increase the risk of respiratory failure in an
identifiable group of patients, (those with simultaneous hypercarbia and
hypoxaemia), oxygen therapy is indicated for all patients with hypoxaemia.
Oxygen relieves pulmonary vasoconstriction and right heart strain and
lessens myocardial ischemia. Improved oxygen delivery to the lungs probably
aids mucociliary transport. Oxygen administration in studies generally
ranged from 24–28%.83,88

Mucolytic agents and percussion

While mucolytic agents may improve symptoms they have not been demonstrated
to improve function or outcome.89
From three RCTs mechanical percussion is not only ineffective but may
decrease FEV1 transiently in patients with acute exacerbations of COPD.89

Methylxanthines
Not only did most studies show little if any additional bronchodilator
effect with aminophylline or theophylline if maximal doses of beta
adrenergics or anticholinergics have been used, but these agents have
numerous adverse effects and drug interactions, sometimes life threatening,
and their use is generally not recommended, particularly in patients with
co morbidities.90

Identifiable risk factors for relapse

From several studies there appear to be identifiable predictors for
relapse. These include:
• lower baseline FEV1 levels;
• higher rates of previous relapse; and
• more bronchodilator treatments or corticosteroids during visit.

However, all have only moderate discriminatory power.89

Predictors of in-patient mortality

Physiological characteristics associated with higher rates of mortality
have been identified, but inclusion criteria showed substantial variability
and predictability of death was less than 90% for any model.

Rationale for referral

While COPD is a common condition and exacerbations frequent, because most
studies are in-patient or emergency department-based, and because there has
been no standard definition of exacerbation or inclusion/exclusion
criteria, recommendations for when to refer are based on present practice.
While factors related to risk of relapse and mortality have been
identified, currently there are no reliable models for risk stratification.
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bronchiectasis, Cochrane Database of Systematic Reviews. Issue 3, Editor. 2001.
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83. McCrory, D.C., et al. Management of acute exacerbations of COPD: a summary and
appraisal of published evidence. Chest 2001; 119(4):1190–209.
84. Russo, R.L. & M. D’Aprile. Role of antimicrobial therapy in acute exacerbations
of chronic obstructive pulmonary disease. Ann Pharmacother 2001; 35(5):576–81.
85. Adams, S.G., et al. Antibiotics are associated with lower relapse rates in
outpatients with acute exacerbations of COPD. Chest 2000; 117(5):1345–52.
86. Allegra, L., et al. Antibiotic treatment and baseline severity of disease in
acute exacerbations of chronic bronchitis: a re-evaluation of previously published
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exacerbations of chronic obstructive pulmonary disease, Cochrane Database of
Systematic Reviews. Issue 3, Editor. 2000.
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dioxide retention during exacerbations of chronic obstructive pulmonary disease.
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 Chronic Renal Failure

Authors: Clinical Assoc Prof Mark Thomas; Dr Sophie Couzos

Reviewers: Dr Dan Ewald (ed); Dr Christine Connors; Dr Paul Lawton; Dr

Paul Snelling

Note: Additional information can be sought from: Couzos S, Thomas M,

‘Chronic Renal Failure’, in Aboriginal Primary Health Care: An evidence-
based approach, second edition, Oxford University Press, Melbourne,
September 2003. This contains more information on the prevention and
management of chronic renal failure, treatment goals and targets, case
management, program implementation, data collection, and performance
indicators.

Summary
Much is to be gained from optimal prevention and management of the
increasing epidemic of chronic renal failure in Aboriginal people and
conversely there is considerable avoidable illness and death where health
care fails. Evidence shows that early recognition, early intervention and
well-timed referral to specialist and tertiary care are all important.
Renal failure is increasingly common in Aboriginal populations, especially
those with diabetes, hypertension, obesity, or a family history of renal
disease.
Social factors such as diet and exercise, combined with minimisation of
smoking and alcohol use, are most important in the primary prevention of
chronic renal disease. Environmental factors such as appropriate housing
and community measures to reduce skin infections are likely to help reduce
renal disease.
All Aboriginal adults should be encouraged to participate in screening
for early renal disease with annual dipstick testing for proteinuria, and
subsequent quantification if positive. People with diabetes should be
tested for microalbuminuria with an ACR. The glomerular filtration rate
(GFR) should be calculated for people with diabetes and microalbuminuria,
and all others with overt proteinuria.
Control of hypertension is one of the major interventions for
controlling the decline in renal function in those with renal impairment
and blood pressure should be kept below 130/85, or even lower in the
presence of proteinuria. The optimal choices of anti-hypertensive are the
angiotensin-converting enzyme inhibitors and angiotensin receptor blockers
(alone or in combination) as they have been shown to delay the progression
of diabetic and non-diabetic-related renal disease by as much as twofold,
and reduce proteinuria by 50%.
Patients with progressive renal failure should be referred to a
nephrologist at or before reaching a calculated GFR of 30 ml/min (and
preferably around 60 ml/min) for further management, including correction
of anaemia, education on end-stage renal failure (ESRF) options and timely
creation of vascular access for dialysis. Aboriginal patients should be
given the same opportunities for ESRF treatment as non-Aboriginal patients,
and those in remote areas the same as those in urban settings.

Burden of suffering
For the most part, the progression from early through to advanced renal
failure is asymptomatic. However, with the onset of end-stage disease,
uraemia and renal replacement therapy, there is considerable physical and
social disruption for most patients. Aboriginal Australians in particular
face a significant and increasing burden of renal disease, mandating
decisive action at all levels of health provision.1 Current and future
projections are of ‘epidemic proportions’ in the NT.2 Maintenance
haemodialysis is the leading cause of hospital admissions among Indigenous
Australians (26% of all episodes of care, and 44% as principal procedure in
1998–99).3 The population-adjusted incidence of new patients accepted on to
ESRF programs in the year 2000 was 400 per million in the total Australian
Aboriginal population. This compared to 300 in Pacific Islanders, 200 in
Maoris and was five times the rate of the Australian Caucasian population
(80 per million).4,5 The racial disparity data from the ANZDATA Registry has
been independently validated.6 The rates of ESRF in Aboriginal populations
vary greatly in different regions, but are generally increasing. The
average annual incidence of ESRF in Northern Territory Aboriginal people
was 440 per million in 1988–93 (approximately ten times the non-Aboriginal
rate), while that in Tiwi people was 1636 per million.7 In the last decade,
the nation-wide incidence of ESRF has risen over twofold, from 170/million
in 1991 to a peak of 430/million in 1997–99.4 Despite likely differences in
the difficulty in access to diagnostic services, the incidence is increased
in remote versus urban centres, and in northern versus southern states.8
Furthermore, ESRF incidence may be underestimated, as many remote area
Aboriginal people decline treatment.9 ESRF in Aboriginal people more often
presents acutely and earlier (median age 48 versus 61 years in non-
Indigenous patients), with a higher proportion of females (57% vs 41%).
Diabetes is a major contributing factor in renal failure in Aboriginal
people with 47% of those with a biopsy-proven cause (20% of total) being
attributed to diabetic nephropathy. In reality, the renal pathology is
multifactorial, representing the cumulative insults of virtually every
recognised risk factor for progressive renal failure10 and indeed
mortality.11 These lifetime risk factors include:
• intra-uterine growth and nutrition, which may impair nephronogenesis12
• low birth weight13
• childhood post-streptococcal infection14
• adult obesity15
• diabetic control16,17
• hypertension18
• smoking18
• albuminuria/proteinuria (correlated with loss of GFR19 as well as all-
cause (predominantly cardiovascular) mortality20
• glomerulomegaly21 (unclear if congenital or acquired secondary to
hyperfiltration associated with focal glomerulosclerosis)22
• socioeconomic disadvantage23
• lack of access to health services24

Most Indigenous patients with renal disease have significant co-morbidities

(alcohol dependency, smoking, frequent infections, poor nutrition,
diabetes, ischaemic heart disease), which contribute to a deterioration in
renal function20 as well as a 50% increased risk of cardiovascular or
respiratory disease versus non-Indigenous patients.
As a result, survival of those with ESRF (i.e. haemodialysis (HD),
peritoneal dialysis (PD) and transplant (Tx)) in 1991–2000 was worse in
Indigenous patients, being 60% at five years, compared to 85% in non-
Indigenous patients (p<.001). Similarly, Indigenous patients with renal
transplant had worse five-year patient and graft survival (70% versus 82%
in non-Indigenous patients).4
Approximately 40% of Aboriginal patients in ESRF programs were not known
to have had renal disease before presenting with renal failure.25 The late
presentation is associated with a lower likelihood of acceptance of
dialysis treatment.
Many Aboriginal people face additional social stress and disruption if
they have to leave their home community for end-stage renal treatment.
Because ESRF mainly affects older people, some remote communities lose
contact with their community elders/leaders through this dislocation. This
sometimes impacts on the choice of treatment, and hence survival and
morbidity. About 90% of the Aboriginal people who received haemodialysis in
Alice Springs were from bush communities, often more than 200 km away. The
family disruption involved in a move to regional dialysis units is
therefore significant. Often there is a failure to match these health needs
with accommodation services. Only a minority of patients (18%) were able to
get Housing Commission accommodation in Alice Springs in 1996.26
Despite the rapidly-expanding patient numbers, only a small number of
satellite HD Units have been established in remote areas of Australia,
limited by funding and staff retention.

Definitions
The definitions used to describe stages of chronic kidney disease are
important in order to clarify optimal specialist referral times, and for
data collection.27,28,29

Diabetic nephropathy
In the absence of a renal biopsy or an alternative explanatory cause a
clinical diagnosis of overt diabetic nephropathy is defined by the presence
of persistent or overt proteinuria (>300 mg/24 hr or >200 microgram/ min).
It is usually accompanied by hypertension, little or no microscopic
haematuria and normal-sized kidneys on renal ultrasound. The American
Diabetes Association states that the diagnosis of diabetic nephropathy in
NIDDM requires an elevated albumin excretion as well as evidence of
diabetic retinopathy.30
Incipient nephropathy is defined by microalbuminuria without overt
proteinuria (30–300 mg/24 hr or 20–200 microgram/min, or an
albumin:creatinine ratio of 3.4–30 mg/mmol). This phase is often
accompanied by glomerular hyperfiltration, with a serum creatinine lower
than expected for age and weight, and GFR greater than normal.

Chronic renal failure

The sustained and irreversible reduction in the glomerular filtration rate
(GFR), accompanied by a rise in serum creatinine, is the hallmark of
chronic renal failure. A low GFR may occur with a normal serum creatinine
in older and smaller patients. The GFR (normally >100 ml/min adult and >50
ml/min child) can be calculated from the serum creatinine (see Diagnosis).
A generally accepted definition of significant chronic renal failure is
a serum creatinine >200 micromol/L or calculated GFR <60 ml/min on two
occasions at least a month apart in the absence of acute illness.

End-stage renal failure

ESRF is usually reached when less than 10% of normal renal function remains
and regular dialysis or renal transplantation is required to maintain
life.31

Diagnosis
The most appropriate screening test is an annual dipstick urinalysis on a
spot urine for proteinuria followed (if positive one plus or more) by
quantitation of albuminuria by albumin:creatinine ratio (ACR). If the ACR
is more than 3.4 on two occasions in the absence of urinary tract infection
or sexually transmitted infection, they should proceed to further
assessment and investigation as per the protocol.
[Editor: The CARPA STM protocol only suggests calculating creatinine
clearance/GFR if the person is hypertensive or diabetic or the ACR is
confirmed to be >100. This difference is because this is the group with the
strongest evidence of benefit of intervention, and less useful calculating
of GFR may be a significant burden on health staff. Given that the protocol
includes measuring EUC on everyone with ACR confirmed to be over 3:4, this
compromise could be revised if, for example, electronic/computer/paper-
based normograms or GFR calculators were widely available. Otherwise the
EUC test is to detect grossly elevated creatinine, which will be less
sensitive for detecting pre-existing renal failure – calculated GFR’s are
probably for the GP to do rather than the health worker. The CARI
guidelines website has a nice sex-specific nomogram for those who can’t do
the rough calculation mentally or manually.]

Microalbuminuria
Microalbuminuria is a recognised early phase of diabetic nephropathy and
indicates leakage of a small protein (albumin) from the kidney that is not
detectable by conventional dipstick tests for proteinuria. Approximately 9%
of diabetic patients with microalbuminuria progress to overt proteinuria
per year.28 It is now proven to be a predictor of the progression to renal
failure in insulin-dependent diabetes mellitus (type 1 diabetes) and non-
insulin–dependent diabetes mellitus (type 2 diabetes). The highest
predictive value for progression to renal failure in diabetic nephropathy
is an ACR two to three times the upper limit of normal.32
A timed urinary albumin excretion rate is generally agreed to be the
most sensitive assay for microalbuminuria.31 Because of the impractical
nature of the required urine collection, an ACR is recommended as the test
of choice. A first morning sample is preferred, but a randomly obtained
specimen may also be used.33 A review of the potential limitations of this
assay for microalbuminuria estimation has been described.32
Making a diagnosis of microalbuminuria, according to the American
Diabetes Association, requires two of three tests (performed over a three-
to six-month period) with elevated results before the patient is considered
to have microalbuminuria.28 This is to reduce the number of false
positives. However, a systematic review concluded that repeated testing is
onerous, unsubstantiated by studies and probably does not improve
diagnostic certainty due to minimal improvements in specificity in low
prevalence situations. This lack of adherence to even single annual
screening tests raised questions of whether the screening strategy of
repeated screening followed by treatment will effectively prevent diabetic
nephropathy.34
[Editor: An unpublished study (Stephen P McDonald, Zhiqiang Wang, Wendy
E Hoy. Menzies School of Health Research. Darwin NT) reports:
Predictive value of dipstick results for subsequent ACR was examined in
3554 observations on 1366 people in a community screening and treatment
program for renal disease. Reproducibility of ACR was examined for both
same-day (n = 120) and same-month (n = 230) collections.
In both groups, variability was less with ACR than with albumin
concentration. It was, however, still substantial: 95% limits of agreement
for a second test range from less than 1/3 to over 3 times the initial
result. This figure is relatively robust to effects of glucose, blood
pressure, gender and obesity. This variability may result in differences
in diagnostic and treatment decisions if not recognised . . . Taking the
mean of 2 repeated tests will reduce the width of the range by 40% (÷2).

We believe these findings are important as they are derived from a

population with similar patterns of UTI and STI and other co-morbidities to
the populations where this protocol is to be used. These factors may
influence the reliability of the ACR test. The CARPA STM suggests that the
best practical assessment will come from the average of two ACR
measurements in the absence of STI and UTI. Though this involves a
significant amount of work for the clinic, it does change treatment
choices, and then does not have to be repeated once the person is known to
be albuminuric / micro-albuminuric.]

Testing with the DCA 2000 (Bayer) point-of-care instrument to assay ACR
from spot urines enables immediate feedback to the patient (within seven
minutes), thereby potentially enabling treatment changes.35,36 This approach
has been successfully used and validated in a number of Aboriginal
community settings.37,38 At present there is insufficient evidence and a
lack of consensus on whether the non-diabetic population should be screened
for microalbuminuria, and CARPA does not advocate it.

Overt proteinuria
The presence of dipstick-positive proteinuria (more than or equal to +1 for
protein) usually indicates overt proteinuria (approximately equivalent to
protein excretion rate of 300 mg in 24 hours, or a protein:creatinine ratio
>30 mg/mmol, or an albumin:creatinine ratio >30). Commercially available
dipsticks are sensitive to albumin in concentrations of 100–200 mg/L, but
may produce a false-negative reading in the presence of a dilute urine
sample. Urinary tract infections, physical exercise, congestive cardiac
failure, menstrual loss and vaginal contamination can cause proteinuria on
dipstick in the absence of renal disease (false-positive). If detected in
the absence of infection, dipstick proteinuria can be quantified by a 24-
hour collection or (much more practicably) by a spot albumin–creatinine
ratio (ACR). There is evidence that an ACR estimate of proteinuria is more
reliable as a predictor of renal decline than a 24-hour urine collection in
non-diabetic patients with chronic renal failure.39,19
 Proteinuria is often the first indication of renal disease. However, it
may be present transiently in people without renal disease. A greater
degree of proteinuria and progressively increasing proteinuria correlates
strongly with the progression of renal failure.28 It is now widely accepted
that overt proteinuria is also an independent risk factor for
cardiovascular disease.30 In the Aboriginal population, proteinuria can
predict all-cause natural death as well as non-renal death, and is
considered a marker of general systemic and possibly vascular compromise.20
Proteinuria has also been related to smoking31 and malignancy, which
suggests that it may be a general marker of chronic poor health as well as
acute disease.40

Serum creatinine and calculated GFR

A reduction in glomerular filtration rate (GFR) is the hallmark of renal
failure, and usually only occurs after longstanding structural changes have
occurred in the kidney. Microalbuminuria, hypertension and overt
proteinuria usually precede any fall in GFR by years.
For routine clinical practice, the GFR is most simply estimated from the
serum creatinine, adjusted for the age, weight and sex of the patient,
providing the serum creatinine is stable. The original Cockcroft and Gault
formula for calculated GFR41 has been shown to both over-estimate and under-
estimate true (isotopic) GFR in various situations. These include: extremes
of renal function, obesity, malnutrition, fluid overload, or use of
cimetidine or trimethoprim (blocking tubular creatinine secretion). Several
modifications have been proposed with varying degrees of additional
complexity.42–45 These formulae can be simplified to the approximation:

Calculated GFR (ml/min) = [140 – age (years)] x weight (kg) x 1.23 (males only)
serum creatinine (micromol/L)

This formula assumes the patient is close to ideal body weight. Using the
actual weight of an obese patient will produce a falsely high, calculated
GFR. To estimate upper limit of normal weight, replace actual weight with
(height (metres)2 x 25) or use a nomogram.
No systematic correlations of calculated and true GFR have been
performed in the Aboriginal population, where muscle mass is frequently
clinically greater than the non-Aboriginal population.
[Editor: The term ‘calculated creatinine clearance’ is interchangeable
(for our purposes) with ‘calculated glomerular filtration rate’ (GFR). We
have used the term creatinine clearance (CrCl) in the STM because several
other resources in common use in the Northern Territory also use this term.
The STM protocol does not emphasise the importance of using lean body
mass in the Cockroft calculation, as described above, as this will make it
more difficult to use. The value of the calculated CrCl in the PHC setting
is to monitor progress/deterioration and to trigger referral to specialist
services at an appropriate stage.
The nephrologists reviewing this chapter point out that the stages of
renal failure are fairly arbitrary, are based on expert and consensus
opinion, and we have chosen to use the categorisation used in the American
K/DOQI discussion document and guidelines. They expect future Australian
guidelines to do likewise. There is little evidence to say that referral to
a specialist should happen by a specific CrCl value. Further, the patient
is not likely to be monitored so closely that this difference will be
detected, unless they are under specialist driven care already for some
reason. The point of referral will be determined by the overall complexity
of the case and the skills and confidence of the PHC team as well as the
calculated creatine clearance.
We do not expect using gross weight rather than lean body mass will
often have a negative impact on care except for very overweight people, in
which case their weight if their BMI was 25 should be used.]
The GFR may be increased above normal (known as ‘hyperfiltration’).
Hyperfiltration can occur acutely following a high protein meal or raised
glucose. A more sustained rise in GFR occurs in the presence of obesity or
the inital phases of diabetic nephropathy. These are commonly seen clinical
situations in Aboriginal patients, and can be identified by the recognition
of a serum creatinine reading lower than expected. Hyperfiltration is
believed to accelerate renal injury (the Brenner hypothesis).
Hyperfiltration is reversed by the use of ACE inhibitors or angiotensin
receptor blockers, accounting for the 20–30% increase in serum creatinine
commonly seen after introduction of either of these two classes of
antihypertensives. Provided the serum creatinine plateaus, this rise
therefore represents the unmasking of the ‘true’ serum creatinine, once
hyperfiltration is corrected.

Summary: Assessing renal function

An increasing serum creatinine concentration is a highly specific indicator
of a decline in renal function and is often accompanied by hypertension.
The presence of proteinuria is also a marker of renal disease, but non-
specific. Overt proteinuria with diabetes can be regarded as clinically
diagnosed diabetic nephropathy. Microalbuminuria is a lesser degree of
renal protein leakage and is a precursor to overt proteinuria. An ACR is
the test of choice for microalbuminuria. Expert groups recommend
confirmation of positive results. Semi-quantitative microalbuminuria
dipsticks have a use where laboratory access is difficult and have value as
a screening tool, but positive results also need to be confirmed with an
ACR. In the presence of a high prevalence of microalbuminuria (>20%), these
dipsticks may not be cost-effective. Point-of-care ACR estimates are
acceptable and valid for assessing microalbuminuria in those with diabetes.

Effect of interventions
The prevention of renal disease has been divided into approaches that
describe the onset and stage of renal disease:
• Primary prevention strategies relate to interventions that may prevent
the onset of renal disease.
• Secondary prevention strategies relate to interventions for screening or
the early detection of existing disease, and optimal strategies to
prevent further deterioration.
• Tertiary prevention strategies relate to the prevention and control of
end-stage renal complications.

Primary prevention
In the prevention of renal disease in Aboriginal populations, the likely
important influence of socioeconomic and environmental factors needs to be
acknowledged. Much emphasis is placed on tertiary level interventions and
the optimal treatment of ESRF, and early screening strategies for chronic
renal failure, when the greatest gains in preventability are likely to be
found in the prevention of the socioeconomic and lifestyle related
antecedents of renal disease in Aboriginal populations.

Intra-uterine growth and renal disease

Increasing ratios of current-weight to birth-weight in adults from a small
Aboriginal community have been correlated with an increased risk for overt
proteinuria. It was proposed that this might be due to impaired
nephrogenesis from intra-uterine malnutrition, compounded by the subsequent
development of a pre-diabetic syndrome (syndrome X) of metabolic
dysfunction.12,46 The prevention of intra-uterine growth retardation (IUGR) in
Aboriginal pregnancies, and the prevention of malnutrition in infants,
should continue to be important goals in primary health care. Whether the
prevention of IUGR is often possible and prevents renal disease is still
uncertain.

Adult obesity, smoking and ethanol excess

These factors are unfortunately often closely-linked, and their
modification can offer great benefits. The calorie load of ethanol promotes
obesity and subsequent diabetes. There is a quantitative relationship
between alcohol intake and the level of blood pressure.47 Smoking
independently trebles the risk of kidney failure in several forms of kidney
disease.93

Skin infections and renal disease

Skin infections with group A streptococci (GAS) can cause
glomerulonephritis. A strong correlation was shown in the NT between past
evidence of infection with GAS and the presence of albuminuria in
adulthood.48 There is a strong rationale that more effective control of GAS
skin infections in childhood is required for the prevention of renal
disease. Control of skin infections is described in CDC guidelines and in
the skin infections chapter of this book.

Secondary prevention
Early detection
• Screening for chronic renal disease (proteinuria or microalbuminuria,
followed by serum creatinine and calculated GFR)
• Screening for hypertension, discussed in the adult health check and
hypertension chapters.

Preventing acute deterioration

• Avoidance of volume depletion, radiographic contrast media and NSAIDS

Managing progressive deterioration and late stages of chronic renal

disease
• Monitoring and early referral to nephrology service
• Treatment of hypertension
• Avoidance of dietary protein excess
• Control of diabetes, smoking and dyslipidaemia
• Treatment of anaemia
• Maintenance of acceptable calcium and phosphate metabolism
Screening for proteinuria
The Australia and New Zealand Society of Nephrology consensus statement
(1999) recommended urinalysis for proteinuria as part of the periodic
examination of Aboriginal and Torres Strait Islander patients.49 The Caring
for Australians with Renal Impairment (CARI) Guidelines (2001) recommended
screening for overt proteinuria in patients at increased risk of renal
disease (Aboriginal and Torres Strait Islander population) in conjunction
with access to referral services. There is currently no evidence to support
the mass screening of the general population for renal disease by urine
dipstick, blood sampling or other means, and this is consistent with
Canadian, US and Scottish guidelines.50–53
Because proteinuria is considered an independent predictor of
progressive renal disease in non-diabetic renal disease54 and a predictor
of cardiovascular disease, it has been suggested that proteinuria screening
of the non-diabetic population may provide a mechanism for modifying the
development and progression of cardiovascular disease. No study has yet
explored this.
Aboriginal population-based screening for microalbuminuria has also been
proposed in the Northern Territory.55 Since it is recognised that those
with diabetes should receive annual screening for microalbuminuria, and a
urinalysis for overt proteinuria is recommended within the periodic health
examination of all Aboriginal adults, the role of population-based
microalbuminuria screening may be limited.
[Editor: The CARPA STM no longer recommends annual ACR measurement for
anyone who is known to have albuminuria or, in the case of those with
diabetes, microalbuminuria. We believe these people have an indication for
aggressive BP control with ACEi and or ARB medication and need their
creatinine/calculated CrCl monitored, not their ACR.
Authors’ reply: As a personal view, rather than an evidence-based one,
serial ACRs or PCRs are actually a very nice quantitative way of monitoring
sequential improvements in the glomerular hyperfiltration – it’s the ‘renal
sphygmo’. BPs are too ‘bouncy’ and creatinines are too late to really get a
feel for how well someone is responding (?complying) with treatment.]
At present, there appears to be little evidence to support screening for
microalbuminuria in the general Aboriginal population. However, as a marker
of general vascular disease and early renal compromise, screening this
population for microalbuminuria may complement other risk factor
assessments (such as blood pressure, weight, diabetes, smoking, lipids
etc.) but this has yet to be shown.

Screening for raised serum creatinine

The serum creatinine representing the referral threshold GFR of 30 ml/min
can vary from 140 µmol/L in a 50 kg 60-year-old female up to 400 umol/L in
a 90 kg 20-year-old male. A high serum creatinine is a late marker of renal
failure. By the time a serum creatinine is elevated above the population
normal range up to 50% of renal function may be lost, particularly in small
elderly females. Screening for raised serum creatinine is not recommended,
but calculation of GFR is critically important in those with any known
renal disease and consistent with local and international guidelines.56
[Editor: Note that the CARPA STM protocol suggests initial referral to a
renal physician earlier in the disease deterioration. This is because of
added difficulties in patient education, logistics and ensuring a venous
shunt is established and matured. In many instances referral to a renal
physician as soon as either a raised serum creatinine or low GFR is
identified will be advisable.]

Preventing acute deterioration

Avoidance of volume depletion, radiographic contrast media and NSAIDS
Radiographic contrast media (such as in intravenous pyelograms) may provoke
sudden and severe deterioration in damaged kidneys, and so caution is
advised. The probability of acute renal failure occurring has been
estimated at 5–10% (>25% increase in serum creatinine levels) and 1–2%
(requiring dialysis).
Non-steroidal anti-inflammatory drugs (NSAIDS) (including the newer COX-
2 inhibitors) can cause a significant decrease in GFR in patients with
renal insufficiency (those with GFR 30–70 ml/min), particularly during
episodes of intravascular volume depletion.57,58,59 NSAIDs can also worsen
hypertension (through sodium retention) and hyperkalaemia (through renin
suppression). Paracetamol is the preferred analgesic for mild-to-moderate
pain in patients with renal impairment.
Intravascular volume depletion (such as following recent inadequate
fluid intake, gastrointestinal losses or inappropriate diuretic use) is
another well-recognised cause of acute renal impairment. The degree of
volume depletion required to cause a renal functional deterioration can be
as little as 2% of body weight in the presence of three at-risk situations:
i. pre-existing renal disease (including patients aged over 65 years); ii.
chronic reduction in intravascular volume (cirrhosis, nephrosis, diuretic
use); or iii. impaired renal compensatory mechanisms (ACE inhibitors
blocking efferent arteriolar constriction by angiotensin II or NSAIDs
preventing prostacyclin-induced afferent arteriolar dilatation). Patients
with renal impairment should have intravenous saline provided in such at-
risk situations.60

Managing progressive deterioration

Monitoring and early referral to nephrology service
Once chronic renal disease is diagnosed as the cause, rate of progression
and co-morbidities must be determined. Earlier referral to nephrologists of
patients with elevated creatinine levels is expected to lead to better
health care outcomes and lower health care costs. Adequate preparation for
dialysis or transplantation (or both) requires at least 12 months of
relatively frequent contact with a renal care team.61 Given the rapid
progression of renal disease in many Aboriginal patients, the time between
the onset of microalbuminuria and development of ESRF can be as short as
18–24 months. People with chronic renal failure need regular review,
including calculated GFR and a care plan guided by specialists.
I recommend that the response to ACEi/ARB therapy in all those with
chronic renal failure be monitored by ACR every three to six months. Whilst
the prime target of monitoring is systemic blood pressure reduction to
120/70 if possible, a steady fall in serial ACR or protein:creatinine
ratios may indicate successful intra-glomerular pressure reduction (a
surrogate marker suggesting improved prognosis) as well as confirming
medication compliance. Anecdotally, patients with proteinuria resistant to
ACEi/ARB therapy appear more likely to have irreversible glomerular
disease. Monitoring proteinuria in non-diabetic chronic renal failure may
also assist with therapeutic adjustments. The degree of reduction in
proteinuria with or without concurrent rise in serum creatinine following
ACEi/ARB therapy can be seen as an indication of the degree of
hyperfiltration present prior to therapy.
[Editor: Though monitoring the albuminuria response to ACEi/ARB
treatment has some theoretical appeal, it is yet to be shown to lead to
better outcomes. The CARPA STM does not advocate monitoring the
effectiveness of ACEi or ARB medication via the ACR. It is the blood
pressure that counts, and ‘full doses’ should be used if tolerated, adding
additional medications as needed to achieve the target BP as mentioned. The
effect on the ACR will not generally change management.
This position is supported by anecdotal experience from the Top End,
described here by Dr Christine Connors:
From auditing at Tiwi, and other communities, we know that the level of
monitoring for diabetes and renal disease is actually very high; the bush
staff are doing an extraordinary job of delivering a high level of
monitoring services. However, the proportion of patients achieving target
BP is suboptimal. My experience is that ACRs are variable and, as Paul
Lawton pointed out, there are many factors that will cause this: time of
day; ‘inflammatory’ process; UTI/STI etc. I know that many people,
especially bush nurses, become confused about this variability, and
basically all of us ignore the results. The evidence is very strong that
achieving BP target is renoprotective, there is currently no evidence that
reducing protein further after meeting target BP will affect outcome.
Again, this is a pragmatic solution for PHC teams, not nephrologists, who
will have greater interest and knowledge about variable ACR. We want PHC
staff to save time (and money) by not doing multiple ACR, and use that
time to make conscious decisions about BP results and take appropriate
action (e.g. put chart in box for GP/chronic disease coordinator review,
refer to GP etc.) or increase drug treatment if seen by GP/CD coordinaotr.
Removing the ACR and focusing on BP is the message for improving renal
outcomes. All remote staff I have discussed this with are very happy with
this decision.]

Treatment of hypertension, with diabetic nephropathy

Hypertension, diabetes and renal insufficiency/failure are very common and
commonly coexist in the one person. All need to be managed as part of
whole-person care. However, for protecting renal function the reduction of
blood pressure to target levels is the most important of all interventions.
Several meta-analyses and recent randomised controlled trials describe
the beneficial activity of both ACEi and angiotensin receptor blockers
(ARB), either alone or in combination, in reducing proteinuria in diabetic
renal disease that is independent of the anti-hypertensive effect of the
drug.62–68 A recent systematic review confirmed the progression of
microalbuminuria to overt proteinuria in those with diabetic nephropathy is
delayed by ACEi.69
Reduced progression of proteinuria is protective against ESRF, but few
studies have shown a reduction in ESRF incidence due to treatment with ACEi
or ARB in those with type 2 diabetes. Over 2.6 years, a 20% reduction (p =
0.07) in the risk of nephropathy progression was reported with ARB
Irbesartan in type 2 diabetics. This outcome was achieved with mean blood
pressure approximating 140/80 in both treatment and placebo groups.70
People with type 2 diabetes and microalbuminuria or overt proteinuria
should receive ACEi or angiotensin blockade therapy, regardless of the
presence or absence of hypertension.28 The evidence that this treatment can
prevent ESRF is still lacking71, though it prevents increasing albumin
excretion rates.71
Tight control of blood pressure reduces the rate of progression of
chronic renal failure by about 50%, and some cases of prolonged
stabilisation of impaired kidney function have been described.72 Diabetic
patients with chronic renal failure or overt nephropathy should aim for a
target of less than 130/80 mmHg.28

Hypertension and non-diabetic renal disease

High blood pressure is a strong and independent risk factor for end-stage
renal disease, as shown in a subgroup analysis of the large Multiple Risk
Factor Intervention Trial.73 The control of hypertension in those with
chronic renal failure before the onset of ESRF is the single most potent
intervention to reduce the progression of renal failure and prevent
cardiovascular mortality in those on dialysis.74
The use of ACEi in those without diabetes who show overt proteinuria in
the presence of hypertension has been shown in numerous systematic reviews
and recent trials to be of benefit in reducing the progression to ESRF.75–81
The protective effect of ACEi in chronic renal disease of non-diabetic
origin is certainly due in large part to a substantial decrease in blood
pressure, but ACEi have some independent effects.81 A Cochrane review is
re-examining the impact of antihypertensive agents other than ACEi on non-
diabetic renal disease.82
Evidence supports counselling patients to incorporate regular physical
activity into their daily routines and is recommended to prevent
hypertension, coronary heart disease, obesity and diabetes.83
A lower-than-usual blood pressure goal has also been shown to be
protective in those with proteinuria and non-diabetic renal disease. In two
randomised controlled trials a low blood pressure goal (<130/80 mmHg)
significantly reduced proteinuria during the first four months after
randomisation. Some guidelines recommend a lower blood pressure goal
(<125/75 mmHg) in non-diabetic chronic renal failure, often necessitating
the use of three or more antihypertensive agents in addition to lifestyle
modification.50,84

Limited dietary protein

Dietary protein restriction (‘low’ protein diet of approximately 0.6 g/kg
body weight/day) slows the progression of both diabetic and non-diabetic
renal diseases, according to meta-analysis. In non-diabetic renal disease,
the risk of renal failure and death is reduced by protein restriction by
about 40% as compared with higher or unrestricted protein intake.85,86,87
However, there is potential for adverse consequences in protein
restriction, so expert guidance should be sought in relation to nutritional
intervention in patients with impending ESRF. Protein-restricting diets are
notoriously difficult to implement and require resource-intensive health
education strategies. The potential for health gain versus the opportunity
costs of diversion from other health issues, and the potentially adverse
consequences of an inadequate caloric intake need to be considered.

Control of diabetes, smoking and dyslipidaemia

Deaths due to cardiac disease and atherosclerosis are the most common cause
of death in patients on dialysis, including Aboriginal patients.88 Chronic
renal failure is associated with lipid abnormalities as well as an
increased risk of cardiovascular events predicted by the presence of
proteinuria.31,89 A recent meta-analysis showed that lipid therapy can
decrease proteinuria and preserve GFR in patients with chronic renal
disease.90
Cigarette smoking was associated with an increased risk of end-stage
renal disease in several large studies.91,92 Cessation of smoking has also
been shown to retard the progression of renal failure in those with
diabetes, but this has not yet been shown in those with non-diabetic renal
disease.60

Treatment of anaemia
Recombinant human erythropoietin (EPO) given intravenously or
subcutaneously increases haemoglobin levels, improves quality of life and
avoids blood transfusion in those with anaemia due to uraemia (generally
late-stage renal disease). The major side effect is hypertension (in up to
30% of recipients). The benefits of subcutaneous EPO is that it can be
self-administered and is more cost-effective than when given intravenously.
However, it is an expensive treatment, costing $4000 to $10,000 per patient
per year, and a rare but serious side effect of pure red-cell aplasia due
to anti-EPO antibodies has recently been described.93
There has also been concern that the increased haemoglobin in the pre-
dialysis period may accelerate renal failure. A systematic review concluded
that treatment with EPO in pre-dialysis patients corrects anaemia, avoids
blood transfusions, and increases quality of life and exercise capacity.
Whilst hypertension may be increased, effects on renal progression could
not be confirmed due to short-term studies.94 The general consensus is that
EPO therapy does not affect the rate of progression of renal failure.

Maintenance of acceptable calcium and phosphate metabolism

There is some evidence that control of calcium and phosphate metabolism
(lowering phosphate levels) may prevent the progression of renal function
loss, although most of the evidence arises from animal studies. Effects on
the progression of chronic renal failure are still unclear.95 However, the
onset of severe renal osteodystrophy due to secondary hyperparathyroidism
can be delayed,96,97 particularly when phosphate binders are initiated at an
early and reversible stage.

Summary of interventions
It is important to detect asymptomatic renal disease through screening for
overt proteinuria and microalbuminuria in those with diabetes. Monitoring
for progression to chronic renal failure with a serum creatinine and
calculated GFR is recommended in those found to have overt proteinuria,
diabetes with microalbuminuria and those with a family history of renal
disease.
The treatment of hypertension to a target level below 130/85 is crucial
to prevent progression. The optimal choice of anti-hypertensive is an ACE
inhibitor, as they have been shown to delay the progression of non-
diabetic-related renal disease in the presence of overt proteinuria.
The use of radiographic contrast media requires caution, and NSAIDS
should be avoided in those with renal disease as acute renal failure can be
precipitated.
Dyslipidaemia should be treated to prevent cardiovascular events in
those with a high absolute risk. This treatment may also prevent renal
disease deterioration. Calcium and phosphate monitoring and treatment are
advised to prevent renal osteodystrophy. Therapy for anaemia using
erythropoietin and aggressive iron supplementation (usually parenteral) can
enhance the quality of life.

Tertiary prevention
Early approaches to ESRF management
Failure to recognise impending ESRF is a major contributor to morbidity and
mortality in patients with chronic renal disease. Delayed referral leads to
emergency dialysis, which has a very high mortality (up to 25%) and
prevents an optimal choice in modality of dialysis and psychological
preparation of the patient for ESRF care. Early and coordinated approaches
to the care of patients with impending ESRF may increase the expected
duration and quality of life.
In Aboriginal populations, preparative processes may increase the
acceptance of tertiary level interventions. A quarter of all Aboriginal
people with ESRF in the Northern Territory withdraw from treatment.88 All
renal units in Australia are now encouraged to develop a pre-dialysis
education program for all clients and to be monitored for the proportion of
clients commencing dialysis who have completed an education program.60

Treatment of ESRF
Options for the treatment of ESRF include:
• Dialysis — peritoneal (continuous ambulatory peritoneal dialysis, CAPD,
or automated overnight PD, APD) or haemodialysis
(home/hospital/satellite)
• Transplantation — cadaveric or living/related/ non-related.

Treatment priorities are to maximise independence and rehabilitation by the

most cost-effective option. This means offering transplantation when
available; encouraging home dialysis (CAPD or home haemodialysis); siting
satellite units for maximal access; and reserving medically supervised
hospital haemodialysis for those patients unable to use other options.

[Editor: Timing of referral to kidney specialist:

Paul Lawton (a key contributor to the protocol) points out that the
‘Stages’ flow chart will indicate referral to kidney specialist at <30
ml/min. There is no evidence of benefit of referral earlier than this at
this stage. This is even more pronounced with the knowledge that the
majority will have ‘the usual’ glomerulomegaly with focal scarring and/or
IgM deposition, for which we have no specific ‘specialist’ therapies. Those
who require earlier specialist nephrologist involvement will be picked up
with the other indications for referral —blood in the urine, nephrotic
syndrome, renal artery stenosis, etc.
The whole point of this protocol in the STM is to reduce the numbers
flying in from remote communities for appointments when they can be equally
well managed in community, given the available evidence. ]

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93. Casadevall N, Nataf J, Viron B, Kolta A et al. Pure red-cell aplasia and
anti-erthyropoeitin antibodies in patients treated with recombinant erythropoeitin.
N Engl J Med 2002; 346(7):469–75.
94. Cody J, Daly C, Campbell M, Donaldson C, Grant A, Khan I, Pennington S, Vale
L, Wallace S, MacLeod A. Recombinant human erythropoietin for chronic renal failure
anaemia in pre-dialysis patients (Cochrane Review). In: The Cochrane Library, Issue
2. Oxford: Update Software, 2002.
95. De Zeeuw D, Apperloo AJ, de Jong P. Management of chronic renal failure. Curr
Opin Nephrol Hypertens 1992; 1:116–23.
96. Gonzalez EA, Martin KJ. Renal osteodystrophy: pathogenesis and management.
Nephrol Dial Transplant 1995; 10:suppl 3:13–21.
97. Brookhyser J, Pahre SN. Dietary and pharmacotherapeutic considerations in the
management of renal osteodystrophy. Adv Ren Replace Ther 1995; 2:1:5–13.
 Diabetes
This section is made up of edited extracts from the following publications
(with permission from the authors and publisher) where further information
can be found:
• Couzos S, Metcalf S, Murray RB. ‘Diabetes’ In: Aboriginal Primary
Health Care: An evidence-based approach. 2nd Edition. Oxford University
Press, Melbourne, September 2003.
• National Aboriginal Community Controlled Health Organisation (NACCHO)
as lead agency of the Chronic Disease Alliance of Non-government
Organisations. ‘Prevention of Diabetes’. In: National Guide to a
Preventive Health Assessment in Aboriginal and Torres Strait Islander
Peoples. Feb 2003 (in press).
Readers are advised to refer to the full documents for detailed information
on the prevention and management of diabetes, treatment goals and targets,
case management, program implementation, data collection, and performance
indicators.

Epidemiology and burden of disease

The overall prevalence of diabetes in the Aboriginal population lies
between 10–30% and is generally 3–4 times higher at any age than the
general population, with an earlier age of onset.1 In northern Australia,
the overall prevalence of type 2 diabetes is 4.5% to 19% in Aboriginal
people rising to 40% in people older than 35 years of age.
Aboriginal and Torres Strait Islanders die from diabetes at an earlier
age and at a higher rate than the general Australian population. They are
10 to 13.5 times more likely to die from diabetes than non-Indigenous
Australians.2
Figure 1 below compares the number of deaths per 100 000 population over
a 16-year period between Northern Territory Aborigines, Northern Territory
non-Aborigines and the Australian population as a whole.3
The AusDiab Study (Australian Diabetes, Obesity and Lifestyle) recently
documented the prevalence of diabetes in the general Australian population
(12 000 persons from regions randomly selected across Australia). It found
that 7.5% of Australians over the age of 25 years suffered from diabetes
(of whom half were previously undiagnosed) and a further 10.6% had impaired
glucose tolerance (IGT), whilst 5.7% had impaired fasting glycaemia (IFG),
during 1999–2000. This study did not include sufficient Aboriginal and
Torres Strait Islander people to report on their prevalence of diabetes.4
The AusDiab study in the general Australian population has confirmed
that for every known case of diabetes, there is an undiagnosed case. Among
the Aboriginal population, most studies support that the true prevalence of
diabetes is twice that determined from known cases, though there will be
great variation between sites due to different levels of screening activity
in recent years.1
The incidence of diabetes has been less frequently reported. An eight-
year follow-up study of a population in remote Central Australia (1987–95)
indicated that 2% of the population developed diabetes every year. This
contrasts with rates of 0.25% per year elsewhere. Obesity (BMI >33)
increased the incidence to 5% per year.5
Hospital admission rates for diabetes are also more common in the
Aboriginal population. There were 10–15 times as many hospital separations
for type 2 diabetes for Indigenous males and females compared with the
total Australian population in 1998–9.2
Diabetes is a significant risk factor for cardiovascular disease — the
primary cause of death among Aboriginal people with diabetes (67% of
Aboriginal diabetic deaths were related to heart disease in 1997–99).
However, the most common cause of death in a cohort of Aboriginal people
with diabetes in the Northern Territory was renal failure. Infections were
the next most common cause of death.6

The major types of diabetes

The diagnosis of diabetes ‘is not based on the presence of a discrete
physiological abnormality, but by an imperfectly chosen point on a
continuum of glycaemia’.7
Type 1 diabetes is also known as insulin-dependent diabetes mellitus
(IDDM). Ninety-nine per cent of diabetes seen in the Aboriginal or Torres
Strait Islander population is type 2.1 In comparison, around 10–15% of
diabetes mellitus is type 1 in the general population.4
Type 2 diabetes, also known as maturity-onset diabetes or non-insulin-
dependent diabetes, is the most common. In type 2 diabetes the pancreas can
secrete excess amounts of insulin though it is insufficient to compensate
for the insulin resistance.
Impaired glucose tolerance (IGT) is an intermediate metabolic state between
diabetes and normal glucose control. Those with IGT are at higher risk of
developing diabetes than the general population.8 Some people with IGT will
progress to diabetes, some will return to normal glucose tolerance and some
will continue to have IGT. IGT, like diabetes, is commonly associated with
hyperinsulinaemia and insulin resistance. Clinically significant
microangiopathic renal and retinal complications are very rare in those
with IGT.9
The use of glycated haemoglobin to diagnose diabetes has been explored
as it has been shown that it can also predict the microvascular
complications of diabetes.10 However, there are limitations in the use of
glycated haemoglobin to screen and diagnose diabetes. A number of expert
committees around the world have not recommended the use of HbA1c (glycated
haemoglobin) measurements to diagnose or screen for diabetes.8,11

Primary prevention: Summary

Three recently published studies have demonstrated that the development of
diabetes in people with IGT can be prevented. The Diabetes Prevention
Study12, conducted in Finland with a 3.2-year follow-up, showed that
(intensive) individual diet and exercise intervention conducted by a
dietitian could reduce the risk of diabetes by 58% (p<0.001) in a high risk
population. This was achieved with seven sessions in the first year and
regular three-monthly sessions after that, during which goals were set on
how to lose weight (>5%), decrease total fat intake to <30% of energy,
decrease saturated fat intake to <10% of energy, increase fibre intake to
>15 g/1000 kcal consumed and to exercise for at least 30 min per day. The
control group were set goals and given general written and oral information
about diet and exercise initially and then annually, but no specific
individualised programs were offered. The incidence of diabetes in the
intervention group was significantly lower than the control group (11% vs
23%). Diabetes did not develop in any of the groups who achieved four or
five goals, however, significantly more people were able to achieve these
goals in the intervention group (49 in the intervention group vs 15 in the
control group, p<0.001 for each of the goals). In those who did not achieve
any of the goals the incidence of diabetes was 38% vs 31% respectively.
The Diabetes Prevention Program was a major clinical trial conducted in
the United States over three years in a group with people with IGT and
therefore at high risk of developing type 2 diabetes. The intensive
lifestyle intervention included instruction on a low fat diet, exercising
for 150 minutes per week and behaviour modification skills. The results
show on average that this group had a 7% weight loss in the first year,
sustained a 5% loss for the study’s duration and maintained 30 minutes of
exercise per day. A 58% reduction in the risk of developing type 2 diabetes
was found compared to the control group who received only basic diet and
exercise advice.13
The Da Qing study reported in 1997 that diet and exercise strategies can
prevent the onset of type 2 diabetes in patients with IGT. Both strategies
were equally effective in preventing the development of type 2 diabetes by
31–46% over six years, although the combination of diet and exercise was
not any more effective than either strategy alone.14
In Aboriginal populations leanness appears to protect against diabetes
in all age groups.15 There is indirect evidence that traditionally oriented
Aboriginal people display insulin resistance despite their leanness and
that this is responsible for their predisposition for the Metabolic
Syndrome upon adopting a Western lifestyle. A reversion to traditional
hunter-gatherer lifestyle has been shown to greatly ameliorate the
abnormalities of carbohydrate and lipid metabolism associated with diabetes
and IGT.16
Dietary aspects other than the impact on BMI appear to be important.
These include a sufficient intake of dietary fibre17,64,18,19 and the
consumption of vegetables, rice and pasta throughout the year.20
People with a high intake of dietary fat, especially saturated fat, are
at increased risk of type 2 diabetes, whilst those who regularly consume
fish derive some protection.11

Physical activity
The effect of physical activity in overweight individuals has been shown to
be beneficial even if they remain overweight. In a prospective trial of
middle-aged men the degree of physical activity required appeared to be
moderate, of at least a 40-minute duration per week. The protective effect
was greater in men at high risk for type 2 diabetes (reduced risk by 64%)
with the same level of physical activity and was still protective even at
lower levels of activity.21
As mentioned above, the US and Finnish diabetes prevention studies found
an important role for physical activity in the prevention of diabetes,
though it was not possible to clearly differentiate the relative roles of
diet and exercise.
Because of the high prevalence of diabetes in the Aboriginal population,
and its great impact on morbidity and mortality, its prevention is very
important. This will need to be multifaceted, combining individual
counselling for high-risk people with population approaches (such as store
food policies, amenities for exercise and promoting a healthy lifestyle).
Promotion of improvements in other fundamental socioeconomic determinants
of health is also likely to be important, though how best to achieve this
is unclear. In general community control and self-determination is thought
to be crucial.
People with the metabolic syndrome and/or IGT have the highest risk of
progressing to full diabetes and its complications and should be targeted
for more intensive interventions.

Primary prevention with medication

The US Diabetes Prevention Program reported in 2002 that metformin (850 mg
twice daily) reduced the incidence of diabetes over 2.8 years by 31%
compared with placebo. Metformin was used by those who were at high risk
for diabetes with high fasting and post-load glucose levels (high enough
for IFG or IGT but not diagnostic for diabetes). The protective effect was
such that 14 people would need to be treated with metformin over three
years to prevent one of them from becoming diabetic, at the expense of
higher rates of gastrointestinal symptoms.13 At this stage CARPA is not
recommending this as routine treatment for IGT, though future studies may
change this.

Other factors
There is evidence that low birth weight and poor growth by 12 months of age
can increase the risk of developing IGT and type 2 diabetes — a link
described by the ‘thrifty-phenotype’ hypothesis.22,1 The understanding of
this relationship (sometimes referred to as the ‘Barker hypothesis’) is
evolving and is beyond the scope of this summary.

Screening
For most people diabetes is asymptomatic and will only become known after
testing. Given that diabetes is common in Aboriginal populations, that
there are effective treatment options and that early detection is
relatively easy, CARPA recommends annual screening for diabetes for all
Aboriginal adults.
[Editor: The optimal age at which to start screening can be debated.
Type 2 diabetes occasionally occurs at ages less than 15 years, but is not
common. Screening people in their early teen years is consequently more
likely to lead to false positive results than screening at an older age. As
a pragmatic compromise the screening age has been kept the same as that
used for other components of the Adult Health Check.
Attempts at annual screening lead to many people actually getting two-
yearly screens. Two-yearly screening would be fine but it may not fit with
local management issues like staff turnover, and staff feeling that they
are responsible for it. There is also value in keeping it linked with other
well- person checks that may be more clearly appropriate annually, such as
smoking. PHC delivery issues probably favour annual screening as part of
opportunistic Adult Health Check.]
Extensive experience in remote and urban Indigenous health practice
tells us that effective screening and management of cases needs local
population registers, coordinated care-planning, recall systems, input from
a range of health professionals and a good relationship between the health
service and the people with diabetes.
A US study concluded that type 2 diabetes screening may be cost-
effective if it involves screening high-risk subpopulations and commences
at a younger age.23 No cost effectiveness study for diabetes screening has
been reported in Australia.
The Australian National NHMRC Evidence Based Guidelines for type 2
Diabetes (2002) recommend that diabetes screening should be offered to all
Aboriginal peoples and Torres Strait Islanders aged 35 years and over, but
may need to be commenced at a younger age in some regions.24 Most primary
care providers to the Aboriginal population have already introduced
diabetes screening at a younger age (around 18 years).25
A fasting blood glucose is currently the most widely recommended
screening test for diabetes. The diagnostic criteria for diabetes have been
based on the levels of hyperglycaemia that adequately predict the
development of microvascular complications of diabetes.26 Diabetes is
present if the fasting plasma glucose is greater than or equal to 7.0
mmol/L. In the absence of symptoms this has to be confirmed on a subsequent
day. A random or casual plasma glucose >11.1 mmol/L (with symptoms or
repeated on a subsequent day) is retained as a diagnostic criterion.
A fasting blood glucose may be less than ideal in the field because of
logistic difficulties. In these instances, a random plasma glucose from
venous blood is an alternative.

Should the diagnostic level of fasting glucose also be used to screen

for diabetes?
This issue was investigated in detail in the Australian National NHMRC
Evidence Based Guidelines for Type 2 Diabetes 2002. A fasting plasma
glucose cut-off of 5.5 mmol/L best defined the upper limit of normality,
and values above this indicated that further diagnostic testing was
required (an oral GTT). Applying the guideline-recommended protocol of
measuring fasting plasma glucose in people with risk factors to the general
Australian population would result in 77% of people with diabetes being
identified (with a specificity of 83%) but 25% of those tested would also
require an oral GTT.24 This has been adopted in the CARPA protocol.

Random blood glucose for screening diabetes

The SANDS study questioned the value of a random blood glucose as a
screening tool and concluded that, if the cut-off was 7.5 mmol/L (meaning
that at this level a diagnostic oral GTT was performed), the test would
fail to diagnose 60% of those with undiagnosed diabetes. The investigators
were able to justify the use of a random blood glucose cut-off of 5.5
mmol/L in screening for diabetes, confirming the diagnosis with an oral
GTT.27 This has been adopted in the CARPA protocol acknowledging that it
will often need to be followed up with diagnostic tests. With very high
prevealence rates, many people will be diagnosed (>11.1, later confirmed)
by random BGL testing and it is very important to make the screening
process easy to implement.

Finger-prick blood glucose useful as a screening test

Capillary glucose levels may be slightly different to venous blood levels.8
Blood glucose meters are frequently unreliable and very few evidence-based
guidelines recommend their use for screening. The Australian National NHMRC
Evidence Based Guidelines for Type 2 Diabetes 2002 clearly recommended that
blood glucose meters not be used to screen for diabetes. However, although
a venous sample is preferred, CARPA realises that there can be an advantage
of having instant feedback, and the option of using a glucometer may
increase the amount of screening that is performed. [Editor: Our experience
is that a major barrier to Adult Health Checks is its uptake and promotion
by primary health care staff during their clinical work, despite
theoretical support.] If other blood tests are being done, for example as
part of an Adult Health Check, then the glucometer should not be used.
A lower (5 mmol) throshold for triggering further diagnostic testing is
recommended to allow for a 10% inaccuracy in the glucometer reading.
Similarly, a high reading of 12 mmol is recomended as being likely to
indicate diabetes, all results in between need follow up.

Case management
Relationship with the health service
As emphasised in the tips for managing chronic disease and in the diabetes
protocol, a trusting relationship between the health professionals and the
patient is very important. This is primarily based on our (CARPA)
experience, but also supported by research into compliance issues.

Lifestyle changes
Weight loss
Weight loss in obese patients with diabetes can improve glycaemic control
and reduce the need for oral hypoglycaemics or insulin. Weight reduction
can also reduce blood pressure in obese hypertensive subjects and can
improve hyperlipidaemia.
In one meta-analysis investigating the effect of weight loss in those
with diabetes, dietary strategies alone had the greatest effect on glycated
haemoglobin levels (a 2.7% reduction). A combination of diet plus
behavioural therapy plus exercise also had a strong effect on reducing
glycated haemoglobin, even though only a small degree of weight loss was
achieved.28 Recognition that improved glycaemic control can occur in the
absence of achieving a target weight is important in relation to compliance
issues, health promotion and evaluation of programs.
For the general population calorie restriction diets and appetite
suppressant drugs have good short-term effects, but most of this weight is
regained a few months after treatment.29 A recent systematic review
concluded that fat-restricted diets are no better than calorie-restricted
diets in achieving long-term weight loss in overweight or obese people
(general population).30 Others have concluded that a combination of advice
on diet and physical activity, supported by behaviour therapy, is more
effective than diet or physical activity alone. Strategies that involve
family support, personal contact with therapist, mutliple inteventions and
walking programs appeared most effective.31
 [Editor: As a person increases their exercise, body fat will decrease
but the net effect on weight or BMI may be less than expected because of
increased muscle mass.]

Diet
A diet high in fibre can lower total cholesterol by 10% in those with type
2 diabetes32 and can improve glycaemic control if ingested in large
quantities, but may be unacceptable.33
A diet high in monounsaturated fat and low in carbohydrate can produce a
more desirable plasma glucose, lipid and insulin profile in the short
term.34,35,36 Modifying the frequency of meals and reducing their size so
that there is ‘nibbling versus gorging’ may alter carbohydrate absorption,
resulting in better glycaemic control.37
The avoidance of sugar in the diabetes diet has been aggressively
promoted in the past. However, simple sugars like sucrose (common sugar)
and fructose (fruit sugar) do not need to be avoided as they have not been
shown to adversely affect the blood glucose level any differently from
complex carbohydrates33, nor do they affect the lipid profile.32 There is no
reason to recommend that people with diabetes avoid naturally occurring
fructose in fruits, vegetables, and other foods.
The health promotion of appropriate diet and physical activity in
several Aboriginal communities in Central Australia was associated with
reduced rates of glucose intolerance over a seven-year intervening
period.38 In the Kimberley, involvement in diet and/or exercise strategies
was associated with protection from increases in plasma glucose.39

Activity
In patients with type 2 diabetes exercise may improve glycaemic control,
hypertension and total serum cholesterol levels. A meta-analysis of
randomised controlled trials demonstrated that exercise in those with type
2 diabetes can reduce glycated haemoglobin from a weighted mean of 8.31% to
7.65% (over a mean period of 18 weeks) without any significant change in
BMI (mean weight 83 kg), compared with control groups with no exercise.40
The physical activity to achieve this outcome was three 45-minute moderate-
intensity aerobic workouts per week (similar to goals specified in
Australian guidelines).41
A community-based exercise program for a Native American population with
type 2 diabetes was able to demonstrate reduced weight and improved
metabolic control after 37 weeks of exercise for approximately two hours
per week.103

Smoking
Smoking is a potent risk factor for vascular disease, and it is
particularly important for those at high risk of cardi-vascular disease,
such as those with diabetes, to be encouraged to quit. See the chapter on
tobacco and smoking for more detail.

Alcohol
People with diabetes should avoid more than about 20 g/day (two standard
drinks). Alcohol consumed in large amounts provides a heavy caloric load,
encourages obesity, adds to psychological stress, damages the liver and
pancreas and raises blood pressure and lipids — all factors which
complicate management. Alcohol can cause severe and life-threatening
hypoglycaemic episodes, particularly among diabetics on insulin or long-
acting sulphonylureas, and can significantly complicate infections such as
pneumonia.

Glycaemic control
Glycaemic control in type 2 diabetes can prevent microvascular disease
(small vessel damage seen in the retina and kidneys) and macrovascular
events (damage to large conduit vessels such as coronary, cerebrovascular
and peripheral vessels) in obese patients.
In those with type 2 diabetes, a six-year Japanese study — which
compared intensive insulin therapy with conventional insulin therapy —
demonstrated a beneficial effect in preventing macrovascular disease in the
intensively treated group. This was noted despite no change in lipid
profiles and hypertension status between the type 2 diabetes groups, and no
difference in weight from baseline after six years. The average BMI (BMI =
21) of the participants was, however, much less than usually seen in
patients with type 2 diabetes, and no blinding was reported.42
This study also demonstrated that intensive insulin therapy (three or
more daily injections) in patients with type 2 diabetes significantly
prevented microvascular complications to a greater degree than conventional
insulin therapy (one or two daily injections of intermediate insulin).
The UK Prospective Diabetes Study (UKPDS) reported 10 years of follow-up
in those with type 2 diabetes, but did not demonstrate reduced diabetes-
related deaths, stroke, amputation, death from peripheral vascular disease,
or all-cause mortality from intensive insulin nor oral hypoglycaemic
treatment (sulphonylureas) when compared with conventional dietary therapy.
The median HbA1c values over 10 years were significantly lower in the
intensive than in the conventional group (7.0% compared with 7.9%). This
degree of glycaemic control appeared to make no difference in influencing
the absolute risk for fatal myocardial infarction, heart failure, or
angina. The aggregate absolute risk for myocardial infarction (fatal and
non-fatal infarction as well as sudden death) was of borderline
significance in favour of intensive glycaemic control. Consequently, the
UKPDS did not support the theoretical risk that exogenous insulin adversely
affected cardiovascular status.43
The situation was quite different and unexpected in overweight type 2
diabetes clients (median baseline BMI = 32) treated with metformin in the
UKPDS. These patients were treated so that fasting blood glucose remained
below 6.0 mmol/L, and were kept on monotherapy until marked hyperglycaemia
occurred. Intensive blood glucose lowering lead to significantly reduced
macrovascular events. There was a 36% lower risk of all-cause mortality,
and 39% lower risk of myocardial infarction. The reduction for aggregate
macrovascular disease (stroke, peripheral vascular disease, infarction, and
sudden death) was 30% greater in the metformin group over 10 years than
conventional treatment. Metformin lead to significantly less weight gain
than sulphonylurea or insulin therapy while achieving the same degree of
glycaemic control.44
The UKPDS demonstrated that intensive glycaemic control in those with
type 2 diabetes, either through insulin or sulphonylureas, can
significantly decrease the risk of aggregated microvascular complications
(in mildly obese or non-obese clients with type 2 diabetes with median
baseline BMI = 27) when compared with conventional treatment such as
regular dietary advice. The absolute risk reduction was 2.8 events
prevented per 100 patients over 10 years. This means that 36 clients with
type 2 diabetes need to be intensively treated in order to prevent one
microvascular event over 10 years, when compared with dietary treatment
alone. However, most of the benefit was due to reduced retinal
complications. The progression of retinopathy after 12 years was reduced by
21%. The need for retinal photocoagulation was also significantly reduced
when compared with diet therapy. However, reno-protection from improved
glycaemic control in type 2 diabetes was not confidently demonstrated.
Whilst intensive treatment with sulphonylurea therapy or insulin lead to a
67% risk reduction in the proportion of patients who had a two-fold
increase in plasma creatinine, the result was not significantly different
from progression in the diet-treated group over 10 years. The progression
of microalbuminuria and overt proteinuria varied between the groups but
differences remained insignificant after 15 years. The progression to renal
failure was reduced but the difference between the treatment groups was
also insignificant. Intensive therapy was also less protective for other
microvascular endpoints such as differences in ankle reflexes, or autonomic
markers.43
There is a special case for insulin treatment in those who have recently
had a myocardial infarct. In the DIGAMI study, intensive insulin therapy
started within 24 hours of infarct (mean age 68 years) and continued
thereafter; this significantly reduced mortality over 3.4 years compared
with conventional therapy. The absolute reduction in mortality was 11%,
implying one saved life for nine patients treated for 3.4 years.45

Oral hypoglycaemic drugs

The timing for the introduction of oral hypoglycaemic drugs has to be
negotiated with the person with diabetes and should be influenced by the
severity of their diabetes (e.g. fasting BGL) and the presence of symptoms
or complications.
In patients with type 2 diabetes, metformin is the drug of choice,46,47
Metformin produces a reduction in fasting (15–20%), post-prandial (45%) and
glycated haemoglobin by 1.2%, which is similar to suphonylurea drugs.46
Further, long-term therapy reduces plasma triglyceride concentrations by
10–20% and reductions in total cholesterol and LDL have been reported,
independent of its glycaemic effect.32,48 In comparison to sulphonylureas,
metformin does not cause weight gain or increase insulin
concentrations.46,47 A systematic review also concluded no increased risk of
lactic acidosis from metformin.49
Alpha-glucosidase inhibitors such as Acarbose can be used as first-line
therapy with diet and exercise, or in combination with sulfonylureas to
lower hemoglobin A1c concentrations an additional 0.5–0.9%.50 These agents
inhibit polysaccharide digestion and therefore glucose absorption, which
decreases post-prandial hyperglycaemia. They have only modest anti-diabetic
action and hence a limited role.
The thiazolidinediones are a new class of oral agents that decrease
insulin resistance. Troglitazone belongs to this class, but was withdrawn
in the US in March 2000 due to associated liver injury. Newer agents have
been approved in Australia (rosiglitazone and pioglitazone) for mono or
combined therapy with metformin or sulphonylurea. These agents lower
hemoglobin A1c concentrations an additional 0.6–0.8% compared with
baseline, alone, in combination or with insulin. There is no evidence to
indicate they are better than other drugs.
Patients should not be started on the glitazones if there is any history
of underlying chronic liver disease, e.g. cirrhosis, and probably chronic
hepatitis. Treatment should be avoided if the ALT is more than 2–3 x upper
limit of normal [Editor: Which is tricky as many of our patients have fatty
liver with mild elevations in ALT which will actually improve on any BG
lowering treatment]. It is recommended to check LFTs at four weeks, then
three monthly and, if the ALT becomes more than three times the upper limit
of normal, treatment should be ceased. Prescribing requires monitoring
alanine amino transferase (ALT) e.g. two-monthly testing in the first 12
months of therapy.51
Most patients with type 2 diabetes over time will require multiple oral
hypoglycaemic therapy for glycaemic control.52

Insulin (in type 2 diabetes)

Those with type 2 diabetes can become insulin-deficient over time because
of the progressive decline in pancreatic beta-cell function and will
require insulin therapy to achieve optimal glycaemic goals.53 The UKPDS
Group reported that, over six years, 53% of type 2 diabetics treated with
sulphonylureas required additional insulin therapy to reach glycaemic goals
(fasting plasma glucose <6 mmol/l).54
When insulin is used in those with type 2 diabetes very high doses are
often required, and consequent increased weight gain can be a problem.55
The use of insulin in poorly controlled type 2 diabetes patients is
controversial and there appears to be no consensus on the optimal
commencement time. The decision can be based on when poorly controlled type
2 diabetes becomes symptomatic, or oral therapy fails to achieve target
glycaemic control. If there is persistant ketonuria, this strongly suggests
a need for exogenous insulin. [Editor: However, because insulin use
requires an additional level of patient education and motivation, it is
crucial to involve the patient, and possibly their carers, in the decisions
about using insulin. This may take more than one attempt.]
The main aim of introducing insulin therapy in patients with type 2
diabetes is to optimise glycaemic control in order to prevent microvascular
diabetic complications and to relieve the symptoms of poorly controlled
hyperglycaemia. The protective effect of insulin was no different from that
achieved with oral sulphonyureas in the 10-year UKPDS, although the rate of
a major hypoglycaemic event every year was almost twice as high (2% per
year) when using insulin. Due to the risk of complications, significant co-
morbidity (e.g. cerebrovascular disease, ESRF, cardiac failure) should be
considered a possible contraindication to tight control in type 2 diabetes.
[Editor: Seek specialist advice re risks and benefits.]
Three meta-analyses have confirmed that combined insulin and oral
hypoglycaemic (sulphonylurea) therapy in type 2 diabetes results in lower
insulin doses than insulin alone to achieve similar glycaemic
control.56,57,58 In addition, combined therapy improved glycaemic control in
type 2 diabetes patients without a significant change in body weight.
Reductions in glycated haemoglobin of 1.0–1.5% with lower insulin doses
were seen in the combined insulin groups.
Common combinations include sulphonylureas plus evening or bedtime
intermediate or long-acting insulin. The combination of sulphonylurea plus
metformin plus insulin has been used infrequently, and is therefore less
well studied. [Editor: The UKPDS data compares early introduction of
insulin with standard non-insulin–based management. This is a different
issue to the use of insulin in ‘failed’ oral Tx. A common problem seen in
clinical practice is; what is the best strategy when diet and oral drugs
have failed? There are only a few options (can be combined):
 • Check and reinforce compliance with diet, exercise and oral drugs
• Switch to or add insulin (which will improve glycaemic control, which
is a beneficial thing)
• Leave glycaemic control and focus on other CV risk factors to decrease
overall risk
One of the major changes in the fourth edition of the CARPA STM is the
promotion of nocturnal insulin in this situation.]

Monitoring glycaemic control

Glycated haemoglobin measurement is the accepted gold standard for
monitoring glycaemic control. Australian guidelines recommend that HbA1c be
measured every three–six months for insulin-treated patients and every six–
12 months for patients with type 2 diabetes who are not on insulin.59
Glycated haemoglobin (expressed as %HbA1c) is measured from red blood
cells and, because cell turnover occurs every three months or so, there is
little value in performing the test at intervals less than three months.60
The optimal glycaemic goal is a HbA1c <7%, although the lower the
glycaemic threshold, the lower the risk of complications. This may be
unrealistic for some people and less stringent treatment goals may be
appropriate for patients with limited life expectancies, in the very young
or older adults, and in individuals with comorbid conditions.61 [Editor: A
goal of HbA1c <7% will not be achievable for many people, and could lead to
a further sense of failure for staff and patients. In the protocol we
stress that any decrease is in HbA1c is beneficial and suggest 8% as a more
realistic target.]
An evaluation of a point-of-care glycated haemoglobin testing program
(DCA 2000) in 42 ACCHSs, in which 2315 Aboriginal people with diabetes were
monitored, showed that point-of-care HbA1c testing served as a catalyst to
enhance patient self-management, was acceptable to Aboriginal health
workers, produced acceptable results, and led to more opportunistic
testing.62,63 A Medicare rebate to cover the cost of cartridges was introduced
in 2000 (item No 73840, $14.15 per tests, 4 x per year).

Self-monitoring of glucose
Self-monitoring is useful for adjusting insulin requirements. For those not
needing insulin it is unlikely to be useful unless it leads to changes in
lifestyle, treatment, motivation or sense of control.
A meta-analysis of trials of self-monitoring of BGL in type 2 diabetes
did not provide evidence for reduction of glycated haemoglobin, nor was
there any effect on body-weight.64 Most of the trials involved clients who
were not on insulin. However, there have been some more recent studies that
suggest a small improvement in HbA1c might be attributable to self-
monitoring in type 2 diabetes.65
The benefits for patients with type 2 diabetes in relation to quality of
life remain to be proven. No matter how hard some patients try to achieve
glycaemic control, their blood glucose values continue to fluctuate in an
alarming way. This can lead to despair and learned helplessness.66
Self-testing for glycouria is unpredictable in relation to glycaemia.
Blood pressure and renal disease
Treatment for hypertension
Hypertension is very common in those with diabetes, thought to be twice
that in those without diabetes. Hypertension in patients with diabetes is
associated with accelerated progression of both microvascular (retinopathy
and nephropathy) and macrovascular (CHD, stroke, peripheral vascular
disease) complications.67 The AusDiab study showed that there is nearly one
untreated and possibly undiagnosed Australian with hypertension for every
person on treatment.4
Lowering blood pressure in those with diabetes is effective at reducing
both macrovascular and microvascular events. Weight loss (even small
reductions such as 3–9% of body weight), increase in physical activity68,
and reduction of sodium intake69 have been shown to improve blood pressure
control.70 A reduction in alcohol consumption from more than two standard
drinks per day reduces blood pressure of both hypertensive and normotensive
people according to two systematic reviews.70,71 (Most of the hypertension
studies have been conducted in the general population without diabetes.)
Non-pharmacological measures should be encouraged as first-line therapy.
Treatment of hypertension in those with diabetes (with or without pre-
existing heart disease) is effective at reducing cardiovascular morbidity
(AMI, stroke) and cardiac death.72 This was shown in several systematic
reviews.73,74,75
In the UK Prospective Diabetes Study (UKPDS) study, lowering the mean BP
to 144/82 mmHg (‘tight blood pressure control’ compared with less tight
control of 154/87 mmHg) achieved significant reductions (44%) in fatal and
non-fatal stroke compared with less tight BP control over nine years. The
21% reduction in risk for myocardial infarction was not statistically
significant, but when all macrovascular diseases were combined — including
myocardial infarction, sudden death, stroke, and peripheral vascular
disease — the group assigned to tight blood pressure control had a
statistically significant (34%) reduction in risk compared with the group
assigned to less tight control.76 Combination therapy with more than one
agent was required in one third of those with type 2 diabetes in the UKPDS
group assigned to tight BP control.
Treatment of hypertension in the UKPDS also significantly prevented
microvascular complications in those with type 2 diabetes by 36%. This was
mainly due to a significant reduction in the risk of requiring retinal
photocoagulation over a median 7.5 years of treatment. Six clients with
type 2 diabetes need to have their blood pressure intensively controlled
over 7.5 years, in order to prevent a two-step retinopathy progression in
one of them. The magnitude of this benefit appears greater than that
achievable through intensive glycaemic control. The deterioration of visual
acuity can also be prevented suggesting the prevention of diabetic
maculopathy. Renal complications could not be prevented by tight BP
control.76
The tighter the control of BP in those with type 2 diabetes, the greater
the reduction in cardiovascular events.72 The HOT study demonstrated that
in patients with diabetes a lower diastolic blood pressure (<80 mmHg) led
to a 51% reduction in major cardiovascular events (fatal and non-fatal
myocardial infarction and strokes and all other cardiovascular deaths) over
3.8 years, compared with a diastolic blood pressure of <90 mmHg.77
The HOPE Study (3577 with diabetes, of whom 98% were type 2, mean age 65
years, mean BMI 28.5, mean baseline BP 142/80 mmHg) was largely a primary
prevention trial for those with diabetes. It compared the use of ramipril
with placebo and found the risk of the aggregate of cardiovascular death,
myocardial infarction, or stroke was significantly reduced by 25% over 4.5
years. There was also a significant relative risk reduction in total
mortality (24%), myocardial infarction (22%) and stroke (33%).78
The MICRO-HOPE substudy assessed the effect of ramipril in those with
diabetes, plus at least one other cardiovascular risk factor (total
cholesterol >5·2 mmol/L, HDL cholesterol <0·9 mmol/L, hypertension, known
microalbuminuria, or current smoking). Subjects had no overt proteinuria
when therapy commenced. Ramipril significantly reduced the risk of overt
nephropathy by 24%, and combined overt nephropathy, laser therapy or
dialysis by 16% over 4.5 years, when the baseline blood pressure on average
was 142/80 mmHg.78
Other studies have shown that the progression of microalbuminuria to
persistent proteinuria can be reduced by ACEI or Angiotensin Receptor
Blockers (ARB) in both hypertensive and normotensive patients with type 1
diabetes and in hypertensive type 2 diabetics79,80 With ACEI, the risk of a
doubling of the serum creatinine was reduced by half over a median follow-
up of three years, as was the combined risk of death, dialysis or
transplantation in type 1 diabetics. A systematic review of trials also
confirmed that ACEI can arrest or reduce the albumin excretion rate in
microalbuminuric normotensive diabetics, as well as reduce or prevent an
increase in blood pressure in both type 1 and type 2 diabetics.81
Overall, the control of hypertension reduces microvascular complications
in those with type 2 diabetes more than glycaemic control does.82 The number
of patients with type 2 diabetes who need to be treated over 10 years to
prevent one patient developing any complication was 6.1 (95% CI interval
2.6 to 9.5) and to prevent death from a cause related to diabetes 15.0
(12.1 to 17.9).76 No studies have as yet shown a reduction in end stage
renal failure (ESRF) incidence or mortality from renal failure, due to
hypertension treatment in patients with type 2 diabetes.

Target blood pressure

The American Diabetes Association recommend a target blood pressure goal of
<130/80 mmHg if it can be safely achieved. There is no threshold value for
blood pressure, and risk continues to decrease well into the ‘normal’
range. Behavioural and lifestyle therapy is warranted for the first three
months if BP is between 130–140 mmHg systolic or 80–90 diastolic, before
commencing antihypertensives, and those with BP >140/90 should be commenced
at the same time as lifestyle advice.67Australian Guidelines recommend a
target <130/85 mmHg.83
Blood pressure should be measured at least annually in those with
diabetes. However, most health care providers will measure blood pressure
more frequently than this. Several evidence-based guidelines suggest
measuring blood pressure at every clinic visit in patients with
diabetes.83,67

Choice of medication
There is evidence that ACE inhibitors have renal protective effects, as
demonstrated by their ability to reduce proteinuria and prevent renal
deterioration more effectively than other classes of anti-hypertensive
agents in diabetic patients. They do not adversely affect glucose control,
they favourably affect lipids and they reduce left ventricular hypertrophy.
The Australian Diabetes Society recommends that ACE inhibitors are the
drug of choice in diabetic patients with microalbuminuria (with or without
hypertension) or overt nephropathy, while beta-blockers or calcium channel
blockers were recommended for diabetic patients without nephropathy but
with angina. The NT Coordinated Care Trial hypertension guidelines have
concluded that the favourable lipid profile associated with ACEI use and
the higher absolute cardiovascular risk in Aboriginal populations support
the first-line use of ACEI regardless of diabetes. Since the introduction
of ARB’s the American Diabetes Association recommend either ACEI or ARB in
hypertensive patients with microalbuminuria or clinical albuminuria/
nephropathy.67

Ischaemic heart disease

Aspirin prophylaxis
There is good evidence that aspirin can prevent adverse vascular outcomes
in those with diabetes. Aspirin is protective in those with diabetes who do
not have heart disease (primary prevention) and in those with pre-existing
heart disease (secondary prevention). Twenty-six poeple with diabetes
needed to be treated with aspirin (75–325 mg/day) over a median of two
years to prevent against a ‘vascular event’ (non-fatal myocardial
infarctions, non-fatal strokes, or vascular deaths)84
Three primary prevention trials — including the Physicians Health
Study,85 the Early Treatment Diabetic Retinopathy Study (ETDRS)86 and the
Hypertension Optimal Treatment (HOT)87 trial — all reported that aspirin
reduced the risk for acute myocardial infarction in those with diabetes,
and to a similar degree to those without diabetes.
A collaborative overview of 145 trials reported secondary prevention
against cardiovascular disease and death from aspirin in subgroups with
diabetes. Diabetic subjects had risk reductions that were comparable to
non-diabetic individuals.88
The American Diabetes Association guidelines recommend aspirin therapy
for all patients with diabetes.89 Contraindications include aspirin
allergy, bleeding tendency, anticoagulant therapy, recent gastrointestinal
bleeding and clinically active hepatic disease. Australian guidelines also
recommend aspirin (75–325 mg/day) for people with type 2 diabetes.90

Lipids
(Also see the separate chapter on lipids.)
Lipid abnormalities — such as elevated low-density lipoprotein (LDL)
cholesterol, and reduced high-density lipoprotein (HDL) cholesterol —
increase the risk of cardiovascular disease in those with or without
diabetes.90 Hypertriglycerideamia is more common in those with diabetes or
IGT, and is an independent risk factor for cardiovascular disease. Alcohol
intake (even modest quantities) can exacerbate hypertriglycerideamia.
Lipid-lowering agents can reduce the risk of cardiovascular disease in
those with diabetes. Reduced risk has been shown in those without pre-
existing heart disease (primary prevention) and in those with previous
acute myocardial infarction (AMI) or angina (secondary prevention).84
Several studies have confirmed that lipid-lowering drugs protect against
CV events in those with diabetes who had previous AMI or angina. The
Scandinavian Simvastatin Survival Study, or ‘4S’, showed that the relative
risk reduction of a major cardiovascular event was of equal magnitude to
that observed in non-diabetic patients (55%, 95% CI 24–73%) over a median
of 5.4 years.91 The LIPID study reduced cardiovascular events in diabetics
over 6.1 years by 16%, but this was not statistically significant. The
Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial
(VA-HIT), led to a 24% decrease in cardiovascular events in diabetic
subjects with prior cardiovascular disease over 5.1 years.92
Weight loss has been associated with improvements in triglyceride
levels, a reduction in total and LDL cholesterol and increases in HDL
cholesterol.93 There have also been reports of a beneficial effect of
exercise on the lipid profile.32,94 Because physical activity is recommended
and shown to be of benefit in weight loss, it is recommended for all
patients with diabetes.41
Dyslipidaemia will improve with a low saturated fat diet replacing
saturated fats with carbohydrate and monounsaturated fats.93 This will also
reduce the risk of coronary heart disease.94
Australian guidelines recommend those with diabetes have annual
assessment of serum lipid levels to assess cardiovascular risk. Lipid-
lowering therapy should be initiated immediately in those with existing
coronary heart disease and a total cholesterol >4 mmol/L. In all those with
diabetes, lipid-lowering therapy should be implemented if dietary advice is
ineffective in reducing total cholesterol to target levels after six weeks
(and total cholesterol is >6.5 mmol/L). A total cholesterol <4 mmol/L (LDL
cholesterol <2.5 mmol/L) is the recommended target. Almost all guidelines
recommend screening using fasting serum specimens for determination of HDL
cholesterol and triglyceride levels in those with diabetes (even though TGs
are only affected by non-fasting).32 When the patient is on drug therapy,
lipid profiles should be repeated every two months to assess progress until
stable and satisfactory. Choice of therapy is detailed in the Australian
Lipid Management Guidelines,94 Australian cardiovascular drug guidelines95
and NHMRC Diabetes Guidelines.32
[Editor: Note that the lipid protocol in the CARPA STM regards diabetics
as being in the highest risk group, along with those who have had a
myocardial infarct. This is outside the scope of many current guideline
recommendations. We believe the combination of: the high incidence of
ischaemic heart disease, the high-risk state of most Aboriginal patients
with diabetes (by virtue of other components of the metabolic syndrome and
the efficacy of lipid treatment as primary prevention of ischaemic heart
disease), make earlier and more aggressive use of lipid-lowering medication
warranted.]

Diabetic retinopathy
Diabetic retinopathy is a specific microvascular complication of diabetes
characterised by microaneurysms, haemorrhages and other abnormalities in
the retina leading to bleeding and new vessel formation in the eye and,
ultimately, blindness. The associated macular oedema occurs from the
increased permeability of retinal vessels. The early changes can only be
detected by eye examination. The case for regular screening and treatment
of diabetic retinopathy is well described in the OATSIH Specialist Eye
Health Guidelines.96
There is little data on the prevalence of diabetic retinopathy in
Aboriginal populations. However, based on unpublished studies from around
Australia, the crude prevalence of diabetic retinopathy in those with
diabetes did not differ between Aboriginal and non-Aboriginal populations
(8–35%).97 It is uncertain what proportion of blindness in the Aboriginal
population is due to diabetes, though we would now expect it to overtake
trachoma as the leading cause.
 Only good glycaemic and blood pressure control and laser
photocoagulation treatment are known to prevent and slow the progression of
diabetic retinopathy. Timely laser therapy reduces the rate of vision loss
by 80–90% among patients with proliferative retinopathy over two years and
this underlies the rationale for regular screenign for diabetic
retinopathy.96
Given that around 20% of those with type 2 diabetes have retinopathy at
the time of diagnosis, screening for retinopathy should be started at the
time of diagnosis. The rate of progression of early retinopathy to high-
risk stage is thought to be only about 1% per year.96 However, we recommend
that in the Aboriginal and Torres Strait Islander population retinal and
eye examinations should be conducted every year, as some will be missed in
some years and other eye conditions will be detected as long as visual
acuity is measured as part of the screening (especially since those with
poor glycaemic control or proteinuria are at greater risk of retinopathy
progression). This is consistant with other reviews and guidelines.96,98
Examinations will be required more frequently if retinopathy is
progressing, and women with pre-existing diabetes who become pregnant
should have close follow-up throughout pregnancy.99
Screening should include visual acuity with vision worse than 6/12
leading to referral.96 Screening can be done by appropriately skilled
clinicians, or better as part of an organised system of retinal
photography. Non-mydriatic fundal photography has enabled retinal screening
to take place without the need for on-site ophthalomologists. It requires
the use of a specialised camera, and photographs can be taken through a
dilated or non-dilated (non-mydriatic) pupil. An ophthalmologist in the
referral centre can then assess photographs.
Indirect ophthalmoscopy is sensitive and specific enough but requires
specialised experience and skill not usually found in primary health care
settings. Screening for DR with a camera is generally more sensitive and
specific than direct ophthalmoscopy.100
Retinal photography has the advantage of possible immediate patient
feedback and the permanent record allows quality assurance and monitoring
of progressive changes. A systematic review of DR screening techniques
supports retinal photography with mydriasis as the preferred method.101 It
has been evaluated in remote Aboriginal community screening programs and
found to be as good or better than indirect fundoscopy.102 There are now a
number of regions successfully using retinal cameras for DR screening in
Australia.
A number of studies have concluded that screening people with diabetes
for retinopathy is cost effective, especially compared to the cost of
caring for people that would otherwise be blind.103,104 The marginal gains in
cost utility of annual over second or third yearly screening were modest in
a US model, though annual screening was more cost-effective for populations
who are at high risk for retinal complications (with poor glycaemic
control).105

Infections
People with poorly controlled diabetes are prone to infections.9 Infections
increase insulin resistance and worsen diabetes control and should be
considered in the differential diagnosis of a sudden deterioation in
glycaemic control.
 Infections in Aboriginal patients with diabetes are very common. The
age-adjusted relative risk for hospital admission resulting from infection
for Aboriginal patients with diabetes presenting to health services in
Central Australia was nearly three times greater than for those who did not
have diabetes. Infection was the most common reason for attendance at a
health service. Infections accounted for 21% of deaths in Aboriginal
patients with diabetes followed for seven years (late 1980s). Furthermore,
deaths occurred at a young age, with a median of 55 years.106 Infection with
diabetic foot complications was the commonest cause for admission in
Central Australia between 1992 and 1997.107
Those with diabetes should receive advice regarding the early
presentation of soft tissue infections and symptomatic urinary tract
infections. Pneumococcal and influenza vaccination is recommended for
Aboriginal patients with diabetes regardless of age.

Feet
This is discussed in detail the following separate chapter.

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 The Diabetic Foot

Author: Dr Sharon O’Rourke (Cairns Diabetes Centre)

Topic Reviewer: Dr Dan Ewald

Introduction
Relevance to the CARPA STM
Diabetes is increasingly common throughout the world. The recent AUSDIAB
survey conducted in Australia found that 7.5% of adults over the age of 25
had diabetes and an additional 16.8% had impaired glucose tolerance.1 The
prevalence of diabetes in Indigenous populations is even higher with rates
of 10 to 20% reported.2 In addition, Aboriginal and Torres Strait Islander
people with diabetes develop diabetes and its complications at least 20
years earlier than non-Indigenous people. Diabetic foot complications are
the commonest reason for hospital admissions.3 People with diabetes are
three to seven times more likely to have a non-traumatic amputation than
people without diabetes.4 The National Diabetes Strategy and Implementation
Plan has advocated a 50% reduction in amputations from diabetic gangrene as
a target for Australia.5
The NHMRC sponsored a National Evidence-Based Guideline for the
Management of Type 2 Diabetes Mellitus, Identification and Management of
Diabetic Foot Disease.6 The guideline is written primarily for general
practitioners in recognition that medical management of type 2 diabetes in
predominantly carried out in general practice. In rural and remote areas it
is often Indigenous health workers and remote area nurses who are
responsible for delivering primary care services and will also find the
guideline useful. The guideline is summarised in this background paper.
Readers are encouraged to source the original document at the Diabetes
Australia web page.

Regional epidemiology
In Central Australia, during the six-year period 1992–97, there were 378
hospital separations of people with diabetes, and foot complications for
174 individuals.7 The number of hospital separations with diabetic foot
complications tripled from 28 per year in 1992 to 90 per year in 1997, and
accounted for 11% of all admissions for diabetes in 1997. This equates to a
rate increase from 98 to 285 per 100 000 per year for hospital separations
with foot complications for people over 15 years of age.8 Each year, two
thirds of these hospital separations are for people with repeated
admissions in the same year. Of the 613 diabetic foot complications, 7%
were amputations, 28% surgical debridements, 34% ulcers of the lower limb
and 28% were infections of the lower limb.
Aboriginal people with diabetes are over-represented in this group,
accounting for 90% of the hospital separations and 90% of the individuals
admitted with foot complications. As is seen in other populations males
were over-represented, accounting for 52% of separations. The cost of
hospitalisations with diabetic foot complications in 1997 was over half a
million dollars.7
 Diabetes-related lower-limb amputation rates for Australia have been
reported using the National Hospital Morbidity Database.9 The Northern
Territory rate was reported as 18.86 (95% CI 15.53–22.19) per 100 000 total
population, or about 36 amputations per year. This compares to 2629 +/- 47
amputations in all of Australia per year or 13.97 (95% CI11.98–15.87) per
100 000 total population. This data needs to be interpreted with caution
since it does not distinguish between multiple amputations in the same
individual, and it is generally accepted that diabetes is not consistently
recorded in hospital records.
In the Central Australian review of hospital separations with diabetic
foot complications mentioned above, the foot complications were
predominantly of the acute type (90%), amenable to early intervention.7
In the past, diabetic foot ulcers and infections often led to
amputation. Fortunately, at least 50% of these amputations can be prevented
with simple inexpensive measures that are readily implemented in rural and
remote locations by a variety of health professionals. Simple screening
techniques to identify those at risk of ulceration and amputation, targeted
education in basic self care of the feet and careful follow-up of these
high-risk patients with regular podiatry and protective footwear will
prevent most ulcers. Multidisciplinary management of active lesions will
prevent or limit the level of amputation.
The Darwin Hospital High Risk Foot Service has reduced major amputations
over three years by almost 50%, from 12 to six major amputations a year.10

Key issues
The key issues in preventing amputations are:
1. How to identify those at risk
2. How to deliver services to protect feet
3. How to manage active foot lesions to minimise limb loss

How to identify people with diabetes who are at risk of ulceration and
amputation
(National Guidelines 1, 2, 3, 4, 5, 6, 7)
The National Guideline has adopted two tiers of risk for diabetic foot
problems.
‘at risk’: people with neuropathy or
peripheral vascular disease or
foot deformity

‘high risk’: people with foot deformity with

(neuropathy or peripheral vascular disease)
or previous ulcer
or previous amputation
Many factors in addition to neuropathy, vascular insufficiency and
deformity interact to result in diabetic foot ulcers. Shoe trauma (rubbing)
is frequently the pivotal triggering event that precedes ulceration or
amputation. Simple, careful, practical clinical assessment of the person
and their feet is the cornerstone to the identification and risk assessment
of diabetic foot problems. Detailed neurological examinations and vascular
assessments are not necessary to identify individuals at risk of ulceration
and amputation.
 Peripheral neuropathy is common, with 12.3% present at diagnosis and 30%
after 12 years in a UK population11, however, not everyone with peripheral
neuropathy is at high risk. Symptoms of pain or altered sensation, signs of
decreased vibration perception or absent ankle reflexes do not reliably
indicate increased risk of ulceration or amputation. It is important to
determine the extent of neuropathy. The 10 g monofilament is a simple,
inexpensive device that predicts ulceration with sensitivity of 90% and
specificity of 86%.12 Failure to feel the monofilament at one non-callused
plantar site is predictive of future foot ulceration.
[Editor: Not all diabetic patients who develop ulcers or foot infections
have neuropathy detectable with the 10 g monofilament. This is said to be
‘common’ in at least one specialist diabetes practice in the Top End (pers.
comm. Dr Di Howard). This may be be because of different patterns of injury
and infection in the Aboriginal population compared to those in which the
monofilament test was validated. The CARPA editorial committee is concerned
that too much emphasis may be placed on the monofilament assessment at the
expense of full assessment of other aspects of diabetic feet.]
A history of claudication strongly suggests peripheral vascular disease
but the absence of claudication does not exclude ischaemia. Pain was
completely absent in 73.8% of 104 people with diabetes, peripheral vascular
disease and an ulcer.13 The presence of palpable pedal pulses is a good
predictor of adequate circulation.14
[Editor: Local experience suggests that skin perfusion may be poor while
peripheral pulses are almost always present, even with advanced foot
disease. (opinion)]
The presence of ischaemia increases risk of amputation. It increases the
risk of a mid-foot or higher amputation 90 times.15 Previous ulceration
proved to be the highest risk factor for development of ulceration (RR
56.8, p = 0.00001).16
Foot deformity — including hallux deformities, claw or hammer toes, bony
prominence and Charcot foot — in the presence of peripheral neuropathy with
loss of protective sensation was associated with twice the risk of
ulceration.12 The presence of callus (a diffuse hyperkeratotic area usually
related to a bony prominence) is highly predictive of ulceration in that
area (RR 11.0, CI 2.8–43.2, p = 0.004).16
Previous amputation increases the risk of ulceration and further
amputation.12,17

Interventions to protect high risk feet

(National Guidelines 3, 7, 8, 10)
Specific foot care education for people with diabetes improves knowledge
and may improve self-care behaviour. The systematic review by Mason et al.
recommended additional research to clarify this issue.18 Inconsistent
interventions, major differences in populations studies, different
endpoints and short duration of follow-up makes the interpretation and
application of studies difficult.
The frequency of foot examinations in people with at-risk feet, but
without a current active problem, should be every three to six months
(consensus statement only).
Reducing plantar pressures is the basis of treating foot ulcers and
preventing ulcers. Plantar pressures may be reduced by 26% by removing
callus19, by 31% with padded socks20, orthotics21 and at least 29% with
running shoes.22
 Regular podiatry review provides an opportunity to reinforce self-care
behaviours and early treatment in people with high-risk feet.23 Podiatry in
combination with protective footwear resulted in a significant reduction in
amputations in a randomised controlled trial of people with high-risk
feet.24
Extra-deep footwear with custom made insoles reduces plantar pressures
by up to 50%.22 This type of footwear is recommended for people at greatest
risk (previous ulcer or amputation, deformity and peripheral neuropathy).
A history of an ulcer or amputation indicates life-long risk of
recurrent foot ulceration and amputation.

Management of active lesions

National Guideline 11: ‘People with diabetes who have foot ulcers or with
high risk feet should be cared for by a multi-disciplinary service which
should include at least a physician and podiatrist and have ready access to
a specialist nurse, orthotist and surgeon.’
Multidisciplinary teams in a number of centres have been successful at
reducing amputation rates by at least 50%.25,26 A similar approach including a
simple recall system reduced hospital admissions, mostly for diabetic foot,
by 32% in one year in remote communities of the Torres Strait.27
In a study of 80 first amputees an ulcer preceded 84% of amputations,
although many different intermediate pathways were identified.28 Careful
monitoring of a ulcer is essential as infection, ischaemia and poor wound
healing may lead to amputation.
In a prospective study of 189 Swedish men and women, at five years there
was a 49% recurrence of amputation with 85% of new amputations preceded by
an ulcer.17 Recurrence rates such as these highlight the need for lifelong
surveillance for people with ulcers or amputations.
A prospective study of Native Americans in a rural setting illustrates
the need for a systematic approach to service delivery.29 After an initial
reduction in amputation rates of 28% with the introduction of screening for
high-risk feet and early treatment, the introduction of a comprehensive
management strategy reduced amputations by a further 48%. The strategy
included a specialised foot care team, consensus guidelines, standing
orders, flow charts, tracking/follow-up and evaluation of the program.
[Editor: The protocol emphasises early, aggressive use of antibiotics in
the management of diabetic foot infection/ulcer. This is supported by the
predominant role of infection in diabetic foot complications seen in the
NT.7,30 Giving antibiotics is relatively easy to do but should not be
regarded as all that is needed. A search for the precipitating cause (e.g.
bad footwear) and relieving pressure and patient education are also needed.
Also note that cheap soft running shoes may be a good choice for many
remote diabetic patients. They can reduce planter pressures and protect
feet from injury.]

Summary of evidence from the National Evidence Based Guideline

for the Management of Type 2 Diabetes Mellitus
There is a direct relationship between glycaemic control and peripheral
neuropathy in people with diabetes.31 Results of randomised controlled
trials in type 1 and type 2 diabetes have shown that improvement in
glycaemic control is effective in reducing the risk of development and
progression of peripheral neuropathy.32,33
 In addition, a healthy lifestyle incorporating good nutrition, regular
physical activity and no smoking will improve glycaemic control and
decrease the risk of developing peripheral vascular disease.
There is evidence from a systematic review of 20 prospective
observational trials that achieving the best possible glycaemic control in
people with type 2 diabetes will prevent or reduce the development of
peripheral neuropathy.34 Several systematic reviews of studies of non-
randomised controlled trials also support the elements of the CARPA
guideline.18,35,36
Level II evidence from randomised controlled trials supports the use
of:37
• Specific foot-care education for people at risk of foot problems
• Therapeutic footwear combined with podiatry in high-risk individuals
• Orthotics to reduce callous

Evidence from well-designed population-based studies or representative

cohort studies is accepted as level II evidence for risk factors and
diagnostic studies. Level II evidence is available for:
• Peripheral neuropathy as a risk for foot ulceration and amputation38
• Assessing for peripheral vascular disease by inquiring about symptoms
of intermittent claudication39

Level III-2 evidence from comparative studies with concurrent controls and
allocation or non-randomised (cohort studies), case-control studies, or
interrupted time series with a control group is available for:40
• Footwear and padded socks to reduce plantar pressure
• Multidisciplinary teams and foot clinics

Evidence from less–well-designed population-based studies or non

representative cohort studies or well-designed case-control studies is
accepted as level III evidence for risk factors and diagnostic studies.
Level III evidence is available for:
• Regular assessment for PVD41
• Employing measures to reduce excessive foot pressures in people with
neuropathy and foot deformities42
• Using a monofilament to detect loss of protective sensation43
• Assessing for peripheral vascular disease by palpation of pedal
pulses44

Specialist diabetic foot-care team

All members of the primary health care team, including Aboriginal health
workers, can be trained to provide essential foot care services, screening,
education for high-risk feet, routine podiatry (including callus
debridement). Active problems, ulcers and infection, need to be managed in
consultation with an experienced medical practitioner and referred to a
Specialist Diabetic Foot-Care Team whenever possible. [Editor: If this is
not possible, try to get specialist advice by phone.]
Date of literature review for this article: 30 September 2001

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33. DCCT The Diabetes Control and Complications Trial Research Group. The effect
of intensive treatment of diabetes on the development and of long-term complications
in insulin-dependent diabetes mellitus. N Engl J Med 1993; 329:977–86.
34. Gaster B, Hirsch IB. The effects of improved glycaemic control on
complications in Type 2 diabetes. Arch Intern Med 1998; 158:134–40.
35. Mayfield JA, Reiber GE, Sanders LJ, Janisse D, Pogach LM. Preventive foot
care in people with diabetes. Diabetes Care 1998; 21:2161–77.
36. National Evidence Based Guideline for the Management of Type 2 Diabetes
Mellitus, op cit.
37. National Evidence Based Guideline for the Management of Type 2 Diabetes
Mellitus, op cit p 75.
38. National Evidence Based Guideline for the Management of Type 2 Diabetes
Mellitus, op cit p 40.
39. National Evidence Based Guideline for the Management of Type 2 Diabetes
Mellitus, op cit p 66.
40. National Evidence Based Guideline for the Management of Type 2 Diabetes
Mellitus, op cit p 86.
41. National Evidence Based Guideline for the Management of Type 2 Diabetes
Mellitus, op cit p 44.
42. National Evidence Based Guideline for the Management of Type 2 Diabetes
Mellitus, op cit p 50.
43. National Evidence Based Guideline for the Management of Type 2 Diabetes
Mellitus, op cit p 60.
44. National Evidence Based Guideline for the Management of Type 2 Diabetes
Mellitus, op cit p 66.
Exercise Program Guidelines

Author: Anne Jones (ASH, Physiotherapy Dept)

[Editor: This section is included because some practitioners may feel more
comfortable with more detailed instructions on promoting exercise among
their clients. Further, some people come to a health service seeking
technical advice on how they should be exercising, and it seems some people
respond well to a ‘prescription’ (medicalisation of exercise) of exercise
and Active Australia has encouraged this from GPs in the past. It was not
included as a protocol in the CARPA STM as it may have limited
applicability. Future feedback from users of the STM will guide its
inclusion in future editions.]

Guidelines
Exercise benefits people with the following conditions:
• Chronic lung disease
• Cardiac disease
• Hypertension
• Diabetes
• Obesity
• Everyone!

How to promote exercise with patients

• Encourage the person to start with an activity that they enjoy. For
example, brisk walking, swimming, football, lifting weights.
• If the person hasn’t exercised for a while, measure the person’s heart
rate and blood pressure taken prior to starting the person on an
exercise program.
• Encourage the person to exercise at a set time each day and to try and
stick to this time.
• Explain to the person that they should not exercise when it is hot or
very cold as this can over stress the body.
• Encourage the person to exercise with another person, as it is more
fun.
• Explain to the person that they need to exercise at a level which
allows them to carry on talking, saying four to five words between
breaths. The person should not be gasping for breath but would be
unable to sing a song if asked to.
• The exercise should cause a light sweat and feel somewhat hard. The
person may be able to exercise only for five minutes or up to 40
minutes.
• Explain to the person that they need to exercise for as long as they
are able to, three to five times a week.
• Encourage the person to warm up by starting with a slow walk for about
five minutes if able. They should then do some stretching exercises.
 The person then does their exercise. After exercising the person needs
to walk slowly for five minutes and do some gentle stretches to cool
down.
• The person will find that exercising will become easier as the weeks
progress. The person needs to then increase the time that they spend
exercising or increase how hard they exercise.
• Initially exercise should begin at 60–70% of maximum heart rate and
progress over four to six weeks to 75–80% of maximum heart rate.

Precautions
• Explain to the person that if they develop increased shortness of
breath, so that talking is difficult whilst exercising, that they
should exercise at a slower pace or stop exercising and get more advice
on their exercise plans.
• Explain to the person that if they develop chest pain, become wheezy,
feel nauseated, become dizzy, become very tired or start coughing up
blood, stop exercising immediately and go to the health clinic.
• Explain to the person that they should not exercise after a meal for
at least one to three hours.
• Explain to the person that they need to take their medication as
directed by the doctor. For example, if they take a bronchodilator and
get short of breath on exercise then they need to take their
bronchodilator 15 mins prior to exercising.

People needing a review by the doctor before commencing exercise

• Recent cardiac surgery, MI or episode of unstable angina
• Moderate to severe cardiac disease
• Recent thoracic surgery
• Severe pulmonary disease
• Unstable diabetes
• Moderate to severe hypertension
• Pregnant women

How to work out a person’s training heart rate

220 – the persons age = maximum heart rate.
Maximum heart rate x 60–80% = training heart rate range.
Let’s say the person is 35 years old:
220 – 35 = 185 (MaxHR)
185 x 0.6 = (60% training percentage) = 111
185 x 0.8 = (80% training percentage) = 148
Training heart rate range = 111–148

Exercise program theory

Exercise has been proven to be beneficial in the treatment and prevention
of many conditions. Physical inactivity is estimated to be responsible for
about 7% of the total burden of disease in Australia (Mathers et al. 1999).
This places it second behind tobacco in terms of importance in health
promotion and disease control (AIHW 2000). Forty-three per cent of adult
Australians did not undertake appropriate levels of physical activity to
achieve health benefits (AIHW 2001).
The exercise guidelines in the CARPA manual were designed from
guidelines and research already undertaken and published in a wide range of
places. Although many of the guidelines have been developed using non-
Indigenous people, population-based studies show that they are applicable
to a wide range of populations (AIHW 2000). These guidelines are applicable
to the Aboriginal population as many of the diseases that exercise can
benefit are seen in the Indigenous population (Swanson 1999, Walsh 2001).
Cardiovascular disease, chronic respiratory disease, obesity, diabetes and
hypertension are diseases prevalent in the Indigenous community.
The National Heart Foundation reports that ‘. . . people who are not
physically active are twice as likely to die from coronary heart disease as
those who are . . .’ (Shilton et al. 2001). Ian Ring (cited in Walsh 2001)
states that mortality from ischaemic heart disease is twice as high in the
Aboriginal population as compared with the non-Aboriginal population, being
six to eight times higher in the age range of 25–64 years. Smoking is twice
as common in Aboriginals as compared with non-Aboriginals, type 2 diabetes
is two to four times higher and obesity and low physical activity is
common. Forty per cent of Aboriginals reported no leisure time physical
activity compare with 34% for other Australians (ABS 1995). In 1995 the
highest levels of physical inactivity was reported in the NT (40%) compared
to all other states (ABS 1995). Over seven million Australians 25 and over
are overweight, two million are classified as obese and three million have
high blood pressure (AIHW 2001).
Research has shown that moderate levels of exercise can:
• Reduce systolic and diastolic blood pressure (AIHW 2001, Chisholm et
al. 1994, NCPAD 2000, Rockville 1995, Shilton et al. 2001) on average
by 11 and 8 mmHg respectively (Taylor 2002)
• Improve exercise tolerance significantly in patients with chronic
respiratory disease (Ries et al. 1997) and cardiac disease (Rockville,
1995)
• Improve the symptoms of dyspnea in chronic respiratory disease patients
(Ries et al. 1997)
• Improve blood lipids by reducing total cholesterol by 6%, reduce low
density lipoprotein by 10% and increase high density lipoprotein by 5%
(AIHW 2001, Chisholm et al. 1994, Shilton et al. 2001)
• Favourably influence body weight (AIHW 2001, Chisholm et al. 1994,
Henry 2002, NCPAD 2000, Shilton et al. 2001, Whedon & Dobbins 2000)
• Prevent 30–50% of new cases of type 2 diabetes (AIHW 2000)
• Help improve quality of life (AIHW 2000)

The exercise guidelines are consistent with all of the guidelines

referenced below (except for ‘How to work out a person’s training heart
rate’). The more accurate way includes using a person’s resting heart rate
in the equation, but this is more difficult and is likely to deter people
from measuring their training heart rate. Therefore, the less accurate
equation was chosen as the recommendation. Having a training heart rate is
needed to determine the intensity level of exercise. Exercising three to
five times a week and preferably for 20–40 minutes has been shown to give
the effects stated above. For those who are unable to exercise for 20
minutes then starting at a level that is obtainable and gradually
increasing the time is better than no exercise. Moderate intensity exercise
has been shown to be all that is needed and using a target heart rate is
the easiest and most reliable measure of intensity of exercise. If the
intensity is too low or high then the benefits of exercise appear to be
reduced (AIHW 2000). Moderate intensity exercise places people at a lower
risk of cardiovascular incident whilst providing safety and beneficial
effects (AIHW 2001). Hagberg and Associates (as cited in Taylor 2002)
reported that moderate activity produced on average 50% greater reduction
in systolic blood pressure as compared to high intensity exercise. They
also reported that the diastolic blood pressure had slightly larger
decreases when moderate exercise was performed as compared with intense
exercise (AHCPR 1995, Chisholm et al. 1994, National Cardiac Rehabilitation
Advisory Committee 2000, Ries et al. 1997, Shilton et al. 2001, Taylor
2002, Whedon & Dobbins 2000).

Guidelines developed from:

Australian Bureau of Statistics (ABS): 1989–1990, 1995 National Health Surveys.
AHCPR (1995): Clinical practice guideline no.17 Cardiac rehabilitation. Table 16
Alternative approaches to cardiac rehabilitation: Randomised controlled trials.
http://hstat.nlm.nih.gov/
Australian Institute of Health and Welfare (AIHW) (2001): Heart, stroke and vascular
diseases: Australian Facts 2001. www.heartfoundation.com.au/statistic
Australian Institute of Health and Welfare (AIHW) (2000): Physical activity patterns
of Australian adults. www.aihw.gov.au/publications/health/papaa/index.html
Chisholm D, Ashwell S, Flower D, Hazel J, Jenkins A, O’Dea K & Zimmett P (1994):
Diabetes and exercise: Series on diabetes No.4
www.health.gov.au/nhmrc/publications/fullhtml/di5.htm
Henry L (2002): Dealing with Diabetes. Muscle and Fitness www.fitnessonline.com
health>illness>specific diseases>article
Mathers C, Vos T & Stevenson C (1999): Burden of disease and injury in Australia.
AIHW Cat No. PHE 17 Canberra:AIHW
National Cardiac Rehabilitation Advisory Committee (NCRAC) of the National Heart
Foundation of Australia (2000): Recommendations for Cardiac Rehabilitation
www.heartfoundation.com.au/prof/04_recom_rehab.html
Pulmonary Rehabilitation Services Ohio State University Medical Centre (2001):
Health for life: Pulmonary Rehabilitation Program Activity Guidelines
http://www.acs.ohio-state.edu/units/osuhosp/patedu/ homedocs.pdf/dis-
cond.pdf/respirat.pdf/act-guide.pdf
Ries A, Carlin B, Carrieri-Kohlman V, Casaburi R, Celli B, Emery C, Hodgkin J,
Mahler D, Make B & Skolnick J (1997): Pulmonary Rehabilitation: Evidence-Based
Guidelines. Chest 112: pp 1363–96
www.chestnet/health.science.policy/quick.reference.guides/pulmrehab.qrg.html
Rockville (MD) (1995): Cardiac Rehabilitation: Evidence-based guidelines. US
Department of Health and Human services, Public Health Services, AHCPR. October; p
202 http://www.guidelines.gov/index.asp
Shilton T, Abernethy P, Atkinson R, Bauman A, Brown W, Naughton G, Oldenburg B, Owen
N & Wright C (2001): Promoting physical activity Ten recommendations from the Heart
Foundation www.heartfoundation.com.au/ prof/docs/promo_physi_act.htm
Swanson N (1999): The Northern Territory Experience: Background to the Preventable
Chronic Disease Strategy). Aboriginal Health Strategy Unit Territory Health Services
Taylor A (2002): Physical Activity: Another resource in the arsenal in fighting
hypertension. Get Active 1(3): p 4.
The national centre on physical activity and disability (NCPAD) (2000): General
Exercise Guidelines www.ncpad.org
Walsh W (2001): Cardiovascular Health in Indigenous Australians: a call for action.
The Medical Journal of Australia 175: pp 351–2.
Whedon B & Dobbins K (2000): Get fit now- Ask me how
www.worldfitness.org/program.html
 Healthy Choices for Food and
Activity

Authors: Vivienne Hobson (DHCS); Fran Keeble-Buckle

Topic Reviewers: Dr Alison McLay (Public Health Nutritionist, Alice Springs);

Angela Peermen (RAN, Oenpelli Clinic); Dr Dorothy McKerras (MSHR)

Introduction
A healthy lifestyle includes, amongst other things, optimal nutritional
intake and participation in adequate physical activity. These two areas
form the basis of much of the preventive component of the NT Preventable
Chronic Disease Strategy. As contributors to the overall burden of diseases
in the general population, lack of physical activity (6.7%), obesity
(4.3%), inadequate consumption of vegetables and fruit (2.7%) and high
blood cholesterol (2.6%) are major risk factors.1
An increasing health issue in Australia, and particularly amongst
Aboriginal people, is overweight and obesity. In the 1994 National
Aboriginal and Torres Strait Islander Health Survey, 36% of men and 29% of
women were classified as overweight and an additional 25% of men and 29% of
women were classified as obese.2 Overweight and obesity are underlying risk
factors for cardiovascular disease, type 2 diabetes and some cancers.
Nutrition and physical activity are core to the prevention and management
of overweight and obesity.
This section is concerned with some key nutrition messages aimed at
preventing overweight and obesity, and guidelines to encourage
participation in physical activity at a level for health gain.

Explanation and expansion of the guidelines

Eat a variety of foods
Research has shown that diets with little variety are associated with
increased risk of mortality.3 Other studies have shown that diets that are
limited in variety are likely to be deficient in at least one nutrient.
Also, by eating a variety of foods, the proportions of major dietary
components such as protein, carbohydrate and fat are more likely to be
appropriate, rather than any being in excess. This is of particular
importance in the prevention of overweight and obesity, which has been
linked with excess fat in the diet.
Consuming a wide variety of foods is the best way to ensure all nutrient
needs are met and minimise the risk of nutrient deficiency diseases. A
varied diet will also minimise risk factors for preventable chronic
diseases, such as cardiovascular disease, type 2 diabetes and certain types
of cancer. It is also a good way to minimise the risk of intake of toxic
substances that may be naturally occurring in some foods or contaminants,
and to minimise the risk of nutrient deficiency diseases. Finally, when the
diet is varied and well balanced the likelihood of nutrient interactions
that may effect the absorption, metabolism or retention of other nutrients
is minimised.3
 It is difficult to measure dietary intake of Aboriginal people because
of a range of cultural, social and ethical factors. In remote areas, it has
been estimated that approximately 95% of the food eaten by Aboriginal
people comes from the community store and takeaway.4 However, this is from
studies about a decade old — and the other 5% relates to bush foods (this
was done in a community where most people did not have the traditional
right to access food from the land the community was on) and many
communities now have takeaway shops.
‘Store turnover’, which measures the through-put of foods through the
community store over a given period, is a validated research tool to
estimate the apparent dietary intake of Aboriginal people in remote
communities. Store turnover studies have shown that most people only have
access to a very limited selection of foods within the store.
The Australian Guide to Healthy Eating is one food guide designed to
demonstrate a varied diet and the approximate proportions of each food
group required in order to meet nutrient requirements. This guide is based
on the NHMRC The Core Food Groups.5 Recently, an Aboriginal and Torres
Strait Islander version of this guide has been developed which also
includes bush foods.

Eat more bush foods

Before European settlement Aboriginal people led a nomadic hunter-gatherer
lifestyle and their diet was varied and rich in nutrients. The food supply
was diverse and affected by geographical location, climate, season and
cultural beliefs. Even in arid areas there was a variety and abundance of
both animal and plant foods.4
The traditional Aboriginal diet is low in fats and sugar and high in
vitamins, minerals, protein and fibre. High sugar foods — such as honey
ants, sugarbag, other nectars and honey — are considered delicacies and are
not available for much of the year or only eaten in small amounts. Meats
from native animals and other wild game meats are generally low in fat,
particularly saturated fat, compared to other contemporary meat sources.
Bush vegetables, seeds and fruits are rich in vitamins and minerals. The
green plum, for example, has the highest concentration of ascorbic acid of
any known plant. Seeds of the acacia species are high in the essential
oils, linoleic and oleic acids.4

Eat more fruit and vegetables

An adequate consumption of fruit and vegetables is protective against
diseases such as coronary heart disease, hypertension, stroke, type 2
diabetes and many forms of cancer. Many of these diseases are of higher
prevalence amongst the Aboriginal population.6
Results from national surveys have shown that Australians do not consume
enough fruit and vegetables. For people living in remote communities in the
NT fruit and vegetable consumption is further compromised because of
limited availability and high costs. The NHMRC publication Core Food Groups
recommends intake of two serves of fruit and five serves of vegetables per
day.5 Note, however, that recommendations ‘per day’ usually mean averages
over some period of time (e.g a week) and so the fact that people do not
eat something the day before a survey does not necessarily mean they do not
meet the recommendations.
The National Nutrition Survey 95 indicates that Australians are not
eating adequate fruit and vegetables.2 Nationally, excluding juice, 42% of
adults did not eat any fruit and 16% had no vegetables on the day of
survey. For fruit, amounts were mostly met in the very young, but fell
sharply to their lowest level during adolescence after which they rose
again with age. Intakes range from 26–60% of recommended when juice is not
included. Intake of vegetables is only 32–60% of that recommended.
Vegetable intake shows a steady increase with age, with males eating more
potato than females, to give a higher total. Adolescents and young adults
are the groups least likely to meet their requirements of fruits and
vegetables.
Territorians have the lowest fruit and vegetable intake in Australia7,
though the NT sample in the National Nutrition Survey may have been too
small to draw strong conclusions. Interestingly, juice intake is higher
than for the rest of Australia. This could be because of reduced
availability, poorer quality and higher cost of fruit in the Territory.
A small number of community stores have been surveyed over the past 10
years and data indicates that the average recorded availability per head
for fruit and vegetables is 103 g per person, which is only 15% of
recommended amounts. Store turnover studies completed in 2001 have shown
that ‘the average person’ is eating only one-third serve of fruit per day
and one serve of vegetables per day.
Market Basket Surveys were carried out in 54 stores across the Northern
Territory between April and June 2001.8 This information provides us with
details about the availability, quality and cost of foods. Analysis showed
that the average number of fresh vegetable choices was 12. For fruit, the
average number of fresh choices available was six. Some stores had no fresh
fruit or vegetables available on the day of the survey and others had very
limited amounts. The price survey showed that on average fruit costs 39%
more and vegetables cost 45% more in remote communities when compared to a
Darwin supermarket chain store. This includes both fresh and tinned
produce. It should be noted that the price of food is already higher in
Darwin when compared to other capital cities.
In a setting where fresh vegetables may be in low supply or of poor
quality, processed vegetables such as frozen, dried and canned should not
be ignored. It may be difficult to increase consumption, particularly in
remote communities, if we promote only fresh produce when the nutritional
value of frozen and canned is similar to fresh produce.

Eat less fatty food and fried food

Fat is the macronutrient with the highest energy value (kilojoules) per
unit weight. Fats and oils may be invisible in the diet, hidden in foods
such as pastries, cakes, confectionery, biscuits and nuts. There is some
evidence that high fat intakes are associated with overweight and obesity.
The results of the 1995 National Nutrition Survey showed that total fat
intake was approximately one third of total energy, with saturated fat
around 12.5%, polyunsaturated fat around 4.5% and monounsaturated fat
around 11.5%.2
A high saturated fat intake is associated with increased plasma LDL
cholesterol, major risk factor for CHD. This has been demonstrated
repeatedly. The first reported association between saturated fat intake and
CHD was the Seven Countries Study, and this has been confirmed in numerous
observataional and experimental studies since then. Trans-fatty acids were
also reported to be associated with CHD in the Nurses Health Study.3 A meta-
analysis of randomised controlled trials has shown that dietary
interventions altering the type of fat reduce cardiovascular outcomes in
the primary prevention situation, but not necessarily total mortality (see
Cochrane Collaboration).
The 2000 Dietary Guidelines for Americans recommends a saturated fat
intake of 10% of kilojoules, and this is a feasible target for Australians
to aim for. With this reduction in saturated (and trans) fatty acids, the
National Heart Foundation (NHF) recommends an increase in polyunsaturated
fatty acids to approximately 8–10% of the total energy intake. Oils rich in
polyunsaturated fatty acid lower plasma total and LDL cholesterol. During
the mid 1960s the population started to increase their intake of
polyunsaturated fats with the introduction of polyunsaturated margarines
and oils and it was around this time that the deaths from CHD started to
decline in Australia3 (although there may be other explanations).
Mono-unsaturated fats found in olive and canola oils may be of
particular benefit in reducing both total and LDL cholesterol and in
reducing risk of CHD.
Omega 3 polyunsaturated fatty acids found in fish oils are of special
benefit in reducing the risk of CHD, and for this reason the NHF has
recommended inclusion of two fish meals per week. The NHF also recommends
inclusion of both plant and marine omega 3 fatty acids as they may protect
against CHD through different mechanisms.9
In remote communities, store turnover has shown that fatty meats
contribute nearly 40% of the total energy in the northern coastal
communities and over 60% in central desert communities. Takeaway foods also
contribute a lot of fat to the diet. In some of the larger northern coastal
communities it has been estimated that 25% of all food purchased comes from
the takeaway with the most popular takeaway foods being pies, chips and
fried chicken legs. Both fatty meat and takeaway foods are high in
saturated and trans fatty acids.10

Eat less sugar and sweet food

Many foods contain naturally occurring sugars, but in other foods sugar is
added during processing to increase palatability and shelf life. Sugars
provide an easily absorbed source of energy, but large amounts are not
desirable. There is an association between sugar intake and dental caries,
and if the sugar is in the form of sugar-sweetened drinks there is an
association with obesity and dental caries, particularly in children. Foods
(and drinks) high in sugar may also displace more nutrient-rich foods in
the diet.
Australian adults obtain about 45% of their energy requirements form
carbohydrates, and about one half of this is from sugars (which includes
the natural sugars found in milk and fruit as well as sucrose from refined
sugar cane). Store turnover studies have shown that Aboriginal people in
remote communities have a much higher consumption of sugar, with refined
sugar contributing approximately 30% of the total energy intake. This
equates to approximately 260 grams (nearly 50 teaspoons) of sugar per
person, per day. 60% of this sugar comes from white sugar per se, with
carbonated drinks providing much of the remaining sugar. Excessive
consumption of sugary foods and limited physical activity contribute to
weight gain and increased levels of triglycerides in the blood.

Drink plenty of water

Water is essential for life. The average adult man requires 3000 ml of
fluid a day and the average woman at least 2200 ml. Approximately 1000 ml
of water comes from solid food and an addition 250 ml comes from the water
of oxidation. The remainder must come from water and other fluids. This
equates to approximately six to eight glasses of fluid a day, and more in a
hot climate.0
The average turnover of water in a 70 kg adult is equivalent to 2500–
3000 ml per day. Water loss from lungs through respiration and skin
(perspiration) is responsible for approximately half of this loss, and at
high temperatures these losses may be even higher. Water depletion can lead
to heat exhaustion, loss of consciousness and heat stroke. Exercise can
exacerbate this water depletion. Another health effect of poor fluid intake
is increased risk of kidney stones, and adequate fluid is also necessary to
prevent constipation.
[Editor: The recommendation to ‘drink more water’ is partly based on the
expectation that this may displace some soft drink consumption.]

Be more active
There has been a growing consensus among epidemiologists, health
professionals and experts in exercise science that moderate amounts of
physical activity can greatly improve health and quality of life and result
in significant savings in health expenditure.11
In 1996 the first US Surgeon General’s report on Physical Activity and
Health was published. This report confirmed the protective effect of
physical activity in relation to prevention of cardiovascular disease,
diabetes and some cancers. Some of the mechanisms for the protective effect
of physical activity in relation to cardiovascular disease are through
lowering the risk of hypertension. Also, physical activity may increase HDL
cholesterol that transports cholesterol away from blood vessel walls and
reduces the risk of development of atherosclerotic plaque.12
Another major disease that is partly caused by inactivity is type 2
diabetes. Physical activity is important in the prevention and management
of type 2 diabetes. Physical activity uses up some of the excess glucose in
the blood, enhances the body’s sensitivity to insulin and reduces central
obesity. Physical activity is also believed to help in the prevention of
hypertension, colorectal cancer and osteoporosis. Studies confirm the
benefits of physical activity in treating mild to moderate unipolar
depression. Some studies have shown that physical activity is beneficial in
treating anxiety, sleep disorders and in improving the quality of life.11
Physical activity is also of major importance in the prevention of
overweight and obesity. In 1997 the NHMRC released a report ‘Acting on
Australia’s Weight’.13 The trends of increasing overweight and obesity in
the Australian population over the last few decades were attributed to the
decline in physical activity in this same period. This decline in physical
activity resulted from a decrease in incidental activity because of greater
use of labour saving devices, as well as a decline in participation in
active recreational activities.
In 1998 the Commonwealth Department of Health and Family Services
published the health response to Active Australia, titled Developing an
Active Australia: A framework for action for physical activity and health.
This document outlined the importance of physical activity in the
prevention of all the National Health Priority Areas (cardiovascular
disease, cancer, mental health, diabetes and injury).14
The first physical activity guidelines in Australia were released in
1997 by the Commonwealth Department of Health and Aged Care. These
guidelines incorporated the current view of physical activity for health,
as well as the previously developed concepts of exercise for fitness. They
stressed the importance of all forms of activities, including simple
movement, to low to moderate intensity physical activity, to more vigorous
activity. The Australian guidelines are:
1. Think of movement as an opportunity, not an inconvenience.
2. Be active every day in as many ways as you can.
3. Put together at least 30 minutes* of moderate intensity physical
activity on most, preferably all, days.
4. If you can, also enjoy some regular, vigorous exercise for extra
health and fitness.

* These 30-minute sessions can be a single session, or accumulated over the

day with each bout lasting at least eight to 10 minutes.15

[Editorial comments: Eat more cereals and legumes. The authors reported
that the forthcoming Australian Dietary Guidelines would recommend that
people eat more cereals, preferably wholegrain. This is to encourage higher
carbohydrate intake. Generally speaking wholemeal flour does not have a
lower glycaemic index than white flour. It is whole-grain foods which have
a lower glycaemic index. One of the main reasons to promote increased
carbohydrate (cereal and legume) consumption is to displace fats and sugars
in the diet.
Basmati rice and oats are specifically mentioned as they have low
glycaemic indexes and their incorporation into a meal will lower the
glycaemic index of the entire meal.

References
1. AIHW. Mathers C, Vos T, Stevenson, C. Burden of disease and injury in Australia.
AIHW Catalogue PHE 17. Canberra. November, 1999.
2. Cunningham J, Mackerras D. Overweight and obesity Indigenous Australians 1994. ABS
Cat 4702. Australian Bureau of Statistics, 1998
3. NHMRC. 2001. Draft Dietary Guidelines for Australians. Canberra.
4. Territory Health Services. Public Health Bush Book. Darwin, 2000.
5. Cashel K, Jefferson S. NHMRC The Core Food Group.
6. SIGNAL. 2001. Eat Well Australia: An Agenda for Action for Public Health Nutrition
2000–2010. Canberra.
7. A National Nutrition Survey Selected Highlights Australia. Canberra: Australian
Bureau of Statistics, 1995.
8. Territory Health Services. Market Basket Survey of Remote Community Store in the
Northern Territory. Darwin, 2000.
9. National Heart Foundation of Australia. Position statement on dietary fats. 1999,
56(4)Supplement S3–S4.
10. Territory Health Services. Background papers to the Northern Territory Food and
Nutrition Policy Volume 4: Food and Nutrients in remote Aboriginal Communities.
11. Sallis, J & Owen, N. Physical Activity and Behavioral Medicine. London: Sage
Publications, 1999.
12. US Department of Health and Human Services. Physical activity and health: A
report of the Surgeon General. Atlanta. GA: Center for Disease Control, 1996.
13. NHMRC. Acting on Australia’s Weight: A strategic plan for the prevention of
overweight and obesity. Canberra: Australian Government Publishing Services, 1997.
14. Australian Sports Commission. Active Australia: A National Participation
Framework. Canberra, 1997.
15. Commonwealth Department of Health and Family Services. Developing an Active
Australia: A Framework for action for Physical Activity and Health. Canberra,
1998.
 Heart Failure

Author: Dr Steven Brady (ASH)

Topic Reviewers: Dr Marcus Ilton (RDH Cardiologist); Dave Corstorpan

(RAN, Nyirripi Clinic)

In the last few years there has been the release of several highly detailed
guidelines for the diagnosis and management of chronic heart failure. These
have included guidelines from Australia1, the USA2 and Europe.3 They give a
detailed description of the clinical trials which have led to marked
changes in the management of chronic heart failure, from one based on
symptom control to one based on accurate diagnosis and a use of
pharmacotherapy and neurohormonal control to improve survival.
The guidelines have very broad agreement about the primary therapies
used for the management of chronic heart failure these being ACE
inhibitors, beta-blockers, diuretics and digoxin and non-pharmacological
measures. The guidelines also discuss in detail the approach to diagnosis
of heart failure, which still remains quite problematic, particularly in a
primary care setting.
The discussion here highlights the important areas that may be
problematic to implement in a very scattered population with scarce
resources.

Overview of diagnosis
Failure of heart to pump sufficient blood for metabolic requirements
The diagnosis of heart failure remains difficult. Surveys in primary care
settings highlight the difficulties of diagnosis and the limited use of
echocardiography.
Signs and symptoms of heart failure are not adequately sensitive and
specific to confirm the diagnosis of heart failure in most circumstances.
Some clinical signs, including a gallop rhythm and raised JVP, both confirm
the diagnosis of heart failure and have implications for prognosis but are
not reliable except in the hands of experienced clinicians.
Heart failure should, however, be suspected in anyone presenting with a
history of new onset fatigue, oedema or breathlessness. This is
particularly the case if the patient has a background of diabetes, chronic
renal impairment, ischaemic heart disease, hypertension or rheumatic
valvular disease.
Initial tests should include an ECG. A normal ECG makes the diagnosis of
heart failure unlikely. A chest X-ray is valuable if able to be performed.
Neither the ECG nor chest X-ray are sensitive or specific enough to form
the sole basis of investigation.
Biochemical markers such as Brain Natriuretic Peptide may become
available as a screening tool in primary care to enable the detection of
patients with heart failure, especially where echo-cardiography is not
easily available and may be suitable as an initial test4,5,6,7 and to guide
therapy or further investigation. However, this is yet to be established in
a primary care setting.
Echocardiography remains an essential part of the diagnosis of heart
failure. Given the very high incidence of rheumatic valvular heart disease
in the Northern Territory8, whenever possible an echocardiogram should be
performed to confirm the diagnosis.
Coronary artery disease is also very common in the Northern Territory.
Given the high prevalence and the early age of onset of ischaemic heart
disease in this population9, coronary artery disease needs to be excluded as
a cause of heart failure in people presenting with left ventricular
systolic dysfunction, if no other cause is apparent. Exercise impairment,
regional wall motion abnormalities and ECG abnormalities make
interpretation of the exercise stress test and other non-invasive tests
difficult. In the population with LV systolic impairment or an ideopathic
dilated cardiomyopathy, coronary angiography is the preferred test to
exclude significant ischaemic heart disease.2 Patients with angina and
heart failure should undergo coronary angiography as revascularisation of
appropriate patients will prolong life and may result in improved LV
function. Other patients with unexplained heart failure may also require
angiography to exclude significant coronary artery disease, although the
efficacy of revascularisation in improving symptoms and survival is less
clear cut.2

Pharmacological treatment
Treatment
Treatment is based on the treatment of acute episodes of acute pulmonary
oedema (or sudden cardiac decompensation), control of possible triggers of
cardiac decompensation and maintenance therapy to maintain adequate cardiac
function for usual daily activities and to reduce gradual decline in
cardiac function.
The mainstays of pharmacological treatment are ACE inhibitors and beta-
blockers to improve survival, decrease hospitalisations and diuretics and
digoxin as symptomatic therapy. The aldosterone antagonist spironolactone
has also been shown to improve survival in patients with severe (NYHA III &
IV) heart failure.
New York Heart Association grading of symptoms in heart failure:
Class I: Cardiac disease, but ordinary activity causes no symptoms
Class II: Slight limitation, with ordinary activity causing symptoms
Class III: Marked limitation, with symptoms on less than ordinary
activity
Class IV: Unable to carry on any activity without symptoms and may have
symptoms at rest

Treatment of acute pulmonary oedema

Intravenous frusemide has been the mainstay of treatment for acute
pulmonary oedema but has been subjected to few randomised controlled
trials. One recent trial10 randomised patients to high-dose intravenous
nitrates and low-dose frusemide versus high-dose frusemide and low-dose
intravenous nitrates. There were fewer requirements for mechanical
ventilation and less progression to myocardial infarction in the group
receiving high-dose nitrates, suggesting a benefit for the high-dose
nitrates group. Whether this may be due to beneficial effects of the
nitrates or deleterious effects of the frusemide is unclear.
 In practice nitrates may be (are and should always be considered in
normotensive or hypertensive patients with LVF) useful in treating acute
pulmonary oedema.

Beta-blockers
Beta-blockers have been shown to improve survival in patients with mild to
severe symptomatic heart failure and should be used in patients with LV
systolic failure in the absence of any contraindication.11 Patients with LV
systolic dysfunction and no symptoms are likely to benefit from beta-
blockers, but this has not been confirmed in clinical trials. Patients with
known ischaemic heart disease should be on beta blockade (particularly if
they have evidence of heart failure) and more widespread therapy with beta-
blockers may decrease the incidence of LV failure.
The benefits of beta blockade occur slowly and may follow an initial
decline in LV function and increase in symptoms. As a rule of thumb, LV
function declines for a month after initiation of therapy and thereafter
improves. Improvement in survival can be demonstrated within six months.
Patients must therefore be stable to begin therapy. Compliance is also
important, as patients who stop and start therapy are more likely to
experience harm than good. Carvidelol is licensed in Australia for the
treatment of heart failure after specialist initiation and this would
appear appropriate for the CARPA protocol. In stable patients this can be
achieved with outpatient and outreach supervision (possibly over the phone)
and does not require hospitalisation.
Overall long-term success with beta blockade is achieved in the same
percentage of patients with diabetes and COPD as in those without, so these
are not contraindications for use. One authority recommends avoiding use in
patients with true asthma (usually have childhood symptoms), severe airways
obstruction (FEV1<50%) or evidence of reversibility on pre- and post-
bronchodilator spirometry. Patients with marked hypotension (SBP <90) and
bradycardia should not be started on beta-blockers. Patients with
borderline low blood pressures may require reduction in other therapies
(particularly diuretics) to allow the introduction of beta blockade.

ACE inhibitors
ACE inhibitors have been shown to decrease progression and mortality in all
stages of heart failure and also led to a reduction in the risk of heart
failure. Widespread use in at-risk patients may reduce the numbers of
patients developing heart failure.12

Angiotensin receptor blockers

Angiotensin receptor blockers (ARBs) remain second-line therapy behind ACE
Inhibitors for the treatment of CCF.1–3 Placebo-controlled trials have shown
clinical and neurohormonal benefits. Trials comparing ARBs to ACE
inhibitors have shown a trend to improved survival with ACE inhibitors.3,13,14
The recent Val-Heft trial15 compared valsarten or placebo to standard
therapy for heart failure including beta-blockers and ACE inhibitors. No
overall advantage on mortality was demonstrated. Valsarten improved
mortality in patients receiving ACE inhibitors and beta-blockers but
worsened mortality in patients receiving both of these drugs in post hoc
analysis.
Therefore ARBs have a role in patients unable to take ACE Inhibitors
because of angio-oedema or cough.2 (Although the AMH defines ACEi-induced
angioedema as a contraindication to using an ARB the American Heart
Association list this as a Class 1 indication for ARB. The low likelihood
of angioedema and the life-saving nature of neurohormonal inhibition leads
me to agree with the ACC/AHA, i.e. to recommend ARBs as the best
alternative to ACEi if there is heart failure and angioedema or cough
associated with use of ACEi.)
The advantage of combining ACE inhibitors and ARBs in patients unable to
take beta-blockers will need to be confirmed in prospective trials.

Reference list
1. Krum H. Guidelines for management of patients with chronic heart failure in
Australia. Med J Aust 2001; 174(9):459–66.
2. Hunt HA, Baker DW, Chin MH, Cinquegrani MP, Feldmanmd AM, Francis GS et al.
ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the
Adult: Executive Summary A Report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines (Committee to Revise the 1995
Guidelines for the Evaluation and Management of Heart Failure). Circulation 2001;
104(24):2996–3007.
3. Remme WJ, Swedberg K. Guidelines for the diagnosis and treatment of chronic heart
failure. Eur Heart J 2001; 22(17):1527–60.
4. Morrison LK, Harrison A, Krishnaswamy P, Kazanegra R, Clopton P, Maisel A.
Utility of a rapid B-natriuretic peptide assay in differentiating congestive heart
failure from lung disease in patients presenting with dyspnea. J Am Coll Cardiol
2002; 39(2):202–9.
5. Koglin J, Pehlivanli S, Schwaiblmair M, Vogeser M, Cremer P, vonScheidt W. Role
of brain natriuretic peptide in risk stratification of patients with congestive
heart failure. J Am Coll Cardiol 2001; 38(7):1934–41.
6. Meyer K. Exercise training in heart failure: recommendations based on current
research. Med Sci Sports Exerc 2001; 33(4):525–531.
7. Nicholls MG, Lainchbury JG, Richards AM, Troughton RW, Yandle TG. Brain
natriuretic peptide-guided therapy for heart failure. Ann Med 2001; 33(6):422–7.
8. Carapetis JR, Wolff DR, Currie BJ. Acute rheumatic fever and rheumatic heart
disease in the top end of Australia’s Northern Territory. Med J Aust 1996;
164(3):146–9.
9. Young MC, Fricker PA, Thomson NJ, Lee KA. Sudden death due to ischaemic heart
disease in young aboriginal sportsmen in the Northern Territory, 1982–1996. Med J
Aust 1999; 170(9):425–8.
10. Cotter G, Metzkor E, Kaluski E, Faigenberg Z, Miller R, Simovitz A et al.
Randomised trial of high-dose isosorbide dinitrate plus low-dose furosemide versus
high-dose furosemide plus low-dose isosorbide dinitrate in severe pulmonary oedema.
Lancet 1998; 351(9100):389–93.
11. Brophy JM, Joseph L, Rouleau JL. Beta-blockers in congestive heart failure. A
Bayesian meta-analysis. Ann Intern Med 2001; 134(7):550–60.
12. Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an
angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-
risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl
J Med 2000; 342(3):145–53.
13. McKelvie RS, Yusuf S, Pericak D, Avezum A, Burns RJ, Probstfield J et al.
Comparison of candesartan, enalapril, and their combination in congestive heart
failure: randomized evaluation of strategies for left ventricular dysfunction
(RESOLVD) pilot study. The RESOLVD Pilot Study Investigators. Circulation 1999;
100(10):1056–64.
14. Pitt B, Poole-Wilson PA, Segal R, Martinez FA, Dickstein K, Camm AJ et al. Effect
of losartan compared with captopril on mortality in patients with symptomatic heart
failure: randomised trial—the Losartan Heart Failure Survival Study ELITE II. Lancet
2000; 355(9215):1582–7.
15. Cohn JN, Tognoni G. A randomized trial of the angiotensin-receptor blocker
valsartan in chronic heart failure. N Engl J Med 2001; 345(23):1667–75.
High Blood Pressure
(Hypertension)

Authors: Dr Andrew Boyden (on behalf of the NVDPP); Ms Susan Anderson; Dr

Sophie Couzos; D Cadilhac;
G Hankey; E Lalor
Acknowlegements: Ms Susan Anderson (National Manager, Food Information Program,
National Heart Foundation of Australia, 407 Elizabeth Street, Surry Hills, NSW,
2012)
Topic Reviewers: Prof Lindon Wing, Prof Andrew Tonkin, Prof Joe Hung, Dr
Michael Stowasser,
Assoc Prof David Sullivan (National Heart Foundation, National Stroke
Foundation)
This chapter is an edited version of a draft prepared for the Chronic
Disease Alliance of Non-Government Organisations: National Guide for
Preventive Health Assessment in Aboriginal and Torres Strait Islander
Peoples.

Burden of disease
Hypertension is a risk factor for cerebrovascular disease, ischaemic heart
disease, peripheral vascular disease and renal disease (with increasing
risk as blood pressure increases) and is a major contributor to the overall
burden of disease in Australia.1
Cardiovascular disease is the leading cause of death amongst the
Aboriginal and Torres Strait Islander population (both male and female) and
the rate was three times higher than that for non-Aboriginal Australians in
1997–99. Cardiovascular disease explains over 30% of the excess deaths in
the Aboriginal and Torres Strait Islander population and accounts for the
highest proportion of excess deaths. Over half (57%) of the total deaths
were due to ischaemic heart disease (heart attack, angina), and a further
18% were due to cerebrovascular disease (stroke). Aboriginal and Torres
Strait Islander people also have an earlier onset of disease so that those
aged 25–54 years are 7–12 times more likely to die from cardiovascular
causes than other Australians.2
According to various cross-sectional surveys that have been conducted in
the Australian general population, there has been a decline in the
proportion of the population with high blood pressure (and/or receiving
anti-hypertensive treatment) over the period from 1980 to 1999–2000. For
men aged 25–64 years, this proportion fell from 45% to 22% and for women
29% to 16%.1
There are no national data available in relation to blood pressure
levels in Australian Aboriginal peoples and Torres Strait Islanders.1
However, a large prevalence survey of the Kimberley Aboriginal population,
conducted in 1989, showed that the prevalence of hypertension was two to
three times higher than among Caucasian Australians. In particular,
hypertension in Aboriginal men was apparent at less than 30 years of age.
The survey also found that many Aboriginal people with hypertension
remained undiagnosed or poorly controlled. Approximately 80% of those found
to be hypertensive were previously undiagnosed. Of those previously
recognised as hypertensive, only in about one-third was the condition
effectively controlled.3 A survey of two country towns in south-eastern
Australia has found that hypertension was more prevalent in those of
Aboriginal descent than in people of European descent.4
There is evidence that hypertension and ischaemic heart disease was less
common in Aboriginal populations in the past. In 1951–57 the systolic blood
pressure in Aboriginal people described as ‘semi-tribal’ was less than that
seen in prevalence surveys after the 1970s.3
Hypertension is very common in those with diabetes, thought to be twice
that in those without diabetes and is one component of the insulin
resistance or ‘metabolic syndrome’, which is common in Aboriginal
populations. Also, it has been shown that hypertension in patients with
diabetes is associated with accelerated progression of both microvascular
(retinopathy and nephropathy) and macrovascular (CHD, stroke, peripheral
vascular disease) complications.5
Low socioeconomic status is also linked with higher mortality rates from
hypertension-related diseases such as coronary heart disease, hypertensive
heart disease, stroke and end-stage renal disease.6 Hypertension is clearly
associated with lower socioeconomic status (SES), but the magnitude of the
difference is only small, with age adjusted mean systolic BP differences of
about 2–3 mmHg between the highest and lowest SES groups. There is little
evidence that adverse psychosocial factors associated with low SES cause
chronic elevations in BP.7

Types of preventive intervention

• Screening blood pressure
• Counselling
• Weight loss
• Physical activity
• Low fat, high fruit and vegetable diet
• Moderate alcohol intake
• Salt restriction with high BP
• Smoking cessation (see other
• Anti-hypertensive medication
• Access to recreational facilities and possibly psychosocial mediators

Evidence of the effectiveness of preventive interventions

Screening
Hypertension is defined as systolic blood pressure of 140 mmHg or greater,
and/or a diastolic blood pressure of 90 mmHg or greater, in people who are
not taking anti-hypertensive medication. The diagnosis of hypertension
should be based on multiple blood pressure measurements taken on several
separate occasions.8
Screening for hypertension involves measuring blood pressure with a view
towards subsequent lowering of blood pressure. There is good evidence that
the early detection and management of hypertension can prevent
cardiovascular morbidity and mortality (see below). The higher prevalence
of undiagnosed hypertension, cardiovascular morbidity and early age of
onset of hypertension-related disease in the Aboriginal and Torres Strait
Islander population supports targeting preventive activities towards this
population.
Counselling and medication
Lowering of blood pressure is effective in reducing stroke incidence and
mortality in those with hypertension. Treatment of hypertension also
decreases mortality from coronary artery disease in patients with high
blood pressure. The effectiveness of drug therapy to lower blood pressure
and reduce fatal and non-fatal stroke, cardiac events and total mortality
has been demonstrated in a number of systematic reviews of randomised
controlled trials.9,10,11 An overview showed that lowering blood pressure by
10–12 mmHg systolic and 5–6 mmHg diastolic, on average, reduces the
relative risk of stroke by about 40% and of coronary disease by about 15%.
This relative reduction in risk is similar, whatever the blood pressure
before treatment and the absolute risk of cardiovascular disease.12
Lifestyle factors are strongly associated with blood pressure control,
and an epidemiological association between blood pressure and excessive
alcohol consumption, obesity and cholesterol levels has been reported for
one Aboriginal population.13 At three or more standard drinks of alcohol
per day, studies have consistently shown that blood pressure increases in
direct proportion to alcohol intake, and reducing heavy alcohol consumption
will reduce blood pressure. At lower levels of drinking the findings are
less consistent.14
A recent randomised controlled trial in the US showed that dietary
sodium restriction, in combination with a diet rich in vegetables, fruits,
and low-fat dairy products, can lower systolic blood pressure. The effects
of sodium restriction were observed in participants with, and in those
without, hypertension, African Americans, those of other races, and women
and men.15 However, meta-analysis of trials did not demonstrate significant
blood pressure reduction from salt restriction in those with or without
hypertension.16 Other meta-analysis in hypertensive subjects showed that
sodium reduction reduces systolic blood pressure in the general population
by a small amount, but the effect is greater among older, previously
hypertensive subjects.17 A more recent meta-analysis involving 58 trials of
hypertensive persons showed that reduced sodium intake (mean reduction of
6.7 g/day for 28 days) dropped SBP by 3.9 mmHg (95% CI: 3.0–4.8 mmHg) and
DBP by 1.9 mmHg (95% CI: 1.3–2.5 mmHg). In 56 trials of normotensive
persons the effect of reduced sodium intake on SBP was 1.2 mmHg (95% CI,
0.6–1.8 mmHg) and on DBP was 0.26 mmHg (95% CI: -0.3–0.9 mmHg). The trials
involved subjects aged between 23–73 years. The results did not support a
general recommendation to reduce sodium intake, but reduced sodium intake
may be used as a supplementary treatment in hypertension.18 These results
have evoked criticism because the trials were of too short duration, or
because dietary sodium intake was not lowered sufficiently in the study
populations.19
Other lifestyle factors also have important preventive implications.
Weight loss, and increase in physical activity, have been shown to improve
blood pressure control in systematic reviews,11 and are supported by the US
Surgeon General.20 The effectiveness of counselling in persuading people to
use these means has not been adequately shown, particularly in the long
term. However, even modest improvements from counselling in primary care
could have large public health benefits. A large randomised controlled
trial confirmed that a low saturated and total fat, high fruit and
vegetable diet results in modest reductions in blood pressure.21,22
Stress management to lower blood pressure has been examined in a number
of trials, but meta-analysis did not confirm a significant reduction.16
Mediating psychosocial causes of cardiovascular disease is particularly
relevant in Aboriginal and Torres Strait Islander population in view of the
much greater relative deprivation.

Frequency of BP checks
Testing the blood pressure of Aboriginal people and Torres Strait Islanders
at every clinic visit is recommended in view of this recommendation for the
general population.23 It is important to minimise missed opportunities to
screen as clinic visits may be infrequent.
The minimum recommended blood pressure screening interval for adults who
are not being treated for hypertension varies according to the initial
blood pressure reading. Generally, those with an initial ‘high-normal’ or
‘normal’ reading and without related significant co-morbidities (e.g.
diabetes, chronic renal disease or overt proteinuria), should be re-
screened within one to two years respectively (see table 1).
However, many Aboriginal and Torres Strait Islander people have
coexisting risk factors — such as family history of cardiovascular disease,
smoking and obesity — as well as co-morbidity and blood pressure screening
should occur annually in this population, commencing at an early age.

Table 1: Suggested follow-up for untreated individuals in relation to various

ranges of blood pressure24
[Editor: Note that this table has been simplified for use in the CARPA STM,
and the prompted recall times have been shortened in view of the added
logistical difficulties encountered in remote practice.]

Systolic Diastolic Action

(mmHg) (mmHg)

<130 <85 ‘normal’ BP, recheck in 1–2 years

130–139 85–89 ‘high-normal’ BP, recheck in 1 year. Offer lifestyle

advice.

140–159 90–99 confirm within 2 months – lifestyle advice

160–179 100–109 evaluate or refer within 1 month – lifestyle advice

>180 >110 evaluate and refer within 1 week (or immediately

depending on

NB: If systolic and diastolic categories are different, allow recommendations for
shorter follow-up (e.g. BP 160/86 evaluate or refer within 1 month).
Table modified from: National Heart Foundation of Australia, 1999, Guide to
Management of Hypertension for Doctors, NHFA (cited in reference to the table:
‘Modified with permission from: The Sixth Report of the Joint National Committee on
Prevention, Detection, Evaluation and Treatment of High Blood Pressure. Arch Int Med
1997; 157:2413–46).
Summary of recommendations

Recommendation Level of
evidence
The Aboriginal and Torres Strait Islander population has a much higher risk of III
developing cardiovascular (CV) disease and an earlier age of onset than the
general Australian population. Ischaemic heart disease (also known as coronary
heart disease) is a major contributor to mortality and morbidity in this
population.
There is some evidence that hypertension is more common and often unrecognised III
in the Aboriginal and Torres Strait Islander population.

Treatment of hypertension decreases mortality from coronary artery disease and I

stroke in patients with high blood pressure.
Modification of risk factors can reduce blood pressure: I
• reducing heavy alcohol consumption will reduce blood pressure;
• reduced sodium intake may be used as a supplementary treatment in those with
hypertension;
• weight loss,
• increase in physical activity,
• diets low in saturated fats and high in fruit and vegetables.

The effectiveness of counselling as part of a preventive health assessment to V

persuade people to modify risk factors has not been adequately shown,
particularly in the long term. However, even modest modifications from
counselling delivered in primary health care services could have large public
health benefits.

Adult (> 18 years) Aboriginal people and Torres Strait Islanders should have V
blood pressure assessed at every visit (at least every 1–2 years). Those with
raised blood pressure detected through screening will require more intensive
follow-up.
References
1. Australian Institute of Health and Welfare (AIHW) 2001. Heart, stroke and
vascular diseases-Australian facts 2001. AIHW Cat. No. CVD 13. Canberra: AIHW,
National Heart Foundation of Australia, National Stroke Foundation of Australia
(Cardiovascular Disease Series No.14.
2. Edwards RW, Madden R. The Health and Welfare of Australia’s Aboriginal and
Torres Strait Islander Peoples, 2001. Australian Bureau of Statistics, Commonwealth
of Australia, 2001.
3. Smith R, Spargo R, Hunter E, et al. Prevalence of hypertension in Kimberley
Aborigines and its relationship to ischaemic heart disease: an age-stratified random
survey. Med J Aust 1992; 156:557–62.
4. Guest CS, O’Dea K, Larkins RG. Blood pressure, lipids and other risk factors
for cardiovascular disease in Aborigines and persons of European descent of
southeastern Australia. Aust J Public Health 1994; 18(1):79–86.
5. American Diabetes Association Treatment of Hypertension in Adults with
Diabetes. Diabetes Care 2002 25:S71–S73.
6. O’Dea K, Daniel M. How social factors affect health: neuroendocrine
interactions. In: Eckersley R, Dixon J, Douglas B. The Social Origins of Health and
Well-being. Cambridge University Press, Melbourne, 2001.
7. Colhoun HM, Hemingway H, Poulter NR. Socio-economic status and blood
pressure: an overview analysis. J Hum Hypertens 1998 Feb; 12(2):91–110.
8. Guidelines Subcommittee of the WHO-ISH: 1999 WHO-ISH guidelines for the
management of hypertension. J Hypertens 1999; 17:151–183. National Heart Foundation
of Australia. 1999 Guide to Management of Hypertension for Doctors. NHFA, 1999.
9. Gueyffier F, Froment A, Gouton M. New meta-analysis of treatment trials of
hypertension: improving the estimate of therapeutic benefit. J Hum Hypertens 1996
Jan; 10(1):1–8.
10. Psaty BM, Smith NL, Siscovick DS, Koepsell TD, Weiss NS, Heckbert SR,
Lemaitre RN, Wagner EH, Furberg CD. Health outcomes associated with antihypertensive
therapies used as first-line agents. A systematic review and meta-analysis. JAMA
1997 Mar 5; 277(9):739–45.
11. Mulrow C. Primary prevention of cardiovascular disorders. In: Clinical
Evidence. Issue 6. BMJ Publishing Group, London, 2001; 96–97.
12. Jackson RT, Sackett DL. Guidelines for managing raised blood pressure
[editorial]. BMJ 1996; 313:64–5.
13. Smith R, Spargo R, King R, Hunter E, Correll R, Nestel P. Risk factors for
hypertension in Kimberley Aborigines. Med J Aust 1992; 156:562–6.
14. National Health and Medical Research Council. Australian Alcohol Guidelines.
Health risks and benefits. Commonwealth of Australia, 2001.
15. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced
dietary sodium and the dietary approaches to stop hypertension (DASH) diet. N Engl J
Med 2001; 344:3–10.
16. Ebrahim S, Smith GD. Lowering blood pressure: a systematic review of
sustained effects of non-pharmacological interventions. J Public Health Med 1998
Dec; 20(4):441–8.
17. Midgley JP, Matthew AG, Greenwood CMT, et al. Effect of reduced dietary
sodium on blood pressure: a meta-analysis of randomized controlled trials. JAMA
1996; 275:1590–7.
18. Graudal NA, Galloe AM, Garred P. Effects of sodium restriction on blood
pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride: a
meta-analysis. JAMA 1998 May 6; 279(17):1383–91.
19. National Heart Foundation of Australia. Salt and Hypertension- professional
paper. NHFA 2002.
20. US Department of Health and Human Services. 1996. Physical activity and
health: A report of the Surgeon General. Center for Disease Control. Atlanta. GA.
21. Moore TJ, Vollmer WM, Appel LJ, Sacks FM, Svetkey LP, Vogt TM, Conlin PR,
Simons-Morton DG, Carter-Edwards L, Harsha DW. Effect of dietary patterns on
ambulatory blood pressure : results from the Dietary Approaches to Stop Hypertension
(DASH) Trial. DASH Collaborative Research Group. Hypertension 1999 Sep; 34(3):472–7.
22. Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, Sacks FM, Bray GA,
Vogt TM, Cutler JA, Windhauser MM, Lin PH, Karanja N. A clinical trial of the
effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N
Engl J Med 1997 Apr 17; 336(16):1117–24.
23. Pearson TA, Blair SN, Daniels SR, Eckel RH, Fair JM, Fortmann SP, Franklin
BA, Goldstein LB, Greenland P, Grundy SM, Hong Y, Miller NH, Lauer RM, Ockene IS,
Sacco RL, Sallis JF Jr, Smith SC Jr, Stone NJ, Taubert KA. AHA Guidelines for
Primary Prevention of Cardiovascular Disease and Stroke: 2002 Update: Consensus
Panel Guide to Comprehensive Risk Reduction for Adult Patients Without Coronary or
Other Atherosclerotic Vascular Diseases. American Heart Association Science Advisory
and Coordinating Committee. Circulation 2002 Jul 16; 106(3):388–91.
24. National Heart Foundation of Australia. 1999 Guide to Management of
Hypertension for Doctors. NHFA, 1999.
 Lipids

Author: Dr Hung The Nguyen (Katherine West Health Service)

Topic Reviewers: Dr Tarun Weeramanthri (Community Physician Darwin);

Kenna Bastani (RAN, Pine Creek); Dr Steven Bryce

Introduction
This background discussion summarises guidelines from a number of sources
world wide.1–7 These guidelines make use of similar, current and best
evidence in published literature and are thus similar in their conclusions
and recommendations. Where possible local information (Northern Territory
(NT) data) are used to address relevance of the topic to remote NT health
practitioners.

Population and high risk strategies: concepts

Population strategies seek to prevent or delay the onset of coronary heart
disease (CHD) in whole populations. The high-risk approach concentrates its
efforts on the smaller number of individuals with cholesterol above a
certain threshold defining hypercholesterolaemia.
This background document concentrates on the targeting of high-risk
individuals in a clinical context. But it must be noted that effective CHD
prevention must involve population (public health and health promotion
strategies) as well as high risk approaches, and that these are not
mutually exclusive.

Need for primary prevention of CHD through lipid control

Diseases of the circulatory system, such as ischaemic heart disease and
cerebrovascular disease, are a major cause of mortality among Indigenous
males and females, accounting for more than one in four deaths identified
as Indigenous. There are almost three times as many cardiovascular deaths
as expected among Indigenous males and females, based on the all-Australian
rates. The rates of death from circulatory diseases are higher for
Indigenous males and females than for their all-Australian counterparts in
every age group from 15 to 74 years, and the steep rise in death rates
begins many years earlier (10–20 years earlier in the NT8) among Indigenous
people than among all-Australian males and females. Ischaemic heart disease
is responsible for the largest number of deaths from circulatory disease
among Indigenous males and females.9 In the NT, from 1979 to 1995, ischaemic
heart disease was the leading cause of death of Indigenous people at 11.7%
of all deaths.
A number of observational data exist that relate the extent of
cardiovascular risk factors in Aboriginal populations. It has been observed
that in more traditional Aboriginal groups total cholesterol (TC) levels
were not generally elevated even when compared to general Australian
populations.10,11 However, high-density lipoprotein-cholesterol (HDL-C) levels
were significantly lower than Australian population, and thus LDL-C/HDL-C
(low density lipoprotein-cholesterol) ratios tended to be high.
 In one study in coastal Arnhem Land, where 78% of the 25–64 year old
Aboriginal population participated, 74% of subjects had LDL-C/HDL-C ratio
greater than 4.5 (abnormally high). In these studies high triglyceride (TG)
were widespread and were much higher in men than women (occurring in 56% of
males and 35% of females in Arhnem Land). Similar observations were noted
in Central Australian Aborigines and represented a high-risk profile for
coronary heart disease (CHD).12 Total cholesterol tended to increase with
age.
In another study in Central Australia TC were elevated in 68% of men and
46% of women over 35 years old. A significant proportion of men and women
under 35 years old had elevated TC (48% and 41% respectively) as well.
There was a similar problem with TG. The rise in TG and TC with age was
reciprocated with a fall in HDL-C.13 The difference in the two studies in
Central Australia relates to the difference in prevalence of other CHD risk
factors, like overweight and obesity and diabetes in the two sample groups.
O’Dea’s group shows that the problem of dyslipidaemia is already present in
young adults and that it would be appropriate for intervention programs to
target young people.12

Lipids in the context of other CHD risk factors

Although lipids are the main focus of this background paper, cholesterol
lowering is only one of a number of interventions to reduce CHD risk. There
is a recent overview of trials of multiple risk factor lifestyle
interventions for preventing CHD that pooled data from 14 randomised
comparisons of multifactorial intervention comprising 1 000 000 person
years of observation.14 The systemic review reports on the main outcome of
decrease in BP of 2.3/1.1 mmHg where anti-hypertensive drugs were not used,
a reduction of smoking prevalence of 4.2% and a net decrease in serum
cholesterol of 0.14 mmol/L. These changes were associated with a non-
significant fall in CHD mortality of 4% and total mortality of 3%. It was
concluded that health promotion interventions resulted in only small
changes in risk factors and mortality rates in the general population,
although there were beneficial effects in individuals within high-risk
groups.14
There are a number of explanations for this, including lack of
motivation leading to poor compliance. These in turn may be linked to poor
socioeconomic status, raising the possibility that until poverty and
deprivation are tackled effectively, the benefit of a healthy lifestyle may
never be realised by a substantial proportion of the population.
It should be noted that for those who are able to make the necessary
changes the benefits might be considerable. Small average reduction in risk
factors may have concealed much larger gains for those who were at highest
risk initially.13 Appropriate lifestyle measures should always be attempted
before resorting to drug therapy.1–6 Lifestyle measures may influence the
whole family and not just the individual at risk. On the other hand people
who do not respond to promotion of lifestyle changes are still likely to
benefit from drug therapy if it is needed.

Measures for lifestyle change include:

Stop smoking
The risks of smoking on CHD increase with the amount of tobacco smoked
daily and the duration of smoking. All patients should be actively
discouraged from smoking. Repeated brief and supportive advice on smoking
cessation should be given to patients by the primary care team. Drug (e.g.
nicotine replacement) therapy should be considered routinely in smokers
with the motivation to quit because they double the quit rate at one year.15

Dietary advice
The main dietary determinant of serum cholesterol is not dietary
cholesterol but saturated fat. Further, there are many components of a
healthy diet that are not related directly to lipids, but which affect CHD
incidence. Diets naturally rich in antioxidants (fruit and vegetables) may
be protective against CHD [Editor: An RCT of antioxidant supplementation
failed to confirm this suspected cause-and-effect relationship, so it may
be a more complex issue of cuisine rather than a specific micronutrient
that is important, i.e. antioxidant supplements are not a substitute for a
healthy diet.]
A number of studies have documented low rates of fruit and vegetable
consumption in Indigenous communities around Australia. Consequently, a
higher intake of fruit and vegetables is recommended. Dietary fibre, oily
fish and mono-saturated fatty acids may also be protective against CHD.
Bush foods, in particular meat, have been known to have low fat content and
organ meats contain long chain highly polysaturated fatty acids.16
Low fat diets in studies with high compliance saw a reduction in serum
cholesterol of 10–15%. By contrast, community-based studies have shown much
smaller average changes. For example, 3% reduction in an American Heart
Association (AHA) step 1 diet and 6% for an AHA step 2 diet (AHA step 1 and
step 2 diets advise less than 30% of total calories as fat).4
In Aboriginal populations, community-based nutrition intervention
programs have been implemented in some communities and have shown some
improvement in nutritionally related health outcomes. In one study of a
community intervention project a reduction in TC of 12% was observed
together with improvements in blood pressure and red cell folate.17
Furthermore, these studies have shown that appropriate facilitating,
planning, implementation and ownership of interventions by community
members and organisations can lead to sustained nutritional improvements.18
A meta-analysis of epidemiological (ecological) studies showed that
there is linear, independent relationship between homocysteine
concentration and cardiovascular risk. Homocysteine levels can be easily
and effectively reduced by supplementation with folic acid alone or in
combination with vitamins B6 and B12.19 Clinical trials are underway to
evaluate the impact of folate supplementation on reducing clinical
cardiovascular events. Until these studies are reported it is not possible
to make a recommendation on vitamin supplementation with folic acid as a
preventive measure for CHD.
It is well known that dietary salt (sodium) intake has an adverse effect
on blood pressure and potential effects on CHD and strokes. Dietary salt
restriction should also be considered. A meta-analysis of primary
prevention dietary intervention has estimated that a reduction in sodium
intake of 30 mmol/d is achievable among normotensive and mildly
hypertensive individuals.20 Dietary sodium intake should be reduced towards
recommended levels of 100 mmol, or 6 g of salt per day.

Obesity and overweight

Obesity (BMI >30 kg/m2) and being overweight (BMI >25) has an adverse
influence on a number of cardiovascular risk factors including BP, plasma
cholesterol, triglycerides, glucose tolerance and is a risk factor for
thrombogenesis in its own right.21 Risk increases substantially in people
with a BMI >30, particularly those people with excess intra-abdominal fat.
Waist circumference offers a simple indicator of risk. However, there are
no primary prevention trials that show that weight reduction impacts
directly on CHD, although observational data suggest an ideal BMI between
18.5–25.21
Realistic targets of 5–10 kg weight loss should be set for overweight
and obese individuals. A successful strategy for weight loss will include
advice not only on diet and exercise but also on behavioural change,
support systems and maintenance of reduced weight.22 [Editor: This is
discussed further in the ‘Overweight and obesity in adults’ chapter.]

Physical activity
Prospective studies support the view that a sedentary lifestyle is
associated with an increased risk of CHD. Physical activity leads to a
reduction in TC and LDL-C and a concomitant increase in HDL-C.23 Moderate
physical exercise decreases mortality. For those who are inactive or not
regularly active, aim to accumulate 30 minutes of moderate intensive
physical activity on most days. For those who are already active, vigorous
aerobic exercise of 20–30 minutes three times per week is recommended.24

Socioeconomic and psychosocial status

There is increasing evidence of a relationship between low socioeconomic
status (SES) and poor health, both for general health and across a range of
conditions including type 2 diabetes, dyslipidaemia and CHD.25 Many
Aboriginal people live in poor socioeconomic circumstances, with limited
incomes and poor household living conditions compounded by low levels of
education, high rates of unemployment and the effects of displacement from
traditional lands and cultural environments. These problems exacerbate
health conditions by acting as a barrier to self-management and control and
increasing the risk of complications. SES impacts upon risk factors for
CHD, including physical inactivity, overweight and smoking.25
There is growing evidence that low SES may be a risk factor in its own
right, as well as impacting on other factors and health service access. Low
mastery (the extent to which people feel control of the forces affecting
their lives) and poor mental health (depression) are related to the
development and progression of CHD.26 Furthermore, there is association
between perceived control (mastery) and positive mental health (lack of
depression) to healthy HDL-C levels. Positive effects on mental health
enhance the immune function and attenuate stress-related changes in
cholesterol.27
Links between psychosocial status and cholesterol may exist via
neuroendocrine pathways. Research is looking more and more into this area.
The practical implication of this is that energy should be focused on ways
to improve health service interaction with people in remote Aboriginal
communities.26 However, the uncritical application to Aboriginal people of
therapies suitable for non-Aboriginal persons may not be effective.
For example, on-going monitoring, education and dealing with variable
‘compliance’ is complicated by cultural differences in basic value systems,
communication patterns and social structure, all of which are potential
barriers to deriving benefit from Western medical knowledge. The value
placed on respect and autonomy in Aboriginal culture may lead Aboriginal
people to regard Western style of intervention as interference,
interruption of lifestyle or invasion of privacy.26
 Educational interactions that are culturally appropriate and orientated
towards communication and empowerment may be necessary. Elucidating
Aboriginal beliefs about the causes of diseases and relating them to
Western biomedical concepts for management of diseases could enhance
mastery.26 Further inroads into the links between mental health and physical
illness is required. [Editor: Some risk factors for cardiovascular disease
are discussed here, but readers should realise that this is not
exhaustive.]

How long to trial lifestyle measures before considering drug

therapy for lipids?
There are no studies to indicate how long a trial period of lifestyle
measures should last before considering lipid-lowering drug therapy. In a
meta-analysis of dietary intervention trials, the total cholesterol
reduction attributable to dietary advice was 6.6% at six weeks, 8.5% at
three months and 6.8% at six months.28 Therefore, it is preferable to pursue
lifestyle changes for at least three to six months in individuals whose
absolute risk for CHD is closer to 3% per year when their chance of
experiencing a cardiovascular event is relatively low.4 Patients at very
high risk may justify drug therapy at an earlier stage. Lifestyle measures
should continue beyond three months irrespective of the use of
pharmacological treatment.

The role of lipid-lowering drugs for high-risk patients

Statins
Statins (HMG CoA reductase inhibitors) influence the rate-limiting enzyme
in cholesterol synthesis. They rapidly lower serum total cholesterol,
especially LDL-C. They also have a lesser effect on TG and very low-
density-lipo-protein-cholesterol (VLDL-C). They also cause a small rise in
HDL-C.29
Pravastatin, simvastatin and lovastatin have been assessed in clinical
trials (pravastatin in primary and secondary prevention (WOSCOPS30, CARE31,
and LIPID32); lovastatin in primary prevention (AFCAPS/TexCAPS33) and
simvastatin in secondary prevention (4S34)). The relative reductions
observed with these three statins were similar, suggesting a class effect
in CHD event reductions and no increase in non-cardiovascular deaths. Other
benefits include a reduction in coronary revascularization procedures and
strokes and may include reduction in the incidence of anginal symptoms,
congestive heart failure, disability and improved quality of life.
Hepatoxity is the most common serious side effect occurring in 1% of
patients. Liver function tests should be monitored before and once during
therapy but not again if normal. Rhabdomyolysis is the most serious adverse
effect occurring in <0.1% of patients.

Fibrates
Fibrates lower serum TG and increase HDL-C levels but have less effect on
LDL-C and TC levels when compared to statins. There have been two primary
prevention clinical trials involving fibrates: the WHO Clofibrate trial and
the Helsinki Heart study of gemfibrozil.35 Both studies showed a reduction in
CHD events. The Clofibrate trial saw an increase in non-coronary mortality.
There was a non-significant increase in non-coronary mortality in the
Helsinki study, which meant all cause mortality was not reduced. Fibrates
cannot be recommended as first line agents for the primary prevention of
IHD.4
There are two secondary prevention studies.7 One clinical trial using
gemfibrozil for about five years saw a significant reduction in non-fatal
MI and coronary deaths compared to placebo. The second clinical trial using
bezafibrate did not see any significant differences between placebo and
treatment group over the six-year trial period.
Fibrates are indicated for mixed hyperlipidemia, hypertriglyceridemia or
when statins are poorly tolerated or ineffective. It is suggested that in
high risk subjects when both cholesterol and TG are >5.0 mmol/L fibrates
can be used.
Fibrates are well tolerated although myopathy is a recognised side
effect.

Resins
Resins (cholestyramine and colestipol) are anion-exchange compounds that
bind bile acids preventing their reabsorption. Two primary prevention
trials involved colestipol (Upjohn study) and cholestyramine (Lipid
Research Clinics Coronary Primary Prevention Study). Both studies showed a
reduction in CHD events.4 They also showed non-significant increases in non-
coronary mortality. Resins are not recommended as first-line agents for
primary prevention of CHD.

Other lipid lowering agents

Nicotinic acid group, fish oil (omega 3 marine TG) and soluble fibre
(ispaghula husk) have not been assessed in primary prevention outcome
studies. Their use should be discussed with a specialist.

Combination therapy
There are no primary prevention studies using combinations of lipid-
lowering agents (statins plus fibrate or statin plus resin for the
treatment of refractory hyperlipidemia, or for enhanced efficacy compared
monotherapy). There is a small risk of myopathy that exists with statins
and fibrates that appears to increase when they are used together and in
the presence of renal impairment.4 A specialist should assess patients who
require combination therapy.
Intervention threshold: When should patients be offered lipid-
lowering drug therapy as primary prevention?

Who to assess
Whole population screening for hyperlipidemia is not recommended.4,5
Lifestyle programs that are directed at whole populations together with a
targeted approach for high-risk people should be adopted. Assessment may be
undertaken systematically by targeting specific groups likely to be at
increased risk of CHD, e.g. diabetics and hypertensives. Patients may be
assessed opportunistically during contact with primary health care
services.
In mainstream populations there is good evidence to screen for primary
prevention of dyslipidaemia in people more than 35 years old.1–6 Below 35
years the risk of CHD is too low to justify widespread screening.1–6 Further,
there are no randomised prospective trials that have assessed long-term
lipid-lowering therapy in this age group (20–35 year olds) so no evidence-
based recommendation can be made. Even so some reputable groups do
recommend starting screening for primary prevention from 20 years old.5 For
patients more than 70 years old there is a lack of evidence of benefit for
intervention. The exceptions for this are members of families of patients
with inherited dyslipidaemia (familial cholesterolaemia) including
children.
Having cited the above argument in mainstream populations one must
consider the differences in Aboriginal populations where there are higher
rates of dyslipidaemia as well as diabetes and CHD at a significantly
younger age of about 10–20 years8 (see above). It is the author’s opinion
that it is logical to adopt the lower age group of 20 years old as the age
to start routine screening for dyslipidaemia for the primary prevention of
CHD in Aboriginal populations of the Northern Territory. This takes into
consideration that atherosclerosis begins long before clinical
manifestations and that more modest interventions, such as diet and weight
loss, can be used early in such individuals.
Patients with a history of CHD, CVD and PVD should be case-managed and
this will include a more aggressive approach to lipid monitoring (see
below).
In certain circumstances cholesterol levels may not be representative of
a patient’s usual levels. These situations include acute illness,
hospitalisation, weight loss, pregnancy, lactation or MI within the
previous 6–12 months. Lipid assessment should be delayed under these
circumstances or interpreted with caution.1–6

Which test?
The best lipid predictor of coronary risk at present is the ratio of TC to
HDL-C.6 The TC/HDL-C ratio reflects both the adverse effect of non-HDL-C and
the protective effect of HDL-C on atherosclerosis, thrombogenesis and blood
viscosity.4
Serum TG is elevated after a fatty meal and often in diabetes, obesity,
alcohol excess and liver disease. Measurement of TG after 12 hours of
fasting is recommended to obtain an accurate measurement of baseline
levels.1–6
 Direct measurement of LDL-C is expensive and is only rarely necessary.
Such tests, when indicated, should be ordered by specialist consultants.
LDL-C can be derived indirectly from Friedewald formula:
LDL-C (mmol/L) = TC – HDL-C – 0.45 x TG [Only valid if TG <4.0 mmol/L]

Exclusion of secondary causes of hyperlipidaemia

Secondary causes of dyslipidaemia should be excluded. Serum TC is usually
raised in hypothyroidism and nephrotic syndrome (therapeutic guidelines).36
Raised TG may be associated with diabetes, alcohol excess and liver
disease. Suggested minimum requirement for further tests to exclude
secondary causes include:
• Electrolyte, creatinine and urea
• Urinalysis
• Fasting glucose
• Liver function test
• Thyroid stimulating hormone (TSH) if serum cholesterol ≥8.0

Remember drugs (β-blockers, thiazide diuretics, oral corticosteroids,

oral contraceptives, phenytoin, cimetidine, cyclosporin, oral retinoids and
protease inhibitors for HIV infection) may affect lipid metabolism.

Risk assessment
The perception of the value of lipid-lowering drug therapy has changed.
Previously concern was expressed that any benefit for CHD might be offset
by an increase in non-cardiovascular mortality. This is not the case for
statins. Of greater interest is the identification of patients whose risk
of developing CHD justifies lipid-lowering drug therapy for primary
prevention.
Intervention trials confirm that those at highest risk of CHD events
have most to gain by treatment. The best way to target patients for statin
therapy is to calculate the absolute risk, not simply cholesterol level,
which is a poorer predictor of risk.36–38 Given that the placebo event rates
for CHD death or non-fatal MI in the CARE and LIPID studies are in the
order of 3% pa, it is logical to target a similar coronary event rate in
primary prevention with a statin.4

Guidelines for risk assessment

A number of tools have been published which can be used for risk
stratification e.g. the Sheffield Table36, the NZ Guidelines37 and the Joint
British Societies Coronary Prediction Chart.38 All three risk assessment
methods use the Framingham risk equation to determine the risk of a major
cardiovascular event. The practical utility of these tools has been
evaluated. Nurses and doctors interpreted the NZ guidelines and Joint
British Chart more accurately and prefer these to the Sheffield table. The
cardiovascular risk assessment using tables and charts was acceptable to
primary health care professionals.4
The main purpose of the above guidelines were to show whether an
individual risk of CHD is increase using age, sex, serum TC, and presence
of HT, smoking, diabetes and electrocardiographic left ventricular
hypertrophy as risk factors. These risk charts, therefore, may
underestimate risk (due to their exclusion) of: Australian Indigenous
populations; diabetics with nephropathy (proteinuria or microalbuminuria);
those with familial hypercholesterolaemia; strong family history of
premature CHD; chronic renal disease (sCr >150 mmol/L); those who have
recently stopped smoking or started antihypertensive drug treatment; or
those who are at the top of their age range (because risk for each age band
(e.g. 55–64) is calculated at the mid point (e.g. 60).4 Risk will be
underestimated as patients approach the next age category).
It can be recommended that a patient should be considered for lipid-
lowering drug therapy for primary prevention following a trial of lifestyle
measures and other appropriate interventions for at least three months when
the TC is ≥5.0 mmol/L and the five year risk of a major cardiovascular
event is 20% using the New Zealand Guidelines. A Microsoft Excel
spreadsheet program is available on the Internet for download and can be
used to calculate absolute risk
(http://www.nzgg.org.nz/library/nzgg-ftp/bloodpressure-calc.exe).
Alternatively, the following tables recommended by others,1,6 including
the National Heart Foundation, can be used to calculate risk of CHD.

Table 2: Patient’s risk category associated with risk factors for CHD (modified
from ref 1)

Number of risk 10-year CHD Risk category

factors risk
0–1 <10% low
2 10–19% moderate
3 20–39% high
>4 ?40% very high

Table 3: Recommended treatment thresholds by risk category (modified from ref 1)

Risk category Threshold for treatment

LDL-C TC/HDL-C ratio

Very high 2.5 4
High 3.5 5
Moderate 4 6
Low 5 7
Table 4: Guide for using drugs to lower plasma TC and LDL-C (modified from ref
6)
Risk category Consider drug Target level**
treatment*
Highest risk TC >4.0
Existing ischaemic heart disease
Existing extra-coronary vascular disease
Diabetes

High risk TC >6.5 TC ≤ 4.0

Positive family history of ischaemia HDL-C ≥ 1.0
heart disease LDL-C ≤ 2.5
Familial hypercholesterolaemia TG ≤ 2.0
Hypertension
Smoking
HDL-C<1.0

Lower risk TC >7.5

Others (35–75 years old)

*It should be emphasised that any lipid lowering is associated with some degree
of heart disease prevention. The benefit is maximised by achieving the
recommended target levels.6,7 Consideration for low HDL-C in assessing the need
for therapy is included (see below).
**The threshold for treatment is based on assessing risk of cardiovascular disease
and Pharmaceutical Benefits Scheme (PBS) guidelines.7
Table 4 is probably the easiest one to use by remote health practitioners.
The underlying philosophy is for health practitioners to assess the level
of absolute risk for individual patients and then to institute appropriate
management based on that risk for CHD and level of TC, HDL-C and LDL-C.

Target cholesterol levels

There is a suggestion from the WOSCOPS30 trial that there may be little
gained in primary prevention by lowering total cholesterol much below 5.0
mmol/L. Overall, the trial data suggest that a 1-mmol/L reduction in serum
TC sustained over five years will reduce the incidence of non-fatal MI and
fatal CHD by 20–25% irrespective of baseline cholesterol and risk.
Serum lipids can be reviewed every six weeks, adjusting dose until
desired target achieved then every year.4

Follow-up lipid assessment

A number of organisations have recommended that lipid assessment should be
performed every five years for those patients at low CHD risk.1–7 For people
with increased CHD risk but TC <5.0 mmol/L, annual assessment is required
with promotion of lifestyle measures.
When to refer
Most patients with lipid abnormalities should be managed successfully
within the primary care setting. However, referral for specialist care
should be considered in:4
• Patients who are refractory to treatment after first drug therapy,
where secondary causes have been excluded and dietary and lifestyle
measures have been tried
• Patients in whom drug therapy is contraindicated or poorly tolerated
• Patients with familial hypercholesterolaemia, to ensure correct
identification and screening of relatives including children
• Patients who are pregnant

Special subgroups
Primary prevention in people with diabetes mellitus
Atherosclerosis is the most frequent complication of diabetes, and
cardiovascular disease the most common cause of death. The United Kingdom
Prospective Diabetes Study (UKPDS) showed that 23% of patients with type 2
diabetes had clinically significant vascular complications at
presentation.39 Serum TC may not differ much from general populations. The
LDL-C particles tend to be smaller and more atherogenic in patients with
diabetes.
A more common abnormality in type 2 diabetes is an elevation in TG,
which is usually associated with low HDL-C. Some patients with type 2
diabetes continue to have high serum TG despite good glycaemic control.
Diabetic dyslipidaemia, especially raised TG and low HDL-C, is linked to
increased mortality from CHD in both males and females.5 In the UKPDS
potentially modifiable baseline risk factors for cardiovascular disease in
patients with type 2 diabetes were LDL-C, HDL-C, hyperglycaemia, HT and
smoking.39
The numbers of diabetic subjects were too small to reach statistical
significance in subgroup analyses of major studies of primary prevention of
CHD in diabetic groups.4 Prospective studies of lipid reduction in people
with diabetes are in progress and a meta-analysis is underway. In secondary
prevention, however, trials of lipid reduction in diabetics have shown
significant reductions in cardiovascular disease in both type 1 and 2
diabetics.31,32,34
The long pre-clinical phase in type 2 diabetes with risk factors like
dyslipidaemia often means that significant cardiovascular disease is
already present but undetected at the time of diagnosis.
It would appear prudent from the above discussion to recommend
aggressive lifestyle modification to lose weight, reduce intake of
saturated fats, increase consumption of fruits and vegetables, take regular
exercise and — where necessary — introduce lipid-lowering drug treatment
for primary prevention in diabetic subjects who will mostly be at high risk
of CHD. The higher absolute risk for cardiovascular disease in patients
with diabetes suggest greater benefit from lipid-lowering therapy than in
non-diabetic subjects for a given TC/HDL-C ratio.

Primary prevention for patients with normal TC and LDL-C but low HDL-C
It is well known that low HDL-C is an independent risk factor for CHD.
Epidemiological data support the protective effect of high HDL-C regardless
of LDL-C levels.41 Low HDL-C with normal LDL-C occurs in up to 30% of
patients with CHD and may represent a larger proportion of the CHD
populations than do those with isolated high LDL-C.42 A decreasing level of
HDL-C is associated with severity of CHD. As yet there is no consensus in
guidelines for targeting low HDL-C in patients at increased risk for CHD.
There are two primary prevention studies to date that address the issue
of whether lowering HDL-C has an impact on outcome from CHD. These are the
Helsinki Heart study (1987)35, 4000 participants using gemfibrozil 600 mg bd
and AFCAPS/TexCAPS (1998)33 6605 participants using lovastatin 20–40 mg/d.
Both studies showed a significant increase in HDL-C levels (6% lovastatin
and 11% for gemfibrozil) with a significant decrease in CHD events over
five years of about 34% for lovastatin (NNT = 50) and 37% for gemfibrozil.
The AFCAPS/TexCAPS populations were patients at risk for CHD but had normal
or mildly elevated TC and LDL-C levels with below average HDL-C levels.
I suggest that these findings support the inclusion of HDL-C levels in
risk factor assessment for CHD and suggest the need for reassessment of
guidelines regarding pharmacological intervention in patients with normal
or mildly elevated TC and LDL-C but low HDL-C levels and who are at
increased risk for CHD. The value of statins, with its relatively low risk
of side effects compared to earlier treatments for low HDL-C, should add
weight to the argument to target HDL-C in the prevention of CHD.

Elevated triglyceride
The mainstay of treatment for elevated triglyceride is physical activity
and reduced fat diet. Elevated triglycerides are usually part of a
metabolic syndrome where patients tend to have multiple risk factors,
including low HDL-C, abnormal glucose tolerance, raised blood pressure and
abdominal obesity. These patients are likely to be assessed as high risk.37
Fibrates are the drugs of choice in these individuals, but treating the
secondary causes (alcohol excess, poorly controlled diabetes and obesity)
first is recommended.
TG persistently above 8 mmol/L requires drug therapy because of the risk
for pancreatitis. Severe isolated hypertriglyceridemia may be referred to a
specialist.

Secondary prevention post-myocardial infarction (MI)

Serum cholesterol and LDL cholesterol are major risk factors for recurrent
cardiac events in patients following MI. In patients with acute MI, TC and
LDL-C decrease shortly after the onset of the MI. The depression of lipids
following MI last an average of six weeks, so it is important to measure
lipids within 24 hours of an acute event to give an indication of the TC
and HDL-C before the event, otherwise measurements should be delayed until
six to 12 weeks after the MI.40 Dietary modification lowers cholesterol but
the changes are small and are poorly maintained as a consequence of limited
motivation and non-compliance with stringent dietary restrictions. Recent
studies using statins have shown falls in cholesterol of 20–30% and clear
benefit in both reductions in vascular events and total mortality.40
It could be summarised from the three major studies that, for patients
with CHD and TC ≥6.0 mmol/L, drug therapy should be initiated. If TC is
between 5.0–6.0 dietary advice is indicated with a follow-up assessment at
six to 12 months. If TC is still within this range lipid-lowering drug
therapy should then be initiated. If TC is <5.0 mmol/L then dietary advice
should be reinforced with yearly follow-up since there is no benefit in
groups with TC <5.0 mmol/L in the CARE trial.
 To be consistent with the NHF guidelines, for patients with existing CHD
and TC >5.0 mmol/L, they should be offered a lipid-lowering agent.
The relative risk reduction observed for pravastatin and simvastatin are
similar suggesting a class effect but there have been no trials for
atorvastatin, fluvastatin and cerivastatin.

Table 5: Major secondary prevention trials for statins in lowering lipids

(modified from reference 39)

4S LIPID CARE
The majority of Patients with Patients with CHD.
patients had had an MI established CHD either Study aim to determine
at least six months MI or unstable angina. whether cholesterol
previously or had lowering was a benefit
angina with a positive for patients with
exercise test. average cholesterol
levels.
Cholesterol TC 5.5–8.0 mmol/L TC 4.0–7.0 TC <6.2
range
Mean reduction TC 28%; LDL-C TC 18%; LDL-C 25% TC 20%; LDL-C 28%
in cholesterol
No. Patients 4444 9014 4159
Treatment Placebo Simvastatin Placebo Pravastatin Placebo Pravastatin
groups 20–40 mg/d 40 mg/d 40 mg/d
Trial period 5.4 6.1 5.0
(y)
Total n 256.0 182.0 633.0 498.0 196.0 180.0
mortality % 11.5 8.2 14.1 11.0 9.4 8.7
RRR 30.0 (p<0.001) 22.0 (ns) 9.0 (ns)
%
ARR 3.3 3.1 0.7
%
NNT 30.0 32.0 143.0
CHD n 189.0 111.0 373.0 287.0 119.0 96.0
mortality % 8.5 5.0 8.3 6.4 5.7 4.6
RRR 42.0 (p<0.001) 24.0 (p<0.001) 20.0 (ns)
%
ARR 3.5 1.9 1.1
%
NNT 29.0 53.0 91.0
CHD n 622.0 431.0 715.0 557.0 274.0 212.0
events % 28.0 19.0 15.9 12.3 13.2 10.2
RRR 34.0 (p<0.001) 24.0 (p<0.001) 24.0 (p=0.003)
%
ARR 9.0 3.6 3.0
%
NNT 11.0 28.0 33.0
n = total number of events. ns = not statistically significant.
RRR = relative risk reduction. ARR = absolute risk reduction.
NNT = number needed to treat to prevent one event during the trial period
Event: 4S – CHD death, non-fatal definite or probable MI, silent MI,
resuscitated cardiac arrest; CARE – CHD death or symptomatic non-fatal MI;
LIPID – CHD death or silent or symptomatic non-fatal MI
References
1. Ontario Association of Medical Laboratories.Guidelines for Lipid Testing. Website
access 12/09/01
<http://www.oaml.com/clp017.html>
2. Institute for Clinical Systems Improvement. Lipid screening in adults.Website
access 12/09/01.
<http://www.icsi.org/guide/LipSxA.pdf>
3. University of Michigan Guidelines for Health System. Screening and Management of
Lipids. Website access 12/09/01
<http://cme.med.umich.edu/pdf/guideline/ lipids.pdf>
4. Scottish Intercollegiate Guidelines Network (SIGN). Lipids and the primary
prevention of coronary heart disease.
Edinburgh (Scotland): SIGN publication; no. 40. website access 12/09/01.
http://www.sign.ac.uk/guidelines/fulltext/40/index.html> 1999
5. Ansell, BJ, Watson KE, Fogelman, AM. An evidence-based assessment of the NCEP
adult treatment panel II guidelines. JAMA 1999; 282(21):2051.
6. National Heart Foundation Australia. Guide for the use of lipid lowering drugs in
adults. November 1998; 548. Website accessed 12/09/01
<http://www.heartfoundation.com.au/prof/index_fr.html>
7. National Heart Foundation and The Cardiac Society of Australia and New Zealand.
Lipid Management Guidelines: 2001. MJA 2001; 175(suppl):S57–S88.
8. Condon JR, Warman G, Arnold L (eds). The health and welfare of Territorians.
Epidemiology Branch, Territory Health Services, Darwin. 2001.
9. ABS. Occasional paper: mortality of Aboriginal and Torres Strait Islander
Australians. 3315.0. 1997.
10. O’Dea K, Spargo RM & Nestel PJ. Impact of westernisation on carbohydrate and
lipid metabolism in Australian aborigines. Diabetologia.1982; 22:148–153.
11. Sladden TJ. Cardiovascular disease risk factors in an aboriginal community.
Unpublished Master of Science thesis, University of Sydney. 1987. Access 12/09/01.
<http://www.healthinfonet.ecu.edu.au/html/html_resource/ theses/sladden.htm>
12. Gault A, O’Dea K, Rowley KG et al. Abnormal glucose tolerance and other coronary
heart disease risk factors in an isolated aboriginal community in central Australia.
Diabetic Care 1996; 19(11):1269.
13. O’Dea K, White NG & Sinclair AJ. An investigation of nutrition-related risk
factors in an isolated aboriginal community in northern Australia: advantages of a
traditionally orientated life-style. MJA 1988; 148:177–180.
14 Ebrahim S, Smith GD. Systematic review of randomized controlled trials of
multiple risk factor interventions for preventing. Coronary heart disease. BMJ 1997;
314:1666–74.
15 Silagy C, Mant D, Fowler G, Lancaster T. Nicotine replacement therapy for smoking
cessation. (Cochrane Review). In: The Cochrane Library, Issue 2. Oxford: Update
Software, 1999. Updated quarterly.
16 Naughton JM, O’Dea K, Sinclair AJ. Animal foods in traditional aboriginal diets:
polyunsaturated and low in fat. Lipids 1986; 21:684.
17 Lee AJ & Bailey APV. Survival tucker: improved diet and health indicators in an
aboriginal community. Aust J Pub Health 1994; 18:277.
18 Lee AJ, Bonson APV, Yarmirr, D et al. Sustainability of a successful health and
nutrition program in a remote aboriginal community. MJA 1995; 162:632.
19 Lonn EM, Yusuf S. Emerging approaches in preventing cardiovascular disease. BMJ
1999; 318:1337–41.
20 Brunner E, Thorogood M, Bristow A, Curle D, Marmot M. Can dietary interventions
change diet and cardiovascular risk factors? A meta-analysis of randomized
controlled trials. Am J Public Health 1997; 87:1415–22.
21 Willett WC, Diez WH, Colditz GA. Guidelines for healthy weight. NEJM 1999;
341:427–34.
22 National institutes of health. National Heart, lung and blood institute. Clinical
guidelines On the Identification, Evaluation, and Treatment of Overweight and
Obesity in adults. 1998.
23. Bowen PH & Guyton JR. Non-pharmacologic and pharmacologic treatment of patients
with low levels of high-density lipoprotein cholesterol. Curr Atherosclerosis
reports 2000; 2:58.
24 Erikssen G, Liestol K, Bjornholt J, Thaulow E, Sandvik L, Erikssen J. Changes in
physical fitness and changes in mortality. Lancet 1998; 352:759–62.
25. National Health Strategy. Enough to make you sick. National Health Strategy
Research Paper 1.Canberra: 1992.
26. Daniel M, Rowley KG, Herbert CP et al. Lipids and psychosocial status in
aboriginal persons with and at risk for type 2 diabetes: implications for tertiary
prevention. Patient Education Counseling 2001; 43:85.
27. Thomas PD, Goodwin JM, Goodwin JS. Effect of social support on stress-related
changes in cholesterol level, uric acid level and immune function in an elderly
sample. Am J Psychiatr 1985; 142:735.
28. Tang JL, Armitage JM, Lancaster T, Silagy CA, Fowler GH, Neil HA. Systematic
review of dietary intervention trials to lower blood total cholesterol in free-
living subjects. BMJ 1998; 316:1213–20.
29. Australian medicines handbook.
30. Influence of pravastatin and plasma lipids on clinical events in the West of
Scotland Prevention Study (WOSCOPS). Circulation 1998; 97:1440–5.
31. Sacks FM, Pfeffer MA, Moye LA, Rouleau JL, Rutherford JD, Cole TG, et al. The
effect of pravastatin on coronary events after myocardial infarction in patients
with average cholesterol levels. Cholesterol and Recurrent Events Trial
investigators. NEJM 1996; 335:1001–9.
32 The Long-term Intervention with Pravastatin in Ischaemic Disease (LIPID) Study
Group. Prevention of cardiovascular events and death with pravastatin in patients
with coronary heart disease and a broad range of initial cholesterol levels. NEJM
1998; 339:1349–57.
33 Downs JR, Clearfield M, Whitney E et al. Primary prevention of acute coronary
events with lovastatin in men and women with average cholesterol levels. JAMA 1998;
279(20):1615.
34 Randomized trial of cholesterol lowering in 4444 patients with coronary heart
disease: the Scandinavian Simvastatin. Survival Study Group (4S). Lancet 1994;
344:1383–9.
35 Frick MH, Elo MO, Haapa K et al. Helsinki Heart Study: primary prevention trial
with gemfibrozil in middle-aged men with dyslipidaemia. NEJM 1987; 317:1238.
36 Moulds, RFW. Sheffield’s tables for primary prevention of CHD: an alternative
approach to lipid Mx. Aust Pres 1998; 21(4):98.
37 Dyslipidaemia Advisory Group on behalf of the Scientific Committee of the
National Heart Foundation of New Zealand. National Heart Foundation clinical
guidelines for the assessment and management of dyslipidaemia. NZ Med J 1996;
109:224–31.
38 Wood D, Durrington P, Poulter N, McInnes G, Rees A, Wray R on behalf of the
British Cardiac Society, British Hyperlipidaemia Association, British Hypertension
Society, and British Diabetic Association. Joint British recommendations on
prevention of coronary heart disease in clinical practice. Heart 1999; 80(suppl
2):S1–S29.
39 Turner RC, Mills H, Neil HA, Stratton IM, Manley SE, Matthews DR, et al. Risk
factors for coronary artery disease in non- insulin dependent diabetes mellitus:
United Kingdom Prospective Diabetes Study. BMJ 1998; 316:823.
40 Scottish Intercollegiate Guidelines Network (SIGN). Secondary Prevention of
Coronary Heart Disease following Myocardial Infarction. Edinburgh (Scotland): SIGN
publication; no.
41. website access 12/09/01 http://www.sign.ac.uk/guidelines/ fulltext/41/index.html>
2000, Jan 26
41 Castelli WP. Cholesterol and lipids in the risk of coronary artery disease –
Framingham Heart Study. Can Coll Cardiol 1988; 4 (suppl):5A.
42 Boden WE & Thomas AP. Raising Low levels of high-density lipoprotein cholesterol
is an important target of therapy. Am J Cardiol 2000; 85(1):645.
 Overweight and Obesity in
Adults

Author: Dr Dorothy Mackerras; Father Frank Flynn (Fellow, MSHR, Darwin)

Topic Reviewers: Alison McLay (Public Health Nutritionist, Alice Springs);

Dymphna Leonard (Public Health Nutritionist, Cairns); Dr Anne Cawley (Wurli
Wurlinjang Health Service); Kenna Bistani (RAN, Pine Creek Clinic);
Dr Penny Roberts-Thompson (Nguiu).

Summary
In overweight and obese people with impaired glucose tolerance or raised
blood pressure, modest weight loss (3–5 kg) achieved using a combination of
increased moderate physical activity (e.g. walking) and improved dietary
quality will reduce the progression to diabetes by about 50% and reduce
blood pressure by about 3 mmHg. Given the high levels of diabetes,
cardiovascular disease and renal failure in Aboriginal people, it would be
sensible to recommend modest weight loss to all overweight and obese
people. The advice should contain both information about moderate physical
activity and dietary quality; it should not focus on cutting calories
(kilojoules) alone. People should not be discouraged from losing some
weight by being told what their ‘ideal’ weight ‘should be’ when this is too
big a target to be achieved realistically. However, it should be noted that
trials showing that progression to diabetes in people with impaired glucose
tolerance could be reduced with lifestyle modification when subjects
received up to 16 counselling sessions. Achieving the same level of effect
in Aboriginal communities would probably require a large commitment in
resources.
[Editor: The studies referred to here utilised 150 minutes per week of
moderate intensity physical activity (such as walking) as well as
resistance training to increase strength and capacity of muscle.
Improvements in dietary quality were achieved with intensive specialist
support (e.g. seven nutrition consultations in the first year, and four per
year thereafter.) While the weight loss achieved was modest, the resources
and commitment required to achieve them were not. While any improvements in
physical activity and diet should be encouraged, it is important not to
assume that a lesser intervention will necessarily achieve an equal effect.
These editorial comments are based on discussions within the editorial
committee and specific technical input from Dympna Leonard, Public Health
Nutritionist, Tropical Public Health Unit Cairns.]
While individuals can achieve some of the goals by their own actions
other important strategies, such as making sure there is a range of foods
available for consumption, will require group decisions and action.

Relevance
Overweight and obesity are important predictors of diabetes, hypertension
and heart disease and these are major causes of morbidity and early
mortality in Aboriginal and Torres Strait Islander Australians. Overweight
and obesity are also becoming more common in Aboriginal, Torres Strait
Islander and non-Indigenous Australians.1 Losing all excess weight is very
difficult and has a low success rate. However, randomised controlled trials
have shown that some of the important risk factors can be substantially
improved after a small amount (3–5 kg) of weight is lost. Therefore, clinic
staff can promote the health benefits of losing some weight to overweight
and obese people and can justify helping these people lose some weight, and
keep it off, even when the ‘ideal’ weight is never achieved. They should
also encourage people in the healthy weight range to stay active to prevent
weight gain.1

Definitions
Body mass index (BMI, also called the Quetelet Index) is defined as weight
(kg)/height(m)2. This usually yields a value in adults in the range of about
17–35 kg/m2 (the units of this ratio tend to be omitted in documents). To
assist practitioners interpret the BMI values, various national bodies have
divided this range up into groups and have given names to the groups such
as ‘underweight’, ‘acceptable or healthy weight’, ‘overweight’ etc.
In the 1970s the cut-off points defining each weight group were lower
for women than men2 based on the fact that women have a higher proportion of
fat at a given BMI than do men. Other studies showed that fat varies with
age, and older people have a higher proportion of fat for a given BMI than
younger people.3 In other words, an old man might have a higher proportion
of fat at a given BMI than a young woman. This means that it is not logical
to base cut-off points on sex alone if the goal is to have the cut-off
points related to percentage of body fat. However, subsequent analyses
revealed that the risk of health outcomes was much the same in men and
women for the same BMI, despite the differences in proportion of body
weight that was fat. So, for the purpose of making guidelines to categorise
BMI that are based on mortality, rather than proportion of body weight that
was fat, men and women could be grouped together. Like many health
phenomena, the relationship between BMI and mortality was a continuous one,
and had a J shape, and so to make categories to guide clinical advice:
The method used to establish BMI cut-off points has been largely
arbitrary. In essence, it has been based on visual inspection of the
relationship between BMI and mortality: the cut-off of 30 is based on the
point of flexion of the curve . . . It may therefore be necessary to
revise the classification of overweight in terms of BMI based on health
risk.3

In 1984, the NHMRC proposed the categories shown in table 1 for use in
Australia with adults.4,5 Note that the decimal places are implied. For
example, someone with a BMI of 19.9 is classified as underweight; the
decimals are not rounded up to 20.

Table 1: 1984 NHMRC cut-off points for weight categories for adults4,5
Group BMI range
Underweight <20
Acceptable/healthy weight 20> to <25
Overweight 25> to <30
Obese >30
More recently the WHO has proposed the groupings shown in table 2.3 The most
important difference between the WHO classification and the NHMRC
classification is that people in the range 18.5–<20 are described as
‘acceptable’ rather than ‘underweight’. This change was made on the basis
that studies from less developed countries indicated that healthy
physically active people in this weight range did not have excess mortality
and that studies in developed countries had not always corrected for deaths
early in the follow-up period or adjusted for smoking. Although the NHMRC
has not endorsed the WHO categories for use in Australia, a modified
version of them that uses the NHMRC category names is now widely used
(table 3) and they were used to analyse the 1995 National Nutrition Survey.6

Table 2: Cut-off points for weight categories for adults recommended by the
1995 WHO Expert Committee3
Category BMI range
Underweight
Severe thinness less than 16
Moderate thinness 16 to <17
Mild thinness 17 to <18.5
Acceptable weight 18.5 to <25
Overweight
Grade 1 25 to <30
Grade 2 30 to less than 40
Grade 3 40 and over

Table 3: Combined NHMRC/WHO cut-off points in common use in Australia at

present 6
Group BMI range
Underweight <18.5
Healthy weight 18.5 to <25
Overweight 25 to <30
Obese 30 and over

Changing the lower cut-off point for the acceptable weight category will
alter the proportion of the population who fall in the ‘underweight’ and
‘acceptable weight’ categories. Table 4 shows the results for the all-
Australian population from the 1995 National Nutrition Survey.7 The
prevalence of underweight and acceptable weight depends on whether the 1984
or 1995 definitions are used. It is important to check which cut-off points
have been used in a report and not to make assumptions based on the names
of the categories that the authors used.

Table 4: Prevalence of different categories of body size in adults aged 19

years and older in the 1995 National Nutrition Survey7, recalculated* excluding
those not measured
Category and BMI cut-off points Men Women
% %
Underweight 0.6 2.3
Acceptable 18.5–<20.0 2.3 6.0
20.0–<25 32.6 42.5
Overweight 45.7 30.2
Obese 18.7 19.1

*The recalculation is necessary as ABS documents tend to include those not

measured as part of the percentage calculations.

There are also some small discrepancies between the NHMRC and WHO cut-off
points. Specifically, 25.000 . . . 0 is classed as acceptable weight in the
NHMRC scheme and as overweight in the WHO scheme; 30.000 . . . 0 has also
moved up one category. The consequence at the population level is more
annoying than real. For example, when we were analysing the 1994 National
Aboriginal and Torres Strait Islander Survey8, only three out of the 7858
adults had a BMI of exactly 25.000 . . . 0 (these days, computers store an
infinite number of decimal places) and would have been affected by this
discrepancy.9 It is more common that the calculation leads to other numbers
such as 24.99 or 25.05 which have not changed their classification. Hence
these small discrepancies in definition do not affect the population
prevalence in an important way.

Table 5: Distribution (%) of Body Mass Index (kg/m2) in Aboriginal and Torres
Strait Islander adults (18 years and older), NATSIS, 199410, recalculated
excluding those not measured
Aboriginal Torres Strait Aboriginal Torres Strait
BMI group men Islander men women Islander
women
Underweight<20 8.2 1.9 13.3 4.8
Acceptable 33.1 25.7 30.9 16.1
20 to 25
Overweight 35.6 30.5 28.8 29.0
>25 to 30
Obese >30 23.0 41.8 27.1 50.1

It is worth drawing the reader’s attention to the fact that the category
cut-off points described for adults are not appropriate for classifying
infants, children or adolescents. Various classifications have been
proposed if BMI is calculated for children and adolescents.8,11–13 However,
the long-term predictive power of these classifications are unknown.

The categories are part of a continuous distribution

The association between weight and risk of mortality or morbidity is
continuous and rising above a BMI in the 20–25 range. Various studies have
reported that the lowest risk is found at BMIs as low as 20 or as high as
25 in different Caucasian groups.3,14 This has lead to different national
bodies making different decisions about the cut-off points based on the
same information. For example, at the time the NHMRC was setting 25 as the
boundary for overweight in Australia, the Americans were setting 27.8 in
men and 27.3 in women as the boundary for overweight and the Canadians were
setting 27 as the boundary for obesity.3 The continuous distribution means
that the risk of adverse outcomes is not equal for every point within the
overweight range. For example, at the lower end around 25.1, the risk is
essentially the same as for someone with a BMI of 24.9 (in the acceptable
range) whereas at 29.9, the risk is essentially the same that of someone in
the obese group with a BMI of 30.1. From this, it is clear that the choice
of the cut-off points to make the categories for guiding clinical practice
is somewhat arbitrary. (One suspects that the choice of 25 rather than
other cut-off points such as 24.9 or 25.5 was related to digit preference.)
However, the consequence of the continuous relationship is that risk
reduces even when a small amount of weight is lost. Although the categories
are based on observational studies a number of trials confirm the view that
small changes in weight lead to reductions in some important intermediate
markers even though the subjects did not lose enough weight to reach the
healthy/acceptable weight range (see below). Hence it is important not to
discourage patients from achieving some level of modest weight reduction by
telling them what their weight ‘should be’. This ‘ideal’ weight might be so
far below the person’s current weight that it is an impossible goal.
In addition, it should be realised that BMI:
. . . appears to be a good measure of overweight and obesity in sedentary
adult white men and women from Europe and North America. However, since
body mass index does not distinguish between weight due to muscle and that
due to fat, its relationship with obesity (excess fat) is likely to differ
in individuals and populations who differ in body build (e.g. highly
muscular individuals) and body proportions (e.g. individuals with
unusually long or short legs).3

This means that when assessing individuals the BMI category is a good
screening tool, but is not a diagnostic tool. Athletes such as footballers
often have a BMI in the overweight range and yet they are not over fat.
Conversely, someone can be in the healthy weight range and still be over
fat. This means that everyone close to the boundary of healthy weight and
overweight should be further assessed, regardless of classification.
Ultimately, the advice you give someone should be in the light of their
other risk factors and lifestyle.

Should cut-off points be different for Aboriginal and Torres Strait

Islander people?
A number of studies have been conducted showing that, for a given BMI,
Aboriginal people have a greater percentage of body fat than do
Caucasians.15 (The opposite may be true of Torres Strait Islanders, but this
is less studied). This has lead to the suggestion that the cut-off points
to define categories should be different for Aboriginal people, e.g. that
the overweight category might be more like 23–<28 than 25–<30. While this
might be true from a theoretical point of view, one needs to consider
several other things.
The current BMI categories are based on risk of mortality, not the
proportion of body weight that is fat, and are simply cut-off points along
a continuous distribution. Different cut-off points could also have been
chosen for Caucasian populations. As indicated above, people near the
boundary of acceptable and overweight should be assessed individually and
their other risk factors taken into account. There are few studies of the
association between BMI and mortality in Indigenous people to determine
whether the BMI associated with the lowest risk of mortality in that group
is different from the BMI associated with the lowest mortality in any other
group.
One analogy might be the difference in risk associated with weight in
smokers and non-smokers (see figure 1).

Figure 1: Schematic diagram of risk levels

in smokers and non-smokers

The curve for smokers is at a higher level than that for non-smokers and so
there are two different ways for an overweight smoker to reduce his/her
risk — one is to stop smoking and the other is to lose weight. But does
this mean that different cut-off points for healthy weight should be set
for smokers and non-smokers? Are we interested in setting cut-off points to
give different groups the same absolute risk, or to define relative
reductions associated with one risk factor across groups? If it is the
first, then we should set different cut-off points for smokers and non-
smokers; if it is the second, then the cut-off points would be the same.
The figure probably reflects the general pattern for Aboriginals (dotted
line) and non-Indigenous Australians (solid line). And so the question
arises: what is the cause of the offset? Is it the central obesity (see
below)? Is it some other factor, such as low birthweight leading to long-
term differences in adult disease? Or perhaps the shape of the two curves
are not similar but different and there really should be different cut-off
points. More research is needed before we can really start to answer these
questions!
As shown below, important improvements in some aspects of heart disease
and diabetes risk factors can be achieved by losing 3–5 kg, even though the
final weight is still in the overweight or obese range. Presumably larger
improvements could be achieved with greater weight loss. This means that we
should be careful not to discourage people from losing some weight because
we have set goals that are too far away to achieve.
[Editor: The relationship of birth weight and early growth to adult
health may be more relevant than ethnicity for explaining differences in
health outcomes at different BMI levels in different populations. ‘In
general the most unfavorable growth pattern is smallness and thinness at
birth, continued slow growth in early childhood, then acceleration of
growth so that height and weight approach the population means . . .’ The
fetal origins of adult disease: no longer just a hypothesis and may be
critically important in south Asia. R. Robinson BMJ 17 Feb 2001.]
Central versus peripheral adiposity
In Caucasians a common pattern is that men tend to put on excess weight on
their abdomen (an apple shape) and women on their hips and thighs (a pear
shape). Visceral (stomach) fat is more metabolically active than
subcutaneous fat and is associated with dyslipidaemias, hypertension and
type 2 diabetes3 and this is one explanation for the observation that
Caucasian men have more heart disease than Caucasian women with the same
BMI. Among Aboriginal people, both men and women tend to put on excess
weight on their stomachs. The different distribution of fat may be one
reason why Aboriginal people have higher levels of chronic diseases than
Caucasians.
The WHO committee’s recommendations for action (see below) class central
obesity as an additional risk factor to overweight3 but only bring in a
consideration of central obesity for people who are in the overweight
range. Given the comments that the cut-off points are screening guidelines
and not diagnostic for excess fat in the body, and the high prevalence of
large waists in Aboriginal people, it would probably be sensible to advise
people in the ‘healthy weight range’ who clearly have pot bellies to lose
some weight. However, measuring waists is difficult. There are at least
three different definitions (at the narrowest point, where the belly button
is and the midpoint between two particular bony landmarks) and these do not
give the same circumference as they are not in the same place. Hence, it
would not seem sensible to make recommendations about numerical cut-off
points. Therefore, at present it would seem best to advise staff to use
their eyes rather than a tape measure to identify who should be advised to
lose weight and for them to ask clients about whether skirts and trousers
are getting looser around the waist.
[Editor: WHR is not specifically mentioned in the protocol. Is this
appropriate given the high prevalence of high WHR in the A&TSI population,
particularly among women? Are the WHO guidelines appropriate for population
where poor growth in adult life is prevalent, and where smoking rates are
high? Would it be more appropriate to advise loss of belly fat at BMI
levels below the 25.0 to 29.9 level?
Waist and WHR are not easy to measure, and ratios and changes in ratio
not concepts which are intuitively easy. The editorial committee chose to
include a mention of the importance of losing ‘belly fat’ even if the
overall BMI is in the healthy range, but believes routine measurement of
WHR may not be well performed or interpreted; guideline threshold waist
circumference values are provided.]

Prevalence of overweight and obesity

The available information about overweight and obesity in NT Aboriginal
adults is derived from the 1994 National Aboriginal and Torres Strait
Islander Survey (NATSIS) and is summarised in ‘The health and welfare of
Territorians’ 16:
. . . One problem with interpreting the data is that many of the
respondents declined to be measured, so it is not clear whether some of
the differences in weight reflect differences in participation rather than
size. The available information does not allow an assessment of whether
the prevalence of overweight and obesity varies substantially with age.

In the Katherine region, where virtually everyone was measured, the survey
found that 46% of Aboriginal adults were overweight or obese (table 6).
This compares with the 1995 National Nutrition Survey figure of 55% for
Australians.
The low measurement rate means that the NATSIS results might not be
representative in all regions of the NT. Therefore, it is possible that the
proportion of obese Aborigines in some parts of the NT is about double the
national prevalence, while in other parts the proportion is much lower.
Despite the low measurement rate the response rate for interviews was very
high, and so we were able to compare the reported characteristics from the
questionnaires of those who were measured with those who declined to be
measured. From these analyses, we concluded that, at the national level,
there was no reason to think that the national figures for weight
distribution in Indigenous Australians were affected by the extent of non-
measurement8 but this might not be true for small areas. The prevalence of
overweight and obesity is higher in Torres Strait Islanders than in
Aboriginal people (table 5). When comparing with the all-Australian
prevalence (table 4) the difference in age structure of the two populations
should be remembered. Among non-Indigenous Australians, overweight and
obesity tends to increase with age, whereas in many locations older
Aboriginal people are less overweight than younger adults. This means that
the prevalence of overweight and obesity in Aboriginal people and the all-
Australian population are more different than appears to be the case at
first glance.

Table 6: NT Aboriginal adults 18 years and older, 199416

Number Per cent
Group Surveyed Measured Underweight Acceptable Overweight Obese
<20 20–25 >25–30 >30
NT ATSIC
Region

Aputula 4380 570 10.9 50.0 37.0 2.2

Alice 2420 1010 7.9 28.7 32.7 30.7
Springs
Tennant 2020 590 10.2 23.7 40.7 25.4
Creek
Katherine 3860 3780 14.0 38.4 30.1 17.5
Nhulunbuy 3650 2430 32.2 35.5 15.3 16.9
Jabiru 4790 2600 18.5 39.8 34.0 7.7
Darwin 4400 3220 8.4 28.6 33.5 29.5
 Table 7: Interventions according to BMI – WHO Expert Group3
BMI range Other conditions Recommendation
18.5 to 24.9 avoid becoming overweight
25.0–29.9 no risk factors avoid weight gain
monitor weight, e.g. yearly
intervene if weight gain
occurs
25.0– 29.9 and risk factors e.g. cease smoking, increase
high abdomen/hip ratio, physical activity, reduce
hypertension, saturated fat, moderate
hyperlipidaemia, glucose weight loss
intolerance, type 2
diabetes, family history
of type 2 diabetes, or
premature coronary heart
disease
30.00 and over as for the overweight group, but moderate weight loss is
a priority as risk factors and conditions are generally
more marked

Evidence for the benefits of losing 3–5 kg

Although observational studies have shown that being obese increases
mortality, the 1995 WHO committee noted that no intervention studies had
shown that obese people who lost weight had lower mortality or fewer
morbidites such as strokes or heart disease.3 A Cochrane review to examine
whether this situation has changed is currently underway. This lack of
information about the benefits of weight loss when no other abnormality
existed lead the WHO Expert Committee to make recommendations about weight
loss in the overweight and obese that depended on the presence of other
factors (table 7).
One of the problems is that there are two sets of studies which investigate
different interventions and have different endpoints. Studies investigating
how to help people lose weight have tended to report only weight loss as
the outcome. Studies with change in chronic disease risk factors as the
endpoint have tended to use combined lifestyle and diet interventions
rather than weight loss alone, and so it is not clear whether the results
are due to weight loss, the other interventions or a mix of the two.
However, there is some evidence that modest weight loss can alter some
important intermediate risk markers and this supports the recommendation
for modest weight loss in those with risk factors.
Mulrow et al.17 reviewed the effects of weight loss on blood pressure
levels. The trials were generally conducted in people with an average
weight of 84 kg and blood pressure of at least 190 mmHg systolic and/or 90
mmHg diastolic. Compared to no change in diet, a diet leading to a weight
loss of 3–9% initial body weight decreased both systolic and diastolic
blood pressure by 3 mmHg, although in neither case was this statistically
significant due to the variability in results among the studies. They also
compared weight loss to anti-hypertensive therapy and found that stepped
care was better than weight loss for reducing blood pressure levels, but
that there was an indication that weight loss would lead to a reduction in
dose of medication. They concluded that it would be reasonable to delay
anti-hypertensive therapy in someone with mild hypertension who was
committed to losing weight but that it is ‘unrealistic to expect a weight-
reducing diet alone to achieve blood pressure control in patients with
severe hypertension or in patients unmotivated to lose weight’. It is worth
noting that many of the people in these trials did not lose enough weight
to achieve the acceptable weight range. Although these results are useful,
their outcome was change in blood pressure; data on change in stroke
incidence or mortality would be more useful, but would require longer and
larger studies.
The effect of weight loss alone on cholesterol levels is not so clear
cut from randomised controlled trials because the trials have generally
involved a diet that had a modified fat and cholesterol content rather than
simple energy intake restriction. Hence, the effects on cholesterol levels
or outcomes such as heart disease or mortality cannot necessarily be
ascribed to weight loss alone. Thus, although multiple risk factor
interventions do reduce cholesterol levels18, their value overall depend on
which outcomes are examined. In the primary prevention situation, they have
only a very small effect on total mortality19,20 although there is generally a
larger effect when heart disease mortality and non-fatal cardiac events are
grouped together.
Until recently, there was no trial examining whether the onset of
diabetes could be delayed in those with impaired glucose tolerance (IGT). A
trial in Finland compared advice regarding diet+exercise to a pamphlet.21
The subjects were recruited by screening high risk individuals (such as
relatives of diabetics), were aged 40–65 years and had a BMI of 25 or
greater. The dietary intervention goals were: weight loss of 5% or more,
total fat intake of less than 30% of energy, saturated fat intake of less
than 10% energy, increasing fibre to 15g/4.2MJ, and frequent intake of
whole grains, fruit, vegetables, low-fat milk and meat, soft margarines and
mono-unsaturated oils. Moderate exercise of at least 30 minutes per day was
recommended and subjects were advised to do both aerobic exercise and
strengthening exercise for the large muscles. Diabetic status was
determined in all but 40 of the 523 randomised subjects. The hazard ratio
(a type of relative risk) was 0.4 (95% CI: 0.3–0.7) at six years of follow-
up (i.e. those in the intervention group were only 40% as likely to have
become diabetic as those in the control group).
By the end of the first year the intervention group had lost 4.2 kg
compared to 0.8 kg in the control group and a greater proportion had
changed various aspects of diet (except alcohol consumption) than the
control group. However, success in achieving specific aspects of the
intervention ranged from 25% for fibre intake to 86% for exercise. In
addition to this intention-to-treat analysis, other analyses were done
according to compliance. In the intervention group, those who lost 5% or
more of body weight had a hazard ratio of 0.3 compared to those with less
weight loss. Among those who did not achieve the weight loss goal, those
who did achieve the activity goal of four hours per week had a hazard ratio
of 0.2 compared to those who did not achieve the activity goal.
Other benefits were reported from this trial. The reduction in blood
pressure level is consistent with that reported in Mulrow et al.’s meta-
analysis.17 Triglycerides, which are commonly raised in Aboriginal people,
also fell although there was no change in cholesterol level. As other work
has shown that controlling hypertension in diabetics reduces the incidence
of important outcomes such as renal failure, these findings are presumably
very beneficial for this group of people.
In 2002, similar results were reported from an American study.22 This study
is particularly interesting because 45% of the study population were from
minority populations — African, Hispanic and Native Americans — who have
very high rates of diabetes. All of these sub-groups had the same benefit
as the larger group. From this it is reasonable to conclude that the
studies conducted overseas can be extrapolated to Aboriginal people in
Australia. The US study also tested metformin in another arm and found that
the lifestyle intervention was more effective in delaying progression to
diabetes than the metformin.22
The BMIs seen in the participants in the trials are quite commonly seen
in Aboriginal groups. It is worth noting that an average weight loss of 4.2
kg in people with a average baseline BMI of 31.3 means that about half the
people in the Finnish trial were still in the obese category at the end of
the first year. In other words, these benefits can be achieved without
people having to lose enough weight to get down to the healthy weight
range. Presumably, if people manage to lose more weight, they will have
additional benefit. In addition, the physical activity was moderate, it was
not strenuous sport-type ‘exercise’.

Table 8: Selected baseline characteristics and results from the Finnish trial20

Intervention Control
group group
n=256 n=250
Baseline characteristics
BMI 31.3 31.0
Total cholesterol (mg/dL) 215 215
Triglycerides (mg/dL) 154 158
Systolic blood pressure (mmHg) 140 136
Diastolic blood pressure (mmHg) 86 86

Change at 1 year
Weight (kg) -4.2 -0.8
Total cholesterol -5 -4
Triglycerides -18 -1
Systolic blood pressure (mmHg) -5 -1
Diastolic blood pressure (mmHg) -5 -3

Diabetes at six years (hazard ratio) 0.4 1.0

All changes at one year are significantly different between the intervention and
control groups except that for total cholesterol

The role of physical activity in prevention

Decreasing physical activity rather than overeating seems to be responsible
for the epidemic of overweight in the Western world. In fact, contrary to
popular perception, we now consume less energy, on average, than our
grandparents, although there are undoubtedly exceptions to this. Research
in the UK has documented a greater decline in physical activity levels than
energy intake over the past few decades, although this may not be the case
in all groups.23 Encouraging enjoyable physical activity in children is an
important strategy for long-term prevention of overweight and obesity.23
 It is certainly true that most people are unable to exercise for the
amount of time that would be needed to achieve a large weight loss without
dieting. As the Finnish study above showed, weight loss with mild physical
activity and mild diet occurred at a rate of about 1 kg per three months.
Despite this, the impact on health was notable. As far as weight control
itself is concerned, the role of physical activity is to prevent the slow
weight gain that tends to occur throughout life and so this should be
encouraged in all age groups. It is also important to ensure that people
understand that activities like walking, dancing or housework are being
encouraged as there is a tendency for people to think of exercise only in
terms of what is aerobic and very energetic. The secondary analysis of the
Finnish study — which found that people who did the exercise but did not
lose weight had a slightly larger benefit than the intervention group as a
whole — is very intriguing. Does this suggest that physical activity might
be an independent protective factor in its own right and not simply a
method to help people to lose weight? (That is, in the same way that an
overweight smoker who quits smoking but does not lose weight will reduce
his/her risk of heart disease.) If so, then people should be told to
increase their activity for its own benefit and not simply because activity
helps to control weight (and, therefore, not to give activity up if weight
loss does not occur). However, a trial of activity in IGT without
concurrent dietary interventions to reduce the subjects’ weight has not yet
been done to answer this question.
One difference between the Finnish and US trials is that the US trial
did not include the large muscle strengthening exercise in its program, but
had only encouraged ‘physical activity of moderate intensity, such as brisk
walking’. However, it should be noted that the subjects in the intervention
groups of both trials received numerous counselling and encouragement
sessions. Hence the same level of result could not be expected from a
single five minute talk.
[Editor: The diet changes and physical activity achieved during the
Finnish and US studies were not ‘mild’. They were significant and
sustained. While it is important to emphasis that small changes in weight
are achievable and can provide great benefits in health, the behavioral
changes in terms of diet and PA need commitment and support to be achieved
and sustained.]

Infant birth weight and maternal weight

As noted above, the cut-off points describing weight categories are based
on risk of mortality. However, the risk of low birth weight babies
increases as maternal pre-pregnant weight decreases. This outcome does not
appear to have been considered by the Expert Committee when they lowered
the cut-off for healthy weight.3 Similarly, the literature discussing the
relationship between maternal weight and infant outcomes does not usually
consider effects on maternal health in the long-term. Hence, it is not
immediately obvious how to weigh up the risks and benefits identified in
the two distinct sets of literature for a population such as Aboriginal
people, who have a high rate of low birth weight and also high levels of
diabetes and other adult chronic disease.
There are two distinct reasons why an infant may be small when it is
born. Firstly, it may be born early (preterm) but be within the expected
size range for its gestational age. Secondly, it may be small for its
gestational age. This is variously called small-for-dates, small-for-
gestational age or intra-uterine growth retardation (IUGR). An infant may
be both preterm and growth retarded. Although the relative contribution of
preterm delivery and IUGR to low-birth weight in the Aboriginal population
is the subject of intense argument at present24–26 both are related to
maternal pre-pregnant weight and/or gestational weight gain.27 Table 9 shows
the factors associated with the two types of low birth weight that were
identified by Kramer27 in a review that considered only deliveries in women
with no underlying chronic illness. Studies published in the last decade
indicate that there are some other important factors for preterm delivery,
including those for the underlying chronic illnesses not considered by
Kramer.27 In particular, urogenital infections, including bacterial
vaginosis, and diabetes28,29 may be important in Aboriginal women. Studies on
Aborigines in WA 30–32 and the NT agree that the factors described elsewhere
in the world are important influences on birth weight.
Rae33 examined the associations between birth weight and various
antecedents using data routinely recorded in antenatal charts in two Top
End communities between 1983–86. She found that the predictors for having
an IUGR infant were maternal pre-pregnant weight of less than 43 kg,
gestational weight gain of less than 8 kg, attending for ante-natal care
after 20 weeks, maternal age less than 19 years and maternal parity less
than four. The effect of pre-pregnant weight was stronger than the effect
of gestational weight gain (39–62 g versus 36–40 g in birth weight for a 1
kg difference in maternal weight respectively). Cigarette smoking was not
well documented in the antenatal records.
Sayers and Powers32 examined the antecedents of 503 Aboriginal infants
born at Royal Darwin Hospital between 1987–90. They found that 15% of the
IUGR was attributable to low maternal weight and 10% to cigarette smoking.
Only diabetes predicted preterm delivery and they estimated that 5% of the
preterm birth could be attributed to it. Overall, they estimated that 28%
of the low birth weight could be attributed to the mothers having a body
mass index of less than 18.5 kg/m2 at delivery, and 18% could be attributed
to mothers smoking more than half a pack of cigarettes per day.
It is worth noting the low weights described by the two authors. The 43
kg of Rae33 is equivalent to a BMI of 16.8 in a woman who is 160 cm tall.
The 18.5 BMI of Sayers and Power32 was a post-partum BMI and therefore
presumably somewhat higher than the women’s pre-pregnant weight. Diabetes
and gestational diabetes are becoming increasingly common in Aboriginal
people at young ages. Given the association with obesity, one would presume
that gestational diabetes is occurring in the heavier women rather than the
thin women, but as the Midwives Collection does not collect maternal weight
it is not possible to confirm this.
Table A.3: Predictors of intra-uterine growth retardation and preterm birth27

Intra-uterine growth retardation Pre-term birth

Established determinants (Kramer 1987)

Direct infant sex Direct maternal pre-pregnancy weight
race/ethnic origin prior preterm birth
maternal height prior spontaneous abortion
maternal pre-pregnancy weight maternal cigarette smoking
paternal height and weight in utero diethy-stilboestrol exposure
maternal birthweight
parity
prior low birthweight infant
gestational weight gain
energy intake
general morbidity
malaria
maternal cigarette smoking
alcohol consumption
tobacco chewing

Indirect very young maternal age

socio-economic status (including maternal
education)

Other proposed predictors of preterm:

maternal diabetes, urogenital infections,
bacterial vaginosis, placental, cervical or
uterine abnormalities
Can low birth weight be improved by altering maternal weight?
The studies described in the previous section are all observational.
Although they describe associations that allow identification of
potentially useful interventions, they do not test whether the proposed
interventions are efficacious. Without proper testing of a proposed
intervention, it is impossible to distinguish between the predictive
factors that are reversible causes and the predictive factors that are only
indicators to identify women at higher risk.
Perhaps the most supportive evidence that altering a woman’s weight
during pregnancy could alter the weight of the infant comes from the
unintended experiment that occurred in Holland during the Second World War.
The amount of food available was drastically reduced from about 1800 kcal
(7.5MJ) per day to 580 kcal (2.5MJ) per day at the height of a siege.34 As
hospital records in the affected towns were kept carefully, the effect of
food restriction at different points during pregnancy could be examined.
The birth weight of those born during the famine was more than 300 g lower,
but the birth weight of those conceived during the famine was not different
from that of non-famine infants.
It would not be ethical to reproduce this study by starving a group of
pregnant women. However, the opposite approach — comparing the effect of a
supplement versus no supplement or placebo — has been tried in a number of
countries. Some trials have tested a combination diet that increased energy
and protein, while others tested the effect of increasing just the protein
content of the diet. Considering only randomised controlled trials, Kramer35
concluded that a balanced supplement of protein and an extra 1 MJ/day of
energy caused an increase of 21 g/week (95%CI: 9 g; 33 g) in maternal
weight gain, an increase of 30g (95%CI: 1 g; 58 g) in birth weight, a non-
significant increase of 0.2 cm (95%CI: 0.0 cm; 0.4 cm) in birth length and
no difference in head circumference. There was a reduction in both IUGR and
preterm birth, both having odds ratios of about 0.8 (95%CI for preterm
birth: 0.6; 1.1) but neither were statistically significant. Thus, the
effect on birth weight was only about half that predicted from the Dutch
results. Kramer (1993) also noted that the effect of supplementation on
birth weight was not larger in women with lower pre-pregnant weight, as had
been predicted from large observational studies (e.g. Naeye et al36).
By contrast, the infants of women randomised to a high protein
supplement but no additional energy intake were significantly lighter than
control infants (-64 g, 95%CI: -124 g; -3 g) and their mothers gained less
weight than the control mothers.35
The results of Naeye et al36 had also predicted that birth outcomes in
obese women would be improved if gestational weight gain were limited. In
another review, Kramer37 examined trials of restricting the intake of obese
pregnant women to between 1200–2000 kcal/day. Contrary to prediction, there
was a statistically significant reduction in birth weight of 153 g (95%CI:
-256 g; -30 g) in the women who were dieted. There was no reduction in the
incidence of pregnancy-induced hypertension or pre-eclampsia and a non-
significant reduction in the preterm delivery rate (OR = 0.5, 95% CI: 0.1;
2.6).
To summarise, increasing maternal intake by about 1 MJ (400 kcal) using
a balanced diet containing a range of nutrients (table 10) will cause a
small increase in infant birth weight, probably in the vicinity of 30 g. At
present, there is no evidence that increasing intake in underweight women
will have a greater effect on increasing birth weight than for normal
weight women. Therefore, it would seem reasonable to advise women who have
a BMI of less than about 18.5 and have a poor quality diet to improve their
dietary quality and put on a small amount of weight before becoming
pregnant. But there is no reason to advise women in the healthy weight
range to ‘fatten up’ during pregnancy beyond the usual recommendations for
gestational weight gain. Advising obese women to restrict their intake will
decrease the birth weight of their infants.
In addition it should be remembered that there are a number of other
factors which lead to low birth weight — such as cigarette smoking38 — that
are common in Aboriginal women. These factors may have at least the same
magnitude of effect on birth outcomes as maternal weight, and advice about
them should also be given. The information available to date would suggest
that smoking rates in pregnant women did not change in the first set of
communities in the Strong Women program.39 Hence this would seem to be a
useful additional focus of intervention for pregnant women.

Table 10: Energy content of typical foods recommended for increasing the
dietary intake of pregnant women
Food kJ kcal

1 slice toasting bread and 1 tsp margarine 611 145

1 medium orange or large apple 255 61

300 ml reduced fat milk 624 149

30g meat (about size of 1 matchbox) 360 86

References
1. NHMRC. Acting on Australia’s weight: a strategic plan for the prevention of
overweight and obesity. NHMRC, Canberra 1997.
2. National Heart Foundation of Australia. Risk factor prevalence study. Report No
1. 1980. National Heart Foundation (undated).
3. WHO Expert Committee on Physical Status: the Use and Interpretation of
Anthropometry 1995. Physical status: the use and interpretation of anthropometry:
report of a WHO expert committee. WHO Tech Report Series, 854, WHO Geneva.
4. NHMRC. Table of acceptable weights for height. Adopted at the 98th Session,
October 1984, Canberra, AGPS, 1984.
5. NHMRC. Definitions of overweight and obesity. Adopted at the 100th Session,
November 1986, Canberra, AGPS, 1984.
6. ABS and HEALTH. National Nutrition Survey Users’ Guide. 1995. ABS Cat No 4801.0.
ABS, Canberra, 1998.
7. ABS and HEALTH. National Nutrition Survey. Nutrient intakes and physical
measurements Australia 1995. ABS Cat No 4805.0. ABS, Canberra, 1998.
8. Cunningham J, Mackerras D. Overweight and Obesity Indigenous Australians 1994.
ABS Cat 4702.0. ABS, Canberra, 1998.
9. Mackerras D. Do we agree on the interpretation of some commonly used indicators?
Aust J Nutr & Diet 1998; 55:63–7, 73.
10. Mackerras D, Cunningham J. Body mass index distribution in adults in the 1994
National Aboriginal and Torres Strait Islander Survey. Proc Nut Soc Aust 1996;
20:169.
11. Harvey PWJ, Althaus M. The distribution of body mass index in Australian children
aged 7–15 years. Aust J Nutr & Diet 1993; 50:151–3.
12. Himes JH, Dietz WH. Guidelines for overweight in adolescent preventive services:
recommendations from an expert committee. Am J Clin Nutr 1994; 59:307–16.
13. Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. Establishing a standard definition for
child overweight and obesity worldwide: international survey. BMJ 2000; 320:1240–3.
14. Manson JE, Colditz GA, Stampfer MJ, Willett WC, Rosner B, Monson RR, Speizer FE,
Hennekens CH. A prospective study of obesity and risk of coronary heart disease in
women. New Eng J Med 1990; 322:882–9.
15. Rutishauser IHE, McKay H. Anthropometric status and body composition in
Aboriginal women of the Kimberley region. Med J Aust 1986; 144(suppl):S8–S10.
16. Arnold L, Warman G, Condon J (eds). The health and welfare of Territorians.
Territory Health Services, 2001.
17. Mulrow CD, Chiquette E, Angel L, Cornell J, Summerbell C, Anagnostilis B, Brad M,
Grim R Jr. Dieting to reduce body weight for controlling hypertension in adults
(Cochrane Review). In: The Cochrane Library, Issue 3, 2001, Oxford, Update Software.
18. Brunner E, White I, Thorogood M, Bristow A, Curle D, Marmot M. Can dietary
interventions change diet and cardiovascular risk factors? A meta-analysis of
randomized controlled trials. Am J Public Health 1997; 87:1415–22.
19. Ebrahim S, Davey-Smoth G. Systematic review of randomised controlled trials of
multiple risk factor interventions for preventing coronary heard disease. Brit Med J
1997; 314:1666–74.
20. Hooper L, Summerbell CD, Higgins JP, Thompson RL, Clements G, Capps N, Davey-
Smith N, Riemersma RA, Ebrahim S. Reduce or modified dietary fat for prevention of
cardiovascular disease. Cochrane Database Syst Rev 2000; (2):CD002137.
21. Tuomilehto J, Lindstrom J, Eriksson JG et al. Prevention of type 2 diabetes
mellitus by changes in lifestyle among subjects with impaired glucose tolerance.
NEJM 2001; 344:1343–50.
22. Diabetes Prevention Program Research Group. Reduction in the incidence of type 2
diabetes with lifestyle intervention or metformin. New Engl J Med 2002; 346:393–403.
23. O’Connor HT, Eden BD (eds). Recommendations for nutrition and physical activity
for Australian children. Med J Aust 2000; 173(suppl):S1–16.
24. Sayers SM, Powers JR. Birth size of Australian Aboriginal babies. Med J Aust
1993; 159:586–91.
25. Coory M. Gestational misclassification and low birthweight in Aborigines. Aust NZ
J Pub Health 1997; 21:84–8.
26. Mackerras D. Size for gestation in Aboriginal babies: a comparison of two papers.
Aust NZ J Public Health 2000; 24:287–90.
27. Kramer MS. Determinants of low birth weight: methodological assessment and meta-
analysis. Bull WHO 1987; 65:663–737.
28. Berkowitz GS, Papiernik E. Epidemiology of preterm birth. Epidemiol Rev 1993;
15:414–43.
29. Lumley J. The epidemiology of preterm birth. Clin Obstet Gynaecol 1993; 7:477–98.
30. Blair E. Why do Aboriginal newborns weigh less? Determinants of birthweight for
gestation. J Paediatr Child Health 1996; 32:498–503.
31. Blair E, Morich P, Stanley F. Why do Aboriginal newborns weigh less? Gestational
age at delivery: estimation, distribution and determinants. Aust NZ J Obstet
Gynaecol 1994; 34:158–63.
32. Sayers S, Powers J. Risk factors for Aboriginal low birthweight in Darwin. Aust
NZ J Pub Health 1997; 21:524–30.
33. Rae CJ. Maternal nutritional status among Aborigines in the Northern Territory:
impact on birth weight. Master of Public Health Thesis, University of Sydney, 1989.
34. Ravelli GP, Stein ZA, Susser MW. Obesity in young men after famine exposure in
utero and early infancy. New Engl J Med 1976; 295:349–53.
35. Kramer MS. Effects of energy and protein intakes on pregnancy outcome: an
overview of the research evidence from controlled clinical trials. Am J Clin Nutr
1993; 58:627–35.
36. Naeye RL. Weight gain and the outcome of pregnancy. Am J Obstet Gynecol 1979;
153:3–9.
37. Kramer MS. Energy/protein restriction for high weight-for-height or weight gain
during pregnancy. Cochrane Database Syst Rev 2000; (2):CD000080.
38. Dollen-Mullen P, Ramirez G, Graff JY. A meta-analysis of randomized trials of
prenatal smoking cessation intervention. Am J Obstet Gynecol 1994; 171:1328–34.
39. D’Espaignet E, Carnegie M, Measey MA, Mackerras D. The NT Strong Women Strong
Babies Strong Culture Program: the first eight years. Manuscript in preparation,
2002.
 Smoking and Tobacco

Author: Dr Rosalie Schultz (adapted from Dr Rowena Ivers1)

Topic Reviewers: Dr Rowena Ivers (MSHR); Central Australian Alcohol

and Other Drugs Services; Janet Fletcher (RAN, Ngukurr Clinic); Sally
Matthews (MSHR), Mt Liebig Clinic staff

Prevalence of use of tobacco

Numbers of users
In the National Aboriginal and Torres Strait Islander Survey conducted
among Indigenous people around Australia in 1994, 54% of Indigenous
Australians stated that they used tobacco.2 However, there are communities
in the Northern Territory where 83% of men and 70% of women smoke.3 By
comparison around 22% of all Australians use tobacco, according to the
Australian Institute of Health and Welfare nationwide survey of all
Australians.4 Australians are exposed to environmental or passive smoke, as
well as a large number using tobacco themselves.

Who uses tobacco?

In both Indigenous5,6 and non-Indigenous people7 use of tobacco is more common
among people with lower levels of education and higher unemployment levels.
Unemployment and lower levels of education are both more common among
Indigenous than non-Indigenous people. Therefore, lower levels of education
and higher unemployment levels may account for some of the extra users of
tobacco among Indigenous people.

Health effects of tobacco

Tobacco causes about 15% of deaths in Australia.8 Illness and death from
tobacco are commonly through9:
• ischaemic heart disease
• chronic obstructive airways disease (chronic bronchitis, emphysema,
asthma)
• lung cancer
• other cancers, including mouth and throat, oesophagus, pancreas,
cervix, kidney
• stroke
• pneumonia

All of these causes of death are more common among Indigenous than non-
Indigenous people.9
Other health problems associated with tobacco use include:
• cataracts and blindness10
• ear infections (which can lead to hearing problems and deafness11)
• infertility12
• SIDS (sudden infant death syndrome) among infants of people exposed to
environmental smoke13
A survey of rural Indigenous people in NSW found that smokers were less
likely than non-smokers to report that they were in very good or excellent
health.5
Chewing tobacco may cause infertility, cardiovascular disease and cancer
in the mouth.14 Chewing tobacco does not expose non-users to environmental
smoke.
Even among people who use very little tobacco, the risk of some of these
illnesses related to tobacco is higher than the risk in non-users. There is
no safe level of smoking.15 There is no information about whether there is a
safe level of chewing tobacco.
People at special risk. The risk of health problems from using tobacco is
greater among people who already have illnesses from tobacco, especially
ischaemic heart disease and chronic obstructive airways disease (‘COAD’,
asthma or emphysema). Diabetes causes thickening of the walls of blood
vessels. Smoking also causes disease in blood vessels. People with any of
these health problems are at particular risk from smoking.16
Children who are exposed to tobacco smoke are at increased risk of
respiratory infections compared with children not exposed to tobacco smoke.
This is true for children born to mothers who smoke, who are exposed even
before they are born. Therefore, pregnant women and people who live with
children have a special reason to stop smoking.17

Helping people quit using tobacco

The Northern Territory Government’s Department of Health and Community
Services (DHCS) has produced a guide to dealing with a number of public
health issues that are prominent in Indigenous communities, the Public
Health Bush Book. It is written for remote clinics and contains a lot of
useful material about tobacco and smoking. Copies were supplied to all NT
clinics and can be obtained through the DHCS.
How people quit
Studies in the USA show that most people who quit using tobacco quit
without any assistance. Quitters quit all at once, without cutting down
first or changing to lighter products.18,19
Despite this, a study of users of tobacco in the USA found that they
believed they would be more likely to quit with health concerns,
legislative changes, restrictions on sales or increased taxes on tobacco.19

Role of health professionals

Many Indigenous tobacco users support the role of doctors and other health
professionals in aiding quitting. They expect the doctor’s job is to
diagnose and give personalised advice, and that health professionals have
detailed knowledge of the body’s internal organs. Health professionals,
particularly doctors, can provide a reason for the Indigenous person to
change.20
Indigenous health workers may feel uncomfortable asking their kinfolk
about private behaviours such as smoking, and non-Indigenous health workers
may be better able to fill that role in encouraging quitting.21

How to do it
The first step to help people quit is to find out whether they use
tobacco.22 When you know that a client smokes you are then in a position to
assess how ready they are to quit, and move them through stages of
behaviour change towards quitting and remaining a non-user.
Encouraging non-users and recent quitters with positive messages about
not smoking may help them to continue not using tobacco and feel good about
their health habits.
A model of behaviour change developed by Prochaska and Di Clemente23 is
well-accepted as a description of the process of changing habits including
smoking, weight control and alcohol use. This model proposes a series of
stages of change which people may move through in their efforts to change.
The stages are in a circle rather than a line, and people may leave the
circle at various points, or continue to go around if they relapse. Health
professionals may be able to facilitate behaviour change by encouraging
progression through the stages from pre-contemplation to contemplation to
determination to action to maintenance, and back to contemplation if there
is a relapse.

Medications to help people quit

Medications have been demonstrated in clinical trials to increase the
likelihood of quitting. Nicotine replacement, such as patches or gum, has
been shown in non-Indigenous people to increase the likelihood of long-term
abstinence. The addition of bupropion, an antidepressant medication,
further increases the likelihood of long-term quitting.24 Bupropion should
not be used in people with previous seizures or psychiatric conditions.25

Health professionals who smoke

Health professionals who smoke are less likely to encourage their clients
to quit.26 Therefore, health professionals who are non-users could
prioritise assisting their colleagues to quit.
References
1. Ivers R. Indigenous Australians and Tobacco: a literature review. Menzies School
of Health Research. Cooperative Research Centre for Aboriginal and Tropical Health,
Darwin, 2001.
2. Australian Bureau of Statistics. National Aboriginal and Torres Strait Islander
Survey 1994: Health of Indigenous Australians (Cat. No. 4395.0). Australian Bureau
of Statistics, Canberra, 1996.
3. Hoy WE, Norman RJ, Hayhurst BG, Pugsley DJ. A health profile of adults in a
Northern Territory Aboriginal community, with an emphasis on preventable
morbidities. Aust N Z J Public Health 1997; 21:121–6.
4. Australian Institute of Health and Welfare. 1998 National Drug Strategy Household
Survey: First results (Cat. No. PHE 15). Australian Institute of Health and Welfare
(Drug Statistics Series), Canberra, 1999.
5. Guest C, O’Dea K, Carlin J, Larkins R. Smoking in Aborigines and persons of
European descent in southeastern Australia: prevalence and associations with food
habits, body fat distribution and other cardiovascular risk factors. Aust J Public
Health 1992; 16:397–402.
6. Hogg RS. Variability in behavioural risk factors for heart disease in an
Australian Aboriginal community. J Biosoc Sci 1994; 26:539–51.
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trends and concerns. Med J Aust 1998; 168:209–13.
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drug caused morbidity and mortality in Australia 1995 (Vol. 2). Australian
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9. Measey M, d’Espaignet E, Cunningham J. Mortality and morbidity attributable to
smoking, Northern Territory 1986–1995. Territory Health Services, Darwin, 1998.
10. Taylor HR. Prevalence and causes of blindness in Australian Aborigines. Med J
Aust 1980;1, 71–6.
11. Strachan DP, Cook DG. Health effects of passive smoking. 4. Parental smoking,
middle ear disease and adenotonsillectomy in children. Thorax 1998; 53:50–6.
12. Baird D, Wilcox A. Cigarette smoking associated with delayed conception. JAMA
1985; 253:2979–83.
13. United States Surgeon General. The health benefits of smoking cessation:
Executive summary. US Department of Health and Human Services, Atlanta, 1990.
14. Council on Scientific Affairs. Health effects of smokeless tobacco. JAMA 1986;
255 (8):1038–44.
15. Single E, Rohl T. National drug strategy: mapping the future. An evaluation of
the National Drug Strategy 1995–1997. Commonwealth of Australia, Canberra, 1997.
16. Rosengren A, Welin L, Tsipogianni A, Wilhelmsen L. Impact of cardiovascular risk
factors on coronary heart disease and mortality among middle aged diabetic men: a
general population study. Br Med J 1989; 299:1127–31.
17. DiFranza J, Lew R. Morbidity and mortality in children associated with the use of
tobacco products by other people. Pediatrics 1996; 97:560–8.
18. Fiore M, Novotny T, Pierce J, Giovino G, Hatziandreu E, Newcomb P, Surawicz T,
Davis R. Methods used to quit smoking in the United States. JAMA 1990; 263: 2760–5.
19. Pederson LL, Bull SB, Ashley MJ, MacDonald JK. Quitting smoking: why, how, and
what might help. Tob Control 1996; 5 209–14.
20. Brady M. Giving Aboriginal people the excuse to stop drinking: the role of the
health professional. Paper presented at the CARPA conference, Alice Springs, 14–15
March 1998.
21. Sibthorpe B. ‘All our people are dyin’: Diet and stress in an urban Aboriginal
community. Unpublished Doctor of Philosophy, Australian National University,
Canberra, 1988.
22. Australian Medical Association and Australian Pharmaceutical Manufacturer’s
Association. Indigenous smoking: issues and responses (draft). Canberra: Australian
Medical Association and Australian Pharmaceutical Manufacturer’s Association,
Canberra, 2000.
23. Prochaske JO, Di Clemente CC. Transtheoretical therapy: toward a more integrative
model of change. Psychotherapy: theory, research and practice 1982; 19:276–88.
24. Silagy C, Mant D, Fowler G, Lodge M. Meta-analysis on efficacy of nicotine
replacement therapies in smoking cessation. Lancet 1994; 343 (8890):139–42.
25. National Prescribing Service. Zyban (bupropion) for smoking cessation: potential
for interactions with psychotropic drugs. Therapeutic Advice and Information
Service, Melbourne, undated.
26. Miwa K, Fujita M, Inoue H, Sasayama, S. Is smoking behaviour in patients with
coronary heart disease influenced by whether their attending physician smokes? Tob
Control 1995; 4:236–8.
 Taking Medicine: Helping clients
make the most of advice and
medicines

Author: Rosalie Schultz (Katherine DMO)

Topic Reviewers: Dr Tarun Weeramanthri (Community Physician, CDC

Darwin); Mt Liebig Clinic staff; Kaz Knudsen (RAN, WA).

Taking medicine is sometimes called ‘compliance’, ‘concordance’ or

‘adherence’.
Forgetting Compliance: Aboriginal health and medical culture, by Kim
Humphery, Tarun Weeramanthri and Joseph Fitz1 provides a comprehensive
review of these issues in the Northern Territory Aboriginal health care
situation. This is a useful background to the subject of uptake of advice
and medication.

Understanding why clients don’t do exactly what you tell them

Forgetting Compliance invites us to consider the entire environment in
which we provide health care services, including social and economic
circumstances, the institutions through which health care is provided (that
is DHCS or Aboriginal-controlled organisations) and their methods of making
decisions, as well as the clinical encounter.1
Humphery emphasises that compliance is not a medical issue, and while we
should not ignore clinical approaches to improve the uptake of treatment
and advice, a medical approach does not have the capacity to address all
aspects of Aboriginal health (p 103). A more far-reaching approach is
needed.
Treatment protocols, even if followed precisely by both health
professionals and clients, are of limited effectiveness. The probability of
benefit for any individual patient receiving treatment, for risk factors
such as hypertension, is modest. For example, it is necessary to treat
around 128 people with diastolic blood pressure 90 to 109 to prevent one
stoke, heart attack or death in five years.2 Deaths of people who diligently
obeyed medical orders contribute to others’ ambivalence about treatment.3
Thus, the choice to take no treatment or intermittent treatment is
justifiable. Non-compliance is neither deviant nor illogical. There is a
conflict between the demonstrated benefit of management of risk factors in
a population and the uncertain benefit for any individual.
Not everyone agrees about the level of power and authority appropriate
for health professionals. However, using the word compliance, or
alternative words such as adherence or concordance, suggests that agreement
with health professionals is normal and appropriate. The effort to improve
compliance is an effort to demonstrate and increase the power of Western
biomedicine and the health professionals (pp 13–14). ‘The power of medical
knowledge is by no means proven or self evident and, to patients, medical
carers may well have a misplaced level of confidence.’3
[Editor: We do not necessarily agree that efforts to implement evidence
based health care, with informed autonomous decision making by clients, is
an effort to increase the power of Western biomedicine and health
professionals. It is, however, often important to differentiate evidence-
based advice from medical wisdom, and to be skilled at communicating the
size of the expected benefits and harms involved in health care choices.]

Treatment protocols
Uptake of medical advice is always imperfect. Studies around the world have
included trials of strategies to improve compliance. A Cochrane review of
clinical strategies to improve adherence4 concluded that:
The full benefits of medications cannot be realised at currently
achievable levels of adherence. Current methods of improving adherence for
chronic health problems are mostly complex and not very effective. More
studies of innovative approaches to assist patients to follow medication
prescriptions are needed.
According to this review the strategies useful to improve treatment
adherence and outcome are:
• Using simple treatment regimens.
• Recalling patients who miss reviews. This ensures
that they remain in contact with the health care system, an essential
prerequisite for continuing long-term treatment.
• Complex interventions which had some effect included combinations of
more convenient care, information, counselling, reminders, self-
monitoring, reinforcement and family therapy. However these
interventions are ‘not very effective’ despite the amount of effort and
resources they consume.4
The conclusion of this systematic review of clinic trials echoes the theme
of Forgetting Compliance, that is the need to look beyond the clinical
encounter in order to give clients the full benefits of available
treatments.

Social issues
The concepts of compliance, adherence and concordance suggest that people
respond to the advice of health professionals only as individuals. However,
people are also members of communities, and respond as members of
communities that have communal histories of contact with health
professionals.1
To understand why people may choose to follow the advice of providers of
health care, it is important to consider the clinical consultation in its
personal, social, and sociopolitical context. If we don’t do this we may
overlook important aspects of the consultation, and fail to account for our
clients’ position.
Here is a list of factors that may affect uptake of health care
advice.1,3,4,5 They have not been rigorously demonstrated to improve treatment
uptake in every situation: nor is this necessarily the goal of health care
providers. However, being aware of these factors may enable us to develop
strategies to improve uptake.
Factors that may affect uptake
of health care advice

Clinical factors

Client factors
• Belief systems, including beliefs about the condition and what should
be done if anything. Consultation is an exchange of information and a
learning experience for both parties. The client can provide you with
useful information about the cause, natural history and appropriate
management of the condition, and vice versa. From agreed information
you can work towards agreed management plans.
• Feeling autonomous in treatment decisions. Start with the client’s
choice of management, and find out how your choice can be incorporated.
• Co-morbidities, including drug and alcohol use, and psychological
illness, and intercurrent illness
• previous treatment uptake history
Treatment factors
• Simplicity of treatment
• Side effects and unpleasant effects of the treatment
• Unexpected symptoms developing while taking treatment
• Length of treatment
• How much behaviour change is needed for the treatment

Health care service factors

• How and where health care services are provided
• How easy it is to travel to the service
• Waiting times
• Atmosphere in clinic, including attitudes and appearances of staff
• Interaction between client and providers, including duration and
closeness of consultation
• Supervision of client and treatment
• Continuing contact between service and client, whatever management is
being used
• General level of client satisfaction with the service
• The organisation and structure of the health care service
• Decision-making within the health care service
• The relative power of the clients and the providers of health care
services

Clinician factors
• Sharing the client’s understanding of the condition
• Empathising with the client
• Agreeing with the client’s intentions regarding treatment plans
• Clear instructions in an appropriate language
• Repetition of instructions to clients and family members
• Written or pictorial instructions
• Using standard treatment plans, followed by all members of the health
care team
• Checking medications taken, or using dosette boxes or Webster packs)

Non-clinical factors
Individual client factors
• Routine and structure in everyday life
 • Living environment including health hardware, crowding, security,
safety
• Living situation including co-habitants and social obligations
• Relationships and interpersonal situations
• Legal and financial situation
• Languages spoken (English competence when medical consultations are in
English)

Community factors
• Support for the health care service and the treatment provided
• Ceremonial and seasonal factors

Factors in the wider society

• The socio-economic situation of clients
• Cultural practices
• Social justice in the health care system and society as a whole

Conclusion
There are many factors to consider in optimising the process of giving
treatment.
At the level of the clinical consultation simpler treatment regimens and
recalling clients for reviews improve treatment uptake and outcomes.
Other factors important in improving uptake and outcomes operate
throughout the society in which the health care service is run. These
include the client’s living situation, community and the wider society. In
this respect it is clear that health care provision is a political issue,
and political action is part of improving health care and health.

[Editorial committee comments: We are very aware that one of the major gaps
between the potential health gains from what health services can offer and
what actually happens may come under this broad banner of ‘compliance’.
This is true for all settings, but as mentioned above there are probably
more reasons, more often for ‘poor compliance’ in Indigenous communities.
In the protocols we have emphasised the importance of having a trusting
ongoing professional relationship between clients and health service staff.
This is, of course, a two-way relationship where the health professional
must also trust and respect the wishes and choices of the client.
Relationship building should be deliberate and a major part of
consultations, especially in the early weeks after diagnosing a chronic
condition.
Some practical clinical suggestions have been included, such as
minimising the number of times a day a person is expected to take
medication.]

References
1. Humphery K, Weeramanthri T, Fitz J. Forgetting Compliance: Aboriginal health and
medical culture. Darwin: Northern Territory University Press, 2001.
2. Medical Research Council Working Party. MRC trial of treatment of mild
hypertension: principal results. British Medical Journal 1985; 291: 97–104.
3. Devitt J, McMasters A. Living on medicine: Social and cultural dimensions of end-
stage renal disease among Aboriginal people of Central Australia. Alice Springs:
Central Australian Aboriginal Congress, 1996.
4. Haynes RB, Montague P, Oliver T, McKibbon KA, Brouwers MC, Kanani R.
Interventions for helping patients to follow prescriptions for medications
(Cochrane Review). In: The Cochrane Library, Issue 3, 2001. Oxford: Update
Software.
5. Hunter P. Health gains when Aboriginal people take control. Australian Medicine
2001 20 August; 11.
 Adult Health Checks:
Sexually transmitted infections

Author: Philippa Binns

Topic Reviewers: Dr Steven Skov; Dr Christine Connors; Robyn Dixson (RAN,

Yirrkala); Katie (RAN, Barunga Clinic); Dr Teresa Yee (Oenpelli)

Sexually transmissible infections (STIs) and their sequelae are extremely

common in the CARPA STM region. There are important regional variations in
the rates of infection. In general terms, rates are higher in remote
communities compared to towns, although there are remote communities with
low rates of infections and there are subgroups of people living in towns
with very high rates. While rates of infection amongst non-Aboriginal
people in the CARPA STM region are higher than the national average, rates
amongst Aboriginal people are very much higher.2 It has been hypothesised
that this relates to lack of access to education and health care rather
than substantial differences in sexual behaviour.1
While incidence rates provide a picture of high rates of infection,
prevalence information provides a different perspective and one that is
more pertinent to the primary health care level. In many communities, a
very high proportion of individuals are affected by these infections. As a
result, in these populations, unprotected sex carries a high risk of
contracting an infection.
Central Australian screening initiatives have provided useful prevalence
information. In 1995 and 1997, 26 remote communities in Central Australian
were involved in a screening program testing for gonorrhoea and chlamydia.
Participation rates ranged between about 50%–80%. It was observed that 24–
29% of 15–24 year olds were infected, as were about 10% of those aged 40–50
years.3
Nganampa Health Council in northern South Australia has conducted
community screening and treatment as a key element of its STI/HIV program
for many years. Initially, prevalence of infection with either gonorrhoea
or chlamydia of 19% was observed4, but these have been drastically reduced
with each year of the program.5
During trials in the Top End in the late 1990s, evaluating a tampon
test, it was found that 17% of women tested had gonorrhoea, 11% had
chlamydia and 25% had trichomonas.6 These results are consistent with
prevalences observed in Central Australia and the Kimberley region.7 Case
note audits in approximately 20 Top End remote communities revealed that
between 42% and 75% of adults had had at least one episode of a bacterial
STI during their life (unpublished data THS AIDS/STD programs).
Trichomonas displays a different epidemiological pattern to other STIs.
The typical STI pattern is for the highest rates to be seen amongst the
younger, more sexually active age groups, particularly 15–29 year olds.
However, high rates of trichomonas infection amongst women persist into
older age groups (NT notifiable disease database). Indeed, Bowden et al.
found that the prevalence of infection of trichomonas was higher amongst
women over 30 years of age.6

Syphilis
Once a person has been infected with syphilis, they generally remain
treponemal test (EIA, TPHA, FTA-Abs etc.) seropositive for life, even after
successful treatment. Treponemal test seropositivity provides a good
indicator of the burden of syphilis infection and one that can be monitored
over time to observe changes, especially in younger age groups. However,
this data must be interpreted with some caution as syphilis treponemal
tests may be positive as a result of yaws and non-venereal endemic
syphilis. These infections were common historically in the CARPA region but
mostly disappeared during the course of the 1950s, with the last known case
of yaws occurring in a Top End community in 1968.8
In the Nganampa Health Council region some 60% of all people aged 30
years were recently found to be seropositive.9 A study of infertility and
STIs revealed that 41% of all women in a large Top End community were
seropositive for syphilis.10 Recent audits of a random sample of 10% of case
notes in approximately 20 remote Top End remote communities revealed that
between 10% and 40% of people were seropositive for syphilis (unpublished
data THS AIDS/STD programs).

Complications of STIs
Pelvic inflammatory disease (PID)
PID will occur in between 10% and 40% of women infected with gonorrhoea or
chlamydia if they do not receive treatment.11,12 In one large Top End
community study it was found that 26% of women have had PID at least once.13
Recent audits of a random sample of 10% of women’s case notes in
approximately 20 remote Top End communities revealed that between 20% and
30% of women appeared to have had at least one clinical episode of PID
(unpublished data THS AIDS/STD programs).

Infertility
In two Top End communities 26% and 30% of women were found to be
infertile.13 Audits of a random sample of 10% of women’s case notes in
approximately 20 remote Top End communities revealed that between 10% and
30% of women appeared to have had no children (unpublished data THS
AIDS/STD programs), with very similar rates observed in women over the age
of 24.
By extrapolating from other studies14–17 in populations with similar rates
of STIs, it is reasonable to assume that at least 50% and perhaps as much
as 70% of this infertility is due to STIs.

Other
Other possible sequelae of STIs include ectopic pregnancy, miscarriages,
premature labour, congenital syphilis, neonatal conjunctivitis, neonatal
pneumonia and enhanced risk of HIV transmission.32

Detecting infection in asymptomatic persons

A large proportion of sexually transmitted infections cause either no
symptoms or very mild symptoms. This is particularly true of chlamydia,
gonorrhoea and trichomonas in women, but also occurs in a substantial
proportion of men with these infections.18–20 Genital ulcers may occur inside
the vagina in women and be clinically unapparent.21,22 People with mild
symptoms may not realise that an STI is the cause or — because of shame, a
lack of access to health care services or an appropriate practitioner — may
not present to a clinic for care. In some settings, it has been estimated
that as few as 5% of all persons in a population with an STI present to a
clinic and receive appropriate treatment.23
This is entirely consistent with experience in the CARPA region. In the
screening programs referred to above, a high prevalence of infection was
detected, even of gonorrhoea in men.3 No data is available as to whether
these people had symptoms. However, the key point is that they had not
presented to the clinic for care at the time they were offered the test.
Data from Top End clinical audits in over 20 remote communities reveals
that only 10%–20% of all STIs detected in remote communities are found in
persons presenting with STI symptoms. Approximately 60% of all infections
are detected by testing apparently asymptomatic persons as part of well-
persons, antenatal or opportunistic testing or as part of a formal
screening program (unpublished data THS AIDS/STD programs). The remainder
are found via contact tracing or follow-up of other infections.
There have been many efforts to describe criteria in order to identify
people at a greater risk of an STI. Many studies have come up with criteria
appropriate to their situation, but very few of them are applicable in a
wide variety of settings. Young age, usually less than 25 years, is common
to most places. In the CARPA region, approximately 60% of all STIs occur in
people under the age of 30 years.24 However, particularly in Central
Australia, there is good data to show that — while STIs are more common in
younger people — high rates continue to occur even up to age 50. There is a
common perception that alcohol use, especially heavy drinking or binge
drinking, is associated with an increased risk of STIs, although there is
no specific data to prove this. In Central Australia, Miller et al. found
that female petrol sniffers were at increased risk of gonorrhoea or
chlamydia as were people with a past history of an STI.5 Several prospective
studies overseas have found that people having one STI are at a
substantially increased risk of another within a relatively short period of
time.25–30
This data shows that if health service strategy is to only offer STI
tests to those persons presenting with symptoms, then it will have very
little impact on a substantial public health problem. Asymptomatic
individuals need testing as well. It is highly recommended that
practitioners have a low threshold for offering testing, and health
services implement a screening strategy. Fortunately, in most instances the
important STIs in the CARPA region can be treated with single doses of
antibiotics.

Screening for STIs

Given the above information it is apparent that STIs, in particular
gonorrhoea, chlamydia and syphilis, adequately fulfil the accepted criteria
for screening as discussed in the introduction. There are high rates of
infection and complications in the CARPA STM region. Most STIs are
asymptomatic and there are acceptable tests, in urine and tampon PCRs and
serology, to detect these asymptomatic infections.
 Single-dose antibiotics are available as a simple, effective treatment.
Community education and feedback would certainly help to ensure that the
benefits of an STI screening program outweigh the intrusion into and
surveillance of their lives. Sufficient planning and resources to provide
adequate follow-up are essential before embarking on an STI screening
program.
There are three ways to maximise the effectiveness of STI screening33:
• Targeting the high risk groups
• Monitor age-specific participation rates and age-specific
prevalence/incidence
• Minimise the interval to treatment
The experience of Nganampa Health Council has shown that targeted
community-wide mass screening for STIs alone can make a significant impact
on the prevalence of STIs in their region. A balance between the time
consuming nature of a well-person check and the resources, organisation and
high participation rates required for a successful community-wide screening
need to be negotiated.
Individual health services will need to decide how to deliver their
screening, but CARPA recommends using the Adult Health Check as an
opportunity for STI testing for gonorrhoea, chlamydia and syphilis from the
age of 15 at yearly intervals. In view of the prevalence in older age
groups this should be continued to at least 50 years of age or older if
risk factors are present. To test for gonorrhoea and chlamydia, a urine PCR
for men and tampon test or endocervical swab for PCR are best for women. To
test for syphilis, syphilis serology on a blood sample should be ordered.
In view of the Nganampa experience and success, communities are
encouraged to consider implementing targeted community-wide mass screening
if resources allow.
Current guidelines for screening for trichomonas remain confusing and
controversial. The PCR test in women has high sensitivity and specificity
but there has been little work in men. The relationship between
asymptomatic PCR-diagnosed trichomonas infection (which can detect a very
low microbial load) and the development of complications remains unclear.
Further information, consultation and research are required before an
appropriate recommendation can be made regarding trichomonas screening in
the general adult population.31

References
1. Fairley CK, Bowden FJ, Gay NJ, Paterson BA, Garland SM, Tabrizi SN. Sexually
transmitted diseases in disadvantaged Australian communities. JAMA 1997; 278(2):117–
18.
2. National Centre in HIV Epidemiology and Clinical Research. HIV/AIDS, viral
hepatitis & sexually transmissible infections in Australia. Annual Surveillance
Report. Sydney: National Centre in HIV Epidemiology and Clinical Research,
University of New South Wales, 2001.
3. Skov SJ. Unpublished discussion paper on secondary prevention strategies to
address the high rates of Sexually Transmitted Diseases in central Australia. Alice
Springs: Tri-State STD/HIV Project, 1996. Ref Type: Report.
4. Skov SJ, Miller P, Hateley W, Bastian IB, Davis J, Tait PW. Urinary diagnosis of
gonorrhoea and Chlamydia in men in remote Aboriginal communities. Med J Aust 1997;
166(9):468–71.
5. Miller PJ, Law M, Torzillo PJ, Kaldor J. Incident sexually transmitted infections
and their risk factors in an Aboriginal community in Australia: a population based
cohort study. Sex Transm Infect 2001; 77(1):21–25.
6. Bowden FJ, Paterson BA, Mein J, Savage J, Fairley CK, Garland SM et al.
Estimating the prevalence of Trichomonas vaginalis, Chlamydia trachomatis, Neisseria
gonorrhoeae, and human papillomavirus infection in Indigenous women in northern
Australia. Sex Transm Infect 1999; 75(6):431–34.
7. Garrow S. Self obtained low vaginal swabs for diagnosis of Chlamydia trachomatis,
Neisseria gonorrhoea and Trichomonas vaginalis in remote clinical practice in
northern Australia. Kimberley Public Health Unit Bulletin November 2001; 11–13.
8. Jacobs DS. A syphilis epidemic in a northern territory Aboriginal community. Med
J Aust 1981; 1(2 Suppl):5–8.
9. Miller P. Unfinished business: syphilis in remote Aboriginal communities on the
Anangu Pitjantjatjara Lands: descriptive epidemiology and disease control
strategies. 1997.
10. Kildea S. A retrospective epidemiological study comparing fertile and infertile
women in a remote Indigenous community in Australia. 1999.
11. Platt R, Rice PA, McCormack WM. Risk of acquiring gonorrhea and prevalence of
abnormal adnexal findings among women recently exposed to gonorrhea. JAMA 1983;
250(23):3205–3209.
12. Stamm WE, Guinan ME, Johnson C, Starcher T, Holmes KK, McCormack WM. Effect of
treatment regimens for Neisseria gonorrhoeae on simultaneous infection with
Chlamydia trachomatis. N Engl J Med 1984; 310(9):545–9.
13. Kildea S, Bowden FJ. Reproductive health, infertility and sexually transmitted
infections in Indigenous women in a remote community in the Northern Territory. Aust
N Z J Public Health 2000; 24(4):382–6.
14. Cates W, Farley TM, Rowe PJ. Worldwide patterns of infertility: is Africa
different? Lancet 1985; 2(8455):596–8.
15. Hornstein MD, Schust D. Infertility. In: Berek JSeae, editor. Novak’s Gynecology.
Baltimore, USA: Williams & Wilkins, 1996.
16. Chigumadzi PT, Moodley J, Bagratee J. Infertility profile at King Edward VIII
Hospital, Durban, South Africa. Trop Doct 1998; 28(3):168–72.
17. Collet M, Reniers J, Frost E, Gass R, Yvert F, Leclerc A et al. Infertility in
Central Africa: infection is the cause. Int J Gynaecol Obstet 1988; 26(3):423–8.
18. Stamm WE. Chlamydia trachomatis infections of the adult. In: KK Holmes et al.,
eds. Sexually Transmitted Diseases. New York: McGraw-Hill, 1999; 407–22.
19. Hook EW, Handsfield HH. Gonococcal infections in the adult. In: KK Holmes et al.,
eds. Sexually Transmitted Diseases. New York: McGraw-Hill, 1999; 451–66.
20. Krieger JN, Alderete JF. Trichomonas vaginalis and Trichomoniasis. In: KK Holmes
et al., edsr. Sexually Transmitted Diseases. New York: McGraw-Hill, 1999; 587–604.
21. Musher DM. Early Syphilis. In: KK Holmes et al., eds. Sexually Transmitted
Diseases. New York: McGraw-Hill, 1999.
22. Farrell N. Donovanosis. In: KK Holmes et al., eds. Sexually Transmitted Diseases.
New York: McGraw-Hill, 1999;: 525–32.
23. Hayes R, Wawer M, Gray R, Whitworth J, Grosskurth H, Mabey D. Randomised trials
of STD treatment for HIV prevention: report of an international workshop. HIV/STD
Trials Workshop Group. Genitourin Med 1997; 7 3(6):432–43.
24. Northern Territory Dept of Health and Community Services. Northern Territory
Notifiable Diseases Database. 2002. Ref Type: Generic.
25. Burstein GR, Waterfield G, Joffe A, Zenilman JM, Quinn TC, Gaydos CA. Screening
for gonorrhea and chlamydia by DNA amplification in adolescents attending middle
school health centers. Opportunity for early intervention. Sex Transm Dis 1998;
25(8):395–402.
26. Fortenberry JD, Evans DL. Routine screening for genital Chlamydia trachomatis in
adolescent females. Sex Transm Dis 1989; 16(4):168–72.
27. Herrmann BF, Johansson AB, Mardh PA. A retrospective study of efforts to diagnose
infections by Chlamydia trachomatis in a Swedish county. Sex Transm Dis 1991;
18(4):233–7.
28. Ramstedt K. An epidemiological approach to sexually transmitted diseases: with
special reference to contact tracing and screening. Acta Derm Venereol Suppl
(Stockh) 1991; 157:1–45.
29. Richert CA, Peterman TA, Zaidi AA, Ransom RL, Wroten JE, Witte JJ. A method for
identifying persons at high risk for sexually transmitted infections: opportunity
for targeting intervention. Am J Public Health 1993; 83(4):520–4.
30. Whittington WL, Kent C, Kissinger P, Oh MK, Fortenberry JD, Hillis SE et al.
Determinants of persistent and recurrent Chlamydia trachomatis infection in young
women: results of a multicenter cohort study. Sex Transm Dis 2001; 28(2):117–23.
31. The Northern Territory Disease Control Bulletin, Centre for Disease Control,
Northern Territory, 2002; 9(1):20.
32. Condon JR, Warman G, Arnold L, eds. The health and welfare of Territorians.
Darwin: Epidemiology Branch, Territory Health Services, 2001.
33. STD Control in remote Aboriginal communities. Office of Aboriginal and Torres
Strait Islander Health, Department of Health and Aged Care. 1999.
 HIV Testing

Author: Kirsty Smith (Coordinator Tri-state Sexual Health Project)

Topic Reviewers: Dr Steven Skov (AIDS-STD unit RDH); Ivor Alexander (RAN,
Nhulunbuy CDC)

Overview
Overall, rates of HIV and AIDS diagnoses in Indigenous Australians are
similar to non-Indigenous rates. Epidemiological data demonstrates that HIV
exposure categories differ between Indigenous and non-Indigenous HIV
infections. There is a higher proportion of heterosexually acquired cases
of HIV infection among Indigenous cases compared with national rates. There
is also a higher proportion of HIV infection of Indigenous women compared
with non-Indigenous women (25% compared with 7% for non-Indigenous cases.1,2
Only 50% of Indigenous HIV infections are attributed to male homosexual
contact.
It is well documented that STIs facilitate the transmission and
acquisition of HIV infection.3
In view of the hyperendemic STI rates in Indigenous populations of
Central Australia and the Top End,1 the potential for an HIV epidemic in
the region remains high. Common reproductive tract infections in this
region include gonorrhoea, chlamydia, trichomonas, bacterial vaginosis,
syphilis and donovanosis. Research performed in a comparable high STI
setting in Africa found that 29.5% of all HIV transmitted was attributable
to reproductive tract infections.4
Testing for HIV has been available in Australia since October 1984. At
that time, AIDS was associated with high morbidity and mortality and an HIV
diagnosis was highly stigmatised due to associations with marginalised
groups and death. National guidelines for pre-test counselling were
produced by a Commonwealth working party in 19925 with the aim of
optimising the information given, obtaining informed consent and preparing
the client to deal with the result, whether positive or negative.
In the last 10 years, advances in HIV treatments have significantly
reduced rates of AIDS notifications and AIDS-related deaths,1 due to
improved health and survival for people living with HIV. Despite these
advances, HIV remains a stigmatised condition that warrants clear testing
guidelines.

Barriers to testing
The promotion of pre-test counselling for HIV helped ensure a standard of
education and training for health care professionals working in the field.
Unfortunately, it also created a mystique around HIV testing which left
many practitioners feeling inadequate to offer testing as they felt they
lacked the ‘counselling skills’ required. A study of the uptake of HIV
testing in six clinics in remote Aboriginal communities of Central
Australia6 attributed the low level of HIV testing to the following:
 • lack of policies and procedures to guide staff on the task of offering
HIV tests
• lack of clear policy, which contributed to staff misconceptions, which
discouraged them from offering testing and providing pre-test
information
• lack of organisational guidelines if an individual did test positive
• difficulties in maintaining confidentiality in small communities

Audits of health services in Central Australia and the Top End of the NT
conducted by the Tristate Project and the THS AIDS/STD Unit respectively in
2000, also demonstrated that a low level of HIV testing was occurring. Of
particular concern was the low number of tests being offered to people with
an STI and pregnant women. Reasons given by non-Aboriginal practitioners
for not offering tests included lack of counselling skills, language
barriers, lack of time, cultural sensitivities, and lack of confidence for
dealing with a positive result.
The Australian National Council on AIDS and Related Diseases (ANCARD)
HIV Testing Policy7 recommends that the terms ‘HIV test discussion’ and
‘post-test counselling’ should replace pre- and post-test counselling to
describe the counselling process. According to the policy:
. . . this change in term is not in any way to diminish the role of this
discussion, but rather to acknowledge the increasing complexity that this
discussion may take on. Further the complexity of discussion will vary
from person to person depending on their risk factors. In definitional
terms, this allows for ‘counselling’ to be provided after the test and
will include the management and continuing needs of the infected person.

In the NT we have adopted the term ‘pre-test information’ in an attempt

to reduce clinician anxiety about pre-test counselling and to normalise HIV
testing.

Confidentiality
Systems to ensure confidentiality are crucial in the provision of HIV
testing, particularly in small communities.8 Currently most health services
in the region have developed coding systems and systems for filing HIV
results, to ensure greater confidentiality around testing. Some health
services have developed policies for dealing with HIV positive results.9,10
All health services need to consider and document this process and ensure
staff are aware of the policy and protocol for testing and for dealing with
results either positive or negative.

HIV pre-test information

Objectives of pre-test information11:
• To provide the individual with sufficient information about the
implications of a positive or negative result
• To enable informed decision-making about testing
• To communicate the health benefits of testing
• To educate patients about maintaining and reducing subsequent
infection risk
• To prepare for a possible positive diagnosis
There are a number of references7,12,13 which outline HIV pre-test information.
According to the ANCARD HIV Testing policy,5 pre-test information ‘should
provide accurate information about safe practices that is appropriate to
the person’s gender, culture, behaviour and language.’ Nganampa Health
Council has developed audio cassettes in Pitjantjatjara to provide HIV pre-
test information for use in clinical consultations where an HIV test is
offered. Other health services (NT Department of Health and Community
Services, Congress Alukura, Ngaanyatjarra Health Service) have produced
videos in language and pictorial storybooks for use in clinical
consultations or with groups.
Clearly there are cultural sensitivities and language issues involved in
STI and HIV testing. For the purposes of the protocol, and with the aim of
increasing the offering and uptake of HIV testing, a checklist has been
avoided in this edition as it is felt that this may deter practitioners
from offering a test due to time constraints or seeming too hard. Instead,
the broad and relevant issues to be discussed when offering an HIV test are
provided, and practitioners are encouraged to develop their own style for
discussing HIV and tailoring the information discussed, language and
terminology used, to the needs of the client.14
Pre-test discussion should include information about:
• HIV and how it is transmitted
• risk assessment
• what a negative and positive test result mean
• the window period (see below)
• ways of maintaining confidentiality around testing
• how and when to get results
• health benefits of knowing a person is positive
• how to prevent transmission of HIV

The window period

The ELISA test will usually begin to detect antibodies from two weeks to
two months after infection. For practical purposes, if the result remains
negative after three months after the exposure, infection is extremely
unlikely to have occurred.
An attempt should be made to ascertain when the most recent behaviour
occurred. Re-testing can then be done if it is possible that the first test
was performed before a sufficient quantity of antibody was generated to
produce a positive result. This is the ‘window period’ — the interval
between infection and the moment when the ELISA result becomes positive.15

Indications for HIV testing

1. Presence of an STI
All persons with an STI should be offered an HIV test. There is a
significantly increased risk of acquiring and transmitting HIV in the
presence of another STI. There is also a medico-legal precedent that a
practitioner may be found negligent if they fail to offer an HIV test to a
person with an STI.15 If the person refuses a test, this should be
documented in their case notes.
2. Exposure to the blood or body fluids of a person whose infection
status is positive or unknown
This may include reuse of injecting equipment, biohazard injuries,
ceremonial practises that involve blood, unprotected sex.

3. Signs or symptoms of HIV or immunosuppression

Seroconversion illness
Clinical manifestations of seroconversion illness of HIV infection which
should prompt HIV testing include the following:

General Neurological
Fever Headache/retro-orbital pain
Pharyngitis Meningoencephalitis
Lymphadenopathy Peripheral neuropathy
Arthralgia Radiculopathy
Myalgia Brachial neuritis
Lethargy/ malaise Guillain-Barre syndrome
Anorexia/ weight loss Cognitive/affective
impairment

Dermatological Gastrointestinal
Erythematous Oral/ oropharyngeal
maculopapular rash candidiasis
Roseola-like rash Nausea/vomiting
Diffuse urticaria Diarrhoea
Mucocutaneous ulceration
Desquamation Respiratory
Alopecia Cough
Not all patients develop all features: about 80% of patients will have an illness
usually lasting about 10–14 days.16

Intermediate immune deficiency

Intermediate immune deficiency lasts, on average, about five years. Most
people maintain full activity and good health, punctuated by minor medical
problems until late in the period. The immune system gradually loses its
ability to function normally at the skin and mucosal surfaces, while
usually maintaining the ability to prevent significant systemic infection.15
HIV testing should be initiated for any infection which looks unusual,
is worse than usual, lasts longer than usual, doesn’t get better with usual
treatment or keeps coming back, for example:
• thrush in the mouth of children or adults
• herpes (oral or genital) if very severe or occurring often
• shingles
• unusual or chronic skin rashes
• chronic diarrhoea in an adult for more than one month
• unexplained weight loss in an adult (more than 10% of baseline weight)
• night sweats or recurrent fevers (lasting more than one month)
• generalised raised lymph nodes lasting three months or more
• TB
• low white blood cells or platelets
 • any neurological symptoms

4. Risk factors
Risk factors in the patient history such as unprotected sex, men who have
sex with men, sharing of injecting equipment, sexual partner of someone
from a high-risk group.

5. Pregnant women
With the appropriate intervention, perinatal transmission of HIV is now
almost entirely preventable. Antiretroviral prophylaxis before, during and
after birth, caesarean delivery and bottle feeding can together reduce the
rate of transmission from around 30% to 2% or even lower.17 These life
saving interventions can only be applied, however, if the woman’s HIV
status is known. HIV risk assessment (without testing) for women in
Australia is an insensitive process as a significant proportion of women
diagnosed with HIV report no risk factors for HIV infection other than
sexual contact with a man of unknown status.16 Of those children born with
HIV in Australia, most of the women were unaware of their HIV positive
status. Consequently, in March 1998, the Royal Australian and New Zealand
College of Obstetricians and Gynaecologists issued its formal policy, which
recommends screening of all pregnant women for HIV as a standard of care.18
It has been the official policy of the DHCS since 1994 to recommend HIV
testing to all pregnant women, regardless of risk assessment.

6. On patient request
HIV screening is not routinely indicated as part of an adult health check,
however, it should be done if requested.

Summary
There are hyperendemic rates of sexually transmitted infections in the
CARPA region, thus the potential for an HIV epidemic is very real. In view
of the considerable advances in HIV treatments available, and to normalise
the process of HIV testing, emphasis on extensive pre-test counselling
using checklists has now shifted to pre-test information which can be
tailored to the needs of individual clients. Appropriate and widespread
testing is encouraged to enable a rapid and effective response to an
emerging HIV epidemic.

Key references for further reading

Stewart, G. (ed) 1994. Could it be HIV? North Sydney: Australasian Medical
Publishing Company Limited.
Stewart, G. (ed) 1997. Managing HIV. North Sydney: Australasian Medical
Publishing Company Limited.

References
1. National Centre in HIV Epidemiology and Clinical Research, 2000, Annual
Surveillance Report 2000, HIV/AIDS, Hepatitis C and Sexually Transmitted Infections
in Australia.
2. Guthrie JA, Dore GJ, McDonald AM, Kaldor JM. HIV and AIDS in Aboriginal Torres
Strait Islander Australians: 1992 –1998. The National HIV Surveillance Committee.
Med J Aust 2000; 172(6):266–9.
3. Cohen MS. Sexually Transmitted diseases enhance HIV transmission: no longer a
hypothesis. Lancet 1998; 351(Suppl III):5–7.
4. Erbelding,E.J. Preventing the Sexual Transmission of HIV. http://www.hopkins-
aids.edu/geneva/hilites_erb_ hivstd.html#proj
5. Department of Health, Housing and Community Services. National Counselling
Guidelines. Canberra: Australian Government Publishing Service, 1992.
6. Miller, P & Torzillo P. Private business: the uptake of confidential HIV testing
in remote Aboriginal communities on the Anangu Pitjantjatjara Lands. AustNZJPublic
Health 1998 Oct; 22(6):700–3.
7. Australian National Council on AIDS and related Diseases, Intergovernmental
Committee on AIDS and Related Diseases, 1998. HIV testing policy. Canberra:
Commonwealth Department of Health and Aged Care, 1998; 18.
8. Skov S, Bowden F, McCaul P, Thompson J & Scrimgeour D. HIV and isolated
Aboriginal communities. Med J Aust 1996; 165:41–2.
9. Miller PJ. Testing for HIV: an information manual for clinic doctors and nurses
on the Anangu Pitjantjatjara Lands. Alice Springs: Nganampa Health Council, 1994.
10. Smith KS 1996. HIV Testing Manual for Remote Health Services. Alice Springs:
Territory Health Services.
11. Australasian Society for HIV Medicine. Could it be HIV? 2nd ed. North Sydney:
Australasian Medical Publishing Company Limited, 2001.
12. Stewart G (Ed). Could it be HIV? North Sydney: Australasian Medical Publishing
Company Limited, 1994.
13. Australian National Council on AIDS, Hepatitis C and Related Diseases,
Commonwealth Department of Health and Aged Care. The Management of HIV/AIDS. A
resource guide for Indigenous primary health care organisations. Canberra:
Commonwealth of Australia, 2000.
14. Territory Health Services. Draft Position paper on HIV testing in the NT, Darwin:
THS, 2000.
15. McMurchie M, Puls D, Nisselle P, Kanwar A. Legal responsibilities in: HIV/Viral
hepatitis: a guide for primary care. Dore G et al. (eds). Canberra: Australasian
Society for HIV Medicine, 2001.
16. Stewart G (Ed). Managing HIV. North Sydney: Australasian Medical Publishing
Company Limited, 1997.
17. Ziegler JB. Antenatal screening for HIV in Australia: time to revise policies?
Med J Aust 1999; 171:201–3.
18. Royal Australian and New Zealand College of Obstetricians and Gynaecologists.
Screening in pregnancy. Statement No. 2.2. Melbourne: RANZCOG, 1998.
 Sexually Transmitted Infections
(STI) in the CARPA Region

Authors: Dr Steven Skov; Dr Kath Fethers (ASH), Kirsty Smith (Coordinator, Tri-
State Sexual Health Project); Stephen Baguley (STI Unit, RDH); edited by Steven
Skov and Dan Ewald

Topic Reviewers: Janet Knox; Peter Knibbs; Mt Liebig Clinic team; Michael
Jenkins (RAN, Manigrida); Ivor Anderson (RAN, Nhulunbuy CDC); Dave Corstorpan
(RAN, Nyirripi Clinic)

This chapter provides an outline of the occurrence of STIs and their

sequelae in the CARPA region, summarises important general principles of
managing STIs and deals specifically with STIs in adult men. The general
principles of managing STIs are the same in men and women. Specific
infections and clinical syndromes in women are covered in the Nganampa
Health Council/ Congress Alukura Women’s Business Manual. Infections in
children should always alert the practitioner to the possibility of child
sexual abuse and be managed after consultation with a paediatrician and the
appropriate child protection authorities.

Key references
KK Holmes et al. (eds) Sexually Transmitted Diseases. McGraw-Hill, 1999.
The nearest thing to an STI ‘bible’. Covers a very broad range of the
discipline from clinical to public health considerations.
There are a variety of guidelines published dealing with the
investigation and management of people with STIs.
International Union against Sexually Transmitted Infections: European STD
guidelines1
http://www.iusti.org/sti/European_Guidelines.pdf
World Health Organisation: Guidelines for the management of sexually
transmitted infections2
http://www.who.int/HIV_AIDS/STIcasemanagement/STIManagemntguidelines/who_hi
v_aids_2001.01/002.htm
Centers for Disease Control: Sexually Transmitted Diseases Guidelines 20023
http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5106a1.htm
National Management Guidelines for Sexually Transmissible Infections. April
2002, Venereology Society of Victoria Inc. Melbourne4

UK National Guidelines: Clinical Effectiveness Group (Association for

Genito-Urinary Medicine and the Medical Society for the Study of Venereal
Diseases)
http://www.mssvd.org.uk/CEG/ceguidelines.htm
The occurrence of STIs in the CARPA STM region
Sexually transmissible infections (STIs) and their sequelae are extremely
common in the CARPA STM region. There are important regional variations in
the rates of infection. In general terms, rates are higher in remote
communities compared to towns, although there are remote communities with
low rates of infections and there are subgroups of people living in towns
with very high rates. While rates of infection amongst non-Aboriginal
people in the CARPA STM region are higher than the national average, rates
amongst Aboriginal people are very much higher. See table 1 over. It has
been hypothesised that this relates to lack of access to health care rather
than substantial differences in sexual behaviour.5
In most populations, younger people (i.e. those under 25 years of age)
are more affected by STIs. In the CARPA region, notifiable disease data
reveals that, on average, about 60% of STIs occur in people under the age
of 30 in this region, with significant rates also occurring in over 30-
year-olds. Of note is that trichomonas infection in women in particular
persists well into older age groups. See figure 1 over.(not shown here)

Prevalences of gonorrhoea, chlamydia and trichomonas

While incidence rates provide a picture of high rates of infection,
prevalence information provides a different perspective and one that is
more pertinent to the primary health care level. In many communities, a
very high proportion of individuals are affected by these infections. As a
result, in these populations, unprotected sex carries a high risk of
contracting an infection.
Particularly in Central Australia there have been many screening
initiatives over the years providing prevalence information. In Central
Australian screening programs involving 26 remote communities between 1995
and 1997, 1693 men and 1458 women were tested for gonorrhoea and chlamydia.
Participation rates ranged between about 50% and 80%. Rates of infection
from these programs are shown in table 2. It was observed that 24–29% of
15–24 year olds were infected, as were about 10% of those aged 40–50
years.11

Table 1: Rates per 100 000 population of Bacterial STIs in the CARPA
region 20006–9

Syphilis Gonorrhoea Chlamydia

Australia 10.1 29.7 74.5
NT non-Aboriginal 18.0 156.0 228.0
NT Aboriginal 547.0 1713.0 983.0
WA Goldfields non- 0.0 11.0 69.0
Aboriginal
WA Goldfields 84.0 2761.0 2064.0
Aboriginal
SA Northern zone 11.0 132.0 145.0
Table 2: Prevalence of infection with gonorrhoea and chlamydia in remote
central Australian communities 1995–97

Men: n=1693 Women: n=1458

(95% CI) (95% CI)
Any infection 20.4% (19–22) 16.0% (14.1–18)
Gonorrhoea 15.3% (14–17) 10.6% (9–12)
Chlamydia 9.7% (8–11) 8.6% (7–10)
Both 4.7% (4–6) 3.6% (3–5)

Nganampa Health Council in northern South Australia has conducted community

screening and treatment as a key element of their STI/HIV program for many
years. Initially prevalences of infection with either gonorrhoea or
chlamydia of 19% were observed12 but these have been drastically reduced
with each year of the program.13–15
In the Top End there was extensive screening conducted in many remote
communities during the work-up and evaluation of the tampon as a self-
administered testing tool for women. During these trials it was found that
17% of women tested had gonorrhoea, 11% had chlamydia and 25% had
trichomonas.16 The proportions of women in communities who were tested was
generally of the order of 10–25%. Although most women were asymptomatic,
they did self-present for testing so there may be some bias in these
estimates of prevalence. However, they are consistent with prevalences
observed in Central Australia, the Kimberley region17 and north Queensland
during the Well-Person’s Health Checks (pers. comm. Prof Robyn McDermott).
Case-note audits in approximately 20 Top End remote communities revealed
that between 42% and 75% of adults had had at least one episode of a
bacterial STI during their life (unpublished data NT DHCS AIDS/STD
programs).
Trichomonas displays a different epidemiological pattern to other STIs.
The typical STI pattern is for the highest rates to be seen amongst the
younger, more sexually active age groups: particularly 15–29 year olds.
However, high rates of trichomonas infection amongst women persist into
older age groups: see figure 1. Indeed, Bowden et al. found that the
prevalence of infection of trichomonas was higher amongst women over 30
years of age.16

Syphilis
Once a person has been infected with syphilis, they generally remain
treponemal test (EIA, TPHA, FTA-Abs etc) seropositive for life, even after
successful treatment. Treponemal test seropositivity provides a good
indicator of the burden of syphilis infection and one which can be
monitored over time to observe changes, especially in younger age groups.
This data must be interpreted with some caution as syphilis treponemal
tests may be positive as a result of either yaws or non-venereal endemic
syphilis, both of which were common historically in the CARPA region. They
mostly disappeared during the course of the 1950s, with the last known case
of yaws occurring in a Top End community in 1968.18 The number of people who
are seropositive from venereal syphilis will naturally increase with age as
more people are infected. But, for people over the age of 40, or perhaps
even 35, seropositivity could have occurred as a result of either yaws or
non-venereal endemic syphilis.
In the Nganampa Health Council region some 60% of all people aged 30
years were recently found to be seropositive.19 A study of infertility and
STIs revealed that 41% of all women in a large Top End community were
seropositive for syphilis.20 Recent audits of a random sample of 10% of case
notes in approximately 20 remote Top End communities revealed that between
10% and 40% of people were seropositive for syphilis (unpublished data NT
Dept Health and Community Services AIDS/STD programs).

Pelvic inflammatory disease (PID)

PID will occur in between 10% and 40% of women infected with gonorrhoea or
chlamydia if they do not receive treatment.21,22 Experienced practitioners
relate that this is a common condition. In one large Top End community
study it was found that 26% of women have had PID at least once.23 A study
of women admitted to Royal Darwin Hospital with PID found that Aboriginal
women were greatly over-represented.24 Recent audits of a random sample of
10% of women’s case notes in approximately 20 remote Top End communities
revealed that between 20% and 30% of women appeared to have had at least
one clinical episode of PID (unpublished data NT DHCS AIDS/STD programs).

Infertility
In two Top End communities 26% and 30% of women were found to be
infertile.23 Preliminary work done by the Tri-State STD/HIV project in four
remote Central Australian communities suggests very similar rates of
infertility (pers. comm. Tri-State STD/HIV Project). Recent audits of a
random sample of 10% of women’s case notes in approximately 20 remote Top
End communities revealed that between 10% and 30% of women appeared to have
had no children (unpublished data NT DHCS AIDS/STD programs), with very
similar rates observed in women over the age of 24.
By extrapolating from other studies25–28 in populations with similar rates
of STIs, it is reasonable to assume that at least 50%, and perhaps as much
as 70%, of this infertility is due to STIs.
Important principles in the provision of STI clinical care
The syndromic management approach
Many STIs cause very similar symptoms and it is common for a person to have
more than one infection. For example, in the Central Australian screening
programs referred to above, 22% of infected persons had a dual infection
with gonorrhoea and chlamydia. It is also common for people to have
atypical manifestations of infection for a number of reasons. Studies from
all over the world have demonstrated that even experienced venereologists
cannot reliably distinguish between different infections on clinical
grounds alone. This has been shown for urethritis in males, vaginal
discharge in females and genital ulcer disease in both sexes.29
An important principle of STI management is to treat symptomatic persons
immediately, or as soon as possible, to limit the possibility of
transmission to others. In many regions of the world diagnostic tests for
STIs are not routinely available. For these reasons, the syndromic
management approach was developed and promoted by the World Health
Organisation.30 This approach, particularly for male urethritis and genital
ulcer disease, has been evaluated in many different settings throughout the
world.29,31–35 These studies consistently demonstrate that syndromic management
for genital ulcer disease and male urethritis is effective at both the
individual and at a population level. The experience is that syndromic
management of vaginal discharge is less effective. It is difficult to
develop algorithms with good sensitivity and specificity that are
applicable in a range of settings.
The syndromic management approach is especially important in the CARPA
region where client mobility is high and follow-up systems are not always
very effective. While diagnostic tests are readily available in the CARPA
region, there are often significant delays in receiving results. All health
services in the CARPA region have endorsed an adaptation of syndromic
management for patients presenting with symptoms of STIs.
The essence of this approach is to offer all clients with symptoms of an
STI a full screen for STIs and immediate syndromic treatment for all the
common infections their symptoms may indicate. For example, a man
presenting with a urethral discharge may have gonorrhoea and/or chlamydia
and he should therefore be immediately treated for both of these.

Full screen for STIs and HIV

All clients presenting with symptoms of an STI should be offered a full
screen for all the common infections in the region and an HIV test. It is
common for a person with one STI to have another and also common for
infections to cause no symptoms. The great majority of syphilis in the
CARPA region is diagnosed via a blood test rather than people presenting
with symptoms. If a person has an STI, they may have been exposed to HIV.
There has been a medico-legal precedent set which found a doctor negligent
for failing to offer an HIV test to a person who, by his presentation with
another STI, was known to have been at risk of HIV.36 If a patient declines
any or all of the STI or HIV tests, this should be clearly documented.
All clients should be fully informed of the nature of any tests in order
to be able to give their consent. Some health services have developed
audiotape, videotape or written resources to assist practitioners in this
process.
Tests should be offered for:
• gonorrhoea and chlamydia
• syphilis
 • HIV

Depending on local prevalences and health service policies, testing for

trichomonas infection may be indicated.

Hepatitis B testing with STIs

[Editor: It was difficult to come to an agreement over the inclusion of
hepatitis B testing in the STI protocols. The decision has to be based on
reckoning and common sense rather than based on evidence, which is lacking.
A summary of the debate is provided here.]

The burden of disease

Infection with hepatitis B is common amongst Aboriginal people in the CARPA
region. Studies from a variety of settings indicate markers of past
hepatitis B infection in 30–72% of Aboriginal people and chronic Hepatitis
B surface antigen carriage in 3–19%.37–43 Higher rates are observed in
rural/remote areas than in urban centres. Chronic carriage of HBV surface
antigen is associated with progression to cirrhosis and carcinoma of the
liver. Hepatic carcinoma has been described as occurring ten times more
frequently in Aboriginal people in the NT.44 Amongst non-Aboriginal
Australians most hepatitis B is transmitted sexually or via injecting drug
use. In developing countries, most hepatitis B transmission results either
from mother-to-child transmission or transmission between young children,
rather than sexually between adults.45 Aboriginal people in remote
communities have similar rates of infection and living conditions to many
developing nations. It is known that 60% of incident cases in NT Aboriginal
people occur in children under 10 years of age.46 It therefore seems
plausible and likely that hepatitis B infection in remote community
Aboriginal people is largely acquired in childhood. The experience of
practitioners is that clinical cases of acute hepatitis B infection are
extremely rare in adult Aboriginal people in the region. In addition, there
is a much more substantial workload involved in the follow-up,
investigation and management of a positive result for hepatitis B compared
to other STIs. The benefits for the individual, and in terms of reducing
further transmission, are much less clear compared to other STIs. For these
reasons the CARPA manual puts caveats on the testing for hepatitis B as
part of STI investigation as summarised in the discussion above.

[Editor: For more detail see the chapter on hepatitis. Some details are
highlighted below.
A 1994 study in AJPH (18(3):286) quoted hepatoma as 10 times more likely
in the NT Aboriginal population than non-Aboriginal and rates equivalent to
those in China.
In the Northern Territory in 1991–95, chronic liver disease (all causes)
and cirrhosis death rates were four times higher for Aboriginal males and
5.5 for Aboriginal females, compared to the non-Aboriginal population.
There were a total of 62 deaths from chronic liver disease (all types) in
the NT during this period.
There were 28 deaths from hepatocellular carcinoma diagnosed in the
Northern Territory between 1991 and 1995. During the period 1987–97 primary
liver cancer was the third most common cancer and the second highest cause
of cancer death in Aboriginal males.
 However, as a health priority, many issues are more significant than
hepatitis B to this population. Furthermore, interventions for higher
priority conditions may use fewer resources and be more appropriate.
Preventing vascular disease (for example) will have a much greater impact
on community mortality than efforts on hepatitis B, such as antiviral
therapy or screening for HCC. This is not to say, however, that an
individual should be refused ‘best care’ if it is deemed by the patient and
clinician to be in that individual’s interest when co-morbidities (and
therefore life expectancy), plus other issues (e.g. preparedness to have a
liver biopsy, or treatment in a larger city or interstate) are considered.

The case against including hepB testing:

It has been argued that most primary health care services using the CARPA
manual will not have the capacity to undertake long-term follow-up and
surveillance of those found to be chronic hepB carriers. We do not know,
but strongly suspect, that of those found to be carriers very few would end
up with a better health outcome because of having their hepB status known
through screening of STI cases. Presumably a proportion of those with
chronic active hepatitis will be identified through being symptomatic
rather than screening.
Further, time and resources spent on investigating and following up on
hepB might be better spent in other STI or other PHC activities. Caution in
overloading clinic staff is an issue dear to the hearts of the editorial
committee, and impacts on the acceptability of the manual as a whole.
There is a risk that clinic staff will not search case notes very well
for a patient’s immune status as clinic notes are often not well sorted and
it can take some time to do well. This could lead to unnecessary re-
testing.
The amount of hepB that is sexually transmitted in the Indigenous
population in the NT is not known, but may be small. We know that the
majority of hepB carriers are infected through non-sexual contact as
children or through vertical transmission from their mothers. If there was
a lot of STI transmission of hepB we should be seeing more acute hepB as
susceptible adults are infected (no data available).
It may be that most of the adults who are not chronic carriers (possibly
85% of the adult population) are immune, from natural exposure as a child.
Contact tracing is often not well done in Indigenous health services for
a multitude of reasons. Further burdening of the contact follow-up systems
may ‘overload’ them further.
Through routine immunisation of Aboriginal children since 1988 and the
catch-up program for children 6–16 years old in 1998, a large proportion of
children up to 20 years old will be immune.
The main strategies to address the burden of disease from hepB are
universal immunisation (underway), and screening of antenatal patients to
allow treatment of the neonates that prevents the vertical transmission of
infection (current practice). ‘High risk’ and contact screening with
follow-up immunisation will probably add marginally to these main
strategies.
The case for including hepB testing
Testing for hepB is a routine part of STI case management in the rest of
Australia, (where infection rates are lower).
The NT health department guidelines from CDC recommend (and fund vaccine
costs for) immunisation of people at high risk, including those with an
STI.
 A high proportion of Indigenous people in the NT are chronic carriers of
hepB (thought to be 10–15%) and there are high rates of STIs. In theory,
these factors combine to make a high risk of sexual transmission of hepB to
susceptible individuals especially those presenting with suspected STI.
These people should be offered hepB immunisation if not immune. However, we
do not know what proportion of the adult population is susceptible to hepB
infection. (An alternative would be to immunise without testing their
immunity first, as was done in the school-age hepB immunisation catch-up
program.)
The CARPA STM includes a protocol for surveillance of hepB carriers with
view to treatment to decrease long-term sequelae of chronic hepB. There are
now effective interventions available for those with chronic active
hepatitis (CAH) from hepatitis B and treatment stops progression and
(presumably) cirrohsis and hepatoma. This should be offered to people with
CAH.

Which tests?
HepBsAg will identify current infection, except those in the early
incubation period, which will be rare. HepBsAb will identify those immune
through vaccination and most of those immune through natural infection. A
few people (Western Pathology says very few) will be hepBcAb positive and
hepBsAb negative after natural infection and are thought to be protected by
the core Ab.
In terms of billing, Western Pathology charges the same for hepB
serology with or without the cAb, i.e. they charge for two tests even if
you ask for hepBsAg, sAb and cAb and that will be $28.55.
This may vary for other labs, but it seems the additional cost of the
HepBcAb is not high, though it will seldom change the decision to immunise.

The compromise
The main strategies for combating hepB are:

1. Universal immunisation, which is under way for all newborn children, and
now covers most people up to 20 years old.
2. Screening pregnant women for carrier status with treatment of the
newborn baby to block the vertical transmission. This is said to be 85–
95% effective at five years, and should be coordinated by the
paediatricians and CDC guidelines.
3. The third strategy, (probably the less important than the other two in
our population of interest), is immunisation of higher risk people, such
as those with STI and their contacts.
We have included a protocol on checking for HepB in those with symptomatic
STI. As with any screening or testing it should not be done if there is not
the capacity to follow through with appropriate follow-up. In the case of
annual surveillance of all adults with chronic hepB, this could amount to a
large workload (possibly 15% of the adult population).]

Using nucleic acid amplification (NAA) tests after treatment

Once an infection is treated and the organisms are dead it takes some time
for the body to clear all remnants of them. NAA tests (such as pcr or lcr)
will detect dead organisms or even parts of organisms. Therefore, if an NAA
test is performed too soon after treatment, one cannot be sure if a
positive result reflects treatment failure, re-infection or merely the
continued presence of dead organisms.47 This phenomena has also been
observed with other non-culture tests for chlamydia.48,49 It is not entirely
clear from the literature how long one must wait after treatment before
using an NAA test, but it is in the range of 1–4 weeks.50–53 Given the
uncertainty, it will be more prudent to wait three to four weeks before re-
testing using an NAA test.

Partner notification, or contact tracing

Partner notification, or ‘contact tracing’, has been considered a
cornerstone of both the individual management of people with an STI and of
STI control in the population. There is a great deal in the literature
evaluating different methods of partner notification in terms of numbers of
partners located, numbers with infection and numbers treated.54–58 Overall, it
appears that the most effective method is that of the practitioner
following up partners on the basis of names provided by the patient55 or at
least offering the patient this option. Whilst, theoretically, contact
tracing is important in limiting the spread of infection within a
population, no studies have demonstrated that this is so.59
There is a great deal of variation in the emphasis placed upon contact
tracing by different health departments and health services. Practitioners
should seek the advice of local authorities in determining the level of
time and effort put into this activity. It should be recalled, however,
that there is a clear duty of care to the sexual partners of people with an
STI — at least to the principal partner — and every effort must be made to
identify, locate and offer treatment to them. If this is not done, the
original client is at high risk of being re-infected and wider transmission
of infection will continue.
Sexual partners should be offered:
• a physical assessment (history and examination)
• a full STI screen (as above)
• the same, immediate treatment as the original client received

Do not wait for test results to come back.

For example:
If the original client had gonorrhoea, treat the partners for gonorrhoea.
If the original client had urethritis (i.e. either gonorrhoea or
chlamydia), treat the partner(s) for both gonorrhoea and chlamydia.
Follow-up of sexual partners of STI patients can be a very ‘high yield’
activity in terms of detecting infection. Clinical audits in the Top End of
the NT found that when sexual partners were tested, an STI was detected in
between 20% and 50% of cases (unpublished data NT DHCS AIDS/STD programs).
The importance of offering a full STI screen is to also identify other
possible infections. For example, in a study of contact tracing in north
Queensland, it was found that nearly half the women and a third of the men
named as contacts had an infection which the index case did not.60 Very
similar findings were made during the Top End clinical audits (unpublished
data NT DHCS AIDS/STD programs).
Partner notification is not easy. Clients are often reluctant to name
names, may be unable to identify partners in a way health staff can use for
follow-up, or may have difficulty with remembering Gregorian calendar time
frames. In some places local, paper-based systems to facilitate contact
tracing have been established.61 These systems help ensure that when sexual
partners are identified that they receive treatment. Contact your local
CDC/Sexual Health Unit for help with resources in how to do contact tracing
and local systems. The local CDC/Sexual Health Unit can also assist in
locating and arranging treatment for people who are not in the community
where the initial diagnosis was made.

Education and promotion of safer sex behaviour

When a person has an STI, it is a prime opportunity to offer them some
education that may prevent them becoming infected again in the future. This
should be done with all STI clients. There are many resources available to
assist with this and all clinics should have a basic resource set to assist
with this. Contact your local CDC/Sexual Health Unit for help with
resources.

Notification of infections
Notification of STIs is important because it is the only way to detect a
change in their occurrence so that health services can develop their
programs appropriately.
By law, STIs must be notified to the health department in all states of
Australia. This legal requirement means that the patient’s consent is not
needed in order to make the notification. Some states require full name
details, others require only a combination of initials and date of birth.
There is some variation in the STIs that are notifiable in different states
as well as in their case definition. Gonorrhoea, chlamydia, syphilis,
donovanosis and HIV are notifiable in all three states of the CARPA region
(NT, SA and WA). Trichomonas is notifiable only in the NT. Herpes and viral
genital warts are not notifiable in any state.
The diagnosis of syphilis is not based on a single laboratory test
result. It requires interpretation in relation to clinical signs, past
serology results and past treatment. Syphilis must therefore be notified by
the practitioner and the appropriate form sent in to the health department.
In some areas there are regional syphilis registers which assume the
responsibility of formal notification of infections
Gonorrhoea, chlamydia and trichomonas are diagnosed on the basis of a
single laboratory report. The regulations in each state vary. In the NT,
they are notified automatically by the pathology company and, in practice,
there is no need for practitioners to also do so. In SA and WA there is
dual practitioner/laboratory notification. Practitioners should be aware of
the particular requirements in those states.
Donovanosis may be notified by the laboratory, but the standard test for
donovanosis — microscopy of a biopsy or smear — has poor sensitivity (i.e.
a high false-positive rate).62,63 Therefore, in the NT, donovanosis may also
be notified on clinical grounds by the practitioner.64 A polymerase chain
reaction (PCR) test for donovanosis is under development and available in
WA.

Detecting infection in asymptomatic persons

A very large proportion of sexually transmitted infections cause either no
symptoms or very mild symptoms. This is particularly true of chlamydia,
gonorrhoea and trichomonas in women, but also occurs in a substantial
proportion of men with these infections.65–67 Genital ulcers may occur inside
the vagina in women and be clinically inapparent.68,69 People with mild
symptoms may not realise that an STI is the cause or — because of shame, a
lack of access to health care services or an appropriate practitioner — may
not present to a clinic for care. In some settings, it has been estimated
that as few as 5% of all persons in a population with an STI present to a
clinic and receive appropriate treatment.70
This is entirely consistent with experience in the CARPA region. In the
screening programs referred to above, high prevalences of infection were
detected: even of gonorrhoea in men.11 No data is available as to whether
these people had symptoms. However, the key point is that, for whatever
reason, they had not presented to the clinic for care at the time they were
offered the test. Data from Top End clinical audits in over 20 remote
communities reveals that only 10% to 20% of all STIs detected in remote
communities are found in persons presenting with STI symptoms.
Approximately 60% of all infections are detected by testing of apparently
asymptomatic persons as part of well-persons, antenatal or opportunistic
testing or as part of a formal screening program (unpublished data NT DHCS
AIDS/STD programs). The remainder are found via contact tracing or follow
up of other infections.
There have been many efforts to describe criteria in order to identify
people at a greater risk of an STI. Many studies have come up with criteria
appropriate to their situation, but very few of them are applicable in a
wide variety of settings. Young age, usually less than 25 years, is common
to most places. In the CARPA region, approximately 60% of all STIs occur in
people under the age of 30 years.7,10 However, particularly in Central
Australia, there is good data to show that, while STIs are more common in
younger people, high rates continue to occur even up to age 50. There is a
common perception that alcohol use, especially heavy drinking or binge
drinking, is associated with an increased risk of STIs, although there is
no specific data to prove this. In Central Australia, Miller et al. found
that female petrol sniffers were at increased risk of gonorrhoea or
chlamydia, as were people with a past history of an STI.71 Several
prospective studies overseas have found that people having one STI are at a
substantially increased risk of another within a relatively short period of
time.71–77
Primary care practitioners in the CARPA region need to be aware of this
situation. Health services will have their own policies for STI testing in
asymptomatic persons. However, it is clear that if health service strategy
is to only offer STI tests to those persons presenting with symptoms, then
it will have very little impact on a substantial public health problem. It
is highly recommended that practitioners have a low threshold for offering
testing. Fortunately, in most instances the important STIs in the CARPA
region can be treated with single doses of antibiotics.
When an infection is detected in an asymptomatic person, there is an
imperative to find the person for treatment as soon as possible. The
individual (especially a woman) is at risk of sequelae and infection can
continue to spread. A person with an STI identified in this way should be
offered a full STI screen if they did not already have one at the time of
the initial test. Significant treatment delays between diagnosis and
treatment have been documented in remote communities. In the case-note
audits in over 25 Top End communities, the average delay between diagnosis
and treatment of an STI in an (apparently) asymptomatic person was 19 days.
Nganampa Health Council found that the delay in treatment of syphilis was
initially 42 days but that this was able to be reduced to 14 days via a
series of health service system improvements.78
Recommended treatment regimens
Urethritis in males
Urethritis in males can be caused by a variety of organisms: Chlamydia
trachomatis, Neisseria gonorrhoeae, Trichomonas vaginalis, Herpes Simplex
Virus, probably Mycoplasma hominis and possibly Ureaplasma urealyticum. In
the CARPA region the only organisms regularly tested for are C. trachomatis
and N. gonorrhoeae, with occasional testing for T. vaginalis. There is
virtually no testing for other organisms as causes for male urethritis.
There is no routinely available data as to the proportion of cases of
urethritis which are caused by any particular organism or no known
organism. The impression of practitioners and sexual health units is that
both C. trachomatis and N. gonorrhoeae are common causes of urethritis, and
there is evidence that infection with both is also common.11,12,79
The CARPA manual therefore recommends immediate single-dose treatment
for both gonorrhoea and chlamydia in men with symptoms of urethritis,
regardless of whether signs of urethritis are also present. This is in line
with the syndromic approach and the known pattern of infection in the CARPA
region. Treating on the basis of symptoms alone will lead to some over-
treatment. However, a number of studies of syndromic management of
urethritis have found that this approach also leads to the fewest number of
infections being missed.29,35,80 It is considered a certain amount of over-
treatment is acceptable in the interest of reducing further spread of
infection as much as possible.
The recommended drugs, when the infection is contracted locally, are 1 g
of Azithromycin, 3 g of Amoxycillin and 1 g of Probenicid. In both Central
Australia and the Top End penicillin resistance, be it chromosomally
mediated or due to penicillinase production, occurs in less than 5% of
cultured isolates.81 Therefore, penicillin continues to be suitable for
first-line treatment of gonococcal infection. The CARPA protocol recommends
that gonococcal infection, which is likely to have been contracted outside
the CARPA region, should be treated with a single injection of 250 mg of
intramuscular ceftriaxone because of the increased risk of penicillin
resistant infection. These recommendations are consistent with all major
texts and guideline references mentioned at the beginning of this section.
If a man re-presents with the same symptoms within one week the protocol
indicates there are a number of possibilities which may not be easy to
elucidate. The protocol recommends that investigations be repeated with a
special effort to obtain a culture specimen for N. gonorrhoeae because of
the possibility of a resistant organism. It is recommended that such cases
be discussed with the local sexual health unit to determine the most
appropriate therapy and follow-up. Given the high prevalence of trichomonal
infection in Aboriginal women in the CARPA region16,82,83, treatment for this
infection should be considered early.

Genital ulcer
The STIs to consider in the differential diagnosis of genital ulcers in the
CARPA regions are syphilis, donovanosis and herpes. Other STI causes of
genital ulcers, such as chancroid or lymphogranuloma venereum, are
extremely rare in Australia.84,85
Other non-STI causes of an ulcer are of course possible; in particular
an infected bite, a burn or other trauma. The guideline intentionally plays
down the possibility of the ulcer not being due to an STI. This is to
reduce the chance of an infection being left untreated. The flow chart is
adapted from a WHO document30 and is designed to reduce unnecessary
treatment of herpes with antibacterials whilst improving syndromic
management of syphilis and donovanosis.
In keeping with the syndromic management approach, it is recommended
that genital ulcers that are not typical of herpes simplex virus are
immediately treated for both syphilis and donovanosis. A single dose of 4
ml of Benzathine penicillin is adequate treatment for primary syphilis.69
Azithromycin as a once-a-week dose has been found to be a very effective
treatment for donovanosis in both formal trials86,87 and from clinical
experience in the CARPA region. Longstanding clinical practice has been to
continue other antibiotic therapy until lesions have fully healed to reduce
the likelihood of recurrences.68 Given its long tissue half-life and some
limited clinical experience, it is possible that limited courses of
azithromycin may be effective. Several of the major guidelines recommend
azithromycin for the treatment of donovanosis, but they vary in their
durations.1–4 No clinical trials have determined what the optimum duration of
therapy should be. Therefore, the CARPA protocol recommends that patients
be closely followed and therapy continued until lesions are seen to be
fully healed with an (arbitrary) minimum of four weeks of treatment.
Three antiviral drugs are commonly used to treat herpes; aciclovir,
valaciclovir and famciclovir. The comparative studies which have been
performed have not shown any differences in effectiveness. They do not
‘cure’ the infection, but do reduce the pain and make the lesions heal more
quickly by a few days. They should only be used within five days of the
start of the primary episode or if new lesions are forming. After this they
are of no use. Herpes often recurs, and treating recurrent episodes with
these drugs has no influence on whether a person will get recurrences. The
main factors determining choice of drug are cost and convenience.
The guideline recommends Famciclovir but there will be local cost
variations which might lead to a different choice.
As with any area of broken skin the ulcer should be kept clean; the
guideline recommends saline for this. If the ulcer hurts, the man should be
given appropriate analgesia. Lignocaine (aka lidocaine) ointment is
effective at relieving the pain of herpetic ulcers.
Famciclovir Valaciclovir Aciclovir
Cost Most expensive Mid-price Cheapest
Dose for primary 125 mg bd for 5 500 mg bd for 5– 200 mg 5 per day
episode days 10 days for 5 days
Other issues Most evidence of
safety in
pregnancy. Not
licensed for use in
primary herpes

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al., ed. Sexually Transmitted Diseases. New York: McGraw-Hill, 1999; 451–66.
66. Krieger JN, Alderete JF. Trichomonas vaginalis and Trichomoniasis. In KK Holmes
et al., ed. Sexually Transmitted Diseases. New York: McGraw-Hill, 1999; 587–604.
67. Stamm WE. Chlamydia trachomatis infections of the adult. In KK Holmes et al.,
ed. Sexually Transmitted Diseases. New York: McGraw-Hill, 1999; 407–22.
68. Farrell N. Donovanosis. In KK Holmes et al., ed. Sexully Transmitted Diseases.
New York: McGraw-Hill, 1999; 525–32.
69. Musher DM. Early Syphilis. In KK Holmes et al, ed. Sexually Transmitted
Diseases. New York: McGraw Hill, 1999.
70. Hayes R, Wawer M, Gray R, Whitworth J, Grosskurth H, Mabey D. Randomised trials
of STD treatment for HIV prevention: report of an international workshop. HIV/STD
Trials Workshop Group. Genitourin Med 1997; 73:432–43.
71. Miller PJ, Law M, Torzillo PJ, Kaldor J. Incident sexually transmitted
infections and their risk factors in an Aboriginal community in Australia: a
population based cohort study. Sex Transm Infect 2001; 77:21–5.
72. Burstein GR, Waterfield G, Joffe A, Zenilman JM, Quinn TC, Gaydos CA. Screening
for gonorrhea and chlamydia by DNA amplification in adolescents attending middle
school health centers. Opportunity for early intervention. Sex Transm Dis 1998;
25:395–402.
73. Fortenberry JD,.Evans DL. Routine screening for genital Chlamydia trachomatis
in adolescent females. Sex Transm Dis 1989; 16:168–72.
74. Herrmann BF, Johansson AB, Mardh PA. A retrospective study of efforts to
diagnose infections by Chlamydia trachomatis in a Swedish county. Sex Transm Dis
1991; 18:233–7.
75. Ramstedt K. An epidemiological approach to sexually transmitted diseases — with
special reference to contact tracing and screening. Acta Derm Venereol Suppl
(Stockh) 1991; 157:1–45.
76. Richert CA, Peterman TA, Zaidi AA, Ransom RL, Wroten JE, Witte JJ. A method for
identifying persons at high risk for sexually transmitted infections: opportunity
for targeting intervention. Am J Public Health 1993; 83:520–4.
77. Whittington WL, Kent C, Kissinger P, Oh MK, Fortenberry JD, Hillis SE et al.
Determinants of persistent and recurrent Chlamydia trachomatis infection in young
women: results of a multicenter cohort study. Sex Transm Dis 2001; 28:117–23.
78. Miller PJ, Torzillo P, Tizard J, Winslow B. Interventions to reduce the
interval to treatment in syphilis: central case management and encrypted email.
Venereology 1998; 11:26–9.
79. Skov SJ. Report of a urine screening program for gonorrhoea and chlamydia
conducted in a remote NT Aboriginal community in 1995. Central Australian Rural
Practitioners Association Newsletter 1996; 15–7.
80. Chandeying V, Skov S, Tabrizi SN, Kemapunmanus M, Garland S. Can a two-glass
urine test or leucocyte esterase test of first-void urine improve syndromic
management of male urethritis in southern Thailand? Int J STD AIDS 2000; 11:235–40.
81. Tapsall J. Annual report of the Australian Gonococcal Surveillance Programme,
1999. Commun Dis Intell 2000; 24:113–7.
82. Knox J, Tabrizi S, Miller P, Law M, Chen S, Garland S. Evaluation of self-
collected samples in contrast to practitioner collected samples for the detection of
Chlamydia trachomatis, Neisseria gonorrhoeae and Trichomonas vaginalis by polymerase
chain reaction among women living in remote areas. In Press 2002.
83. Voolmann T, Morey F, Rich G. Trichomoniasis is a problem in Aboriginal women:
fact or fiction? Venereology 1995; 8:34–6.
84. Roche P, Spencer J, Lin M, Gidding H, Kirk M, Eyeson-Annan M et al. Australia’s
notifiable diseases status, 1999: annual report of the National Notifiable Diseases
Surveillance System. Commun Dis Intell 2001; 25:190–245.
85. Thomson J, Lin M, Halliday L, Preston G, McIntyre P, Gidding H et al.
Australia’s notifiable diseases status, 1998. Annual report of the National
Notifiable Diseases Surveillance System. Commun Dis Intell 1999; 23:277–305.
86. Bowden FJ, Mein J, Plunkett C, Bastian I. Pilot study of azithromycin in the
treatment of genital donovanosis. Genitourin Med 1996; 72:17–9.
87. Skov S, Tait P, Kaldor J, Bowden F. A field trial of azithromycin in the
treatment of donovanosis in central Australia: a step towards eradication?
Venereology 1998; 11:11–4.
 Adult Health Checks:
Introduction, background and
principles
[Editor: The main reference for this section is the recent edition of the
RACGP ‘Red Book’ guidelines for preventative activities in general
practice. These recommendations have been reviewed in light of local
patterns of disease, local experience at the clinic level and recent new
evidence. The second edition of Aboriginal Primary Health Care: An
evidence-based approach, to be published by Oxford University Press, will
contain a detailed review of the evidence for the various components of the
Well Person Health Check (WPHC, as they call it). An extension of this
literature review work was undertaken by a consortium of chronic disease
NGOs (the Chronic Disease Alliance). This plans to produce a stand-alone
publication that reviews the evidence behind the WPHC.
There are few variations between the overall recommendations to come out
in these documents and those presented in the CARPA STM. Where the
recommendations do vary, it is in those largely based on expert opinion and
the difference is likely to be due to regional variations in disease
patterns or health service policy or capability.]

The Adult Health Check (AHC) has roles in both primary and secondary
prevention of diseases.
Primary prevention reduces the likelihood of disease occurring, e.g.
assessing risk factors and providing appropriate health education.
Secondary prevention aims to detect disease before it becomes
symptomatic, e.g. screening, BP checks, pap smears. There are some further
components that seek to identify late stages of disease that can still
benefit from health care interventions (e.g. trichiasis surgery).
The AHC involves questioning, examining or testing people who feel well
to see whether they are likely to have particular health problems.
The purpose is to:
• Identify health problems that may lead to disease, e.g. smoking
• Detect diseases early to improve chances of a cure

• Prevent complications in people who have diseases

• Provide people with information about their health, about health
risks, and assist people in changing unhealthy behaviours (brief
interventions)
• Provide a non-threatening way for people to engage with the health
service about health concerns

The following criteria for screening are recommended before embarking on an

AHC program:1,2
1. The disease must be a substantial health problem in the population to
be screened.
2. The screening test should accurately identify a high proportion of
persons with the condition of interest.
3. The detection and management of the condition should result in an
improved outcome.
 4. The screening should be safe, acceptable to the population, easy to
use and of relatively low cost.
5. There must be sufficient planning and resources to adequately follow
up the screening program.
6. In Aboriginal communities, Aboriginal people must be sure that the
benefits of the program outweigh the intrusion into and surveillance
of their lives.
7. There should be an evaluation process and monitoring of
effectiveness, which includes effective feedback to the community and
community-based health staff.

Screening may have adverse effects such as invasion of privacy,

inappropriate or wasteful use of health resources, and distress due to
false positive results. With planning, the impact of these possibilities
can be minimised.
The organisation of the screening process depends on the clinic and
community preferences and resources. The options are:
• Community-wide (mass) screening: large numbers of people over a short
period of time
• Targeted screening: directed at a particular segment of the community
at high risk (e.g. 15–25 year olds for sexually transmitted diseases)
• Individual opportunistic: when the person presents to the clinic for
some other reason
• Self-initiated: by a well person
• Clinic initiated: inviting people to the clinic for a check up

The AHC as described in the CARPA STM is based on the above screening
criteria and is specific for remote Aboriginal communities. In many
instances there is no good evidence to support what, when or how we should
screen in this population. The recommendations are based on existing
evidence-based guidelines, prevalence of certain diseases in these
communities and opinions from experts in the field.
In general terms, because of the prevalence of certain conditions, the
recommended screening for risk factors and problems fall into three main
categories:
1. Chronic diseases
2. Sexually transmitted infections (STIs)
3. Women’s cancers

Chronic diseases
Australian Aboriginal and Torres Strait Islander people die of
cardiovascular disease at twice the rate of other Australians. This
difference is even greater among those aged 25–64, where the death rate is
seven times those of other Australian men and ten times those of other
Australian women.3 When risk factors for cardiovascular disease are
considered in general terms, Aboriginal and Torres Strait Islander people
are more likely than other Australians to smoke tobacco, not participate in
leisure-time physical activity and be obese. There is no national data with
respect to hypertension, however data from the Kimberley region suggest
that hypertension is two to three times more common amongst Indigenous
people. In the Northern Territory, hospital admissions for hypertension are
greater for Aboriginal people compared with non-Aboriginal people.4 There is
no definitive national data available regarding blood cholesterol levels
among Aboriginal and Torres Strait Islander people compared with non-
Aboriginal Australians.3 However, some observational data exist that show
high rates of dyslipidaemia exist in central and northern Australian
Aboriginal people, in particular elevated cholesterol and triglycerides and
low HDLs.9,10,16 Indigenous Australians have one of the highest rates of type 2
diabetes in the world, with prevalence in 25–55 year olds being seven to
eight times higher than their non-Indigenous counterparts. The overall
prevalence is two to four times greater. As a cause of death, Aboriginal
and Torres Strait Islanders die from diabetes at almost three times the
rate of other Australians. Rates of renal disease are also higher. In 1997
the incidence rate for Indigenous Australians beginning end-stage renal
disease treatment was nearly nine times that of non-Indigenous
Australians.21

Body measurements
Obesity and excess abdominal fat are risk factors for diabetes,
cardiovascular disease and renal disease. Weight and height for body mass
index (BMI) and waist circumference are the recommended measurements.
The RACGP recommend routine screening for BMI and waist circumference
(Level III evidence) every two years (Level V evidence).22
Because of the high rates of obesity and associated morbidity in
Indigenous Australians the CARPA STM recommends BMI and waist circumference
measurements be included in all yearly Adult Health Checks.

Blood pressure
The risk of myocardial infarction, stroke and renal disease increases with
elevated blood pressure.
The RACGP recommend screening for hypertension should commence at age 18
and continue every two years in the general population.22 This is based on
Level I evidence. However, because Indigenous Australians are more likely
to die of the complications of hypertension, the CARPA STM recommends blood
pressure checks are done at every yearly Adult Health Check as well as
opportunistically as appropriate.

Lifestyle issues
Tobacco use
In 1998 it was estimated that 10% of the total burden of disease (including
cardiovascular disease and respiratory tract disease and cancers) in
Australia was attributable to tobacco smoking.5 The prevalence of tobacco
use among Indigenous Australians is much higher than among other
Australians. Nationally, approximately 54% of Indigenous Australians smoke
compared with 22% of all Australians.12
Based on Level I evidence, the RACGP recommends screening everyone from
age 10 years at every opportunity.22 As Indigenous people die younger from
tobacco-related illness than non-Indigenous people, and the prevalence of
smoking-related diseases are higher amongst Aboriginal Australians6, this
approach is very important. The CARPA STM therefore recommends screening
for tobacco use at every Adult Health Check as well as incorporating
inquiring about tobacco use as part of routine history-taking at any
presentation. In order to keep the protocol as simple as possible the STM
advocates starting at 15 years old along with the other components of the
Adult Health Check.
Alcohol use
Excessive alcohol consumption can lead to increased risk of
trauma/accidents, hypertension, cardiovascular disease and liver disease.
Less Aboriginal people consume alcohol than in the general Australian
population, but those who do are more likely to do so at hazardous or
harmful levels.7
Based on Level II evidence the RACGP recommend screening to detect
problem drinking three-yearly from age 14 years.22 In those at higher risk
for drinking and its complications it is suggested that screening should
occur at every presentation.
The CARPA STM therefore recommends including questioning about quantity
and frequency of alcohol consumption at yearly Adult Health Checks. In
higher risk individuals screening should occur whenever they present to the
health centre.

Other substance misuse

Substance misuse may include use of marijuana, kava, petrol and solvent
sniffing, pituri use, analgesic abuse and other substances such as heroin
and amphetamines. The use of kava, petrol and marijuana is particularly
prevalent in some communities in the Northern Territory, and this can have
associated significant health and social problems.6 There is good evidence
to include verbal questioning (US preventive task force) about substance
use and advice on harm reduction. The CARPA STM therefore recommends
questioning at the Adult Health Check. This recommendation depends on the
prevalence of each substance misuse in the community e.g. where petrol
sniffing is common. A positive finding should be followed up with
appropriate counselling or referral.

Physical activity
Regular moderate exercise reduces all causes of mortality, incidence of
cardiovascular disease, diabetes, hypertension, obesity, osteoporosis,
colon cancer, falls, anxiety and depression. Based on Level III evidence
the RACGP recommends counselling all adults and children to participate in
physical activity on most days of the week, for an accumulated time of 30
minutes per day.22
The CARPA STM recommends asking about physical activity at the Adult
Health Check yearly. Physical activity can include walking, playing sport,
heavy housework, and hunting. Activity totalling at least 30 minutes on
most days per week is should be advised. Any increase in activity up to
this amount should be encouraged.

Nutrition
Although there is insufficient evidence to recommend for or against a
routine search for malnutrition there is evidence that nutritional
counselling is effective in changing diet.13 Based on the effectiveness of
dietary advice and the association between poor diet and nutrition-related
diseases — such as cardiovascular disease, diabetes, hypertension and
anaemia which are important causes of morbidity and mortality for
Aboriginal people — it is reasonable to provide general dietary advice. The
CARPA STM therefore recommends asking about nutrition and dietary intake at
the Adult Health Check and use the opportunity for brief intervention
advising on healthy nutrition as per Dietary Guidelines for Australians.14
Type 2 diabetes
The NHMRC, based on Level III evidence, recommend assessing all Aboriginal
and Torres Strait Islanders aged 35 years and over for diabetes.8 Plasma
glucose performed by a laboratory is most accurate. A fasting sample is
preferable, however, a random sample can be used. If the screening test is
negative then three-yearly testing is recommended. The NHMRC do not
recommend screening using a blood glucose meter.
There is evidence from cross-sectional studies that the prevalence of
impaired glucose tolerance in Aboriginal populations is high and is
apparent at early ages.9,10 The American Diabetes Association (ADA), also
recognises recent reports of the emerging problem of type 2 diabetes in
children and adolescents in many countries.15 There is an association
between type 2 diabetes in children and obesity, decreased physical
activity and a family history. As such the ADA Consensus Panel recommend
testing children from age 10 every two years if they are overweight and
have two other risk factors (family history, race/ethnic group with high
incidence, signs of insulin resistance). They also recommend using clinical
judgement to test for high-risk patients who do not meet these criteria.
As our population has such high rates of diabetes this suggests that
screening should start at an earlier age than the NHMRC recommendation of
35 years. CARPA therefore recommends yearly screening from age 15 years
with the well person’s check, which fits in with much of remote clinic
current practice.
[Editor: There are reports from mass screening e.g. from the Torres
Strait (with incomplete coverage) of about half of the female population
over 35 years old having diabetes, and half the male population over 45
years old having diabetes in some communities. This supports screening from
an age younger than 35 years.]
The preferred test is fasting plasma glucose. However, choosing the test
that is best and cheapest to diagnose and screen for diabetes will depend
on the individual’s willingness to return for repeat testing. Random finger
prick blood sugar levels using a glucometer are useful in that they provide
immediate feedback to the individual. However, they lack sufficient
accuracy for screening for undiagnosed type 2 diabetes (Level I-A
evidence).22 If a random BGL is 5.0 mmol/L or more then a venous blood
sample should be sent to the laboratory. This is because capillary whole
blood glucose of 5 mmol/L is the equivalent of venous plasma glucose of 5.5
mmol/L.8
Fasting plasma glucose has the highest sensitivity and specificity for
screening for type 2 diabetes, but if someone will not come back for
testing then random plasma glucose can be substituted (Level I-A
evidence).22
Furthermore, if a BGL is markedly elevated (e.g. 12 mmol/L), and the
person is unlikely to return for further testing, then glycated haemoglobin
could be measured.11 However, concerns regarding its use for screening and
diagnosis refer to the cost, the inability to define impaired glucose
tolerance and the precision required with the test. On the other hand,
laboratory, personnel and logistic costs being less than those of obtaining
a fasting blood or oral glucose tolerance test (Level III evidence)22 make
the HbA1c a reasonable option in these circumstances.
CARPA therefore recommends a fasting venous sample. If this is not
possible then a random venous sample is acceptable. A glucometer is useful
for immediate feedback but is not accurate for screening. If a BGL is 5.0
or more then a venous sample is warranted.
Lipids
Mass screening for lipid levels in the general population, regardless of
age, is not currently recommended. However, the RACGP, Heart Foundation and
The Cardiac Society of Australia and New Zealand recommend five-yearly
testing for hyperlipidaemia at age 45 for men (I-A evidence), women (III-C
evidence) and those aged less than 45 years of age but at higher risk for
coronary artery disease (V-A evidence).22,17 Aboriginal and Torres Strait
Islanders as a group are considered to have a higher absolute risk of
coronary artery disease.17 The age at which testing lipids should commence
in this high risk group is not known but the earlier onset of CHD and
contribution of cardiovascular disease to mortality in Aboriginal men and
women suggests it should be at an earlier age. Data from O’Dea shows that
dyslipidaemia is already present in young adults and that it would be
appropriate for intervention programs to target young people.16 There are no
randomised prospective trials that have assessed lifestyle interventions or
long-term lipid-lowering therapy in those aged less than 35. The benefits
and risks of testing at an early age and instituting treatment must be
considered. In view of this lack of evidence the CARPA STM recommends
commencing testing lipids from age 25 in the general Aboriginal population
and, if normal, to repeat five-yearly. If an individual has any other risk
factors for CHD then we suggests doing lipid measurements five-yearly from
age 15. Other risk factors would be a significant family history of CHD,
familial hyperlipidaemia, overweight or obesity and possibly smoking. Of
course, if a person has other confirmed diseases such as diabetes or
impaired glucose tolerance, renal disease, hypertension or known ischaemic
heart or cerebrovascular disease, then testing would be according to the
corresponding care plans.
Based on guidelines from the RACGP, Heart Foundation and the Cardiac
Society of Australia and New Zealand the CARPA STM recommends measuring
total cholesterol, triglycerides, HDL-C and LDL-C (calculated) levels on a
fasting blood sample (III-B evidence).22 If a fasting sample cannot be
collected then a random levels are still worth doing.

Renal disease
Major expert bodies show little support for screening the general
population for proteinuria.22,13,18 However, with an incidence rate for
Indigenous Australians beginning end-stage renal disease treatment at nine
times that of non-Indigenous Australians21, and success in improving the
clinical profiles and mortality after implementation of a community-based
renal protective program19, attempts at early detection of renal disease by
screening appear justified. The program suggested a marked treatment
benefit in those with overt albuminuria or hypertension, including in non-
diabetic people. The benefit was not clear in those with microalbuminuria
alone. There is no evidence to suggest the optimal age to implement
screening nor the screening frequency.20
In view of the burden of renal disease, the evidence for the prevention
of renal disease and the low cost of screening using dipstick urinalysis
the CARPA STM recommends yearly urinalysis commencing from age 15. A
Norwegian study26 found that subjects with a positive urinary dipstick
analysis for leucocyte esterase, nitrites, haemoglobin or glucose had a
higher urinary albumin excretion rate. Although this finding was
statistically significant the numerical difference was small. Despite this,
at this stage experts in the field still suggest a reading of ‘one +’ or
more (indicative of macroalbuminuria) needs to be followed by exclusion of
other causes — such as contamination, renal tract abnormalities or a
genitourinary tract infection — by sending the urine for ACR, MC&S and PCR.

Brief interventions
There is good evidence from other populations that brief advice from health
professionals (doctors, nurses and others) can help about 6% additional
smokers to quit.12 Systematic reviews and two subsequent randomised
controlled trials have found that antismoking advice improves smoking
cessation in people at high risk of smoking related disease.23 Based on this
and other Level 1-A evidence,22 CARPA recommends brief advice regarding
quitting smoking at the Adult Health check.
There is weak evidence from systematic reviews and RCTs that sedentary
people can be encouraged to increase their physical activity. Interventions
that encourage moderate rather than vigorous exercise, and do not require
attendance at a special facility, may be more successful.23 Based on this
evidence the RACGP22 recommends, as does CARPA, that all adults and children
are advised to participate in physical activity on most days of the week,
for an accumulated time of 30 minutes per day. This amount is based on the
National Guidelines for Physical Activity for all Australians.24
There are few studies that have evaluated brief interventions for
reducing alcohol consumption in the Aboriginal group. However, a meta-
analysis of RCTs addressing brief interventions in heavy alcohol drinkers25
found that heavy drinkers receiving brief intervention were twice as likely
to moderate their drinking six to 12 months after an intervention compared
with those who received no intervention. Similar to the RACGP guidelines,22
CARPA recommends that brief intervention techniques to reduce alcohol
consumption should be used with all potential problem drinkers.
Although not in the primary health care setting, systematic reviews have
found that advice on eating a cholesterol-lowering diet (i.e. advice to
reduce fat intake or increase the polyunsaturated to saturated fatty acid
ratio in the diet) leads to a small reduction in blood cholesterol
concentrations in the long term.23 Based on the effectiveness of dietary
advice13 and the association between poor diet and nutrition-related
diseases — such as cardiovascular disease, diabetes, hypertension and
anaemia which are an important causes of morbidity and mortality for
Aboriginal people — it is reasonable to provide general dietary advice.
CARPA recommends using the opportunity of the Adult Health Check to provide
brief intervention advising on healthy nutrition as per Dietary Guidelines
for Australians.14

References
1. Mitchell H, Irwig L. Screening as a strategy for disease control. Med J Aust
1991; 155:237–242.
2. Scrimgeour D. Screening issues for Aboriginal people. CARPA Newsletter October
1996; 24.
3. Australian Institute of Health and Welfare (AIHW) 2001. Heart, stroke and
vascular disease: Australian facts 2001. AIHW Cat. No. CVD 13. Canberra: AIHW,
National Heart Foundation of Australia, National Stroke Foundation of Australia
(Cardiovascular Disease Series No 14).
4. Condon JR, Warman G, Arnold L, eds. The health and welfare of Territorians.
Epidemiology Branch, Territory Health Services, Darwin, 2001.
5. Mathers C, Vos T, Stevenson C. The burden of disease and injury in Australia.
Canberra: AGPS, 1999.
6. Plant E, Condon J, Durling G. Northern Territory health outcomes: Morbidity and
Mortality 1979–91, Territory Health Services, 1995.
7. NHMRC Guidelines for Preventative Interventions in Primary Health Care:
Cardiovascular disease and cancer. NHMRC, AGPS, 1997.
8. NHMRC Draft Diabetes Guidelines. 30 November 2000.
9. O’Dea K, Patel M, Kubisch D., Hopper J, Traianedes K. Obesity, diabetes and
hyperlipidemia in a central Australian Aboriginal community with a long history of
acculturation. Diabetes Care 1993; 7:16:1004–10.
10. O’Dea K, Lion RJ, Lee A, Traianedes K, Hopper JL, Rae C. Diabetes
hyperinsulinaemia and hyperlipidemia in a small Aboriginal community in Northern
Australia. Diabetes Care 1990; 8:13;830–5.
11. Couzos S, Metcalf S, Murray R, O’Rourke S. Systemic review of existing evidence
on primary care guidelines on the management of non-insulin-dependent diabetes in
Aboriginal and Torres Strait Islander populations. Kimberley Aboriginal Medical
Services. Canberra, ACT: Council for the Office for Aboriginal and Torres Strait
Islander Health Services, Commonwealth Department of health and Family Services,
September 1997.
12. Ivers, R. Indigenous Australians and tobacco: A literature review. Darwin:
Cooperative Research Centre for Aboriginal and Tropical Health, 2001.
13. Canadian Task Force on Periodic Health Examination. The Canandian guide to
clinical preventive health care. Ottawa: Supply and Services, 1994. http://www.hc-
sc.gc.ca/hppb/healthcare/pubs/clinical_preventive/index.html http://www.ctfphc.org/.
14. National Health and Medical Research Council. Dietary guidelines for Australians.
Canberra: AGPS, 1998.
15. Consensus Statement: Type 2 Diabetes in Children and Adolescents, American
Diabetes Association. Diabetes Care 2000; 23:3;381–9.
16. McDermott R, Rowley K, Lee A, Knight S, O’Dea K. Increase in prevalence of
obesity and diabetes and decrease in plasma cholesterol in a central Australian
Aboriginal community. MJA 2000; 172:10;480–4.
17. Lipid Management Guidelines. MJA 2001; 175 supplement.
18. US Preventative Taskforce (USPSTF) Guide to Clinical and Preventive Services. 2nd
edition
http://odphp.osophs.dhhs.gov/pubs/GUIDECPS/.
19. Hoy W, Baker P, Kelly A, Wang Z. Reducing premature death and renal failure in
Australian Aboriginals: A community-based cardiovascular and renal protective
program. MJA 2000; 172:473–8.
20. Couzos S, Murray R. Aboriginal Primary Health Care: An Evidence-based Approach.
Oxford University Press, 1999.
21. Cass A, Gillin AG, Horvath JJ. End-stage renal disease in aboriginals in New
South Wales: a very different picture to the Northern Territory. MJA 1999;
171(8):407–10.
22. Guidelines for preventive activities in general practice. Australian Family
Physician May 2002; special issue.
23. Clinical Evidence. BMJ Publishing Group, Issue 7, June 2002.
24. National Physical Activity Guidelines for Australians
http://www.health.gov.au/pubhlth/publicat/document/physguide.pdf.
25. Wilk A, Jensen N, Havighurst T. Meta-analysis for randomised control trials
addressing brief interventions in heavy alcohol drinkers. Journal of General
Internal Medicine 1997; 12(5):274–83.
26. Clausen P, Jensen J, Borch-Johnsen K, Jensin G, Feldt-Rasmussen B. Prevalence of
positive urinary dipstick analysis (leucocyte esterase, nitrite, haemoglobin or
glucose) in a population of 3645 adult subjects: consequence for measurement of
urinary albumin excretion rate. Scand J Urol Nephrol 1998; 32(6):399–404.
 Acute Respiratory Infections in
Adults and Children Over 5
Years of Age

Author: Dr Colin Mathews (ASH physician)

Topic Reviewers: Dr Paul Torzillo; Dr Andrew Bell; Top End DMOs; Dr Penny
Roberts-Thomson (Nguiu); Malcolm Auld (RAN, Bonya Clinic); Rin Riemersma (RAN,
Finke); Leone Radnedge (RAN, Utopia)

Introduction
Respiratory tract infections (RTI), including pneumonia, represent a high
proportion of the burden of ill health and death throughout the world.
In developed countries, such as the United States, figures show that
RTIs are the seventh most important cause of morbidity and sixth commonest
cause of death (the mortality rate being 10%) with the cost to the country
being over 20 billion dollars annually.1,2,3
In Australia it has been reported that pneumonia occurs in 200 per 100
000 adults and accounts for 2% of hospital admissions each year, the
mortality being 7–10%. One organism alone, the pneumococcus, affects 50–100
per 100 000 at the extremes of life and has a case fatality rate of 12–
14%.4,5,6
RTIs are more important in under-developed countries and among
Indigenous populations, and are claimed to be the commonest cause of
morbidity and mortality.7,8,9
In Aboriginal people lung disease, mainly acute respiratory infections,
result in 12% of hospital admissions for males and 9% for females, this
being a five-fold greater morbidity and increased mortality compared to the
non-Indigenous population. For the pneumococcus the rate of infection is as
high as 1500 per 100 000 for children under two years, but remains at about
100 per 100 000 for the 15–64 year age group.10,11
A number of different pathogenic organisms are implicated in acute
respiratory infections (ARI), which involve the upper respiratory tract,
causing colds, influenza, sinusitis, pharyngitis and the lower respiratory
tract resulting in bronchitis and pneumonia.
The incidence of RTIs caused by the various pathogens differs from area
to area and from time to time. Precise figures implicating specific
causative agents are difficult to obtain for various reasons. At the best,
there is delay in making the diagnosis because it takes several days to
culture an organism from pathology samples and several weeks to get
information on serology tests.
In practice, most serious attempts at categorising agents are deficient
due to a large group of ‘No pathogen identified’.
These may be due to patients receiving early antibiotic treatment,
having inadequate sputum, inappropriate sampling or the limitations of the
procedures currently used.
Significant issues in the Northern Territory and remote
Indigenous communities
• Persistent high rates of invasive pneumococcal disease and the
overwhelming likelihood that this is the major pathogen involved in
community acquired pneumonia (CAP).
• The implications of a probable increase in intermediate level penicillin
resistance in invasive pneumococcal isolates.
• The importance of the frequency of underlying disease, including chronic
lung disease/bronchiectasis.
• Confusion engendered by the fact that people with underlying lung disease
often wheeze with pneumonia.
• The lack of accurate clinical predictors of pneumonia in adults leading
to a high possibility of incorrect diagnoses and assessments in this
area. Health workers are encouraged to seek early medical consultation.
• The use of predictors of severity and poor outcome as the basis for
immediate medical consultation.
• The disproportionately high morbidity and mortality from ARI in the
Indigenous population.
• The lack of ready access to hospital-based investigations, such as X-
rays, experienced by many patients because of their remote location or,
at times, a reluctance to submit to a system foreign to their culture.
• The difficulties involved in decisions to transfer patients to a larger
centre, including the assessment of severity and urgency, the reluctance
to leave the ‘safety’ of home and the organisation and cost of
evacuation.
• The pressing need for more effective and greater utilisation of
preventive measures, including interventions for environmental health
factors, smoking and vaccinations.4,10
• In the Northern Territory, the rates of pneumococcal disease are also
higher in the non-Indigenous population than in the rest of Australia.

As noted, these diseases are worldwide and many of the problems needing
attention are also relevant elsewhere.
There may also be some other poorly understood contributing factors in
local respiratory illnesses. As some Alice Springs physicians report;
‘Experience and common sense suggest there are defective immune responses.
We see people who attend early in their illness, receive appropriate
management (confirmed by pathology results), have the right temperature and
white cell responses but get progressively worse and die’ (pers. comm.).

Clinical aspects
Typically patients with RTI present with the general features of infection
(fever, sweating, lethargy, anaemia) and the specific symptoms involving
the respiratory tract (nasal discharge, facial pain, cough, sputum
production, chest pain, dyspnoea). There is usually a short period between
the onset of illness and the manifestations implicating the respiratory
tract, and in epidemics the incubation period is usually short.12 These
comments do not apply to some chronic disorders, particularly tuberculosis,
which is dealt with in a separate chapter.
It is common for patients to seek care early in the illness and it may
be possible to assess the severity and expected course at this stage. In
the Northern Territory, however, distance from help and cultural
differences frequently delay the presentation during which time the disease
may progress to become less responsive to therapy.

Disease severity
Significant factors indicating severe disease are2,13,14:
• Body temperature <36?C
• Respiratory rate > 30/min
• Pulse rate >120/min
• Systolic blood pressure <90 mm Hg
• Altered mental status
• Evidence of multi-lobar disease
• Indication of extra-pulmonary infection
• Hospital admission in the previous year
• Reduced oxygen saturation
• Associated conditions

Other circumstances, many of which affect Indigenous populations and are

particularly significant in the Northern Territory, alter the pattern of
disease leading to higher susceptibility and greater severity. These
include11,16:
• Environmental exposures: Air pollutants, camp fires, smoking, petrol
fumes, Infections associated with overcrowding
• Co-morbidities: Asthma, allergy, chronic lung disease, diabetes,17 renal
failure, alcohol, chronic liver disease, neoplastic disease,
immunosuppression

Comments on allergy
There is thought to be less allergy in Aboriginal than Caucasian patients,
but it is so common in the latter group it is part of remote practice.
However, Dr John Weiner, visiting allergist, advised he sees a number of
Aboriginal people from the bush who are allergic to couch grass causing
asthma. Prof Anne Woolcock, Australia’s (late) asthma guru, wrote in
several articles about increasing dust mite allergy in north Queensland
Aboriginal communities.

Complications
Most RTIs are treated and respond to appropriate antibiotics, or
spontaneously resolve (viral). Some progress to complications, and there
may also be long-term consequences.
Short-term complications12
• Lungs: abscess, atalectasis
• Pleura: pneumothorax, effusion, empyema
• Other sites: pericardial, cerebral, hepatic

Long-term consequences18,19
• Bronchiectasis
• Chronic airway limitation, and other lung function abnormalities

Aetiological agents
A number of pathogens are implicated in RTIs and their distribution varies
in time, place and setting. There are different ways of classifying these
infections and their manifestations and it is useful to consider more than
one approach.
A. Classification by causative organism
• ‘Typical’ pathogens: Streptococcus pneumoniae, Haemophilus influenzae,
Moraxella catarrhalis, other gram negative bacilli
• ‘Atypical’ pathogens: Mycoplasma pneumoniae, Chlamydia pneumoniae and
C. psittaci, Legionella species
• Aerobic bacteria: Staphyloccus aureus, Pseudomonas aeruginosa,
Bordetella pertussis (Mycobacterium tuberculosis)
• Anaerobic bacteria: Bacteroides fragilis, Streptoccus anginosus,
Fusobacteria
• Rickettsiae: Coxiella burneti (Q fever), louse borne, murine and scrub
typhus
• Viruses: Influenza, para-influenza, rhino- and corona- viruses, herpes
simplex and zoster, cytomegalovirus

B. Classifications by clinical syndrome 2,6,12,15

• Community-acquired pneumonia: Typical and atypical agents, aerobic

bacteria, C. burneti
• Aspiration pneumonia: Typical and anaerobic bacteria
• Hospital acquired pneumonia: Typical, aerobic and anaerobic bacteria
• Acute bronchitis: Typical and atypical agents, P. aeruginosa, B.
pertussis. Viruses group 3 d i
• Otitis media: Typical agents. C. Pneumoniae, Streptococcus pyogenes

C. Distribution patterns
Although some organisms causing pneumonia lead to classical features, such
as pneumococci typically causing lobar consolidation, none of the signs or
symptoms are specific for a particular organism. It is therefore difficult
or impossible to differentiate the causative organism on clinical grounds
(as mentioned earlier, this difficulty extends into hospital and research
medicine.)
In practice, it is appropriate to focus on the most important pathogen,
S. pneumoniae, which is probably the commonest cause of infection and is
certainly the leading cause of death from CAP in Central Australia. The
protocol is based on this but is modified for the Top End in the wet season
where melioidosis is the major cause of mortality from ARI.6,37 [Editor: For
details see melioidosis chapter.]

Comments about specific organisms

Pneumococci It is generally agreed that these are the most significant
pathogens causing CAP throughout the world, in Australia and in our region,
where the highest rate of infection in any community has been demonstrated.
It is important that treatment protocols and preventative measures be
directed against this organism.
There are many serotypes with variations of importance in time and
place. Furthermore, the frequency and pattern of antibiotic use influences
the patterns of sensitivity, which in turn dictates the appropriate
medication and vaccine for specific groups. 6,8,10,20,21
Haemophilus influenzae Worldwide, this is historically the second most
important CAP pathogen and it is interesting that in the two small
studies from north Queensland and Alice Springs, greater numbers of
this organism were recorded. Thompson suggests that this may relate
more to colonisation than invasion and further assessment comparing
blood culture and bronchoscopy specimens with sputum samples would be
appropriate.22,23

Melioidosis and acinobacter Local variations are exemplified by the

significance of these bacteria in the Top End, with their resulting severe
disease and high mortality. (See chapter on meloiodosis).37

Staphylococcus While numbers of this pathogen invading the lung are small
the complications and mortality are high and it is important that this
infection be identified promptly.

Atypical agents Although the studies included have revealed relatively few
infections with these organisms, they are becoming more important in
developed areas. There is an impression that they are uncommon in north
Australia, but they are not routinely investigated. Although Thompson found
no positive serology for atypicals and there were only two cases of
chlamydia in the series in Alice Springs, there have been reports of two
cases of Legionella longbeachae and up to five cases of mycoplasma a month
during 2001. Recent studies have demonstrated a better patient outlook if
antibiotics covering these agents are included in treatment, even if there
is no positive evidence of their presence. However, in the protocol, these
concerns need to be balanced against the need to focus on the best
antibiotic regimen for the predominant pneumococcal disease.22–25

Diagnosis of respiratory tract infection

In children, studies have indicated useful predictive values for clinical
features in making the diagnosis of pneumonia. By contrast, in adults there
is little data to help. Fever, tachycardia, changes in alertness, etc. may
occur in many disorders and even more specific findings such as dyspnoea
and cough, are present in other conditions e.g. asthma, cardiac failure and
metabolic acidosis. The constellation of findings helps to make a diagnosis
of pneumonia, but when in doubt it is advisable to seek help and often to
treat because of the potential harm of untreated infections.15,29,30,31

Management
When a diagnosis of pneumonia is made (or strongly suspected) antibiotic
use is mandatory. The appropriate treatment depends on the actual or likely
organism, the usual antibiotic for those bacteria and the pattern of
antibiotic resistance. Each of these aspects varies in time and place and
advice on the local situation, which may be subject to review.8,31,32
The rapid emergence of antibiotic resistance in all pathogenic organisms
in all infections is of major concern for the ongoing management of
illness. Contributing to this state has been inappropriate use of
antimicrobials, both from prescribing practices of the medical profession
and poor compliance to treatment regimens by patients.
To minimise the effects of this situation, greater efforts need to be
made to apply evidence-based measures in diagnosing and treating patients,
using correct doses, administration measures and courses, and withholding
drugs if advisable. However, many decisions are difficult when managing
seriously ill patients infected with unknown organisms and sensitivity
patterns, and empirical treatment may be needed.
 However, in many cases, resistance is only partial and not all in vitro
(laboratory) findings are translated into in vivo responses. Therefore,
larger doses of a standard antibiotic may be used effectively in people
with a normal immunity profile. Thus, penicillin can still be used for
pneumococcal and other infections, and newer broad-spectrum antibiotics
kept for the future or for other pathogens.8,31,32

Practical antibiotic regimens

It is clear that in each location, the initial treatment must be on
empirical grounds, with management of the individual patient being modified
according to the clinical course of the disease and the availability of
information, such as laboratory results and radiological findings.
Regimens also differ according to the severity of the disease and
whether it is acquired in the community or hospital (or institution). Other
factors, such as cost and practicality, are also important.1,28,32,33
Following are examples of CAP protocols and some results, which may have
some relevance to the decisions made here:
An article from Post-Graduate Medicine in November 1999 recommended:

a. For chest infection with typical organisms: amoxycillin, alternatives

being amox/clavulanate, macrolides or cephalosporins including
cefuroxime and third generation agents.

b. For CAP, which may include atypical organisms: beta-lactams, new

generation macrolides or doxycycline, alternatives being
cephalosporins or fluoroquinolones.

This is a fairly typical example of advice for developed countries.15

In Pakistan in the early 1990s the WHO recommended oral co-trimoxazole
for non-severe pneumonia, with clinical failures receiving oral
Amoxycillin. A study of children in two communities showed a cure rate of
91% and 92% despite the fact that in vitro resistance to the drug was shown
to be up to 45% during the same period.
This is an example of an undeveloped country using an economical regimen
that appeared effective.34
[Editor: Cure rates in community trials will vary depending on the
proportion of cases that were caused by susceptible organisms. Of prime
importance in this would be the proportion that was caused by viral
infection and hence not responsive to antibiotic treatment.]
A study of the empirical treatment of CAP in the Royal Prince Alfred and
Gosford hospitals compared the efficacy of a penicillin-based protocol with
third generation cephalosporins. The penicillin protocol was:
Clinical condition Treatment

For mild to moderate CAP IV Benzyl penicillin and oral macrolide

For those with COAD IV Ampicillin and oral macrolide

For severe CAP IV Benzyl penicillin, Erythromycin and Gentamicin

For penicillin sensitivity IV Cephalothin

Adherence to the protocol was not good, but retrospective analysis
indicated the outcomes were the same in each group. This is an example of
Australian practice, though the study was considered of poor design with
selection and adherence bias.13

The protocol for CAP in the Top End (NT) published in December 2000 is:
No risk factors Risk factors
Mild pneumonia penicillin penicillin

Moderate pneumonia penicillin ceftriaxone + gentamicin

Severe pneumonia ceftriaxone (ceftriaxone or

ceftazidime or meropenem)
+ gentamicin
Note: For atypical pneumonia, add or substitute erythromycin or ciprofloxacin. Risk
factors include alcohol or kava excess, diabetes, chronic renal disease, chronic
lung disease, steroid therapy.33

The current recommended initial therapy for patients admitted to Alice

Springs Hospital is:14

Moderate pneumonia IV Penicillin 1.2 g 6-hourly

Roxithromycin 300 mg daily

Moderate pneumonia IV Penicillin 1.2 g 4-hourly

with risk factors O Roxithromycin 300 mg daily
IV Gentamicin (5 mg/kg) daily
for 2/7

Severe pneumonia IV Penicillin 1.2 g 4-hourly

IV Erythromycin 1 g 6-hourly and
IV Gentamicin (5 mg/Kg) daily
for 2/7

Critically ill patients IV Ceftriaxone 2 g daily

Admit to ICU IV Erythromycin 1 g 6-hourly
IV Gentamicin (5 mg/kg) daily
for 2/7

The local hospital regimens are given for information and to show that
penicillin is also a drug of first choice for in-patients.

Parenteral vs oral antibiotics

There has been an ongoing debate amongst CARPA practitioners about the
recommendation to treat all pneumonia with parenteral penicillin. There is
no data to inform this debate but there is a wealth of clinical experience
and common sense.
There is benefit in standardising treatment (both drug and method of
giving it) for pneumonia across the CARPA region. This includes making it
easier to give IM injections if people expect them.

The case for only recommending parenteral

penicillin is that:
• It can be given once a day, except for severe cases.
• It can be linked to reviewing the patient daily, and this may be
skipped otherwise.
• High penicillin levels can be achieved, adequate to cover the
increasing frequency of intermediate resistance in the pneumococcal
isolates.
• It is currently accepted practice by ‘most’ community people.
• It ensures some level of compliance, at least if the people return to
the clinic.
• It helps to ensure that cases with under-recognised severity receive
more adequate treatment.

The case against only recommending parenteral penicillin is that:

• It is painful.
• Many community-based staff feel they can assess if a person is likely
to take oral antibiotics as needed.
• Some patients may feel offended at not being ‘trusted’ to take oral
antibiotics.
• It may be over-treating many people.
• It may be ‘disempowering’ for some patients if they feel like they have
less control over their treatment that oral treatment might offer.

Further investigation
If a system for transporting specimens to the hospital laboratory is
practical, blood and sputum tests for moderately ill patients are
recommended.
In other settings, the diagnosis of pneumonia is dependent on the
demonstration of consolidation on chest X-ray. In remote areas, the
diagnosis is clinical but, under some circumstances, late referral for X-
rays may be indicated. If considered, the decision should be made in
consultation with a doctor.
‘Simple’ pneumonia usually improves in two days and settles in six days.
If symptoms become worse in the first week or persist beyond that time,
further action may be needed.
Clinical features which indicate complications — such as effusion,
collapse, bronchiectasis, antibiotic resistance or other diagnoses —
include:
• Increasing shortness of breath
• Coughing blood (apart from rusty sputum in the first few days)
• Chest pain (other than early pleurisy)
• Shift of the trachea from the mid-line
• Reduced breath sounds on one side
• Persistence or late onset of bronchial (tubular) breath sounds
Post-acute management
It is prudent to consider background factors that may have contributed to
the illness and predispose to slow convalescence or recurrence such as:
• Poor housing conditions and overcrowding
• Poor nutrition, excess alcohol
• Active (or passive exposure to) smoking
• Other co-morbidities

Of these factors, nutrition, smoking, excess alcohol and petrol sniffing

are all amenable to individual level intervention as described elsewhere in
the CARPA manual and reference book.
It is important that the patient’s immunisation status is checked and
appropriate vaccination given, especially for pneumococcus and
influenza.4,35,36

References
Note: A number of references have been taken from several large documents &
for convenience, these are abbreviated in the list below.
PD1A 2000–Pneumococcal Disease in Australia. MJA 3rd October 2000, Vol 173
Supplement.
ICARI.1997 International Conference Acute Respiratory Infections Canberra. 7–10 July
1997

1. Andreson D. & Collignon P. Antibiotics for CAP. MJA 2 April 2001; 174 (7).
Editorial.
2. Bryan S. Acute CAP Diagnosis and Treatment. Journal of Sth Carolina Med
Association Jan 2001.
3. Garabaldi A. Epidemiology of CAP. Am J Med June 1985; 78(6B).
4. Indigenous Paediatric Respiratory Workshop Alice Springs August 2001. Comments.
5. Tsirgiotis & Ruffin CAP: A perspective for family practice. Aust Fam Physician
July 2000; 29(7).
6. Jenkins C. How to treat CAP. Australian Doctor September 1997.
7. Hunter’s Tropical Medicine and Emerging Infections Diseases 8th Edition 2000,
edited by G. Thomas Strickland.
8. PDIA Gilbert GL. Retreat of the Pneumococcus.
9. Mathews C. Unpublished PNG.
10. Torzillo et al. Invasive pneumococcal disease in Central Australia. MJA 20
February 1995; 162.
11. Australian Lung Foundation COPD 2001. Case Statement.
12. Harrison’s Principles of Internal Medicine 2000. CAP Outpatient Management.
13. Dobbin C. et al. The efficiency of an antibiotic protocol in CAP. MJA 2 April
2001; 174(7).
14. Segasothy M. Department of Medicine Communications, ASH.
15. Singh & Arrieta. Of bugs and drugs. Post Grad Med November 1999; 106(6).
16. Atkins & Meikle. Central Australia Respiratory Outreach Project. Report, May
2001.
17. Patel S. et al. Frequent hospital admissions for bacterial infections among
aboriginal people with diabetes in Central Australia. MJA 19 August 1991; 155.
18. Chang A. 2001. Chest Infections from 3–12 months in CARPA reference Book. Alice
Springs: CARPA, 2003.
19. Woodcock A & Hensely M. Chronic Respiratory Consequences of ARI ICARI, 1997.
20. McIntyre et al. Pneumococcal Disease in NSW. PD1A 2000.
21. Krause et al. Invasive Pneumococcal Disease in NT. PD1A 2000.
22. Alice Springs Hospital. Infection Control Unit Annual & Monthly Reports, 2000,
2001.
23. Thompson J. CAP in NE Australia: A hospital based study. Aust NZ J Medicine 1997;
27.
24. Torzillo P. Communication 1998. Alice Springs.
25. Segasothy M. Personal Communication. ASH.
26. Semin. Respiratory Infection September 1994; 9(3). Macdonald et al. CAP: The
future microbiology laboratory.
27. Colacino J. Rapid diagnosis for viral respiratory disease. ICARI, 1997.
28. Thomson R. Laboratory diagnosis of respiratory infections. Current Opinion in
Infectious Diseases 1999.
29. Klugman K. Antimicrobial Resistance. ICARI 1997.
30. Collignon & Turnidge, Antibiotic resistance in Strep. pneumoniae. PD1A 2000.
31. Turnidge et al. Rapidly emerging antimicrobial resistance in S. pneumoniae. MJA
15 February 1999; 170.
32. Paterson & Playford. Controversies in Health. MJA 6 April 1998; 168.
33. Currie et al. Antibiotic protocol for adult CAP in the Top End. NT Disease
Control Bulletin, December 2000; 7(4).
34. Qazi S. Antibiotic strategies in developing countries. ARI Experiences in
Pakistan. ICARI 1997.
35. Lehmann D. Efficiency & effectiveness of pneumococcal vaccines. PD1A 1997.
36. Lehmann D. Application of polysaccharide pneumococcal vaccine. ICARI 1997.
37. Currie et al. Melioidosis, The Top End prospective study. NT Disease Control
Bulletin. December 2000; 7(4).
 Chickenpox and Zoster

Authors: Christine Selvey; Geoff Cross; Dr Dan Ewald

Topic Reviewers: Kenna Bistani (RAN, Pine Creek); Dr Anne Cawley (Wurli-
Wurlingang); Kaz Knudsen (RAN, WA); Dr Ian Dumbrell (Port Keats)

Overview
Chickenpox is a highly infectious disease. The incubation period is 10–20
days.1,2 The main symptom is a vesicular rash, where the virus is found in
great numbers. The severity of the disease is largely related to the extent
of the rash. In general there is no way of predicting disease severity in
individuals, however, there are a number of important considerations. The
disease tends to be more severe in adults than in children, with adults
more likely to develop varicella pneumonia (16% of previously healthy
adults with chickenpox had radiological evidence of varicella pneumonia in
a study of US military recruits — only a quarter of these were
symptomatic.3 Severe pneumonia occurs in 0.25% of all adult cases of
chickenpox3). People with impaired immune systems are also more at risk of
severe or complicated or even fatal infection. The overall case fatality
rate in Australia is approximately three per 100 000.4 It is much higher
than this in immunosuppressed individuals. The case fatality rate in
children with leukaemia has been shown to be 7–14%.5
Most people are infected and become immune as children. The person or
their carer may not notice this, as many cases will be clinically very
mild, or subclinical. In Australia 75% will have developed immunity by age
12.1 A study conducted in antenatal clinics in the Top End of the NT in
1999 found that 92% of women were seropositive but only 51% gave a definite
history of chickenpox6, i.e. the sensitivity of a clear history of past
chickenpox is low for immunity. However, the specificity is very high, with
only 1.6% of adults with a clear history of prior chickenpox being
serosusceptible.7
After chickenpox the virus lies dormant in nerve cells. It may
reactivate in later life leading to Herpes zoster (shingles), which can be
a serious disease. Severe neonatal infection can result from perinatal
maternal varicella infection.
There are vaccines that offer protection against chickenpox and zoster.1
Details of the vaccines and their use and some detail on the
epidemiology can be found in the latest edition of the Australian
Immunisation Handbook.

Antiviral treatment
In an RCT in healthy adults with varicella early acyclovir treatment
(initiated within 24 hours of rash onset) reduced total time to full
crusting of lesions from 7.4 days to 5.6 days and reduced the maximum
number of lesions by 46%. There was no effect if given after 24 hours.8
Another trial showed similar results in children, shortening the duration
of the illness.9
 There are some that argue for acyclovir to be given to all contacts, for
adults to reduce the risk of severe disease and for children to reduce
discomfort, severe disease cases and to reduce the need for parents to stay
home with a sick child, leading to lost income. An Australian review of the
benefits of acyclovir treatment of varicella in 1996 conclude that
acyclovir should be used for those with altered cell mediated immunity,
newborns in the first two weeks of life, preterm infants in hospital,
severe varicella or shingles and in pregnancy. They do not recommend
acyclovir for healthy individuals without severe disease, or as a
prophylactic agent, or for treatment of post-varicella syndromes. Treatment
is not recommended for asthmatic patients receiving inhaled or low dose
oral steroids.10
The protocol does not describe how to use antiviral treatments in
varicella or exactly who should be offered treatment. This will need to be
discussed with a specialist. It is, however, important to identify those
who need to be discussed with a specialist, as some individuals may derive
important benefit from treatment.
The above-mentioned RCTs used acyclovir 800 mg five times a day PO for
five days in adults, or 20 mg/kg QID PO in children. Famcyclovir 500 mg TDS
PO, or Valacycolvir 1 g TDS PO are much more convenient and better absorbed
but they are not approved for this indication, however, they are the
treatment of choice in many centres. (Valcyclovir and Famcyclovir are more
expensive than acyclovir, however when the dosing is taken into account,
the difference is not so big.)

Bacterial complications of the rash

The recommendations made about cutting fingernails short, giving treatment
to reduce itch (and hence scratching) and being alert to the possibility of
secondary bacterial infection of the skin lesions is based on consensus of
clinical opinion and common sense. We did not search for, nor find, any
systematic evidence about how best to reduce the likelihood for bacterial
infection. In the CARPA region, bacterial skin infections are extremely
common (see section on skin infections), so treatment with penicillin is
frequently likely to be needed.

Chickenpox in pregnancy
A detailed discussion of this problem can be found in the paper by Heuchan
and Isaacs.11 The approximate risk of VZV embryopathy (congenital
abnormalities) is 0.4% if the mother is infected in the first trimester and
2% if infected in the second trimester. The risk to the foetus is highest
in the third trimester. If the mother is infected within five days of
giving birth there is a high incidence of neonatal varicella, which has a
25% mortality.12 In the third trimester, the mother herself is at higher
risk of more severe disease.
If an exposed pregnant woman is not immune VZIG should be given, ideally
within 48 hours, but is effective up to 96 hours post-exposure. If a
pregnant woman develops clinical varicella, expert advice should be
obtained urgently, and consideration given to acyclovir in the mother and
VZIG or acyclovir in the neonate, depending on timing.

Varicella zoster vaccine

The recommendations for use of the varicella zoster vaccines are likely to
change with the next edition of the Australian Immunisation Handbook. In
the NT, CDC recommendations are likely to be in line with national
practices, which will depend on the Commonwealth’s willingness to fund
widespread use of the vaccines. (pers. comm. Vicki Krause 2002).

Varicella zoster immunoglobulin

Varicella zoster immunoglobulin (VZIG) can prevent or reduce the severity
of chickenpox if given within 96 hours of exposure. It is recommended for
use when non-immune individuals at risk of severe disease have had
significant exposure to chickenpox or zoster (e.g. neonates of non-immune
mothers, all premature infants born at less than 28 weeks, pregnant women,
immunocompromised individuals) (see Australian Immunisation Handbook,
seventh edition, p 236). Specialist advice should be sought.

Zoster
After initial infection with the varicella virus it remains dormant in the
dorsal root ganglia. Re-activation may occur later in life leading to
varicella zoster (shingles). Eighty per cent of cases in Australia are over
the age of 40 years. The virus tracks down the sensory nerve to the skin
where it causes a characteristic pattern of skin rash that matches the
dermatome of the nerve(s) involved. Severe pain and paraesthesia are common
and up to 30% of older people with zoster may suffer postherpetic
neuralgia. There is excellent evidence (meta-analysis of four RCTs) that in
adults over 50 years of age oral acyclovir (800 mg five times/day for 14
days) started within 48-72 hours of the onset of the rash decreases the
incidence of post-herpetic neuralgia at six months by 50%, and decreases
the duration of severe pain in the acute infection.13 Valacyclovir (1 g TDS
PO) and Famcyclovir (500 mg TDS PO) are more convenient and have been
demonstrated to be at least as good as acyclovir for this indication.14,15
Adults below 50 years old are less likely to get post-herpetic neuralgia
and the benefit in this group is less clear. If presenting within 72 hours
of the onset of rash, oral acyclovir (or Fam/Val) should be given to adults
over 50, anyone with involvement of the ophthalmic branch of trigeminal
nerve, and those under 50 with severe pain/parasthesia.
Contact with zoster can lead to chickenpox (if not immune) but does not
lead directly to zoster. Repeated bouts of zoster are rare. Zoster in young
adults is a cause for investigation as it may indicate an underlying immune
deficiency. If the zoster involves the ophthalmic branch of the facial
nerve, it may involve the eye. Management should be discussed with an
ophthalmologist.

References
1. Varicella Zoster in The Australian Immunisation Handbook draft for 8th
edition, NHMRC Commonwealth Department of Health and Aged Services. Unpublished.
2. Mandell, Douglas and Bennett’s Principles and Practice of Infectious
Diseases. 5th Edition. Churchill-Livingstone, 2000.
3. Weber DM, Pellechia JA. Varicella Pneumonia. JAMA 1965; 192:52.
4. McIntyre P, Amin J, Gidding H, Hull B, Torvaldsen S, Tucker A et al. Vaccine
preventable diseases and vaccination coverage in Australia, 1993–98. Commun Dis
Intell 2000; 24(suppl):S1–83.
5. Feldman, Hughes & Daniel. Varicella in children with cancer: 77 cases.
Paediatrics 1975; 56(3):388–97.
6. O’Grady KA, Merianos A, Gilbert L. Usefulness of a self reported history of
chickenpox in adult women in the Top End. Northern Territory Disease Control
Bulletin, Dec 1999; 6,(4)1-3.
7. Weber DJ, Rutala WA,Hamilton H. Prevention and control of varicella-zoster
infections in healthcare facilities. Infect Control Hosp Epidemiol 1996 Oct;
17(10):694-705.
8. Wallace, MR, Bowler, WA, Murray, NB, et al. Treatment of adult varicella with
oral acyclovir. Ann Intern Med 1992; 117:358.
9. Dunkle, LM, Arvin, AM, Whitley, RJ, et al. A controlled trial of acyclovir
for chickenpox in normal children. N Engl J Med 1991; 325:1539.
10. Acyclovir for the prevention and treatment of Varicella Zoster in children,
adolescents and pregnancy. J Paediatr Child Health. 1996 Jun; 32(3):211–7.
11. Heuchan, Isaacs D. The management of Varicella-zoster virus exposure and
infection in pregnancy and the newborn period. Med J Aust 2001 Mar 19; 174(6):288–
92.
12. Enders G, Miller E; Cradock-Watson J; Bolley I; Ridehalgh M. Consequences of
varicella and herpes zoster in pregnancy: prospective study of 1739 cases. Lancet
1994 Jun 18; 343(8912):1548–51.
13. Wood MJ, Kay R, Dworkin RH, Soong SJ, Whitley RJ. Oral acyclovir therapy
accelerates pain resolution in patients with herpes zoster: a meta-analysis of
placebo-controlled trials. Clin Infect Dis 1996 Feb; 22(2):341–7.
14. Tyring S, Barbarash RA, Nahlik JE, Cunningham A, Marley J, Heng M, Jones T,
Rea T, Boon R, Saltzman R. Famciclovir for the treatment of acute herpes zoster:
effects on acute disease and postherpetic neuralgia. A randomized, double-blind,
placebo-controlled trial. Collaborative Famciclovir Herpes Zoster Study Group. Ann
Intern Med 1995 Jul 15; 123(2):89–96
15. Beutner KR, Friedman DJ, Forszpaniak C, Andersen PL, Wood MJ. Valaciclovir
compared with acyclovir for improved therapy for herpes zoster in immunocompetent
adults. Antimicrob Agents Chemother 1995 Jul; 39(7):1546–53
 Coral and Marine Cuts

Author: Prof Bart Currie (MSHR)

Topic Reviewers: Michael Jenkins and Dr Meredith Arnold (Maningrida Clinic);

Robyn Dixson and staff (Yirrkala Clinic)

Infections from the sea may be from coral cuts and abrasions, or venomous
or non-venomous animal spine penetration and exposure to sea or fresh
water. The infecting organisms can be either human skin bacteria or
specific fish or marine or fresh/brackish water bacteria. The specific
bacteria live in various environments, often including the mucous layer of
the skin of fish. Most of the zoonotic bacteria are also fish pathogens.
Bacterial populations and risk of infection to both fish and humans are
increased by pollution in waterways/estuaries. Specialised laboratory
culture techniques should be requested if specific pathogens are suspected.
The common human skin pathogens are Streptococcus pyogenes (especially
common in tropical areas, e.g. northern Australia) and Staphylococcus
aureus.

Important specific pathogens include

• Aeromonas species — fresh or brackish water — may progress to myositis or
sepsis with metastatic complications (especially if underlying systemic
illness)
• Vibrio vulnificus, V. alginolyticus, V. parahaemolyticus and other non-
cholera vibrios — salt or brackish water — may progress to blistering
cellulitis, myositis and fulminant septicaemia (especially if underlying
liver disease or diabetes)
• Mycobacterium marinum — especially fish tanks but also swimming pools —
nodular lesion(s), can spread locally or occasionally disseminate in
immunocompromised people — other Mycobacteria occasionally occur also
• Edwardsiella tarda — e.g. fish spine puncture — may progress to
osteomyelitis, septic arthritis, meningitis and septicaemia (especially
if underlying illness such as cirrhosis, iron overload)
• Erysipelothrix rhusiopathiae — from many fish — specific-looking local
lesion (‘fish rose’), sometimes diffuse cellulitis but occasionally
endocarditis and septicaemia with high mortality (especially if
underlying illness)
• Streptococcus iniae — especially with aquaculture, both saltwater and
freshwater, (e.g. farmed barramundi) — cellulitis may progress to
arthritis, endocarditis, meningitis and septicaemia

Management
• Initial first aid is especially important — vigorous cleaning of wound.
Scrubbing with brush also important if coral cuts or abrasions. There
does not appear to be any evidence to suggest using an antiseptic agent
to scrub the wound is better than using saline.
• Appropriate cultures if established infection on presentation — notify
laboratory of ‘?marine pathogen’.
• For mild infections:
i. A mild/early cellulitis is likely to be S. pyogenes which can be
treated with penicillin. IM procaine penicillin would be appropriate as
is recommended for non-marine infections. Other organisms can cause
cellulitis (including S. aureus) so it is important to review the
response to treatment.
ii. If there is a boil, then S. aureus should be suspected and treatment
should be with flucloxacillin or dicloxacillin. Some clinicians use
cotrimoxazole for mild marine infections.
iii. If it is not responding to treatment within 48 hours, suspect a non-
sensitive organism, and do cultures if possible.
• For more severe infections the specific marine pathogens may need to be
covered by initial therapy (before laboratory identification of the
organism), in addition to covering S. pyogenes and S. aureus. This is
complicated. The drug of choice for Aeromonas species is
ceftriaxone/cefotaxime or ciprofloxacin. The drug of choice for Vibrio
species is doxycycline, but ciprofloxacin also works. Therefore, a
reasonable empirical regimen for more severe infections is ceftriaxone
plus doxycycline. An alternative combination for critically ill patients
is meropenem/imipenem plus ciprofloxacin.

References
1. Antibiotic Guidelines Version 11, 2000; 181–2.
2. Lehane L & Rawlin GT. Topically acquired bacterial zoonoses from fish: a review.
Med J Aust 2000; 173:256–259.
 Dental Health: The context of
remote dental health and
services in Central Australia

Author: Bruce Simmons (Oral Health Services, DHCS, Central Australia)

Topic Reviewers: Dr Peter Tait; Dr Dan Ewald

Historical dental anthropological work has demonstrated that Indigenous

peoples across the world, including Australia, very rarely experienced
tooth decay, gingivitis and periodontal disease. Severe attrition resulted
though from the use made of teeth not only chewing unprocessed foods but as
a tool e.g. chewing hide, gut etc to soften and modify with saliva for
binding, clothing etc. Attrition eventually resulted in the exposure of
pulp chambers, pulpal necrosis, dental abscesses, gross infections and
ultimately quite large spiralling draining sinuses to the bone surface. So
dental pain and infection was well understood, and bush medicine included
ways of managing it. A dental anthropologist from Adelaide University, Dr
Murray Barrett, described how people at Yuendemu reported that tooth decay
was caused by a ‘little brown snake’. This belief could be related to the
spiralling draining sinuses running from the root apices of ‘dead’ teeth to
the bone surface.
Changing diets and lifestyles have increasingly impacted on the teeth
and the surrounding soft and hard tissues. Tooth decay is an ever
increasing problem, especially in the very young, but across all ages.
Gingivitis is endemic because very few people brush their teeth regularly,
or even occasionally, and periodontitis is an increasing problem,
particularly for smokers and diabetics. Remote-living Aboriginal people in
Central Australia have been shown to have three times the tooth loss of
non-diabetic people.
Aboriginal people are used to tolerating pain and discomfort generally,
and more specifically pain from dental and periodontal infections. This
should not be taken as an indication that Aboriginal people prefer to
tolerate and accept dental and oral pain to receiving preventive or early
interceptive treatment for their conditions. Research into service delivery
methods at Utopia in 1999 clearly demonstrated considerable interest in and
support for both oral health promotion and treatment services. It appears
to be generally true that Aboriginal people see medical health service
providers and dental health service providers in different lights, although
both health service providers are often the option of last resort when
dental pain becomes intolerable. Nonetheless, dental health service
providers’ professional care is often sought for ‘check-ups.’ Preventive
and interceptive care is often accepted after a person attends for either a
check-up or an acute problem.
On the other hand, medical health service providers are viewed almost
exclusively as sources for dental and periodontal pain relief and possibly
referral to a dentist. People are attending mainly at a point of severe
stress. Three stories that relate to this phenomenon are now told.

Story 1
Medical Practitioner Toby McLay worked with me on dental mobiles in the
early 1980s at Utopia. He was a wonderful supporter of early interceptive
dental care, and with his assistance a large proportion of the Aboriginal
population was regularly screened and their dental caries successfully
treated. Even so, some people still experienced pain from severe tooth
decay or periodontal disease, and Toby decided that it would be a much
better service and more efficient use of resources not to have to wait some
months for the next dentist visit or take people into town for treatment.
By working with me, he soon learnt to give local anaesthetic and extract
teeth. He reported good acceptance and good outcomes for the extractions he
subsequently performed. I was very pleased too because it enabled me to
focus more on the screening and early interceptive work that people wanted.
In my experience almost all Aboriginal people out bush who attend the
dentist would prefer to keep their teeth unless they become so painful or
loose and sore to bite on that they are intolerable.

Story 2
I was meeting with the health council at Bonya a few years ago when Banjo
Madrill told me that the elders wanted the dentist to come out to Bonya so
that people with toothache didn’t have to go to town where they could be
unhappy, stuck, or get into trouble. At the time I tried to explain that it
wasn’t economically possible for the dentist to be travelling out to
communities to perform a few extractions. Rather, I said I needed to make
the trip worthwhile by checking up and treating as many children and adults
as possible to prevent toothache and worry. I guess this concept would be
quite foreign in many ways to traditional healings, concepts that address
problems when they become intolerable.
At a recent dental visit to Bonya, in fact, almost all the people in the
area came for a check-up and treatment. During the visit, the remote area
nurse Malcolm Auld worked with me and learnt about techniques of local
anaesthetic and extractions. Another dentist visit and he could take over
most of the extractions needed by the community.

Story 3
I had a number of discussions with remote nursing staff at the time of
drafting the dental sections for the CRANA Procedures Manual which include
local anaesthetic and extraction techniques. There was general interest in
the topic of dental health and considerable frustration and disappointment
expressed by the nurses at their inability to address the needs of people
who came in with toothaches. Most said that they couldn’t spare ambulance
space for dental patients to come to Alice Springs, but that they were also
tired of the people who continually attended their clinic with ongoing
dental pain. A few nurses expressed their interest in learning dental
extractions, though most showed anxiety and mild anger when the idea of
their taking on another treatment task was proposed. The question was
raised and warmly supported about why PATS couldn’t be used to refer people
in to Alice Springs to see a dentist for severe dental pain and related
inflammation and infection.

The first three editions of the CARPA manual have focussed on emergency
relief of pain and management of inflammation and infection associated with
dental and periodontalat (gum) diseases. One might almost suppose that
dental infections were short-term, opportunistic infections, when in fact
they are chronic diseases that cannot be addressed without considerable
surgical and/or medical treatment as well as addressing the underlying
causative factors.
As dental decay and periodontal disease continue to worsen so it becomes
clearer to local communities that they need to address both the causative
factors as well as the treatment needs. The Katherine West Health Board has
sent a delegation to the Melbourne Dental School asking for help. Clearly
the outcomes of dental diseases present a significant and growing health
problem for community members.
A question therefore for the editors of the fourth CARPA manual to ask
is what dental information should be included in this edition. Is it
sufficient to describe the temporary relief of pain and management of
inflammation and infection, or should other treatments be included and if
so which?
The CRANA editorial team reported that there were sufficient remote area
nursing staff without regular dental services who wanted to learn about
dental anaesthetics and extractions to justify making these techniques
essential components of the manual.
Some further information for the editors to consider is that Australia
is well into a period of growing crisis for public dentistry in particular.
Levels of new dentist and dental auxiliary graduates are increasingly
falling behind workforce demand. Private dental practice is becoming
increasingly lucrative, impacting negatively on recruitment and retention
on the rural and remote, and the public dental health, workforce in
particular.
Salaries are being markedly increased with no hope of reversal for at
least 10 years. Rising personnel costs are being matched by operational
cost increases for infection and quality control, IT systems etc., so the
funding picture is grim. The result is a decrease in service provided by
visiting dental teams.
Solutions for remote communities appear to lie partly in health
promotion activities, but also in increasing the on-site capacity of health
staff to definitively address at least acute dental needs. Over time, with
increased familiarity and acceptance, local health staff, including
Aboriginal health workers, might take on more preventive and early
interceptive oral health care. But here and now it seems the need for
remote practitioners to learn to provide simple dental extractions has
arrived.
It goes without saying though that we also need a much bigger remote
dental workforce to meet the growing treatment needs, as well as to provide
training to remote practitioners in emergency dental care and oral health
promotion.

[Editor: There was some discussion about the possible use of temporary
fillings such as ‘Cavit’ rather than oil of cloves for dental pain.
Potential problems with oil of cloves include it being irritating to the
surrounding gum tissue (hence need to squeeze out the excess oil). Against
using temporary filling is the possibility of it preventing a dental
infection from draining, leading to deeper infection. Using a temporary
filling also assumes that the tooth can be adequately cleaned out first,
and this may not be the case.]
 Eye Conditions

Authors: Dr Tze Foon Lai; Dr Johnny Wu; Dr Tim Henderson; Dr Wilfred Win Law
(Department of Ophthalmology, ASH)

Topic Reviewers: Prof Hugh Taylor; Kenna Bistani (RAN, Pine Creek); Bernard
Egan (RAN, Bilman Clinic); Robyn Dixson (RAN, Yirrkala); Colin Watson (RAN,
Nyirripi Clinic)

[Editor: In this section the authors have collated more detailed and
expanded instructions on the appropriate care of common (or frightening,
e.g. penetrating eye injury) eye conditions seen in remote community
clinics.
The evidence for the specialist care of diabetic retinopathy, cataract
and trachoma has been collated by the Centre for Eye Research Australia for
the Commonwealth Department of Health and Ageing, Office for Aboriginal and
Torres Strait Islander Health in Specialist Eye Health Guidelines for use
in Aboriginal and Torres Strait Islander Populations. Cataract, Diabetic
Retinopathy, Trachoma (Commonwealth of Australia, 2001).
Though these guidelines are written for specialists, they also offer a
good review of the evidence for most aspects of primary clinical care of
these conditions. Many aspects of trachoma control and primary prevention
of cataract and diabetic retinopathy are in the realm of population-based
public health measures, and hence beyond the scope of the CARPA STM.
Good management of systemic aspects of diabetes are very important in
minimising diabetic retinopathy, this is covered in detail in the diabetes
chapter.
Cataract is not specifically dealt with in the CARPA STM. However, using
the protocols (including the ‘older persons adult health check’) will
direct people with significant visual disability from cataract to
specialist eye services where appropriate treatment should follow. Other
protocols also cover the potentially modifiable risk factors for cataract
such as smoking, diabetes, alcohol and the judicious use of medicines that
can be a risk factor for cataract.)

History and examination

Using the E chart or the letter chart?
Visual acuity is the ‘vital sign’ in ophthalmology. It should be the first
step in the examination and should be performed accurately. The only time
visual acuity should not be obtained before treatment starts is in chemical
injuries, when washing out the eye is the most important thing to do
first.1,2
1. Patient is seated at an appropriate distance depending on the chart
used. The standard distance is 6 m (20 feet). It does not matter which
chart is used, the size of the figures is what is important. The
patient should be briefed precisely what is required of them to allow
an accurate assessment of their vision.
2. Test the vision:
 i. Unaided or with glasses if worn for distance
(driving/TV spectacles).
ii. Using a pinhole if not able to see 6/6
Always test one eye at a time while covering the other effectively. If
you ask the patient to use their hand make sure it is the palm of the
hand, as they can inadvertently get a very good pinhole effect between
their fingers of the eye that is supposed to be covered.
If patients are literate it is easier to have them call out the
letters. If using an E chart ask the patient which way the three limbs
of the E point (not the two white gaps between them, which point the
opposite way).
3. Record the vision for each eye with and without the pinhole. Take the
number written on the chart corresponding to the line the patient can
see (this is written below or above each line of letters, depending on
the chart), i.e. if the patient reaches the line numbered 24 and
completes this line then take this number. For example:

RVA 6/24 with glasses LVA 6/6

6/9 with p.h. 6/6

(6 = the distance from the chart in metres, 24 = the number of the

line corresponding to the distance a person with ‘normal’ vision would
be able to see this letter).

Tip: Children are usually easier to examine when they do not realise
that a procedure is being done. Therefore do not miss the opportunity to
have a good look at the child’s eye whist he or she is busy reading the
letters initially.
For very young children, visual acuity can be assessed by observing
whether they can pick up ‘hundreds and thousands’ cake decorations.6 Other
tests such as letter matching or preferential looking for babies are also
employed.

Using an ophthalmoscope
Whenever possible put dilating drops (Tropicamide 1% eye drops) in the eyes
to be examined, only after checking pupils.
1. Switch on the ophthalmoscope and make sure it is working.
2. Turn all the dials to zero.
3. Darken the room.
4. Hold the ophthalmoscope at arm’s length from the patient and keep the
eyepiece right up against your own eye. Unless you have one eye with
poor vision use the ophthalmoscope ‘Right eye to Right eye and vice
versa. (This avoids kissing the patient by mistake!) It also makes it
easier for the patient to look straight ahead while being examined. For
each eye check the red reflex from a distance and compare both eyes.
The red reflex is a reflection of the light directed into the eye. If
it is speckled, dull or totally absent, there is opacity interrupting
the passage of light, which is usually caused by a cataract but can be
due to other causes, e.g. vitreous haemorrhage.
5. Then approach from the temporal side of the eye aiming for the centre
of the head. Find something that looks like a blood vessel and, while
looking at it, turn the dial on the ophthalmoscope to bring it into
 sharp focus. Then follow the vessels until you find the optic disc.
Once at the disc look up and temporally along the vessels then follow
the lower vessels temporally. Finally, look temporal to the disc into
the central area of vision known as the macular. This is bright for
patients but if they can tolerate it the best way of looking at the
very central part of the retina is to ask the patient to look straight
at the light.1,3 This usually causes the maximal pupil constriction, and
dilating drops may be necessary to see any real detail.

Visual field testing

The visual fields map the peripheral extent of the visual world. Testing
the visual field may give clues to the site of lesion and the diagnosis.
The visual field may be tested in various ways.
Confrontation test6
1. The patient is seated directly opposite the examiner closing his/her
eye on the same side.
2. An object, such as a red top pin, is then brought into view from the
periphery and moved centrally. The patient is asked to indicate when
he/she first sees the test object.
3. Each quadrant is tested and the location of the blind spot
determined, careful use of this technique can allow assessment of the
size of the blind spot.
4. The patient’s field is thus compared to that of the examiner.
Crude testing of the field can be performed as follows6:
1. The patient is seated directly facing the examiner.
2. The patient is asked to cover one eye.
3. The examiner hold up both hands in front of the unoccluded eye, palms
facing the patient, one on either side of the midline. Ask whether the
two palms appear the same.
4. This can be useful in picking up a bitemporal hemianopia (patients
may also miss the temporal letters on the Snellen chart when their
visual acuity is measured).
The patient is asked to count the number of fingers in each quadrant of the
visual field while presenting two fingers on one side and one on the other.
How to evert or double evert an eyelid
See CRANA Clinical Procedures Manual.

Eye injuries
Ocular injuries, however trivial, are a frightening experience for the
patient [Editor: and practitioner!], who may have a deep-rooted fear of
blindness. The incidence of injuries varies with the environment and
protective measures taken.
Trauma to the eye is managed differently according to the kind of injury
the eyeball has received. There are two broad categories, sharp
(penetrating) and blunt (non-penetrating) trauma, but if the force hitting
the eye is severe enough then both types of injuries will result,
irrespective of the size of the object.4,10
In the assessment of eye injuries, a thorough history should be taken to
elicit:
 • Mode, extent of injury to the eye. Record, in the patient’s own words,
the events leading up to the injury and the direction the blow came
from, e.g. if a stick injury, did the stick hit the eye end on or from
the side. This information helps you to judge the amount of direct
trauma to the eyeball. For sharp trauma, establish whether the object
that caused the injury was intact on withdrawal from the eye. If the
object is available do not discard it or any of its pieces. If the
penetrating object is still in the eye do not be tempted to remove it.
• Other relevant injuries (head/neck)
• Tetanus prophylaxis
• Past ocular, medical and drug history including hepatitis/HIV status
Visual acuity (VA) should always be measured despite the eye being sore and
swollen shut. If the eye is too painful to open2:
• Explain the importance of obtaining a visual acuity to the patient and
relatives/parents.
• Instil some topical local anaesthetic drops. Warn the patient this
will sting for approximately 30 seconds. This is especially important
for children and their parents.
• Allow the anaesthetic to work. Ask the patient if he or she can open
the eye after about 30 seconds or so. The patient may need help if the
lids are swollen. Even if it means reading letters one at a time
between opening the eye and the patient ‘having a break’, a visual
acuity must be obtained.
• It may be necessary to exert gentle pressure to reduce lid oedema or
even to use lid retractors to hold tight swollen lids open enough to
check vision.
Do not be put off by an unenthusiastic patient and always encourage a
patient further. The letter on the next line down may appear blurred but if
the patient can read them, then this blurring is of significance.
For children, if the child is frightened or crying, this should be
performed with great care to avoid aggravating any pre-existing injury. If
at any time during the examination suspicion of a ruptured globe develops,
no further diagnostic examinations should be performed.9
Do not force the eyelids open if there is any chance of a penetrating
injury. Beware deep lacerations of the upper lid. Do not forget the VA of
the other eye need to be recorded.
VA not only is a good indication of the severity of a condition; it may
also be required for medicolegal reasons1,2,6,7 and to give some idea of the
potential vision that may be recovered if multiple procedures are
contemplated to rehabilitate the eye.6
Examine the eye systemically from the outside in.2
• Eyelids: Look for laceration, bruising and surgical emphysema. (It
classically feels like the sensation of walking on dry leaves. Once
felt never forgotten). The presence of surgical emphysema suggests a
bony fracture into a sinus.
• Conjunctiva: This is often red and swollen. Look for foreign bodies
and lacerations. If the patient was (at the time of the injury)
wearing a contact lens, this may have been displaced. It needs to be
found and removed. If possible, ask the patient to remove the lens
themselves (most patients are very good at this). If there is any
suspicion of a full-thickness laceration of the eyeball do not try to
 open the eyelids, and any contact lens can be left in place as it may
be holding things in check.
• Cornea: Look for abrasions (these may look like tiny yellow (when
fluorescein is used) dots or straight lines). Locate, and if possible
remove, any foreign bodies.
• Anterior chamber: Look for hyphaema, a fluid level of blood that can
look bright red, dark red or even black. Try to judge how much of the
anterior chamber is filled by roughly assessing how far up the cornea
the top of the fluid level is situated, e.g. an anterior chamber
totally filled with blood has a 100% hyphaema, one in which the blood
level only comes half the way up has a 50% hyphaema. Measuring the
height in minutes is helpful to indicate if it is settling with time.
• Iris and pupil: Check the pupils for size, shape and reactions to
light. The pupil may be fixed and dilated or be an abnormal shape. Any
tear of the iris will cause a distortion of the pupil. Any abnormally
shaped pupil may indicate a ruptured eyeball. If the iris is
protruding through a wound, this is known as iris prolapse. A peaked
pupil is the characteristic sign of a perforating corneal wound (best
to draw it).
• The deeper layers of the eyeball will not be visible without
specialised equipment, but if there is an ophthalmoscope available
check for a red reflex.
• Exclude a blow-out fracture of the orbit by testing the patient’s eye
movements. Testing for numbness on the upper part of the patient’s
cheek in the area below the eye, with either cotton wool or gently
with a disposable needle. Compare with other side. Any numbness on the
side of the injury suggesting that there might be a fracture in the
orbital floor.
• X-rays: The floor and medial wall of the orbit are the weakest. A
blow-out fracture may be confirmed by asking for ‘occipitomental’ and
‘A-P’ views. These do not have to be performed as an emergency.
Practice points
Penetrating injuries of the eye can easily be missed because they may seal
themselves, and the signs of abnormality are subtle. Any history of high
velocity injury (particularly a hammer and chisel injury) should lead one
strongly to suspect a penetrating injury and request orbital X-rays on up-
gaze and down-gaze to identify metallic fragments.

Eyelid abrasions/lacerations
Treatment
Eyelid abrasions should be cleaned and debrided to prevent infection.
Tetanus immunisation should be updated for deep, dirty or devitalised
wounds.
Prophylactic topical antibiotic ointment (Chlorsig) four times daily is
indicated to prevent periorbital cellulitis.
Referral to ophthalmologist needed if:7,9
• Full thickness cut or those involving the lid margin.
• The lacrimal ducts have been involved.
• There is any suspicion of a foreign body or penetrating injury.
Periorbital or ocular contusion
History
Usually minimal pain and visual disturbance. The degree of periorbital
oedema varies.
Examination
Periorbital ecchymosis and oedema are found superiorly and/or inferiorly
and may involve the contralateral eye.
Subconjunctival haemorrhage.
Full oculomotor movement with minimal pain.
Treatment
Plain X-ray films and/or computed tomography (CT) scanning of the orbit is
needed if orbital fracture is suspected (subject to availability).1,6,7
Ocular involvement: refer to ophthalmologist.
Non-ocular involved cases: reassurance, cool compress and non-urgent
follow-up.

Orbital fractures
Blow-out fracture
History
Orbital floor (‘blow-out’) fractures are common when orbit is struck by
objects larger than or of similar size to the orbital opening, such as a
ball (especially squash ball), fist, or the dashboard of an automobile.9,10
Examination
Limitation of upward gaze is the most apparent clinical sign.
Others include lower eyelid ecchymosis, nosebleed, orbital emphysema,
and hypaesthesia of the ipsilateral cheek and upper lid (results from
disruption of the infraorbital nerve as it traverses the orbital floor).

Medial wall fracture

History
This can be caused by the same forces that cause orbital floor fractures,
also with blows to the bridge of the nose.9,10
Examination
Orbital emphysema, epistaxis, a depressed bridge of the nose, and
enophthalmos (sunken eye).
It there is nasal septal fracture or haematoma, the nose is deviated and
nasal breathing can be impaired. The nasolacrimal drainage system can be
disrupted, resulting in epiphora (tearing), lacrimal sac mucoceole, or
dacryostenosis (blockage of the tear-draining system).

Orbital roof fracture

It is less common than inferior or medial wall fractures but is more life
threatening. Central nervous system involvement, pneumocephalus, or an
intracranial foreign body should be considered in the assessment. Late
complications include brain abscess and infectious meningitis.9,10
Examination
 • Cerebrospinal fluid leakage (rhinorrhea). Rhinorrhoea is usually
transient because dural tears are generally self-sealing.
• Superior and lateral subconjunctival haemorrhage.
• Optic nerve can be involved on this injury.
Treatment
• Refer to ophthalmologist.
• With orbital emphysema, expulsion of air into the orbit can
dramatically increases with sneezing, coughing, or blowing the nose,
all of which can cause a sudden rise in paranasal sinus pressure.
Therefore, patients should be forewarned against blowing their nose,
and coughing episodes should be vigorously treated with antitussives.1,7

Subconjunctival haemorrhage
History
Blunt trauma, forceful sneezing and eye rubbing are usually reported. It
can also occur spontaneously.
Examination
• Painless, bright red accumulation of blood, usually limited to one
section or quadrant of the eye. The size of the clot and the area
affected varies from patient to patient.
• For spontaneous subconjunctival haemorrhage, measure the patient’s
blood pressure7 and consider checking their coagulation status.
• Whenever a traumatic subconjunctival haemorrhage occurs, a more severe
underlying ocular injury should be ruled out. Accumulated blood can
hide a retained foreign body or an occult scleral laceration.
Treatment
In uncomplicated cases, reassurance alone is adequate.2,7 Patient should be
told that the haemorrhage could take several weeks to completely disappear.
It may appear to become larger over the first several days secondary to
gravity and local spread under normal conjunctiva, turned yellow and
gradually resorbs over two to three weeks.2

Conjunctival laceration
History
A conjunctival laceration is common when a sharp object, such as a
fingernail or glass, strikes the eye.
Examination
It is essential to look for any deeper or more severe injury to the globe.
Treatment
Small isolated conjunctival laceration rarely requires treatment.
Prophylactic antibiotic ointment or drops (e.g. Chlorsig) to prevent
secondary infection.

Corneal abrasion
History
 • A history of mild trauma to the eye, possibly caused by dust,
fingernail scratch, tree branch, contact lens, make-up brush, or
foreign body.
• Photophobia and involuntary lid closure (blepharospasm).
• Pain and foreign body sensation may be quite severe as when the
epithelium is scratched, abraded, denuded it exposes the underlying
epithelial basement layer and superficial corneal nerves.
• Vision is disturbed if the abrasion is in the central cornea.
Examination
• Instil a drop of topical local anaesthetic if the patient has severe
spasm of the eyelids that prevent examination.
• Conjunctival hyperaemia, swollen eyelids and tearing.
• Pen light may reveal a surface irregularity.
• Linear corneal abrasions should alert the examiner a foreign body is
possible.
• Slit lamp examination shows an epithelial defect but often a clear
cornea. Minimal cellular reaction is seen in the anterior chamber. If
corneal haze or moderate to severe flare and cells noted in the
anterior segment, especially with an associated discharge, bacterial
superinfection should be considered.
• Fluorescein dye is absorbed by areas devoid of epithelium and outlines
the defect, best seen when illuminated by light with a blue filter.
Differential diagnosis1
• Viral keratitis (herpes simplex or zoster), often with corneal
dendrites.
• Corneal or conjunctival foreign body, especially under the conjunctiva
of the upper lid, which can cause ‘ice-skate track’ abrasions as the
foreign body is repeated swept linearly over the epithelium.
• Recurrent erosion, which is identical to primary epithelial defects
but occurs long after the initial corneal trauma.
• Ultraviolet corneal injury (welder’s flash).
Treatment
Foreign body’s management described as below. The aims of treatment are 7:
• To prevent infection: Topical local antibiotic drops and/or ointment.
[Editor: The issue of eye patching for corneal abrasion has been the
subject of review. We found one systematic review of RCTs (seven,
total of 550 patients) with meta-analysis (309 patients) (Flynn CA,
Damico F, Smith G. Should we patch corneal abrasion? A meta-analysis.
Journal of Family Practice, 1998; 47(4):264–70).]
They included a variety of eye-pad options trialed in people over six
years old. Abrasions related to infection or contact lenses were
excluded. Primary outcome was healing at one to two days, secondary
outcomes were symptoms and complications.
There was no significant difference in the likelihood of healing at
one or two days. There was no significant difference in the risk of
complications. Two of seven studies reported faster healing in the no-
patch group and five found no difference. Four of seven studies found
no difference in pain between groups and two studies found
statistically less pain in the no-patch group.
Conclusion: Eye patching was not found to improve healing rates or
reduce pain in patients with corneal abrasions. Given the theoretical
harm from loss of binocular vision and possible increased pain or
 infection risk, we recommend no-patching in treating corneal
abrasion.]
• To relieve pain: Instil a cycloplegic (e.g. cyclopentolate 2%); give
oral analgesia if necessary.
Practice points2,7
• Although patients often request them, under no circumstances should
topical local anaesthetics be prescribed or given to the patient. Not
only do anaesthetics retard wound re-epithelilisation, but the loss of
the cornea’s normal pain response presdiposes the patient to a much
more severe injury.
• Patients with a large central abrasion or high-risk abrasion should be
referred to an ophthalmologist for management and follow-up care.
• A pressure patch is never used for more than 24 hours.
• If visual acuity is markedly decreased, more severe ocular injury
needs to be ruled out.
Follow-up
All abrasions are monitored daily until they have completely resolved. If
healing takes longer than two or three days, the patient should be referred
to an ophthalmologist.

Corneal laceration
A corneal laceration can be either full or partial thickness. A full
thickness laceration should be suspected when the results of the Seidel
test are positive.11,12
The test is performed by applying a dry strip of fluorescein over the
wound or a drop of 1% fluorescein whist observing the cornea at the slit
lamp with the cobalt blue light. A slow leak of aqueous fluid (a positive
test) is diagnosed with progressive dilution of the green fluorescein dye
like a yellow-green waterfall.
Treatment
A shield should be placed over an eye suspected of having a corneal
laceration until the patient can be examined by an ophthalmologist.8
A pressure patch should never be applied to a potentially open eye.8

Foreign body
History
It is not uncommon for the patient not to recall a foreign body having
entered the eye.7 Pain and ocular foreign body sensation are the common
symptoms, but a high-speed foreign body may cause no more than a transient
irritation.
Examination
Slit lamp examination of the conjunctivae and cornea is preferable to
definitely locate the particle and assess the degree of injury. The upper
and lower lids must be everted to search for debris.1,7,12,20 Linear abrasions
are highly suggestive of a foreign body embedded in the superior
conjunctiva; discovery and subsequent removal of the particle provides
prompt relief to the patient.20
Treatment
Conjunctival foreign bodies are often swabbed away easily with a moist
cotton-tipped applicator following local topical anaesthesia. If this
fails, foreign bodies can be removed with an 18 or 25 gauge needle.20 An 18-
gauge needle has a wider diameter and is used for large foreign bodies,
while a 25-gauge needle is narrow and useful for small particles.
Manipulation of the needle may be stabilised by attaching it to a
tuberculin syringe or inserting a cotton-tipped applicator in the plastic
end.
If the foreign body is located in the cornea, the depth of the particle
should be established before removal is attempted.20 Foreign bodies that lie
deep within the stroma occasionally have the potential to penetrate into
the anterior chamber when manipulated. Referral to an ophthalmologist is
advisable for removal of dangerously deep foreign bodies that pose the risk
of an aqueous leak. It should be remembered that the cornea is a very tough
structure and it is quite difficult to penetrate through it.
The needle is held tangential to the surface of the cornea and never
pointed in a perpendicular direction toward the patient. Improper
angulation could drive the sharp point into the cornea with abrupt patient
movement, but if held correctly, it is unlikely that the force will be
sufficient to penetrate through Bowman’s membrane or the stroma.20 The
examiner’s hand should be stabilised on the side of the patient’s face or
nose so that any movement goes with the patient.
Sterile irrigation can be used to dislodge superficial foreign bodies
from the ocular surface. Irrigating solution should not be pointed directly
at the foreign body but rather at a slight angle since pressure exerted
from the irrigation stream straight onto the particle could embed it more
deeply into the cornea.
Not all foreign bodies require removal and, in fact, deeply embedded,
non-toxic foreign bodies such as glass may best be left in situ rather than
subject the eye to additional scarring by extraction. Such particles should
be lodged well below the corneal surface, allowing the epithelium to heal
over them.20
Following removal, cyclopentolate 2% and antibiotic ointment
(Chloramphenicol) should be instilled into the eye followed by firm double
padding. Padding protects the eye whilst still anaesthetised but may be
removed after two hours if the patient prefers.
Follow-up
Patients treated for corneal foreign bodies should be examined the next day
to evaluate the level of healing and detect signs of infection. Foreign
bodies from potentially contaminated substances — such as vegetative matter
— deserve careful follow-up, since introduction of micro-organisms at the
time of the injury could precipitate corneal ulceration.
Practice point
Any foreign body on or close to the visual axis should be left for removal
by an ophthalmologist.
Iron-containing foreign bodies deserve special consideration. Within a
few hours of the injury, the iron partially decays, and rust stains the
adjacent epithelial cells as well as Bowman’s membrane.13 The rust ring must
be removed as it will act as a continued source of irritation, delays
healing process and can permanently stain the cornea.
Wooden splinters are particularly dangerous as they may easily penetrate
the eye and cause severe infection.13
 Fluorescein stain is a useful diagnostic adjunct to the evaluation of a
patient with anterior segment trauma; however, fluorescein instillation
should follow examination of the anterior segment, since subtle flare may
be masked by fluorescein in the tear film. As the fluorescein stain pools
within zones of corneal disruption, the extent of the corneal injury from
the foreign body is highlighted. Additionally, fluorescein is useful in the
detection of perforations of the globe, because aqueous leakage through the
wound will be observed as a bright green stream and then washed away. This
percolation of aqueous through the injury site is known as Seidel’s sign.20
Patients who have been hammering/chiselling/ drilling/grinding will need
an X-ray to exclude the presence of an intra-ocular foreign body. X-rays
are very useful but not conclusive, and only useful if they have been taken
with eyes looking up and down. Each X-ray department has its own protocol
on which X-ray views should be taken. Be sure to write ‘to exclude an
intra-ocular foreign body’ on the form, and ask for ‘non-screen film’,
because this has fewer speckles (which may be misinterpreted as intra-
ocular foreign bodies) on it.

Globe rupture/penetrating injuries

Severe trauma may result in globe rupture, gross lid and conjunctival
swelling, sometimes hyphema, restricted eye movement and ocular contents
may be visible outside the eye.
Treatment
In situations where a penetrating foreign body is visible it should not be
removed, as intra-ocular contents may be lost in the process.
Initial treatment includes loose fitting shield (Cartella shield or
plastic cup cut in half) over the injured eye, systemic antibiotics (e.g.
cephazolin 1 g three times a day), anti-emetic, analgesias, and intravenous
fluids as necessary.2,8 Keep patient nil by mouth and urgent referral to an
eye care facility is mandatory.8 Transport should be smooth and avoid
depressurisation (please refer to RFDS guideline).
[Editor: Previous editions of the CARPA STM had specifically recommended
pethidine over morphine for pain relief in penetrating eye injury. ‘The
principle is to avoid opiates if possible in penetrating eye injury because
of the theoretical possibility of retracting the iris when it is the only
thing preventing collapse of the eyeball. The risk of posterior synechiae
is of minor importance’ (communication Tim Henderson ASH ophthalmologist).
An enquiry through the National Prescribing Service revealed; The evidence
for pethidine having a lesser pupillary constriction effect is weak1, though
the pupillary effect of morphine may last longer.2 The emetic effects are
likely to be similar for equi-analgesic doses, and an anti-emetic would be
given in this circumstance anyhow.
Our recommendation is that if an opioid is needed, then Tramadol or
morphine can be used.
1. Ghoneim MM, et al. Comparison of four opioid analgesics as supplements to nitrous
oxide anesthesia. Anesth Analg 1984; 63:405–12.
2. Zachny JP, et al. A dose-response analysis of the subjective, psychomotor and
physiological effects of intravenous morphine in healthy volunteers. J Pharmacol Exp
Ther 1994; 268:1–9.]
Injuries to the iris
History
Blunt eye contusion can injure the iris sphincter muscle, resulting in
pupillary constriction (traumatic miosis) during the first several hours,
followed by dilatation (traumatic mydriasis).
Patient complains of pain, photophobia, and asymmetry in pupil size. An
accommodative spasm and paralysis may be associated, resulting in blurred
vision and difficulty with near tasks.
Examination
Hyphema, perilimbal conjunctival injection, anisocoria, and sluggish pupil
response
Treatment
The management of traumatic hyphema is variable and controversial.9 There is
no consensus as to whether patients should be at strict bed rest or allowed
limited ambulation or whether they can watch television or read. There is
also no agreement as to the efficacy of hospitalisation, ocular occlusion,
patching of the traumatised eye, cyclopegics, topical corticosteroids, and
antifribrinolytic agents.
Accepted practice is reduced activity, bed rest for 72 hours and topical
steroids.

Injuries to the lens

History
Trauma is the most common cause of dislocation of the ocular lens. Other
causes include congenital dislocation, systemic syndrome (e.g. Marfan,
homocystinuria), inflammation, and congenital glaucoma with buphthalmos.3,4,9
Treatment
A non-cataractous, dislocated lens may be stable and asymptomatic for
years. Children and their families, however, should be forewarned of the
symptoms of pupillary block glaucoma and be advised to wear eye protection
for sports and hazardous labour.9
Surgical considerations for removal of a dislocated lens include
pupillary block glaucoma, corneal touch, inflammation, and decreased vision
uncorrected by other means.9,10

Traumatic retrobulbar haemorrhage

History
• Significant sharp or blunt trauma to the globe/
peri-orbital region.2
• A markedly swollen red eye, painful, decreased vision.
Examination
• Proptosis, eyelid and peri-orbital ecchymosis.
• Diffuse and massive subconjunctival haemorrhage and chemosis. The
posterior border of the subconjunctival blood cannot be visualised.
• The pupils and extra-ocular motility are evaluated carefully. The
presence or development of a relative afferent pupillary defect may
 indicate optic nerve injury caused by compression or a traumatic optic
neuropathy.
• Markedly elevated intra-ocular pressure; significant resistance on
repulsion of the globe can be found and the peri-ocular area is tense.
• Extra-ocular movements may be limited.
• Intracranial penetration should be suspected in cases in which
retrobulbar haemorrhage resulted from a penetrating injury.
Differential diagnosis 2

• Orbital cellulitis, which often can be ruled out by the patient’s

history.
• Orbital fracture.
• Carotid-cavernous fistula, which is possible after severe head trauma.
• CT scan may be useful (if available).
Treatment
For suspected retrobulbar haemorrhage, patients should be referred to an
ophthalmologist urgently. Emergency lateral canthotomy and inferior
cantholysis can be performed by those who are experience in this procedure.

Scleral laceration or rupture

History
• Usually, sharp objects or missiles (e.g. metal-on-metal projectile
injury, broken glass, knife wound, and bullet).
• Severe blunt trauma (e.g. from a fist, bottle, or club).
• Red eye, pain, decreased vision, and possible inadvertent lid closure
(blepharospasm).
Examination
• A defect is noted in the conjunctiva or sclera, with or without
subconjunctival haemorrhage.
• Marked haemorrhagic chemosis (swelling) may obscure the underlying
scleral injury.
• Uveal or vitreous prolapse occurs through the scleral wound, which may
appear as a brownish discolouration beneath the conjunctiva, sometimes
mistaken for blood.
• Pupil may be abnormally shaped (e.g. peaked).
• The intra-ocular pressure is low in most cases. Less commonly, the
intra-ocular pressure is normal or elevated.
• The anterior chamber (cornea to iris) depth may be increased making it
look ‘deep’.
Differential diagnosis1,2
• Conjunctival laceration without scleral injury.
• Intra-ocular foreign body.
• Clear or haemorrhagic chemosis without obvious scleral injury.
Treatment
• If globe rupture is suspected, the eye is shielded and the patient
immediately referred to an ophthalmologist. No patching is used. A
light pad may be necessary to absorb any discharge or bleeding.
• In cases of partial-thickness lacerations of the sclera, the patient
is refer to an ophthalmologist for evaluation and possible surgical
repair
 • In cases of suspected or confirmed full-thickness lacerations,
intravenous antibiotics are administered and the patient is immediately
referred for ophthalmological evaluation and surgical repair.
• The patient’s tetanus status should be updated.
Follow-up
The focus and frequency of follow-up vary depending on the extent of the
injury

Traumatic optic neuropathy

History
A history of traumatic injury to the globe or orbit (causing direct injury
of the optic nerve) or to the forehead or temporal region (causing indirect
injury of the optic nerve) is reported. Optic nerve injury manifests as a
reduction in visual acuity not explained by refractive error or injury to
the cornea, lens, or retina.
Visual acuity is decreased.
Examination
• Decreased visual acuity.
• Colour vision and red saturation are decreased and may be accompanied
by a visual field defect.
• The optic disc appears normal. If an atrophic disc is seen on
examination, a chronic process is ongoing or the nerve sustained injury
at least six weeks previously.1
• Disc haemorrhage and oedema may be seen.
• A new relative afferent pupillary defect in a traumatised eye suggests
the diagnosis (i.e. no retinal pathologic conditions or chiasmal
damage).1,6
Aetiology
• Injury to the optic nerve from a sharp injury or compression by
fragments of bone, foreign body, blood, or oedema can lead to traumatic
optic neuropathy.
• A shearing injury from blunt trauma has also been implicated.
Differential diagnosis1,2
• Optic chiasm injury.
• Optic nerve head avulsion.
Treatment
Once the diagnosis is suspected, the patient is immediately referred to an
ophthalmologist for complete assessment and management.
Follow-up
The prognosis depends on the mechanism of injury and degree of damage
sustained by the optic nerve. With a clinically evident relative afferent
pupillary defect, the optic nerve must have sustained a fairly severe
injury; therefore ultimate visual functioning may be poor.

Ocular burns
A burn may result from contact with heat, flame, chemicals, electricity or
radiation, with chemical and radiation being the most common causes of
burns to the eye.14
Management
The underlying basis of management of burn injuries is to preserve the
globe vision and to prevent and treat complications.16
The management is based on an understanding of the protective mechanisms
of the globe, the reaction of ocular tissues to injury and the healing
processes of various ocular tissues. These latter include the blink, Bell’s
phenomenon, the tears, protective bony structure of the orbit and shielding
of the eyes and face by the hands and arms.16

Alkali burns
Causes of alkali burns15
• Ammonia (NH3): fertilisers, refrigerants and cleaning agents
• Lye (Sodium hydroxide Na OH): drain cleaners
• Potassium hydroxide KOH (Caustic potash)
• Magnesium hydroxide Mg (OH2): sparklers, flares and fireworks
• Lime (calcium hydroxide): plasters, mortar, cement and whitewash
• Motor vehicle airbag injuries. (Note: a side product of the explosive
reaction, which produces inflation of the airbag, releases alkali,
which can burn the eyes, though eye injury in this case is usually
mechanical effect)
• Household cleaners, fertilisers, and refrigerants contain ammonia.
Plaster, cement, mortar and whitewash contain fresh lime. Sparkles and
flares contain magnesium hydroxide.
With alkali burn the corneal epithelium is rapidly and extensively lost.15,16
The epithelium is an effective barrier against microbial pathogens and its
loss deprives the cornea of one of its most effective barriers, defence
mechanisms and subsequently delays corneal stromal healing. The rapidity
with which alkali penetrates the cornea is reflected by the rapid rise in
pH in the aqueous. Ammonia causes the most severe form of alkali burn and
the rise in pH may occur within seconds.15 It usually returns to normal with
or without external irrigation within 30 minutes to three hours. The more
severe the burn, the deeper the injury and the greater likelihood of
ischaemic change. The corneal epithelium has a strong regenerative power;
the corneal re-epithelialisation is dependent upon the limbal stem cell
population, if this is severely damaged then poor recovery is likely with
chronic scarring and loss of vision.
Alkali also acts directly on collagen resulting in trabecular meshwork
distortion, therefore an early increase in intraocular pressure may result,
and while damage to the nerve endings may produce corneal anaesthesia.
Keratocytes may be completely obliterated, which further limits the
possibility of a good recovery as they are pluri-potential cells with the
unique ability to remodel damaged stroma.
In acute alkali injury there may also be damage to the corneal
endothelium, to the lens, the iris and the ciliary body. There maybe an
acute rise in intra-ocular pressure and, in extremely severe injury,
hypotony may result. Hypotony indicates very severe injury — the ciliary
body has been so badly involved that aqueous production has dropped — hence
also intra-ocular pressure.

Acid burns
Causes of acid burns15
• Sulphuric acid (H2SO4): car battery acid
 • Sulphurous acid (H2SO3): fruit and vegetable preservatives, bleach and
refrigerants
• Hydrofluoric acid (HF): penetrates easily into the corneal stroma due
to the presence of the fluoride ion
• Hydrochloric acid (HCL)
• Nitrous acid (HNO2)
• Acetic acid (CH3COOH)
• Fruit preservatives
• Glass-etching (HFI)
The description above of the response of alkali may apply equally to acid
burns.8,15,17 However, acid burnsare usually not as severe, since the
coagulation of proteins in the corneal epithelium and superficial stroma
caused by acid neutralises the acid and produces a barrier to deep
penetration.
Superficial complications — such as vascularisation and scarring of the
cornea — may occur, but corneal stromal thinning and sterile ulceration and
perforation, along with the intra-ocular complications, are much less
likely. The exception to this is an injury caused by hydrofluoric acid,
which penetrates the cornea rapidly because of the presence of the fluoride
ion. These injuries may be associated intra-ocular inflammation, including
corneal endothelial damage and cataract formation.

Thermal burns
The response of the bulbar tissues to thermal injuries varies. Generally
the instantaneous nature of the injury produces a burn that is limited to
the superficial layers. In flame injuries frequently the globe is spared.
In contact injuries, however, the severity may vary from superficial
epithelial loss to perforation, if a burning object remains in contact with
the eye wall and burns through it. Molten metal can collect in the fornix
and remain in contact with the globe for some time while it cools.

Chemical injury
History
• A history of chemical exposure.
• Severe pain, redness, blurred vision and eyelid spasm.
Examination
Signs vary depending on the severity of the injury and the time since the
chemical exposure.
In mild to moderate injuries1,17:
Initial signs include corneal epithelial loss, chemosis and conjunctival
hyperaemia, subconjunctival haemorrhage, intact episcleral and conjunctival
vessels, and mild peri-ocular skin involvement (first-degree burns).
Chronic signs include minimal corneal scarring.
In severe injuries1,17:
Initial signs include severe chemosis; corneal oedema and opacification;
loss of conjunctival and episcleral vessels, which causes a very white-
appearing sclera; severe peri-ocular skin involvement (second or third
degree burns); and a marked anterior chamber reaction, which may not be
visualised.
Chronic signs include: foreshortened fornices (loss of normal conjunctival
cul-de-sac) with symblepharon formation (conjunctival and globe adhesions);
severe eyelid abnormalities such as trichiasis (misdirected eyelashes),
entropion (lid turned in), and ectropion (lid turned out); severe tear film
abnormalities (loss of mucus producing cells in the conjunctiva); corneal
scarring and opacification and phthisis bulbi (shrunken, blind eye).
Treatment
As with other ocular injuries, the history guides the evaluation and
treatment.
The severity of the chemical injury is directly related to:
• The nature of the chemical
• Whether or not the chemical was diluted with volume
• The volume of chemical that entered the eye
• The speed at which first aid was given, both on site and in the
casualty department
In cases of severe exposure, initial treatment precedes the ocular
evaluation. Copious irrigation with at least two litres of normal saline
solution 0.9% over one hour is performed as an initial treatment in the
emergency room. Topical local anaesthetic is instilled initially and every
10 to 15 minutes to make this a much less painful procedure. Lid speculum
is used if significant orbicularis spasm is present.8,9
The clinician should sweep the conjunctival fornices with a moistened
cotton-tipped applicator to remove any retained foreign matter, especially
lime, which exists as particulate matter.
It is also essential to evert the upper and lower lids to ensure that no
retained chemical is present after sweeping the fornices.
In cases of less severe exposure or questionable history (e.g. the
patient reports getting a drop of cleaner in the eye but washing it out at
home), less copious irrigation with pH measurements is performed initially.
Irrigation continues until the conjunctival pH normalises (i.e. 7.3 to
7.6); the pH is checked with the pH section of a urinalysis strip or litmus
paper. Two to three normal readings should be obtained at five to 10 minute
intervals widely, and the eye should be reassessed.
The possibility of a ruptured globe is carefully assessed. Minimal
pressure is placed on the globe during lavage when this diagnosis is a
possibility or is indicated by the history (very rarely related to
chemical/burn injuries). Specific treatment actions are as follows:
• Cyclopegic agents (e.g. homatropine 5%) and mydriatic agents (e.g.
phenylephrine 2.5%) are instilled to dilate the pupil. Note: In severe
injury, some researchers discourage instillation of phenylephrine
because of the possibility of further vasoconstricting the conjunctival
vessels.1
• Topical antibiotic ointment is instilled and a pressure patch is
placed over the eye.
• Immediate referral to an ophthalmologist is needed once the initial
lavage is complete.
• Management of severe burns includes treatment of the intra-ocular
pressure problems, exposure, scarring, and tear film dysfunction;
therapy involves corticosteroid administration, ascorbate or citrate
supplementation (in cases of alkali burns only), and surgery (e.g.
conjunctival grafts, corneal transplants).
• The most important aspect of treatment of a chemical injury is the
speed and efficiency of the washing out procedure.
Follow-up
Patients are usually monitored daily for several days.
Prognosis
The prognosis mainly depends on the type of injury.
Even in the most severe alkaline injuries the primary care physician can
play a significant role in reducing the chronic sequelae. By instructing
the patient to irrigate at the place of injury (e.g. home, work) using a
sink, shower, or garden hose — rather than immediately summoning the
patient to the emergency room — the chronic sequelae can be reduced. As
stated, the prognosis is directly affected by the adequacy of the lavage
immediately after exposure.
Practice points
Sometimes what seems like a mild injury on the first day can develop into a
more serious condition later. Warn the patient of this and refer all
chemical injuries for thorough assessment.

Thermal injury
History
• A history of exposure to a hot object (e.g. curling iron, tobacco ash,
electrical arc, explosion).
• A red painful eye, tearing, a foreign body sensation, and decreased
vision.
Examination
• Burns of the eyelids and peri-ocular region.
• Corneal whitening indicates an epithelial or a stromal burn.
• Conjunctival chemosis and injection.
• Corneal epithelial defect is evident.
• Minimal anterior chamber reaction.
Differential diagnosis1
• Corneal abrasion or infection (especially if no history available).
• Ultraviolet injury (welder’s flash).
Treatment
• Associated alkaline injury should be ruled out or confirmed if the
thermal burn was caused by fireworks or flares (magnesium hydroxide).
• Double pad the worse eye for 24 hours with chloramphenicol ointment
and cyclopentolate drops, and prescribe chloramphenicol ointment four
times a day for the other eye and for the padded after this time.
• Analgesias (e.g. paracetamol, NSAIDS).
• Cold compresses are useful.
• In cases of deep burns of the cornea, patients should be referred
immediately to the ophthalmologist.
• Peri-ocular burns are treated with ophthalmic preparations. Skin
preparations may enter the eye and cause epithelial toxicity.
Follow-up
An ophthalmologist or oculoplastic surgeon is consulted if severe peri-
ocular injury accompanies the ocular injury. Cicatrisation (scarring) of
the eyelids from severe burns may lead to exposure and corneal scarring.
Practice points
Light induced burns to the eye: ‘flash burns’,‘arc eye’.1
 Patients exposed to the light of an arc-welding lamp may develop very
painful red watery eyes a few hours after exposure. Although the eyes are
very painful it is only the very front surface of the eye (the corneal
epithelium) which has been affected, and this will heal completely in two
to three days.

Conjunctivitis
The conjunctiva is a thin, transparent mucous membrane that lines the inner
surface of the lids and outer surface of the eye. Conjunctivitis,
inflammation of the conjunctivitis, is a common presenting problem to the
doctor and can be broadly classified into the three common causative
factors: viral; bacterial; or allergic conjunctivitis.
Conjunctivitis in young children is extremely important because the eye
defences are immature and a severe conjunctivitis with membrane formation
and bleeding may occur. Serious corneal disease and blindness may result.
Conjunctivitis in an infant less than one month old (ophthalmia neonatorum)
is a notifiable disease. Such babies must be referred to the
ophthalmologist. Venereal disease in the parents must be excluded.

Viral conjunctivitis
Viral conjunctivitis occurs in clusters or mini-epidemics (pink eye). Most
often it is caused by an adenovirus, a highly contagious organism with an
incubation period of four to 10 days. Other viral causes include coxsackie
and enterovirus, which also occur in epidemics.7,8,18,21
History
• Acute onset. Red eye, photophobia, watery discharge, gritty and
uncomfortable feeling.
• The second eye is usually involved three to seven days after the
first, and the symptoms are less severe in most cases.
• This type of conjunctivitis usually lasts longer than bacterial
conjunctivitis and may go on for many weeks.
• Photophobia and discomfort may be severe if the patient goes onto
develop discrete corneal lesions.
Examination
• Visual acuity is normal (when the patient is not looking through a
film of tears or discharge) Chemosis, watery discharge. In severe
cases, erythema and oedema are often found in the lids.
• A follicular response (lymphoid aggregation) in the conjunctiva is
evident in most cases.
• Pre-auricular adenopathy is common; patient may report tenderness in
this region. Bacterial conjunctivitis is almost never associated with
pre-auricular adenopathy, which can be a differentiating feature.
• Subepithelial infiltrates can develop in the cornea two to three weeks
after the acute infection. They result from the body’s immune response
to viral antigens and can cause decreased vision and photosensitivity.
Treatment
Just as there is no cure for a cold, there is no treatment one can give a
patient with a viral conjunctivitis. Treatment is symptomatic and includes
(i) cold compresses, (ii) artificial tears and (iii) topical
vasoconstrictors (such as phenylephrine 0.12%) (iv) topical Chloramphenicol
drops/ointment (to prevent secondary infection, and provide lubrication)
and (v) avoidance of bright light.18
Viral conjunctivitis is extremely contagious and strict hygienic
measures are important for both the patient and the doctor — for example,
washing of hands, sterilising of instruments and so on.
Patients are counselled that they (and especially their tears) are
infectious, so their handkerchiefs, towels, pillows etc. need to be kept
separately: if other members of the family use them they may contract the
virus.
Reassure the patient that their vision is unlikely to be affected, but
the condition, although self-limiting, can take as long as three to four
weeks to disappear.
Warn the patient that if their vision becomes blurred (even after they
clear tears/discharge away from their eye) they should return. This symptom
means that the infection may have spread to the cornea and the patient
should be referred within 24 hours.
Practice points
• In view of the chronic course of some cases the patient may return for
further treatment, but steroids must not be given without
ophthalmological supervision.
• Never pad a discharging eye.
• If possible clear away debris and mucus with sterile normal saline
solution before using medication.
• If there is no improvement after two days with antibacterial, review
diagnosis and consider taking swabs after a 24–hour period without
antibacterial.
• Viral conjunctivitis is infectious until redness and weeping resolves
(usually 10–12 days after onset). Patients should avoid touching their
eyes and sharing towels, and should wash hands before and after
instilling medications, e.g. lubricant drops.
• Appropriate cultures and susceptibilities should be considered if
clinically indicated.

Bacterial conjunctivitis
Incidence/prevalence
Currently there is no good evidence on the incidence or prevalence of
bacterial conjunctivitis.
In adults, bacterial conjunctivitis is less common than viral
conjunctivitis; although estimates vary widely (viral conjunctivitis has
been reported to account for 8–75% of acute conjunctivitis).21,22
Staphylococcus species are the most common bacterial pathogens, followed by
Streptococcus pneumoniae and Haemophilus influenzae.23
In children, bacterial conjunctivitis is more common than viral, and is
mainly caused by H. influenzae, S. pneumoniae, and Moraxella catarrhalis.24
History
• Red eye, irritation, purulent discharge, adhesion of the lids
(especially in the morning).
• There may be a history of contact with a person with similar symptoms.
Examination
• Normal visual acuity.
• A mucopurulent discharge is found in the fornix and on the lid margin
associated with conjunctival papillae.
 • In cases of diffuse conjunctivitis, erythema and oedema of the lids is
sometimes observed
• N. gonorrhoea and N. meningitidis cause a ‘hyperacute’ conjunctivitis
characterised by an exuberant mucopurulent discharge.7,36 Because the
organism can rapidly invade the cornea, causing tissue destruction and
ocular perforation, infection with Neisseria species results in a
potentially serious form of conjunctivitis.7,36
Treatment
The aim is to achieve rapid cure of inflammation and to prevent
complications, with minimum adverse effects of treatment. Chloramphenicol
eye drops should be instilled hourly for 24 hours, decreasing to four times
a day, and chloramphenicol ointment applied each night for a week to hasten
recovery.25
Practice points
Swabs for microscopy, Gram’s stain and culture are performed in any cases
suggestive of conjunctivitis caused by Neisseria species.
Most case do not require extensive investigation because broad spectrum
antibiotics eradicate the infection and conjunctival swabs are only
necessary in cases where significant improvement does not occur within
three to four days of treatment.
Gonococcal or chlamydial conjunctivitis (see below) should be considered
in patients who do not respond to treatment, and should be referred to an
ophthalmologist for investigation

Gonococcal conjunctivitis
Gonococcal conjunctivitis is seen both sporadically and in epidemics in
Central and Northern Australia.36 The rare sporadic cases outside these
areas should be treated in consultation with an ophthalmologist. Patient
requires both topical and systemic antibiotic treatment.36
Treatment35,36
For sporadic cases, three days of therapy is adequate. Procaine penicillin
(child: 50 mg/kg up to) 1.5 g intramuscularly daily for three days. or
Amoxycillin (child: 75 mg/kg/day) for children or 3 g plus probenecid 1 g
for adults for three days.
In the epidemics, all household and classroom contacts should be treated
and single dose therapy of above regimen has been adequate to date.

Gonococcal ophthalmia in neonates

This is highly contagious and may rapidly lead to blindness. Patient should
be admitted for both topical and systemic antibiotic treatment.36
Cefotaxime 50 mg/kg intravenously, eight hourly or Ceftriaxone 50 mg/kg
intravenously, daily for seven days.
In areas where the prevalence of penicillin-resistant N. gonorrhoea is
low, or where the organism from the neonate or mother is known to be
penicillin-susceptible, use29 Benzylpenicillin 15 mg/kg intravenously, 12
hourly during the first week of life, and 7.5 mg/kg six hourly, thereafter,
for a total of seven days.
Co-infection with Chlamydia trachomatis and N. gonorrhoea is common in
some areas. Thus treatment of C. trachomatis conjunctivitis should be used
in addition to the beta-lactam antibiotic.
Prognosis
Most bacterial conjunctivitis is self-limiting. One systemic review of
randomised controlled trials reported clinical cure or significant
improvement on placebo within two to five days in 64% of people (99% CI 54%
to 73%).25
Some organisms cause corneal or systemic complications, or both; otitis
may develop in 25% of children with H. influenzae conjunctivitis, and
systemic meningitis may complicate primary meningococcal conjunctivitis in
18% of people.26
Conjunctivitis in children is more likely to be bacterial than viral,
warranting heightened awareness of possible systemic complications.

Adult chlamydia conjunctivitis

History
• Acute or subacute onset. Patients are usually young with a history of
chronic bilateral conjunctivitis with a mucopurulent discharge.
• There may be associated symptoms of venereal disease.
Aetiology
Ocular inoculation usually results from chlamydial infection of the
genitalia.
Examination
• Unilateral or bilateral.
• Diffuse conjunctival injection with a scant mucopurulent discharge and
many lymphoid aggregates in the conjunctivitis (follicles). The cornea
is usually inflamed (keratitis) and an infiltrate of the upper cornea
(pannus) may be seen. Pre-auricular adenopathy are sometimes seen.
Investigations
Conjunctival swabs for antigen detection, polymerase chain reaction or
ligase chain reaction test, or culture should ideally confirm the
diagnosis, as successful treatment requires systemic therapy. There is no
evidence that additional topical therapy provides any benefit.
For neonates (inclusion conjunctivitis) and children under 6 kg, use
erythromycin 10 mg/kg orally, six-hourly for 21 days.
For adults and children over 6 kg, use azithromycin (child 20 mg/kg up
to) 1 g orally, as a single dose.27
In areas where trachoma is prevalent, the treatment of all household
contacts is recommended. When the prevalence of trachoma in the community
is above 20%, a community-based treatment program should be considered
where practicable.36

Allergic conjunctivitis
History
The prevalent symptom is intense itching.19 Almost always bilateral. Usually
associated with a history of exposure to: pollen (hay fever), medication
(topical eye preparation), insect bites, chemicals (e.g. make-up). There
may be a family history of atopy. Similar symptoms may have occurred at the
same time in previous years.
Examination
• Conjunctival injection and chemosis. The discharge is clear and
stringy.
• Because of the fibrous septa that tether the eyelid (tarsal)
conjunctivae, oedema, results in round swellings (papillae). When these
are large they are referred to as cobblestones.
Treatment
For treatment of acute allergic conjunctivitis, the patient should be
instructed to go home and lie down, with their eyes closed, and covered
with a cold flannel for comfort.
The swelling of the conjunctiva settles spontaneously over a few hours,
and requires no treatment.7 Reassure the patient and his/her parents that
this is an acute allergic response and that the patient should avoid the
causative factor from now on if identified.
Hay fever can affect the eyes badly and unfortunately antihistamine
tablets seldom help. Topical sodium cromoglycate ‘Opticrom’ and the more
recently introduced Iodoxamide ‘Alomide’ drops used four times a day for
many weeks are very effective.2,7 These take two weeks to modify the mast
cell population so must be used regularly for some time for maximum
benefit.
Systemic allergy evaluation is performed with consideration of
desensitisation treatment and removal of allergens from the patient’s
environment.
Systemic antihistamines are administered in severe cases. Several
topical preparations may be useful such as: topical
vasoconstrictor/antihistamine combinations, topical antihistamines, mast
cell stabilisers, topical NSAIDS.
If these treatments fail, patients should be referred to an
ophthalmologist for further treatment for consideration of topical
corticosteroid.

Corneal ulcers
Examination
• A white corneal opacity. Most corneal ulcers are easily visible with
the naked eye, have many causes and can be situated anywhere on the
cornea.
• A corneal ulcer is likely to be infected and the infection can spread
inside the eye. Assume a corneal ulcer is infected until proven
otherwise.1,2
Treatment
Corneal ulcers always need referral, even if they are very small.1,2,6,7

Cellulitis (pre-septal or post-septal)

Pre-septal cellulitis is the less serious of the two, and involves the
eyelids. Orbital cellulitis is the more severe condition that affects the
contents of the orbit. Orbital cellulitis is a medical and ophthalmic
emergency, as the infection can spread to the brain and the situation can
become life threatening in a matter of hours.1

Pre-septal cellulitis
History
Warm, red, tender swelling of the lids may extend over the nasal bridge to
the opposite side. This may be associated with a stye, traumatic or
surgical lacerations.
Examination
• Usually a low-grade fever and elevated white blood cell count.
 • The eye is usually white or may be red if there is a bacterial
conjunctivitis secondary to an underlying cause, e.g. discharging eye.
• Normal visual acuity.
• There is neither proptosis, i.e. the eyeball is not pushed forward,
red desaturation or RAPD.
• Blood cultures are usually negative unless the organism is Haemophilus
influenzae or Streptococcus pneumoniae.
Aetiology
• Upper respiratory tract infection or sinusitis (commonly arises from
infection in ethmoid sinuses). The most common causative organisms in
adults are Streptococcus species, Staphylococcus aureus, and mixed
flora.
• Lid trauma (blunt or perforating). The most common causative organisms
are Streptococcus pyogenes, S. aureus and fungus (if organic material
was involved).
• Superficial lid infections such as a stye (hordoleum) or impetigo.
• Conjunctivitis.
• Dacryocystitis.
• Surgical procedures that violate the orbital septum — such as
strabismus, retinal detachment repair, and orbital surgery — can lead
to the disorder.
Differential diagnosis 1

Orbital cellulitis, orbital pseudotumous, carotid-cavernous fistula.

Investigation: FBC, swabs of an open wound, purulent nasal drainage,
conjunctival discharge, or any weeping vesicles for microscopy, culture and
sensitivity. Computer tomography of orbits and sinuses if indicated. Blood
cultures are performed if H. influenzae or S. pneumoniae is suspected.
Treatment36
Refer to hospital for admission if systemically unwell.
Children under five years: For the severely ill child, give cefotaxime
50 mg/kg up to 2 g intravenously, eight-hourly, or ceftriaxone 50 mg/kg up
to 2 g intravenously, daily, until clinically improved, followed by
amoxycillin/clavulanate 15 mg/kg up to 500 mg orally, eight-hourly to
complete a total treatment period of one week.
When associated with local lesions such as styes, dacrocystitis or
impetigo that suggest staphylococcal or streptococcal infection,
di(flu)cloxacillin should be added to the regimen above.
Adults and older children: di(flu)cloxacillin 500 mg (children 12.5
mg/kg up to 500 mg) orally, six-hourly. In severe, use di(flu)cloxacillin 2
g (children: 50 mg/kg up to 2 g) intravenously, six-hourly.
Follow-up
The focus of follow-up is to ensure that orbital cellulitis does not
develop. Warn the patient that if their symptoms increase, they should
return for further examination. The patient does not need referral unless
the diagnosis is in doubt or the condition deteriorates.

Orbital cellulitis
History
Symptoms are the same as those for preseptal cellulitis. But the patient is
in severe pain, is feverish and systemically unwell and shows evidence of
orbital involvement.
Examination
• Low-grade fever. Both lids are red, swollen and tender, which can be
so severe that the patient cannot open their eyes.
• Normal visual acuity.
• Proptosis (when viewed from above the patient’s head, and (if
possible) with the eyelids pulled out of the way, the eyeball will be
seen to protrude further out of the socket when compared with other
eye).
• Conjunctival chemosis, sluggish pupillary reflex.
• Eye movements are restricted. Early restrictions of movement can be
difficult to detect but the patient will tell you that they see double.
This is a very important sign.
• The signs of severe disease are reduced visual acuity, red
desaturation, and presence of an RAPD indicating optic nerve
compression.
Investigations
• Same as that for cases of preseptal cellulitis.
• A fundoscopic examination may reveal retinal haemorrhages, venous
congestion, and disc oedema.
• A CT scan displays diffuse infiltration of orbital fat may progress to
abscess formation.
• Blood cultures are usually negative.
Differential diagnosis
Differential diagnoses are the same as those for preseptal cellulitis.
Treatment
• Urgent referral to ophthalmologist and intravenous antibiotics.
• Urgent surgical drainage of the sinuses or of an abscess may be
required, lest vision be lost.
Practice points
• The adequate examination of children presenting with orbital
cellulitis can be difficult. Therefore, have a high index of suspicion
and refer early.
• The possibility of orbital cellulitis should always be kept in mind,
especially in children, and patients should be referred immediately.

Acute red eye

Acute angle closure glaucoma
Acute glaucoma should always be considered in a patient over 50 (can occur
younger than 50, but rarely) with a painful red eye. The diagnosis must not
be missed or the eye will be permanently damaged.
History
• Acute onset, characteristically in the evening when the pupil becomes
semidilated. The patient may have had similar attacks in the pasts that
were relieved by going to sleep (the pupil constricts during sleep, so
relieving the attack).
• Intense ocular pain and photophobia.
• Blurred vision and halos are seen round light fixtures due to oedema
of the cornea.
• It can be associated with vasovagal symptoms such as diaphoresis,
nausea, and vomiting.
Examination
• A fixed and mid-dilated pupil.
• Lid oedema and conjunctival injection.
• Hazy cornea with fragmented light reflex.
• Vision is impaired according to the state of the cornea.
• On gentle palpation, the eye feels harder than the other eye.
• The anterior chamber seems shallower than usual, with the iris being
close to the cornea.
• If the patient is seen after the resolution of a reversible attack the
signs may have disappeared — hence the importance of the history.
Associated factors and diseases
• Women are affected three to four times more commonly than men.1
• The average age of presentation is 60 and increases thereafter.1
• Shorter, smaller, far-sighted eyes with narrow chamber angles.1
• Stress, a darkened room, and drugs that can dilate the pupil may
precipitate an acute angle-closure attack.1 Many systemic medications
with anticholinergic or sympathomimetic action carry a warning against
use in persons with glaucoma. This applies to patients with a narrow
chamber angle only, not to patients with open-angle glaucoma. Because
most glaucoma cases are open-angle, these medications are rarely
contraindicated in medical practice.
• Two studies have shown that the incidence of mydriasis-induced acute
angle glaucoma is only approximately 0.02%.32,33 [Editor: This is ~2 in
10 000, so don’t let this put you off using mydriatic drops to examine
the fundus when needed.]
Treatment
• Acute angle-closure glaucoma is an ophthalmic emergency and requires
immediate referral to an ophthalmologist.
• Initial medical treatment to lower the IOP involves a topical B-
blocker (e.g. timolol 0.5% — 1 drop), carbonic anhydrase inhibitors
(e.g. Diamox 500 mg intravenously or 250 mg orally two times), and
osmotic agents if Diamox fails to reduce IOP (e.g., oral isosorbide 50–
100 g or intravenous mannitol 1–2 g/kg given over 45 minutes — 500 ml
of mannitol 20% contains 100 g of mannitol).1
• In most cases, laser iridotomy (creating a full thickness opening in
the peripheral iris) reopens at least a portion of the angle with
marked lowering of the IOP. This is the definite treatment of acute
angle-closure glaucoma, but cannot always be done in the acute stages.
Follow-up
• After an acute-angle closure event, a portion of the angle may remain
closed because of scarring of peripheral iris tissue to the cornea,
causing chronic angle-closure glaucoma.
• Chronic angle-closure glaucoma may also occur without any symptoms,
just like open-angle glaucoma. Treatment involves medications and
incisional surgery such as trabeculectomy.
• Laser iridotomy may be recommended for individuals with very narrow
angles who are at significant risk for the development of either acute
or chronic angle-closure glaucoma. Such patients are described as
having occludable drainage angle.
Acute iritis/uveitis
Acute iritis is usually idiopathic, but the commonest systemic association
is in patients who are HLA-B27 positive.34
History
• The patient who has had past attacks can often feel an attack coming
on before physical signs are present.
• Painful, photophobic, red eye with reduced vision.
Examination
• Reduced visual acuity.
• The diagnosis is made on the slit lamp, but the history obtainable
from the patient is often typical.
• Small and maybe irregular pupil (this is more likely if the patient
has suffered with recurrent attacks of iritis).
• Ciliary flush, anterior chamber flare (cells and proteinaceous
exudate), keratitic precipitates on the cornea or may settle to form a
collection of cells in the anterior chamber of the eye (hypopyon).
Treatment
The diagnosis is difficult without the use of a slit lamp and the patient
should be referred to an ophthalmologist.
Where the patient has had previous episodes and is confident as to the
similarities with this acute presentation, topical steroids (Prednefrin
Forte two hourly)30 and homatropine 2% three times daily can be commenced
while ophthalmic review is arranged.

Medications
There are a wide variety of topical ophthalmic preparations available as
diagnostic aid and rationale treatment for many eye diseases. Drugs
administered topically act either within the eye or on its surface.
Blinking distributes and eliminates drugs dissolved in tears. As tears
containing the drug pass through the lacrimal drainage system and into the
nasopharynx, it may be absorbed through the mucosa into the systemic
circulation (without first having to pass through the liver) and lead to
systemic side effects.31,35
Choice of preparation is limited by the range of products available.
Adverse effects due to nasal drainage and systemic absorption are more
common with eye drops than with ointments.35
Ointments are appropriate to use at night, in children, and when action
depends on sustained concentrations of drug, e.g. antivirals. Drug action
is prolonged by decreasing drug dilution and drainage. Ointments are often
difficult to self-administer, blur vision may cause contact dermatitis.

Diagnostic medications
Topical fluorescein35
Fluorescent stains the cornea at epithelial defects (orange when
concentrated, bright green when diluted) taken up by devitalised tissue.
Indications
It is used to diagnose corneal abrasions and ulcers, fit rigid gas
permeable contact lenses, test patency of lacrimal passage (Jones tests),
detect aqueous leak and for applanation tonometry.
Dosage
Eye drop, 1 drop (0.25% ideal for applanation tonometry).
Paper strips, moisten tip with a drop of either sterile 0.9% normal
saline solution or topical anaesthetic; avoid abrading the cornea.
Specific considerations
It is safe to use in pregnancy and lactation.
Patient counselling
Fluorescein stings initially, and can cause temporary yellow staining of
skin, urine, nasal secretions and tears. It can permanently stain soft
contact lenses and clothes (comes out with soap and water but is
unresponsive to dry cleaning).

Rose Bengal 35

Stains nuclei of corneal and conjunctival epithelial cells at defects in

the precorneal tear film (where mucus layer is deficient); also stains
‘sick ‘ cells (supravital stain) and abnormal mucin.
Indications
It is used to demonstrate superficial corneal and conjunctival tissue
changes, especially herpes simplex epithelial disease, Sjogren’s syndrome
and keratoconjunctivitis sicca.
Dry eye syndrome: rose Bengal causes intense stinging; use topical
anaesthetic first or instil only a fraction of a drop.
Dosage
Eye drops, 1 drop.
Specific considerations
It is safe to use in pregnancy and lactation.
Patient counselling
Rose Bengal stings initially (stings more than fluorescein) and can cause
temporary red staining of skin, urine, nasal secretions and tears. It
permanently stains soft contact lenses and clothes.

Ocular local anaesthetics35: Amethocaine, lignocaine, oxybuprocaine and

propavacaine
Indications
They block nerve conduction reversibly and provide short-term ocular
surface anaesthesia.
Specific considerations
Prolonged use impairs corneal epithelial healing, prevents reflex ocular
protection and masks progression of keratopathy; use only for short
procedures (<20 minutes).
Corneal scrapings: use preservative-free drops (preservative may affect
microbiological culture).
Adverse effects
Common: stinging on instillation, punctate epithelial epithelial damage of
cornea (do not use long term because of epithelial toxicity, i.e. acute
corneal ulceration).
Rare: allergy.
Dosage
1 drop, repeated in five minutes if necessary; maximum five doses.
Specific considerations
It is safe to use in lactation. However, for pregnancy lignocaine is
classified as Australian Drug Evaluation Committee (ADEC) A and others not
categorised.
Patient counselling
Warn patients (especially children) about the initial stinging.
Close eyes after instillation and dab away tears without rubbing eyes.
Practice points
• Never prescribe for home use; anaesthetics are toxic to epithelial
cells and thus will delay or prevent wound healing.
• Topical anaesthetics increase corneal permeability and intra-ocular
bio-availability of other topical drugs; they also reduce the initial
stinging of other topical drugs and should be instilled first.
• Single-use drops are useful if infection is suspected.

Table 2: Comparison of ocular local anaesthetics35

Drug Amethocaine Oxybuprocaine Propavacaine Lignocaine

Duration 20 10–20 10–20 20–30
(minutes)
Duration 20 10–20 10–20 20–30
(minutes)
Sting 30 10 10 30
(seconds)
Punctate +++ ++ ++ +
epithelial
damage

Mydriatics and cycloplegics1,35

Mydriatic and cycloplegic agents can be used for diagnostic and therapeutic
purposes. Mydriatics dilate the pupil, and cyclopegic agents paralyse the
ciliary muscle. Dilating the pupil is necessary for adequate examination of
the internal ocular structures.
Therapeutic benefits are numerous: paralysing the ciliary muscle reduces
pain associated with traumatic iritis, prevents posterior synechiae
formation (adhesion between the iris and lens), and stabilise the blood
ocular barrier during bouts of intra-ocular inflammation.
Topical anticholinergics are the main drugs used for both mydriasis and
cycloplegia. Phenylephrine (a sympathomimetic) is used to supplement
anticholinergic mydriasis.
Diagnostic use
• Adult, 1 drop tropicamide 0.5% or 15, repeated in five minutes (add
phenylephrine 2.5% if dilation is inadequate).
• Child one to 12 years, 1 drop proxymetacaine followed by 1 drop
cyclopentolate 1%, repeated in five minutes.
• Infants under one year, 1 drop of proxymetacaine followed by 1 drop
cyclopentolate 0.5%.
• Preterm infant (<32 weeks), 1 drop proxymetacaine followed by 1 drop
cyclopentolate 0.1%.
• Examine after 20 minutes (30 minutes for darkly pigmented eyes and for
cycloplegic refraction).
Therapeutic
Iridocyclitis, 1 drop homatropine 5% every four to six hours, or 1 drop
atropine 1% three to four times daily (phenylephrine 10% three times daily
is occasionally used as an adjuvant).
Postoperative, 1 drop atropine 1% three to four times daily.
Patient counselling
To reduce initial stinging, shut eyes and avoid rubbing eyes after
instillation. Enlarged pupils result in blurred vision and glare from
bright light (suggest dark glasses). It is generally inadvisable to drive
while vision is disturbed (approximately the duration of action). Report
back if eye becomes painful or red, or vision deteriorates.
Practice points
• Do not use after head injury or if anterior chamber angle is narrow.
• Reversal of mydriasis with a cholinergic agent (pilocarpine) is not
recommended and can precipitate an angle-closure attack in susceptible
patients.

Anticholinergic
Atropine, cyclopentolate, homatropine, tropicamide35
They act by reversibly blocking acetylcholine receptors on iris sphincter
and ciliary muscle.

Contra-indications
Iris clip intra-ocular lens implant.
Specific considerations: Coexisting conditions
Significant head injury: uses only short-acting agents, and with care;
consult patient’s neurosurgeon or intensivist. Always make a note that
pupils were dilated intentionally.
Narrow anterior chamber angle: mydriasis may rarely precipitate acute
closed angle glaucoma.
Previously treated acute closed angle glaucoma: should be dilated under
specialist supervision as not all laser iridotomies remain functional.
Lenticular subluxation: small risk of anterior lens displacement.
Children
Use with extreme caution if at all in neonates, preterm infants and
children with spastic paralysis or brain damage, as they have increased
susceptibility to systemic reactions. One drop of 0.5% atropine can cause
systemic reactions in infants. In young children, long-term cycloplegia may
induce amblyopia.
Adverse effects
Common: sting (especially 1% cyclopentolate), intolerance to bright light
(glare) blurred vision (especially near vision), transient intra-ocular
pressure elevation (especially in ocular hypertensives).
Infrequent: contact allergic blepharitis (atropine), persistent ocular
irritation (mucus discharge, severe watering discharge, superficial
punctate keratopathy and characteristically no itch), punctal stenosis with
prolonged use (years), insomnia, drowsiness (cyclopentolate).
Rare: systemic toxicity, e.g. dryness of skin and mouth, fever, facial
flushing, tachycardia, irritability, disorientation, ataxia, visual
hallucinations, incoherent speech, delirium, psychosis, seizures,
hyperactivity in children.
Special considerations
It is safe to use in pregnancy and lactation.

Table 3: Comparison of Ocular Anticholinergics35

Drug Effect Peak effect Duration Systemic side

effects
Atropine 1% Mydriasis 30–40 mins 7–10days +++
cycloplegia 3–6 hours 7–14 days
Cyclopentolate Mydriasis 30–60 mins 1 day ++
0.5–1% cycloplegia 25–75 mins 6–24 hours
homatropine Mydriasis 20–30 mins 6 hours–4 +
2% cycloplegia 30–90 mins days
10 hours–2
days
tropicamide Mydriasis 20–40 mins 6 hours rare
0.5–1% cycloplegia 30–40 mins 2–6 hours

Sympathomimetics
Phenylephrine
It is a relatively selective alpha 1 agonist; stimulates pupil dilator
muscle. Maximal mydriasis occurs after 60–90 minutes; duration of action is
five to seven hours. It does not affect accommodation.
Specific considerations
Caution: With recent myocardial infarction or unstable angina. Blood
pressure elevation can occur with repeated doses of 10% drops.
Elderly: Increased risk of systemic adverse effects.
Children: Increased risk of systemic adverse effects, especially
hypertension and intraventricular bleeding in the first two to four weeks
of life in preterm infants. Do not use 10% drops in preterm infants.

Drug interactions
MAOIs (antidepressants): hypertensive crisis may result; avoid use while
taking phenelzine or tranycypromide, and for 14 days after ceasing MAOI.
Methyldopa, alpha antagonist hypertension may occur; avoid combination.
Adverse effects
Common: rebound miosis, hyperaemia, stinging on instillation.
Infrequent: liberation of iris pigment (probably has no deleterious
effects).
Rare: systemic effects (most frequently with 10% drops), e.g. hypertension,
tachycardia, tremor, anxiety.
Dosage
Generally used as an adjunct.
Mydriasis: 2.5%, 1 drop once only as adjunct if mydriasis difficult, 10%, 1
drop once only as adjunct for rapid maximal mydriasis.
Uveitis: 10%, 1 drop three times daily as adjunct to mydriatic if trying to
release posterior synechiae.
Episcleritis: diagnosis (vasoconstriction test) 2.5% 1 drop once only;
episcleral vessels should blanch after five minutes.
Dilating drops are contraindicated in patients with known angle-closure
glaucoma. Dilating drops may be less effective in patients with dark irides
or intra-ocular inflammation. Administration of dilating drops to premature
infants or children with cardiac disease or hypertension is high risk.
These agents should be used cautiously in these patients.
Special considerations
It is not recommended to be used in pregnancy as theoretically it can
induce placental vasoconstriction and fetal hypoxia. It is safe to use in
lactation.
Practice points
Can reduce systemic absorption of the drug by pressing on the tear duct and
closing eyes for three minutes after instilling drops

Antibacterial agents
Bacterial conjunctivitis35
Acute bacterial conjunctivitis is frequently a self-limiting condition,
lasts for two to three days.25
Antibacterial is used to hasten recovery, prevent complications and
limit the spread of infection to other people.
Drug choice
There are few comparative randomised controlled studies that compare
antibiotics, and none have found a significant difference in rates of
clinical or microbiological cure.
Aminoglycosides are active against gram-negative bacteria. Framysetin
and especially, neomycin are associated with contact allergic reactions.
Framycetin and, especially, neomycin are associated with contact allergic
reactions. Gentamicin and tobramycin are more expensive, are active against
Pseudomonas, and are indicated for neonatal gram-negative conjunctivitis.
Neomycin-polymycin combination is inexpensive and broad spectrum, but
can cause contact allergy.
Sulfacetamide is irritant, avoid use.
Antiseptics (e.g. aminacrine, Aminopt) are ineffective, even for mild
conjunctivitis.

Chloramphenicol
Chloramphenicol (chlorsig ointment, eyedrops) is the most common antibiotic
used. It is bacteriostatic against Staphylococcus aureus and
Enterobacteriaceae by inhibiting the protein synthesis at the ribosomal
level.37 It is bactericidal against Haemophilus influenzae, penicillin-
susceptible Streptococcus pneumoniae, and Neisseria meningitidis, but not
group B streptococci.37
It is a broad spectrum antibiotic active against many gram-positive,
gram-negative (except Pseudomonas species), and anaerobic bacteria,
rickettsiae, chlamydiae and mycoplasma.37
It has good ocular penetration and is safe in pregnancy and not
expensive.
Contra-indications
Allergy to chloramphenicol.
Rare: allergic reactions, e.g. angioedema, anaphylaxis, contact dermatitis,
dermatitis (often moderately severe).
Adverse effects
Local stinging, burning and unpleasant taste.35 Topical chloramphenicol may
very rarely cause aplastic anaemia as an idiosyncratic reaction resulting
from systemic absorption.38 There has been much debate about the association
but it remains tenuous.
Dosage35
Bacterial blepharitis: Massage ointment into lid margin two to three times
daily. Blepharitis can often be managed with diluted baby shampoo used to
wash the lid margins.
Bacterial conjunctivitis: 1 drop every two to four hours for two days;
then if there is improvement, 1 drop four times daily for five days.
Ointment may be used as an adjunct to drops at night, or as a single
agent three times daily, e.g. in children.
Prevention of infection (after superficial trauma or surgery): 1 drop
four times a day until epithelium healed (rarely more than four days).

Ceftriaxone
It is a broad-spectrum cephalosporin. It is a popular agent due to its
broad spectrum and its long half-life, allowing for once-daily dosing in
non-central nervous system infections.
In ophthalmology, it is used as empirical treatment of orbital
cellulitis and penetrating eye injuries.
Adverse effects39
It can cause dose-dependent asymptomatic and reversible biliary sludge
formation (pseudolithiasis), especially in children. This has been mistaken
for gallstones on ultrasound scans and usually resolves after ceasing
treatment. Pancreatitis and cholecystitis have also been reported.
Associated symptoms may include nausea, epigastric distress, vomiting and
right upper quadrant abdominal pain.
Dosage36,37
Adult: 1 g IM/IV daily, maximun 4 g IV daily. Child: 50 mg/kg IM/IV as a
single daily dose or divided dose 12-hourly.
Specific considerations37
Neonates and preterm infants: Ceftriaxone is not advisable as it binds to
serum proteins and displaces bilirubin from albumin and this may increase
risk of bilirubin encephalopathy. Therefore, cefotaxime is preferred in
neonates and preterm infants.

Antivirals
Viruses are obligate intracellular pathogens that use the host’s metabolic
processes for their survival and replication. Antiviral agents are designed
to target the pathogen while leaving uninfected host cells essentially
unaffected from their toxic side effects. To date, the most effective
antiviral agents target viral enzymes and proteins that are essential for
viral assembly.
 Topical antivirals are indicated for treatment of herpes simplex
keratitis and herpes zoster ophthalmicus with corneal involvement.
Antivirals improve cure rates and reduce recurrences versus placebo. There
is no good evidence of differences between topical antiviral agents.41

Aciclovir35
Aciclovir is the common antiviral agent used.
Adverse effects
Common: mild transient stinging sensation.
Infrequent: superficial punctate keratitis, allergic reactions.
Dosage
Apply about 1 cm of ointment into the lower conjunctival sac, five times
daily for 14 days or for three days after corneal epithelium healed,
whichever is shorter.
There is conflicting evidence about the role of debridement before
application of topical antivirals.40,42
Specific considerations
It is safe to use in pregnancy (ADEC category B3) and lactation.
Practice points
• Herpes simplex keratitis is best managed by an ophthalmologist.
Treatment usually requires topical steroid to suppress inflammation and
topical antiviral to prevent viral replication. Therapy may be
prolonged.
• For frequently recurring herpes simplex epithelial keratitis, advise
patients to keep a spare tube of ointment and start treatment at the
first sign of recurrence.

Drugs for allergic and

inflammatory conditions
Allergic conjunctivitis
There are two main types, seasonal (hay fever) and perennial. Drug
treatment is aimed at symptom control.19,35
Treatment regimens35
Identify triggers (e.g. pollens, house dust mites, cosmetics, ophthalmic
drugs, contact lenses and solutions); avoid where possible.
Mild symptoms: irrigate with normal saline solution twice daily, use
artificial tears four to eight times daily, and cold water compresses as
required.
Moderate symptoms: use topical drugs, e.g. ketorolac, levocarbastine.
Topical decongestant-antihistamine combinations are not recommended in the
long term due to rebound conjunctivitis.
Severe symptoms: ophthalmology referral; topical corticosteroids may be
required.
Recurrent disease: use topical mast cell stabiliser as a preventative.
Factors influencing drug selection
• Response to cromoglycate may be delayed.
• Topical levocabastine and NSAIDs are expensive.
• Consider potential for adverse effects (e.g. raised intra-ocular
pressure with corticosteroids).
Excessive mucus35
• Decongestants include naphazoline, phenyl ephrine, tetrahydrozolinea
and xylometazoline.
• Antihistamines combined with decongestants in eye preparations include
antazoline and pheniramine.
Mode of action
Alpha-adrenoreceptor agonists constrict conjunctival blood vessels,
reducing ocular redness and discomfort.
Contra-indications
Narrow anterior chamber angle.
Drug interactions
Monoamine oxidase inhibitors (MOIs): wait 14 days after ceasing MOAI before
using decongestants; risk of hypertensive crisis.
Adverse effects
Common: rebound hyperaemia, stinging on instillation.
Others: mild mydriasis, blurred vision, epithelial erosion, narrowing of
the tear duct, acute and chronic conjunctivitis with prolonged use
(months), corneal and conjunctival pigment deposition with prolonged use
(years).
Comparative information
All decongestants have similar efficacy, adverse reactions and cost.
Dosage
Phenylephrine, 1–2 drops every three to four hours as required. Others, 1–2
drops every six to 12 hours as required.
Special considerations: It is safe to use in pregnancy and lactation.
Patient counselling
Although advertised as being useful for relieving eye redness due to minor
irritations (such as dust, smoke and contact lens wear), a cool compress is
beneficial and is safer.
Seek medical attention if symptoms do not improve within 48 hours.
Do not use continuously for more than five days.
Practice points
Decongestant eye drops, used widely in non-prescription products, are not
recommended, as their benefit is doubtful and rebound hyperaemia leads to
overuse.

Levocabastine35
It is a selective H1 antagonist.
Adverse effects
Stinging, mild ocular irritation, headache
Dosage
Adult and child more than six years, 1 drop twice daily, increasing to
three to four times daily if necessary.
Specific considerations
It should be avoided in pregnancy as there is no human data available (ADEC
B3) and can be use in lactation if needed

Mast cell stabilisers35

Cromoglycate, lodoxamide35
They act by inhibiting mast cell degranulation by unknown mechanism.

Adverse effects
Generally well tolerated, stinging on instillation.
Comparative information
Cromoglycate may take three to six weeks to take effect; lodoxamide’s
effects occur more rapidly (one to two weeks).
Dosage
Cromoglycate: 1 drop four to six times daily; Lodoxamide: adults and
children over four years, 1 drop four times daily.
Special considerations
Cromoglaycate is safe to use in pregnancy and lactation, however there is
limited data on lodoxamide.
Patient counselling
These drugs can take four to six weeks to reach full effect.
Practice points
Mast cell stabilisers have delayed onset of action; trial for at least two
to four weeks before evaluating effect. For best results, start treatment
one month before the onset of the hay fever season, or give in combination
with a low potency topical steroid for the first month

Anti-inflammatory agents
Anti-inflammatory agents are used most frequently to suppress immunologic
mechanisms of all types, both externally and within the eye. Suppression of
severe external inflammation is necessary to prevent synechiae (scarring),
some forms of glaucoma, and postoperative inflammation. Topical
administration allows excellent penetration into the anterior chamber. Some
agents penetrate easier than others depending on the chemical composition.
Topical corticosteroids should be used with caution because they can
cause cataracts and glaucoma and potentiate herpes simplex viral
replication.35

Non-steroidal anti-inflammatory agents (NSAIDs)35

NSAIDs inhibit cyclo-oxygenase, decreasing prostaglandin synthesis and
prostaglandin-mediated inflammation.
They are prescribed for 1) inhibition of miosis during cataract surgery
(diclofenac, flubiprofen), 2) allergic conjunctivitis (ketorolac) and 3)
prevention of inflammation after cataract surgery (diclofenac, ketorolac),
and can also be used as an alternative to steroids or as steroid-sparing
agents (e.g. episcleritis, allergic conjunctivitis, inhibition of
postoperative inflammation) and analgesia following photorefractive
surgery.
Contra-indications
Aspirin or NSAID induces anaphylactoid reactions (e.g. asthma, urticaria or
rhinitis).
Specific considerations
ADEC category C, although short-term low-dose use should not be a concern
in pregnancy. They are safe to be used in lactation.
Adverse effects
Commonly cause stinging on instillation and ocular irritation.
Practice points
These agents have an insignificant effect on intra-operative miosis (marked
indication) and are used more as an alternative or adjuvant to topical
steroids.
May mask symptoms of ocular infections.

Ketolorac35
Ketolorac is used for short-term (two to four weeks) treatment of seasonal
allergic conjunctivitis and prevention and reduction of inflammation after
cataract surgery.
Adverse effects
Common: local allergic reactions, superficial keratitis.
Rare: systemic allergic reactions.
Dosage
1 drop four times daily.
Practice points
Start drops 24 hours before cataract surgery then continue for two to four
weeks if needed.

Corticosteroids35
They act on intracellular receptor-mediated inhibition of inflammatory
cascade, fibroblast and keratocyte activity.
They are indicated for allergic and selected inflammatory conditions of
lids, conjunctiva, cornea, iris and ciliary body, including postoperative
inflammation.
Contra-indications
Ocular infection, especially herpes simplex epithelial keratitis and fungal
keratitis.
Adverse effects
Topical ocular steroids, alone or in combination with antibacterials,
should not be prescribed without close supervision by an ophthalmologist as
they have major, potentially vision-threatening, adverse effects.
Common: Ocular hypertension (usually reversible) proportional to dose,
potency, penetration and duration of treatment; retarded corneal healing,
rebound inflammation.
Infrequent: Opportunistic infection.
Rare: Refractive changes, ptosis, chemosis, lid swelling, exophthalmos
(slowly, incompletely reversible).
Cataracts: Posterior subcapsular cataracts may occur with long-term
(greater than one year) high-dose use; mostly asymptomatic and partially
reversible.
Dosage
Titrate to disease severity and treatment response. Usual: 1 drop (or
application of ointment) two to four times daily. Intensive: 1 drop every
hour.
Specific considerations
Contact lens wearers: risk of indiscriminate long-term use of steroids to
relieve ocular irritation.
Glaucoma: may be aggravated.
It is safe in pregnancy and lactation.
Practice points
Do not prescribe ocular corticosteroids for longer than two weeks without
supervision by an ophthalmologist unless facilities are available to
monitor corneal epithelium and intraocular pressure, and never without
first staining with fluorescein to exclude an ulcer of any sort.

Therapy of tear deficiency states

The tear film is a highly complex layer responsible for vision (the primary
ocular refractive surface) and ocular comfort. A large percentage of
patients have tear film abnormalities and experience symptoms related to
‘dry eyes.’ Tears contain mucous, lipid and aqueous components but the most
common cause of tear deficiency states is lack of the watery component.
Such conditions are mild in most cases and caused by senile atrophy of the
lacrimal gland, or by neural or humoral factors.19 Patients with ocular
surface abnormalities usually respond well to artificial lubricants,
although the symptomatic relief may be only temporary.19,35
Drug choice19,35
Use of ocular lubricants provides symptomatic relief. Patient preference
after an empirical trial usually determines final choice.
Topical drops should be given as frequently as is necessary to alleviate
symptoms. These may vary from two or four times daily to every hour
depending on severity of symptoms.
Preservative-containing: if drops are used infrequently, use an inexpensive
lubricant containing a preservative that prevents microbial contamination.
Preservative-free preparation: if drops are required more than four to six
times daily, unpreserved lubricants such as Polytears and Genteal should be
considered to avoid the ocular surface toxicity caused by preservatives. It
is non-irritant but more expensive and packaged in bulky single-dose
containers that are harder to use. Single-use vials can be used safely more
than once (if uncontaminated and kept refrigerated) but must be discarded
24 hours after opening. Ointments are also beneficial as nocturnal ocular
lubricants, the major difference between them being the inclusion of
lanolin in Lacri-lube. Practitioners should be aware that lanolin can act
as a sensitiser at the ocular surface and, if ocular inflammation is
increasing, it may be reduced by introduction of a lanolin-free ointment.
Lacrisert is a sustained-release lubricant designed to sit in the inferior
conjunctival recess and provide continuous tear film supplementation.
However, sufficient tears to dissolve the lubricant are required.
Eye ointments/gels
Used before bedtime if symptoms interrupt sleep or occur on awakening, and
may be used throughout the day if dry eye is severe. Some people have
incomplete lid closure at night and may benefit from having lids taped
closed overnight.
Specific considerations
It is safe to use in pregnancy and lactation.
Patient counselling
Lubricants can be used safely as often as possible.
Practice points
• Reduce evaporation by using cold water, humidifiers, avoiding air
conditioners that dry the air, and hair driers, and by wearing wrap-
around glasses or even swimming goggles.
• Patients often find a suitable lubricant by trial and error.
• Encourage regular use if required (e.g. hourly).
• Ocular delivery system is usually a last resort; it is difficult to
insert and often poorly tolerated.

References
1. Palay DA, Krachmer JH. Ophthalmology for the Primary Care Physician. Mosby-Year
Book, Inc. USA, 1997.
2. Okhravi N. Manual of Primary Eye Care. Torino, Italy: Reed educational and
Professional Pulishing Ltd, 1997.
3. Berson FG. Basic Ophthalmology for Medical Students and Primary Care Residents.
6th ed. United States of America: American Academy of Ophthalmology, 1987.
4. MacCumber MW. Management of Ocular Injuries and Emergencies. United States of
America: Lippincott-Raven Publishers, 1998.
5. Specialists Eye Health Guidelines for use in Aboriginal and Torres Strait
Islander populations. Office for Aboriginal and Torres Strait Islander Health,
Commenwealth Department of Health and Aged Care, 2001.
6. James B, Chew C, Bron A. Lecture Notes on Ophthalmology. 8th ed. United Kingdom:
Blackwell Science.Ltd, 1997.
7. Elkington Ar, Khaw PT. ABC of Eyes. Great Britain: British Medical Journal,
United Medical Journal, 1990.
8. Manolopoulas J. Emergency Primary Eye Care: Tips for diagnosis and acute
management. Australian Family Physician 2002; 31(3):233–7.
9. Catalano RA. Eye injuries and prevention. Pediatric Clinics of North America
1993; 40(4):827–39.
10. Cassen JH. Ocular Trauma. Hawaii Medical Journal 1997. 55:292–4.
11. Pavan-Langston D. Manual of ocular diagnosis and therapy. Boston, United States
of America: Little Brown, 1980.
12. Bartlett JD, Jannus SD, eds. Clinical ocular pharmacology 189. USA: Butterworth,
Stoneham.
13. Zuckerman BD, Lieberman TW. Corneal rust ring. Arch Ophthalmol 1960; 63:254–65.
14. White WL, Hollsten DA. Burns of the Ocular Adnexa 1994. 5:74–7.
15. Hammerton ME. Burns to the eye: an overview 1995; 24(8): 998–1003.
16. Hammerton ME. Management of Ocular Burns 1995; 24(8):1006–20.
17. Wagoner MD. Chemical Injuries of the Eye: Current Concepts in Pathophysiology and
Therapy. Survey of Ophthalmology 1997; 41(4):275–313
18. Coote MA. Sticky Eye, Tricky Diagnosis. Australian family Physician 2002;
31(3):225–231.
19. Hall AJ. Itchy Burning Eyes: Diagnosis and Management. Current Therapeutics 1999;
11:34–36.
20. Class’e JG. Anterior segment disease Update. Optometry Clinics. 1(4):59–70.
21. Wishart PK, James C, Wishart MS, Darougar S. Prevalence of acute conjunctivitis
caused by chlamydia, adenovitus, and herpes simplex virus in an ophthalmic casualty
department. Br J Ophthalmol 1984; 68:653–5.
22. Fitch CP, Rapoza PA, Owens S et al. Epidemiology and diagnosis of acute
conjunctivitis at an inner city hospital. Ophthalmology 1989; 96:1215–20.
23. Seal DV, Barrett SP, McGill JI. Aetiology and treatment of acute bacterial
infection of the external eye. Br J Ophthalmol 1982; 66:357–60.
24. Gigliotti F, Williams WT, Hayden FG, et al. Etiology of acute conjunctivitis in
children. J Paediatr 1981; 98:531–56.
25. Sheikh A, Hurwitz B, Cave J. Antibiotics for acute bacterial conjunctivitis. In:
The Cochrane Library, Issue 4. Oxford, 1999.
26. Bodor FF. Conjunctivitis-otitis media syndrome: more than meets the eye. Contemp
Pediatr 1989; 6:55–60.
27. Bowman RJC, Sillah A, Van Dehn C, et al. Operational comparison of single-dose
azithromycin and topical tetracycline for trachoma. Investig Ophthalmol Visu Sci
2000; 41:4074–9.
28. The WHO Western Pacific Region Gonococcal Antimicrobial Surveillance Programme.
Surveillance of antibiotic resistance in Neisseria gonorrhoeae in the WHO Western
Pacific Region,1999, Commun Dis Intell 2000; 24: 269–71.
29. Centers for Disease Control and Prevention. 1998 Guldelines for the treatment of
sexually transmitted diseases. Morb Mortal Wkly Rep 1998; 47(RR-1):60.
30. The Loteprednol Etabonate US uveitis Study Group. Controlled evaluation of
loteprednol etabonate and prednisolone acetate in the treatment of acute anterior
uveitis. Am J Ophthalmol 1999; 127:537–44.
31. McClellan K. Topical Eye Preparations. Current Therapeutics 1995, January; 61–6.
32. Wolfs Rc, Grobbee DE, Hofman A, de Jong PT. Risk of acute angle-closure glaucoma
after diagnostic mydriasis in nonselected subjects: the Rotterdam Study. Invest
Ophthalmol Vis Sci 1997; 38(12):2683–7.
33. Patel KH. et al. Incidence of acute Angle-Closure Glaucoma After Pharmacologic
Mydriasis. Am J of Ophtham 1995; 120:709–17.
34. Stawell RJ, Hall AJ. Eyes signs in Systemic Disease. Australian Family Physician
2002. 31(3):217–22.
35. Australian Medicines Handbook 2002. South Australia: Australian Medicine Handbook
Pty Ltd; 375–400.
36. Therapeutic guidelines: Antibiotic version 11 ed. Victoria, Australia:
Therapeutic Guidelines Limited, 2000; 47–53.
37. Reese RE, Betts RF, Gumustop. Handbook of Antibiotics. 3rd ed. Philadelphia, USA:
Lippincott Williams & Wilkins, 2000; 383–98 & 440–5.
38. Walker S, et al. Lack of evidence for systemic toxicity following topical
chloramphenicol use. Eye 1998; 12:875.
39. Lopez AJ, et al. Ceftriaxone-induced cholelithiasis. Ann Intern Med 1991;
115:712.
40. Wilhelmus KR, Coster DJ, Jones BR. Acyclovir and debridement in the treatment of
ulcerative herpetic keratitis. Am J of Ophtham 1981; 91:323–7.
41. Jensen KB, Nissen SH, Jessen F. Aciclovir in the treatment of herpetic keratitis.
Acta Ophthalmol 1982; 60:557–63.
42. Parlato CJ, Cohen EJ, Sakauye CM, Dreizen NG, Gakentine PG, Laibson PR. Role of
debridement and trifluridine (trifluothymidine) in herpes simplex dendritic
keratitis. Arch Ophthalmol 1985; 103:673–5.
 Heat Illness

Author: Dr Claire McGrath (Emergency Department, ASH)

Topic Reviewers: Kenna Bistani (RAN, Pine Creek); Helen Collinson (RAN,
Adelaide River); Monica Ostigh (RAN, Jabiru)

Heat stroke exists when the core body temperature exceeds 40–41ºC. It
usually results from a prolonged exposure to extreme heat or physical
activity during extreme heat. In the Central Australian context it is more
likely to occur in tourists who are not acclimatised, where the actual
ambient temperature need not be excessive.
Mortality increases significantly when cooling is delayed. Immersion in
iced water results in rapid reduction of core temperature to less than
39ºC. This treatment is advocated but is not practical in most rural
clinics in Central Australia. The combination of atomised tepid water from
a spray bottle and standing fans cools at a comparable rate to immersion
and is much more amenable to our conditions. When the temperature falls to
39ºC cooling measures should cease to avoid a hypothermic overshoot. If
excessive shivering occurs this can further aggravate the hyperthermia.
Treatment options include reducing the cooling mechanisms or IV
Chlorpromazine 25–50 mg.
The absence of sweating is usual but not always present. The diagnosis
should not be based on the absence of sweating.
Antipyretics such as paracetamol and aspirin are contraindicated because
the pathophysiology of fever is different and liver damage from the
hyperthermia may be exacerbated.
Fluid requirements are modest unless there has been prolonged exposure.
250–500 ml/hour of N Saline or Hartmanns should be sufficient. Pulmonary
oedema occurs in heat stroke and may be exacerbated by too much fluid.
All patients with heat stroke have signs of CNS dysfunction — delirium,
coma, and seizures.
Cerebral oedema is a feared complication and can also result in
convulsions, which should be treated with IV Diazepam or midazolam.
A urinary catheter should be inserted in any one whose initial core
temperature exceeds 40ºC or whose temperature fails to fall below 39ºC
after one hour of appropriate cooling methods. If there is heavy
proteinuria (2 plus or more) or haematuria (which may represent
myoglobinuria) the administration of mannitol 12.5 gm loading, followed by
12.5 mg/L of IV fluid should be considered after consultation with a doctor
or emergency department. Urine flow then needs to be maintained at 50
ml/hour or more (adult).
A full examination should be performed to exclude other injuries that
may have occurred before or during the exposure to heat. e.g. a fall
because of wandering during a delirium; or a snake bite. Remember that such
an event may have precipitated the prolonged exposure.
[Editor: There have been cases of hyponetremia in the Top End, brought
about by the combination of drinking large amounts of water while sweating
‘saline’; this possibility should be kept in mind in the Top End.]

Medline keywords: Heat stress, mannitol; hyperthermia and resuscitation,

dehydration and heat stress

References
1. Eichner ER. Treatment of suspected heat illness. International Journal of Sports
Medicine 1998 June; 19Suppl2S150–3.
2. Noakes TD. Fluid and electrolyte disturbance in heat illness. International
journal of Sports Medicine Jun1998; 19suppl2S146–9.
3. Rosen et al. Emergency Medicine. Fourth edition, 2000.
 Hepatitis: The management of
chronic hepatitis B virus
infection in Aboriginal
and Torres Strait Islanders

Authors: Dale Fisher; Sarah Huffam

Topic Reviewers: Ivor Alexander (RAN, Nhulunbuy CDC), Steven Skov, Dan Ewald

This background paper quite deliberately focuses on hepatitis B. While the

authors acknowledge that most observed abnormal liver enzyme tests are
related to fatty deposits in the liver secondary to diabetes or
dyslipidaemia, it is clear that most controversy for health care providers
in remote Aboriginal communities comes from the management of patients with
hepatitis B. Abnormal liver function tests are also recognised frequently
in a setting of kava or alcohol abuse. The management of such abnormal
liver function relates to management of these underlying problems and as
such we will not expand on these issues here. Other causes of chronic liver
disease — such as hemochromatosis, Wilson’s disease, auto immune hepatitis
and (thankfully still) hepatitis C — are rare at best.

Summary
Over the last five to 10 years, treatment options for patients with chronic
hepatitis B have evolved considerably. The mainstay of management of this
common worldwide problem remains primary prevention. As universal
vaccination in the NT was introduced initially in the late 1980s, concerns
over ensuring optimal management of chronic hepatitis B infection will
remain for decades yet. Those with chronic infection require an emphasis on
avoidance of exacerbating hepatic insults, particularly alcohol. As well as
this there is increasing utilisation of more sophisticated therapy
including antiviral drugs for those with progressive inflammation and
fibrosis. Furthermore, medical and surgical developments have increased the
options for those with stable cirrhosis as well as decompensated disease
and hepatocellular carcinoma.1 The literature provides some guidelines to
assist primary health providers in the broader community deliver best care
to patients with hepatitis B.2,3 They do not, however, commit to guidelines
for screening of hepatocellular carcinoma and this is because of a lack of
evidence as to its value. Such guidelines designed for general
practitioners for the general population assist with testing and
indications for specialist referral, but do not offer specific information
for the remote Aboriginal and Torres Strait population known to have
Australia’s greatest hepatitis B burden.
The summary of hepatitis B, published by the Gastroenterological Society
of Australia in 2000, is an excellent resource for those wishing further
reading.3 The core issues to be addressed by this chapter are the role of
testing and follow-up in the primary care setting of remote Aboriginal
communities. The issue of referral for consideration of the newer
specialised treatments is also addressed. Finally, even in the absence of
satisfactory evidence, we must define a guideline for screening for
hepatocellular carcinoma, which does not exist in the broader community but
is a constant (and appropriate) question emanating from primary health care
providers in this endemic setting.

Natural history of endemic chronic hepatitis B virus infection

The need for any intervention is a function of the natural history of the
disease to be treated. Of those infected with hepatitis B virus (HBV) at
birth or early childhood, 95% will become chronically infected. Each year
5–10% will lose their envelope antigen (e Ag) status and 10% will remain
HBe Ag positive for life. Hepatitis B surface antigen (HBs Ag) will be lost
in 1–2%/yr of those chronically infected.
Of those remaining HBs Ag positive around 25% will progress to end-stage
liver disease.4 There is a 200-fold increased risk of hepatocellular
carcinoma (HCC) in chronically infected patients. Patients without
cirrhosis, and with negative HBe Ag and negative DNA, have a low risk of
HCC. However, most patients who develop HCC are HBe Ag negative.
The risk of a patient developing sequelae of HBV associated cirrhosis is
related to male gender, young age of acquisition, concurrent hepatitis C or
HIV and alcohol misuse. Patients with chronic HBV that are HBV DNA negative
and have normal ALT levels have little liver-related mortality. A
longitudinal study of 92 such patients over 15 years showed no liver
related deaths.5 Survival in patients with hepB cirrhosis is 71% at five
years, with death being due to bleeding, sepsis or HCC.6
Early diagnosis of HCC allows for a variety of treatment options aimed
at cure as well as prolonging length and improving quality of life.
Treatment modalities range from transplantation to radio and microwave
frequency ablation, resection and hemihepatectomy, intra-arterial
chemotherapy and embolisation and percutaneous intralesional ethanol
injections, each requiring extensive work-up and attendance at tertiary
referral hospitals.1 The natural history of HCC is dismal, with survival
beyond two years rare.

Screening for hepatitis B and vaccination

Opportunistic screening for hepatitis B infection in the context of
sexually transmitted infection, prenatal care or biohazard injury should be
followed with vaccination if the individual is not immune. Universal
vaccination of newborns for hepatitis B commenced in the NT in 1988 for
Aboriginal children, and vaccination of non–Aboriginal children was
commenced in 1990 and actively promoted in 1993. A ‘catch-up’ program was
conducted in 1998 to vaccinate children age 6–16 years. The efficacy of
vaccination is related to development of HBs Ab and will occur in >95% of
infants undergoing recommended protocols.7 For the purposes of this chapter
we will assume the reader has a good understanding of the essential role of
primary prevention via vaccination (including immunoglobulin
administration), contact and family screening and the overall importance of
counselling and education.
The role of antiviral therapy
Alpha-interferon was the first drug to become available for treatment to
prevent progression of liver disease. Success is defined as loss of
viraemia and normalisation of liver function tests and occurs in 40% of
those treated with a six-month subcutaneous course. The side effect profile
is high.
More recently, lamivudine became available as an alternative antiviral
agent for patients with active chronic HBV infection. The seroconversion
rate in those treated is up to 73% at four years.8 Those most likely to
respond will have a high ALT and low-level viraemia together with a high
degree of activity on biopsy. Patients, to receive treatment, need serial
blood tests demonstrating an elevated serum ALT and HBV viraemia. They must
consume little alcohol over six months and then undergo a liver biopsy.
Treatment is a daily tablet, for possibly years. The drug is very well
tolerated with few side effects reported. Success is defined as loss of
viraemia and normalisation of ALT at which time treatment may stop.
Survival of patients treated successfully with loss of HBe Ag, viraemia
and possibly sAg is significantly better than those not treated and those
treated without seroconversion.9
It is unlikely that there is any role for interferon in the Aboriginal
and Torres Strait Islander population at this stage. Lamivudine is less
toxic and taken orally. It also has cumulative benefit although there is
concern over the selection of resistant strains.8
Future treatment options likely to become available include other
nucleoside analogues and more acceptable preparations of interferon plus
combination approaches. Currently, both interferon and lamivudine require
initiation and monitoring via a hospital based liver clinic. They are
funded via the S100 scheme.
Studies in hepatitis B patients being immune suppressed for other
reasons, notably renal transplant or chemotherapy, have a decreased risk of
hepatitis flare when given lamivudine.10
Transplantation for end-stage and decompensated HBV cirrhosis is now
widely accepted since the recognition of improved graft survival with
lamivudine. This involves extensive assessment of a variety of patient
factors. Once accepted, the patient must live within ready access of a
major centre and be available to respond immediately to a page. Waiting
times are generally in the order of three to nine months and dependent
largely on blood group status. For a period post operatively the patient is
required to remain close to the major centre. Regular specialist follow-up
is lifelong and immunosuppressive drugs are taken daily. The side effect
profile including the risk of sepsis is significant. Management is
complicated where co-morbidities in the form of renal disease, hypertension
and diabetes exist.

Relevance in the remote Aboriginal and Torres Strait Islander

population
In Australia, 90 000 Aboriginal people live in remote communities, many of
which are accessible only by aircraft especially in the wet season. Most
have much worse social and economic circumstances, education, living
conditions and health status than other Australians.11,12,13
Aboriginal and Torres Strait Island people have death rates over three
times higher than the Australian population overall with life expectancy
approximately 20 years less than other Australians.11,12,13,14 The major causes
of death in Aboriginal people include cardiovascular and respiratory
disease, injuries and poisoning. Furthermore, there are increasing trends
in cancer, diabetes, chronic liver disease and suicide. In the Northern
Territory in 1991–95, chronic liver disease (all causes) and cirrhosis
death rates were four times higher for Aboriginal males and 5.5 for
Aboriginal females, compared to the non-Aboriginal population. There were a
total of 62 deaths from chronic liver disease in the NT during this period14
(figures 1 and 2 below).

Incidence and prevalence of hepatitis B

Studies from 1989–93 in 24 Northern Territory urban and rural schools of
children aged nine to 17 years, and teachers, demonstrated serological
markers of HBV infection in 18.7% of school children. This included 46.9%
of 439 Aboriginal children, 13.7% of 556 children from ‘low prevalence’
(e.g. Caucasian) groups and 32.1% of 109 ‘other’ ethnic groups. 12.8% of
school staff from low prevalence backgrounds and 37.9% from ‘other’
including Aboriginal and Asian backgrounds had HBV markers.15
 Other studies have shown HBs Ag detected in 8–26% of rural Aboriginal
populations.16,17,18
Liver cancer death rates have almost tripled in the period from early
1980s to the early 1990s (figures 3 and 4). Where serology was undertaken
in patients with HCC one study demonstrated HBs Ag was positive in 7/11
Aboriginal cases (63.6%) and 2/4 non-Aboriginal cases. The median and mean
age was 59 years.19 Aboriginal people are 12 times more likely to die from
liver cancer than Australians generally.14
There were 28 deaths from HCC diagnosed in the Northern Territory
between 1991 and 1995. During the period 1987–97 primary liver cancer was
the third most common cancer and the second highest cause of cancer death
in Aboriginal males.11
However, as a health priority, many issues are more significant than
hepatitis B to this population. Furthermore, interventions for higher
priority conditions may be less consumptive of resources and more
culturally appropriate. Preventing vascular disease (for example) will have
a much greater impact on community mortality than efforts on hepatitis B
such as antiviral therapy or screening for HCC. This is not to say,
however, that an individual should be refused ‘best care’ if it is deemed
by the patient and clinician to be in that individual’s interest. This is
still the case when co-morbidities (and therefore life expectancy), plus
other issues e.g. preparedness to have a liver biopsy, or treatment in a
larger city or even interstate, are considered.

The role of new therapies and of HCC screening in ATSI populations

Investigation and treatment of asymptomatic individuals needs to be
justified in any health care setting. In remote Aboriginal communities
where the general burden of disease is high, and resources are scarce, this
is particularly important. Local health care workers are generally
overburdened and need to prioritise their efforts for maximal gain to their
patients in terms of length and quality of life. The financial cost for an
investigation in a patient living remotely may be significantly greater
especially if it involves travel. The cost benefit of any screening,
investigation and treatment in an asymptomatic individual may not be
considered worthwhile, if cultural factors, co-morbidity, life expectancy
and personal priorities are taken into account.
For so many reasons the decision to screen, investigate and treat needs
to be justified in Aboriginal and Torres Strait Islanders living in remote
communities. The collorary is that not screening, investigating or treating
equally needs justification, especially when mortality is documented to be
so high and increasing.
By defining a guideline we necessarily generalise about a population’s
characteristics and needs with respect to a particular disease. Aboriginal
and Torres Strait Islanders living in remote communities live with endemic
chronic HBV infection, and guidelines are needed for primary health care
providers despite the fact that such guidelines are not laid down for the
broader community.
While defining guidelines, however, it is acknowledged that it is always
essential that clinicians adapt them to suit an individual patient’s needs.
The need for guidelines is well discussed in the setting of CARPA
protocols.20
Screening/surveillance for HCC
In the case of screening/surveillance for HCC, where there is a dearth of
evidence, experts disagree on protocols and thus we can be comfortable that
no sensible management plan can be deemed ‘wrong’. Surveillance for HCC is
practised widely by hepatologists but there is no published and accepted
protocol. There is no randomised controlled trial showing benefits from
surveillance, however, many believe that patients identified early have a
greater opportunity to access curative therapy. One group has attempted
guidelines in this field but undertaken screening only in those with
clinical or biopsy-proven cirrhosis.21
A 16-year longitudinal study screening for hepatocellular carcinoma in
hepatitis B sAg positive Alaskan Indigenous people showed benefit in
screening by AFP alone.22 While screening with AFP is a reasonable
compromise, the highest yield comes from a combination of AFP and
ultrasound.23 Whether early diagnosis and intervention benefits the
individual remains controversial. Furthermore, the appropriateness of
dedicating resources required for such programmes is also debatable.
Patients being screened and monitored will require a good understanding
of the reasons to investigate and consider treatment, particularly as they
are likely to be asymptomatic at the appropriate time to intervene.

Antiviral therapy
Regarding antiviral therapy, clearly selected individuals can benefit.
Patients being considered for treatment will require a good understanding
of the reasons surrounding investigation and follow-up. They will need to
understand the possibility of treatment failure. It should be seen that in
the context of that individual’s care that treatment is being considered,
because it is likely, that the sequelae of hepatitis B will possibly have
an impact on that individual’s prognosis.

Recommendations
After negotiation and discussion with a person with chronic HBV infection,
they should have a monitoring/ surveillance plan. This should fall into one
of three streams based on their serology and LFTs (see flow chart at end of
article).
Before committing to follow-up, education should emphasise its purpose,
which is to decrease the risk of decompensated liver disease and
hepatocellular carcinoma. Compliance with attendance and modification of
other lifestyle factors, particularly alcohol, has a greater priority than
biochemical testing. It should be remembered that other causes might result
in abnormal liver function tests and in particular include diabetes,
obesity, dyslipidaemia, medications, alcohol and kava consumption.
A person may move between categories. We also recommend some flexibility
for primary health providers in determining the follow-up category. For
instance, the intensity of follow-up can be downgraded or even removed for
a number of reasons as listed below.
• Patient choice if appropriate decision-making opportunities ensured
• Unacceptable patient compliance with regards follow-up and life-style
issues including alcohol consumption
• Existence of significant co-morbidities, thus altering the patient’s
prognosis for other reasons, including age
 • A belief after discussion with the patient and relevant others that
treatment options are culturally/socially inappropriate even if
screening does demonstrate significant early and asymptomatic disease.

The management of chronic HBV infection is complex, and made more so by

factors in this population including remoteness, co-morbidities, patient
desires and resources. These guidelines outline many of the issues
necessary to consider and provide a simple guide to facilitate follow-up
and appropriate and timely referral for further investigation and
consideration of treatment.

References
1. Badvie S. Hepatocellular carcinoma. Postgrad Med J 2000; 76:4–11.
2. Farrell GC. Chronic Viral Hepatitis. Med J Aust (Practice Essentials,
Gastroenterology) 1999; 26–33.
3. Gastroenterological Society of Australia. Hepatitis B; New tests, new treatments,
new recommendations. An information booklet for health care providers from the
Digestive Health Foundation, 2000, 2nd edition.
4. Mahoney FJ. Update on Diagnosis, Management and Prevention of Hepatitis B Virus
Infection. Clin Microbiol Rev April 1999; 351–66.
5. de Franchis R, Meucci G, Vecchi. The Natural History of Asymptomatic Hepatitis B
Surface Antigen Carriers; Annals of Internal Medicine. 1993; 118:191–4.
6. De Jongh FE, Janssen HLA, de Man RA. Survival and prognostic indicators in
Hepatitis B surface antigen positive cirrhosis of the liver. Gastroenterology 1992;
103:1630–5.
7. Mahoney FJ. Update on diagnosis, management and prevention of hepatitis B virus
infection. Clin Microbiol Rev. April 1999; 12(2):351–66.
8. Strasser SI, McCaughan. Therapies for chronic hepatitis B: emerging roles for
nucleoside analogues. Aust NZ J Med 2000; 30,556–8.
9. Niederau C, Heintges T, Lange S. Long-term follow–up of HBe Ag–positive patients
treated with interferon alfa for chronic hepatitis B. N Engl J Med 1996; 334:1422–7.
10. Han DJ, Tae HK, Park SK, Lee SK et al. Results on Pre emptive or prophylactic
treatment of Lamivudine in HBsAg (+) renal allograft recipients: comparison with
salvage treatment after hepatic dysfunction with HBV recurrence. Transplantation Feb
15, 2001; 71:367–94.
11. Condon JR Warman G, Arnold L (editors). The Health and Welfare of Territorians.
Darwin: Epidemiology Branch, Territory Health Services, 2001.
12. Australian Bureau of Statistics and Australian Institute of Health and Welfare.
The health and welfare of Australia’s Aboriginal and Torres Strait Islander peoples.
Canberra: Australian Bureau of Statistics, 1999. 4704.0. 1997.
13. Cunningham J, Paradies Y. Mortality of Aboriginal and Torres Strait Islander
Australians 1997. Canberra: Australian Bureau of Statistics. Occasional Paper,
3315.0. 17–4–2000.
14. Dempsey KE, Condon JR. Mortality in the Northern Territory 1979–1997, Darwin:
Territory Health Services, 1999.
15. Gardner ID, Wan X, Simms PA et al. Hepatitis B virus markers in children and
staff in Northern Territory schools. Med J Aust 1992; 156:638–41.
16. Burrell CJ, Cameron S, Hart G et al. Hepatitis B reservoirs and attack rates in
an Australian community. A basis for vaccination and cross infection policies. Med J
Aust 1983; 2:492–6.
17. Holman CDJ, Bucens MR, Quadros CF et al. Occurrence and distribution of Hepatitis
B infection in the Aboriginal population of Western Australia. Aust NZ J Med 1987;
17:518–25.
18. Campbell DH, Sargent JW, Plant AJ. The prevalence of markers of infection with
Hepatitis B virus in a mixed race Australian community. Med J Aust 1989; 150:489–92.
19. Wan X, Mathews JD. Primary hepatocellular carcinoma in Aboriginal Australians.
Aust J Public Health 1994; 18:286–90.
20. Scrimgeour D. Screening issues for Aboriginal People. CARPA Newsletter number 24,
October 1996; 4–10.
21. Llovet JM, Bruix J. Early Diagnosis and treatment of hepatocellular carcinoma.
Balliere’s Clin Gastr 2000; 14:6.991–1008.
22. McMahon BJ, Bulkow L, Harpster A. Screening for hepatocellular carcinoma in
Alaska natives infected with chronic Hepatitis B: A16-year population based study.
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Follow-up of hepatitis Bs Ag positive patients*
 Melioidosis

Authors: Prof Bart Currie (MSHR); Dr Dan Ewald

Topic Reviewers: Robyn Dixson (RAN, Yirrkala Clinic); Michael Jenkins (RAN,
Maningrida Clinic); Liz Stephenson (RAN, Nhulunbuy CDC); Dr Penny Roberts-
Thomson (Nguiu Clinic); Dr Steven Skov

This material is extracted from papers prepared by Bart Currie (MSHR) and
others involved in the Top End Prospective Melioidosis Study. In particular
a review paper: Bart J. Currie. Menzies School of Health Research, Darwin
and Northern Territory Clinical School, Flinders University. ‘Melioidosis:
an Australian perspective of an emerging infectious disease’. Recent
Advances in Microbiology 2000; 8:1–75.

Overview of melioidosis
Introduction
Melioidosis is an infection with the bacterium Burkholderia pseudomallei,
previously known as Pseudomonas pseudomallei until the mid-1990s. It is an
environmental organism found in soils and water across the Top End of
Australia and in Asia.
‘It is in the dirt and you can’t kill it with a big stick’ (memories of
a doctor’s introduction to melioidosis in the Torres Strait). B.
pseudomallei is characteristically resistant to penicillin, ampicillin,
first and second generation cephalosporins, gentamicin, tobramycin, and
streptomycin.
Until new therapies recently became available it was the commonest cause
of fatal community-acquired bacteremic pneumonia at Royal Darwin Hospital
(and possibly also Katherine and Gove Hospitals). In 2000 (an unusually wet
year) there were two cases in Central Australia.

Clinical picture
B. pseudomallei can cause infection in almost any part of the body. Most
infection is thought to be acquired through percutaneous inoculation,
although inhalation and ingestion are also possible.
Most cases occur in the wet tropics, during the wet season, though rarer
temperate cases do occur and some people may become infected while visiting
the wet tropics and develop the illness after returning to cooler/ dryer
climates. The incubation period has been ascertained from the Top End study
to be one to 21 days, with a mean incubation period of nine days.
Pneumonia is the commonest presentation of melioidosis. As well as
severe septicaemic pneumonia, with mortality often over 50%, many patients
present with milder forms of pneumonia, which respond well to appropriate
antibiotics. Other presentations of melioidosis include skin abscesses or
ulcers, abscesses in the internal organs (such as the prostate, spleen,
kidney and liver), fulminant septicemia with multi-organ abscesses and
unusual neurological illnesses, such as brainstem encephalitis and acute
flaccid paraplegia.
 People without symptoms or a known history of disease can also be found
to be positive on serological testing, indicating asymptomatic infection. A
small proportion of these people can ‘re-activate’ from latent infection
many years later in life, analogous to tuberculosis. However, re-activation
represents probably less than 5% of Top End cases, with the vast majority
of presentations following infection during the current wet season.

Diagnosis
Diabetes is the most important risk factor for melioidosis, with around 40%
of cases in the NT being diabetic. In addition, excessive alcohol
consumption, chronic renal disease, chronic lung disease and excessive kava
drinking are risk factors for melioidosis. While the majority of patients
with melioidosis have one or more of these risk factors, melioidosis can
also occur in children and healthy adults. However, severe disease and
death are extremely rare in people without (above mentioned) identified
risk factors.
The likelihood of diagnosis is increased by using selective culture
media (modified Ashdown’s broth), frequent sampling (sputum, throat, rectal
and ulcer swabs) and collection of blood cultures. Clinicians should liaise
with laboratory staff to ensure selective media are available including for
remote communities.

Treatment
Early diagnosis and appropriate antibiotic therapy decrease mortality. Once
melioidosis is confirmed the usual treatment recommended is: Initial
intensive therapy for at least 14 days with: intravenous high dose
ceftazidime or meropenem plus high dose cotrimoxazole, in hospital.
A long period of eradication therapy for at least three months is needed
to avoid relapse/recrudescence. This is usually done with oral monotherapy
using high dose cotrimoxazole.
The duration of the intensive and eradication therapy may need to be
prolonged in deep-seated infections, bone, joint and CNS infections.
In patients in ICU with melioidosis septic shock, a G-CSF protocol has
been associated with decreased mortality.

Melioidosis in more detail

Epidemiology
Excellent summaries of what is known about the global distribution of
melioidosis are provided by Dance (Dance, 1990; Dance, 1991; Dance, 2000b).
The majority of cases of melioidosis currently being diagnosed are from
South-East Asia, most notably Thailand (Punyagupta, 1989; Chaowagul, et
al., 1989; Vuddhakul, et al., 1999), with an estimated 2000–3000 cases each
year (Leelarasamee, 2000), Malaysia (Puthucheary, et al., 1981;
Puthucheary, et al., 1992; Vadivelu, et al., 1997), Singapore (Chan, v,
1985; Tan, et al., 1990; Yap, et al., 1991; Yap, et al., 1995; Singapore
Committee on Epidemic Diseases, 1995; Lim, et al., 1997) and northern
Australia (see below).
The two locations where melioidosis is arguably the most important
single bacterial pathogen for humans are some north-eastern provinces in
Thailand and the Top End of the Northern Territory of Australia.
Melioidosis is the commonest cause of fatal community-acquired bacteraemic
pneumonia at Royal Darwin Hospital (Currie, 1993a). Average annual
incidence of melioidosis in the Top End between 1989 and 1998 was 16.5/100
000, with a rate of 34.5/100 000 for the year spanning the 1997–98 monsoon,
which was particularly wet (Currie, et al., 2000c).
Re-activation of latent infection, analogous to tuberculosis, is well
recognised and led to concerns of disease in soldiers returned from
Vietnam, with estimates from serology studies of around 225 000 potential
cases, termed the ‘Vietnamese time bomb’ (Spotnitz, 1966; Clayton, et al.,
1973). However while occasional cases of re-activation of B. pseudomallei
still occur in Vietnam veterans (Mackowiak & Smith, 1978; Chodimella, et
al., 1997) it is rare in comparison to the numbers exposed.
Although the endemic area for melioidosis has generally been stated to
be between the latitudes 20?S and 20?N (Dance, 1991; Leelarasamee &
Bovornkitti, 1989), Winton in outback western Queensland the location of
the first description of melioidosis from Australia, is below this latitude
and just inside the tropics at 22?S. However, by far the majority of human
cases still occur above 20?S, with disease recognised across northern
Australia.
There is considerable variation across northern Australia, with less
disease in the Kimberley in the far north west (Inglis, et al., 2000a) than
in the adjacent Top End of the Northern Territory. Even within the Top End
there are variations, with melioidosis clearly more common in some
Aboriginal communities than others (unpublished data).
In addition to newly recognised foci of melioidosis in Australia and
globally, there has been a steady increase in the number of cases of
melioidosis diagnosed in the Northern Territory, beyond the increase in
population (Currie, et al., 2000c). In the 19 years after the first
reported case in the Northern Territory from 1960 (Crotty, et al., 1963),
there were 36 further cases diagnosed (average two cases per year), with 10
in the five years from 1975–79 (Rode & Webling, 1981). From 1984–90 there
were 54 confirmed cases (average nine cases per year) (Woods, et al.,
1992). In the 10 years from October 1989 there were 252 culture-confirmed
cases (average 25 cases per year) (Currie, et al., 2000d). Recent years
have seen over 40 cases diagnosed each year (Currie, et al., 2000c).
While increased awareness of melioidosis amongst clinicians and the
public and improved laboratory diagnosis clearly account for some of the
increased numbers, it is considered unlikely that large numbers of cases
were being missed in the Northern Territory from 1980 onwards. Dance has
discussed possible reasons for a genuine increase in melioidosis incidence
(Dance, 2000b). These include an increased number of individuals with risk
factors for melioidosis, such as diabetes, alcohol excess and renal
disease, all of which are emerging problems in the Indigenous population of
northern Australia. In addition it is possible that there has been an
increase of B. pseudomallei in the environment.

Environmental aspects
The understanding of B. pseudomallei as a widely distributed environmental
saprophyte has recently been summarised by Dance (Dance, 2000a). Although
originally considered a zoonotic infection (Stanton & Fletcher, 1932),
zoonotic infection is in fact very rare, with only three possible cases
described from Australia (Low Choy, et al., 2000). It is now clear that
both animals and humans acquire infection from organisms present in soil
and surface water. Furthermore, molecular typing has shown that animals and
humans can be infected by the same environmental clone of B. pseudomallei
(Currie, et al., 1994; Haase, et al., 1995b).
 Many factors are likely to influence the presence and distribution of B.
pseudomallei in the environment. These include temperature, rainfall and
humidity, sunlight and UV irradiation, pH of soil and water and other
chemical factors such as soil composition, vegetation and use of
fertilisers (Dance, 2000a).
An extensive and meticulous epidemiological investigation into a dry
season cluster of melioidosis cases in a remote Kimberley (north-west
Western Australia) coastal community suggested contamination of the local
water supply and chlorination failure were responsible for transmission of
B. pseudomallei (Inglis, et al., 1998; Inglis, et al., 1999). Five cases
(three fatal) occurred over a six-week period (Inglis, et al., 1999).
Further studies showed contamination of a water storage tank and of spray
formed in a pH-raising aerator unit. Typing of the isolates by pulsed-field
gel electrophoresis confirmed clonality of the human and environmental
isolates (Inglis, et al., 2000a).
A similar situation has been documented from the Northern Territory.
Nine cases of melioidosis with four deaths occurred over a 28-month period
in members of a small remote Aboriginal community in the Top End (Currie,
et al., 2000e). Typing by pulsed-field gel electrophoresis showed isolates
of B. pseudomallei from six of the cases to be clonal and also identical to
an isolate from the unchlorinated community water supply. It was considered
possible that the clonal bacteria persisted and were propagated in biofilm
in the unchlorinated water supply system. B. pseudomallei has also been
isolated from rural bore water in the Darwin region (Currie, et al.,
2000c). These case clusters and the 1980s Queensland piggeries outbreak —
which was terminated by adequate chlorination of the water supply
(Ketterer, et al., 1986) — have public health implications for quality of
water standards and prevention of melioidosis in endemic locations such as
northern Australia.

Mode of infection
Recent reviews support the predominant role of percutaneous inoculation of
B. pseudomallei (Leelarasamee & Bovornkitti, 1989; Dance, 1990; Currie, et
al., 2000c). In the Northern Territory presentations with pneumonia
following presumptive inoculating skin injuries have been documented
(Currie, et al., 2000c), suggesting haematogenous spread to the lung rather
than inhalation or spread from the upper respiratory tract. This is
analogous to post-primary tuberculosis, with disease from haematogenous
spread localising in the upper lung zones, where highest alveolar oxygen
tension exists (Citron & Girling, 1987). Furthermore, septicaemic
melioidosis pneumonia cases are often more systemically ill than suggested
by initial chest X-ray, supporting the concept of spread to, rather than
from, the lung (Currie, et al., 2000c).
Despite the presumptive percutaneous inoculation in cases of melioidosis
with a well defined cutaneous exposure event, subsequent disease mostly
occurred at distant sites without evidence of active melioidosis at the
inoculation site (Currie, et al., 2000c).
Epidemiological studies in patients with genitourinary melioidosis in
the Northern Territory have to date not shown any evidence of sexual
transmission of B. pseudomallei (unpublished data).
It has been noted that, despite the large bacterial load in severely ill
patients with septicaemic pulmonary melioidosis, person-to-person
transmission is extremely unusual (Kunakorn, et al., 1991; Dance, 2000a).
This supports the primary importance of host risk factors for development
of melioidosis.

Asymptomatic infection, incubation, acute and chronic disease and

latent infection
Serology studies suggest that most infection with B. pseudomallei is
asymptomatic (Nigg, 1963; Strauss, et al., 1969a, Ashdown & Guard, 1984;
Kanaphun, et al., 1993), with severe clinical disease occurring mostly in
those with risk factors such as diabetes, renal disease and alcoholism
(Guard, et al., 1984; Leelarasamee & Bovornkitti, 1989; Suputtamongkol, et
al., 1994a). Studies in north Queensland also suggested that for those with
risk factors such as diabetes and alcoholism there is an increased
prevalence of asymptomatic infection (seropositivity) as well as of
clinical disease (Ashdown & Guard, 1984). Although this association may
reflect confounding factors such as increased exposure, a case control
study from Thailand demonstrated a significant interaction between diabetes
and occupational exposure for melioidosis cases (Suputtamongkol, et al.,
1999). This is consistent with an increased susceptibility to infection in
diabetics exposed to B. pseudomallei.
Seropositivity in the Top End varies from under 5% to 13% (Currie, et
al., 2000c). To date there is no definitive evidence for development of
immunity to melioidosis with natural exposure to B. pseudomallei. Re-
infection with a different strain of B. pseudomallei following successful
treatment of melioidosis has been documented (Desmarchelier, et al., 1993;
Haase, et al., 1995a).
The incubation period for melioidosis has been ascertained in the Darwin
prospective melioidosis study, which commenced in October 1989. Of the 206
B. pseudomallei culture confirmed cases of melioidosis up to September
1998, 52 (25%) had likely inoculating events (Currie, et al., 2000c). These
were specifically recalled situations where usually percutaneous exposure
to soil or muddy water occurred during the monsoon. In the 25 cases where a
clear incubation period could be determined between the inoculating injury
and the onset of symptoms, the incubation period was one to 21 days (mean
nine days). This is consistent with a reported series of nosocomial
melioidosis cases from Thailand, where incubation period was three to 16
days (mean 9.5 days) (Sookpranee, et al., 1989a). Rapid onset of
melioidosis (even within 24 hours of inoculation) has been seen in presumed
aspiration following near drowning (Achana, et al., 1985; Lee, et al.,
1985), as well as in a small number of patients with heavy environmental
exposure in the Darwin series. It is likely that inoculating dose, mode of
infection, host risk factors and differential virulence of infecting B.
pseudomallei isolates all influence the incubation period (Howe, et al.,
1971; Bovornkitti, et al., 1985).

The Darwin study has also characterised presentations as acute or

chronic disease. Acute disease is most common and was defined as symptoms
being present for less than two months on presentation. Chronic disease was
defined as illness with symptoms for longer than two months duration on
presentation. Of 252 cases of culture-confirmed melioidosis in the 10 years
until September 1999, 222 (88%) presented with acute illness and 30 (12%)
with chronic illness, with no fatalities in the latter group (Currie, et
al., 2000a).
Intracellular survival of B. pseudomallei in human and animal hosts is
likely to explain the ability for latency, with possible parallels to
environmental ‘latency’ with the recently described ability of B.
pseudomallei to survive inside free-living amebae (Inglis, et al., 2000b).
It has long been recognised that, analogous to tuberculosis, B.
pseudomallei has the potential for re-activation. Hence the concern of the
‘Vietnamese time bomb’ in returned soldiers (see above). Latent periods
from exposure to B. pseudomallei in an endemic region to onset of
melioidosis in a non-endemic region have been documented as long as 26
years (Mays & Ricketts, 1975) and 29 years (Chodimella, et al., 1997) from
the USA and 19 years (Newland, 1969) and 24 years (Kingston, 1971) from
Australia. However documented cases of re-activated B. pseudomallei are
very uncommon. The small numbers of such cases in the USA in comparison to
the estimated 225 000 seropositive soldiers who returned from Vietnam
(Spotnitz, 1966; Clayton, et al., 1973), suggest re-activation of B.
pseudomallei is an infrequent event.
The vast predominance of cases of melioidosis occurs in the monsoonal
wet seasons of the various endemic regions. Seventy-five per cent of cases
in north-east Thailand were in June to November (Suputtamongkol, et al.,
1994a) and 85% of cases in the Northern Territory were in November to April
(Currie, et al., 2000a). These data support the concept that, in addition
to most infections with B. pseudomallei being asymptomatic, most cases of
melioidosis in endemic areas are recent infections presenting with acute
illness, predominantly in the wet season (Ashdown & Guard, 1984; Guard, et
al., 1984; Chaowagul, et al., 1989; Dance, 1991; Currie, et al., 2000c).
The Darwin study data suggested that only 3% of cases of melioidosis are
from re-activation of B. pseudomallei from a latent focus (Currie, et al.,
2000a).
In summary, from the Darwin prospective study 85% of cases of
melioidosis occurred in the wet season (November to April), with 88%
presenting with acute illness and 12% having chronic illness (sick for more
than two months). Incubation period was one to 21 (mean nine) days amongst
the 97% of cases considered due to recent infection with B. pseudomallei.
Only 3% of cases overall were considered to be re-activation from a latent
focus. It remains unknown what proportion of asymptomatic seropositive
people have latent infection with the potential for re-activation.

Risk factors for melioidosis

The most important risk factors for melioidosis are diabetes, alcohol
excess and renal disease (Leelarasamee & Bovornkitti, 1989). The importance
of diabetes as the most commonly associated risk factor for melioidosis has
been well documented in the major melioidosis endemic countries
(Puthucheary, et al., 1981; Guard, et al., 1984; Chaowagul, et al., 1989;
Suputtamongkol, et al., 1994a; Puthucheary, et al., 1992; SCED, 1995;
Suputtamongkol, et al., 1999; Currie, et al., 2000d).
The rates of diabetes in Thai studies of melioidosis cases were 23%
(Punyagupta, 1989), 32% (Chaowagul, et al., 1989) and more recently 60%
(Suputtamongkol, et al., 1999), compared to a rate of 37% in the Darwin
prospective study (Currie, et al., 2000d). Studies in the Northern
Territory and Thailand showed adjusted risk ratios of diabetes in cases of
melioidosis versus controls of 12.9 (95%CI 5.1–37.2) (Merianos, et al.,
1993) and 5.9 (95% CI 4.0–8.9) (Suputtamongkol, et al., 1999),
respectively. The Thai study also showed a statistically significant
predisposition to bacteraemic disease versus non-bacteraemic disease in
diabetics with melioidosis (OR 1.32; 95%CI, 1.05–1.66) (Suputtamongkol, et
al., 1999). Furthermore, logistic regression demonstrated a significant
interaction between diabetes and occupational exposure (Suputtamongkol, et
al., 1999), consistent with Ashdown and Guard’s earlier serology studies
suggesting diabetics to be at increased risk for infection with B.
pseudomallei as well as for developing melioidosis (Ashdown & Guard, 1984).
The importance of alcohol excess as a risk factor for melioidosis was
recognised in the Northern Territory (Rode & Webling, 1981) and in north
Queensland (Guard, et al., 1984), but is not as evident in studies from
Thailand (Chaowagul, et al., 1989, Suputtamongkol, et al., 1994a).
Alcoholism appears to be even less common as a risk factor in Malaysia
(Puthucheary, et al., 1992) and Singapore (SCED, 1995). This may well
reflect the differences in alcohol consumption by the various populations,
but further comparative studies will be informative. In Thailand 12% of
melioidosis cases had a history of heavy alcohol consumption
(Suputtamongkol, et al., 1999), compared to 39% in the Darwin study
(Currie, et al., 2000d).
Chronic renal disease is also a recognised risk factor for melioidosis
in the endemic region (Chaowagul, et al., 1989; Suputtamongkol, et al.,
1994a; Puthucheary, et al., 1992; SCED, 1995; Suputtamongkol, et al., 1999;
Currie, et al., 2000d). Renal disease was present in 27% and 20% of
patients in the Thai studies (Chaowagul, et al., 1989; Suputtamongkol, et
al., 1999), compared with 10% in the Northern Territory study (Currie, et
al., 2000d).
Other risk factors identified for melioidosis include chronic lung
disease (present in 27% of cases in the Northern Territory study) (Currie,
et al., 2000d), thalassemia (in 7% of Thai patients with an OR of 10.2;
95%CI, 3.5–30.8) (Suputtamongkol, et al., 1999) and probably various
malignancies, steroid therapy and tuberculosis, although their roles as
independent risk factors are yet to be confirmed (Suputtamongkol, et al.,
1999).
The association of melioidosis with the consumption of kava has recently
been recognised in Australia (Currie, et al., 2000c). Kava is an extract of
the root of the plant Piper methysticum and was introduced to remote
Aboriginal communities by missionaries as an alternative to alcohol. Kava
consumption was noted in 8% of melioidosis cases in the Northern Territory
study and whether kava is an independent risk factor for melioidosis and
other infectious diseases is currently being assessed (Currie, et al.,
2000d).
Overall, risk factors are less commonly present in children compared to
adults (Dance, et al., 1989a; Lumbiganon & Viengnondha, 1995; Edmond, et
al., 1998). Although fulminant melioidosis can occur in healthy
individuals, severe disease and fatalities are uncommon in those without
defined risk factors.
In the Northern Territory study, 51/252 cases (20%) had no identified
risk factor and there was only one fatality in this group (Currie, et al.,
2000d). This was an elderly male, and recent multivariate analysis has
shown age over 50 to be an independent risk factor for fatal melioidosis
(Currie B & Jacups S, in preparation).
In summary, diabetes is the most important risk factor for melioidosis,
with alcohol excess, chronic renal disease and chronic lung disease also
important. Severe disease and death are unusual in the absence of risk
factors.
 Table 1: Clinical presentations of melioidosis over 10 years in the Top
End from; Currie, et al., 2000d

Number Died Mortality

rate
Bacteraemic
Pneumonia – Septic 37 31 84%
shock
– Other 29 0 0%
Genitourinary – Septic 5 4 80%
shock
– Other 18 0 0%
Osteomyelitis/septic – Septic 1 1 100%
arthritis shock
– Other 3 0 0%
Other – Septic 7 7 100%
shock
– Other 17 0 0%
Non-bacteraemic

Pneumonia 61 4 7%
Genitourinary 14 0 0%
Skin abscess 32 0 0%
Soft tissue abscess 10 0 0%
(es)
Neurological 10 2 20%
Ostermyelitis/septic 5 0 0%
arthritis
Other 3 0 0%
Total 252 49 19%

Clinical features
As noted already, there is an enormous spectrum of disease with B.
pseudomallei infection. The majority of those infected are asymptomatic,
but it remains unknown what proportion of asymptomatic seropositive people
have latent infection with the potential for re-activation. Re-activation
appears to be a rare event in endemic regions (Currie, et al., 2000a), but
presumably accounts for those cases with latency of up to 29 years
(Chodimella, et al., 1997).
Table 1 shows the clinical presentations of the 252 cases in the 10 year
prospective study from the Top End of the Northern Territory (Currie, et
al., 2000c). As noted above, 88% presented with acute illness and 12% with
chronic illness (symptomatic for >2 months) (Currie, et al., 2000a). In the
Top End, 46% of cases were bacteraemic and overall mortality was 19%
(Currie, et al., 2000d).
Pneumonia is the commonest clinical presentation of melioidosis in all
studies (Howe, et al., 1971; Guard, et al., 1984; Punyagupta, 1989;
Chaowagul, et al., 1989; Leelarasamee & Bovornkitti, 1989; Dance, 1990;
Puthucheary, et al., 1992; SCED, 1995; Simpson, et al., 1999), accounting
for half of the Northern Territory cases (Currie, et al., 2000c). The
diversity of presentations other than pneumonia was demonstrated in the
Thailand series of 686 cases presented at the National Workshop on
Melioidosis in November 1985 (Punyagupta, 1989). Of those without
bacteraemia in the Top End study, 24% presented with skin ulcers or
abscesses — well recognised presentations of melioidosis, as are septic
arthritis and osteomyelitis (Punyagupta, 1989; Leelarasamee & Bovornkitti,
1989; Subhadrabandhu, et al., 1995; Popoff, et al., 1997). Also well
recognised, whatever the clinical presentation, are abscesses in internal
organs, especially spleen, kidney, prostate and liver (Punyagupta, 1989;
Leelarasamee & Bovornkitti, 1989).

Antibiotic therapy
B. pseudomallei is characteristically resistant to penicillin, ampicillin,
first and second generation cephalosporins, gentamicin, tobramycin, and
streptomycin (Eickhoff, et al., 1970; Leelarasamee & Bovornkitti, 1989;
Chaowagul, 2000). It has been shown to be susceptible to various newer
beta-lactam antibiotics, especially ceftazidime, imipenem, piperacillin,
amoxycillin/clavulanate, ceftriaxone and cefotaxime (Chau, et al., 1986;
Cheong, et al., 1987; Ashdown, 1988; McEniry, et al., 1988; Dance, et al.,
1989b; Yamamoto, et al., 1990; Smith, et al., 1994).
Emergence of resistance in B. pseudomallei during therapy has been well
documented (Dance, et al., 1988; Dance, et al., 1989b; Godfrey, et al.,
1991; Dance, et al., 1991; Toohey, et al., 1994; Smith, et al., 1994;
Jenney, et al., 2001).
The carbapenems — imipenem and meropenem — have the lowest minimum
inhibitory concentrations against B. pseudomallei (Ashdown, 1988; McEniry,
et al., 1988; Dance, et al., 1989b; Yamamoto, et al., 1990; Smith, et al.,
1994; Smith, et al., 1996). Furthermore, in vitro time-kill studies to
measure the rate of bacterial killing showed the carbapenems to perform
better against B. pseudomallei than ceftazidime (Smith, et al., 1994),
including for various resistant isolates (Smith, et al., 1996). It was
suggested that this might reflect enhanced penetration through the cell
wall or preferential binding to different penicillin binding proteins. A
surprising finding of the time-kill studies was that, unlike for imipenem,
meropenem and piperacillin, bactericidal activity of ceftazidime was not
confirmed (Smith, et al., 1994; Sookpranee, et al., 1991). Another
theoretical advantage of carbapenems is the demonstration of a post-
antibiotic effect against B. pseudomallei which is not present for
ceftazidime (Walsh, et al., 1995a).
Most recently, high dose imipenem has been shown in another comparative
trial from Thailand to be at least as effective as ceftazidime for severe
melioidosis, with no differences in mortality between the groups and fewer
treatment failures in those given imipenem (Simpson, et al., 1999).
Another trial in Thailand suggested cefoperazone/ sulbactam plus
cotrimoxazole may be a useful alternative for the initial intensive
therapy, although numbers in the study were inadequate for a conclusive
result (Thamprajamchit, et al., 1998). A study in mice has suggested useful
efficacy for cefpirome, especially when used in combination with
cotrimoxazole (Ulett, et al., 1999).
The duration of initial intensive therapy should be at least 10 days
(Chaowagul, 2000). The Northern Territory guidelines state at least 14
days, with longer required if critically ill, or for extensive pulmonary
disease, deep-seated collections or organ abscesses, osteomyelitis, septic
arthritis and neurological melioidosis (Currie, et al., 2000d; Group,
2000/2001).
Ceftazidime infusions through a peripherally inserted central catheter
(PICC line) using an elastomeric infusion device (Baxter, Sydney) have
enabled early discharge for hospital-in-the-home therapy (Currie, et al.,
2000d). The absence of any postantibiotic effect with ceftazidime gives
such a continuous infusion a theoretical advantage over intermittent dosing
(Walsh, et al., 1995a).

Subsequent eradication therapy for melioidosis

Following initial intensive therapy, using ceftazidime or imipenem or
meropenem, possibly in combination with cotrimoxazole, subsequent
eradication therapy is considered necessary for preventing recrudescence or
later relapse of melioidosis.
Both duration of eradication therapy and the best antibiotics to use
remain uncertain. Molecular typing of isolates from recurrent melioidosis
has confirmed that by far the majority are true relapses from failed
eradication, rather than new infection (Desmarchelier, et al., 1993;
Chaowagul, et al., 1993; Haase, et al., 1995a; Mohandas, et al., 1995;
Currie, et al., 2000a).
There are a number of reasons for failure of eradication therapy.
1. The most important factor responsible for most recrudescence or
relapse of melioidosis is poor compliance with eradication therapy
(Chaowagul, et al., 1993; Rajchanuvong, et al., 1995; Currie, et al.,
2000a; Jenney, et al., 2001). The reasons for poor compliance are
complex and multifactorial, but availability and cost of medications
and access to follow-up assessment are critical, as is the ability to
recognise medication side effects and arrange alternative therapy where
appropriate. We aim for regular follow-up of cases during the
eradication phase, with free antibiotics and action plans for
defaulters, analogous to tuberculosis programs (Currie, et al., 2000d).
2. Relapses have been found to be 4.7 times (95%CI: 1.6–14.1) more
common in patients with severe disease compared with those with
localised melioidosis (Chaowagul, et al., 1993).
3. Use of ceftazidime in the initial intensive therapy was also
associated with a halving of relapse (Chaowagul, et al., 1993).
4. Duration of eradication therapy is also critical, with relapses
following oral therapy of eight weeks or less more likely than if
eradication is given for longer than 12 weeks (Suputtamongkol, et al.,
1991, Chaowagul, et al., 1993). Hence the recommendations that
eradication therapy should be for 12–20 weeks (Rajchanuvong, et al.,
1995, Chaowagul, 2000) or ‘at least 3 months’ (Group., 2000/2001,
Currie, et al., 2000d).
5. The choice of agents for the eradication therapy is important. Both
amoxycillin/clavulanate (Rajchanuvong, et al., 1995) and oral
quinolones (ciprofloxacin or ofloxacin) (Chaowagul, et al., 1997) have
been found to be less effective in preventing relapse than
‘conventional’ eradication with chloramphenicol (given usually only for
the first four to eight weeks), cotrimoxazole and doxycycline.

Reports on in vitro susceptibility of B. pseudomallei for quinolones

generally show resistance or intermediate results (Chau, et al., 1986;
Ashdown, 1988). Disc diffusion techniques can give false-sensitive results,
hence the cautions against use of quinolones (Ashdown & Currie, 1992).
However, quinolones are still being used in some circumstances, possibly
with the consideration of the noted excellent postantibiotic effect of
ciprofloxacin (Walsh, et al., 1995a) and their ability for intracellular
activity and potential activity in the presence of biofilm (Vorachit, et
al., 2000). At present quinolones are not recommended as first-line agents
for eradication of B. pseudomallei, although there is currently a study
comparing azithromycin plus ciprofloxacin against doxycycline plus
cotrimoxazole (Chaowagul, 2000).
The most important recent trial of eradication therapy was a comparison
of doxycycline alone (the most commonly used eradication regimen in the
Northern Territory until 1998) versus ‘conventional’ chloramphenicol (first
four weeks only), cotrimoxazole and doxycycline combination (Chaowagul, et
al., 1999a). Relapses were significantly commoner in the doxycycline-alone
group, resulting in a recommendation that doxycycline not be used alone as
first-line eradication therapy (Chaowagul, et al., 1999a). Similar failures
of doxycycline alone as eradication therapy were being noted in the
Northern Territory (Currie, et al., 2000a), with some B. pseudomallei
relapse isolates showing acquired doxycycline resistance (Jenney, et al.,
2001).
Since changing to eradication therapy with cotrimoxazole alone in the
Northern Territory, relapses have been almost exclusively in non-compliant
patients (Currie, et al., 2000d), consistent with the hypothesis that it is
cotrimoxazole which is the critical component in the ‘conventional’
combination therapy. Current trials in Thailand will hopefully ascertain
whether it is still beneficial to have combination therapy for the
eradication phase of melioidosis treatment, or whether cotrimoxazole alone
is adequate.
In summary, initial intensive therapy should be with ceftazidime or
imipenem or meropenem, possibly with cotrimoxazole added, for a minimum of
14 days —longer (four to eight weeks or more) if critically ill, extensive
pulmonary infection, deep-seated collections or organ abscesses,
osteomyelitis, septic arthritis or neurological melioidosis. Subsequent
eradication therapy should be for a minimum of three months, with high dose
cotrimoxazole or conventional combination therapy.
In patients with septic shock, preliminary data suggest addition of G-
CSF in addition to state of the art intensive care management may increase
survival.

Protocol issues requiring special consideration

Who to treat/cover for melioidosis when you only have clinical
suspicion of the diagnosis?
The risk factors of melioidosis are common (diabetes, alcohol abuse, renal
failure, steroid treatment, chronic lung disease), and presentation to a
remote health centre with fever and/or signs of pneumonia is relatively
common. There is therefore a potentially large group of people being seen
in remote settings (in the Top End) who should be suspected of having
melioidosis.
Early treatment is important for survival, so waiting for failure of
standard penicillin treatment regimens may lead to poor outcomes. However,
experience from the Royal Darwin Hospital (RDH) suggests that a policy of
treating moderate or severe pneumonia in a person with one or more risk
factors for melioidosis with cefriaxone 2 g (high dose) and evacuating to
hospital seems to work well. This protocol has been in place for 10 years.
Decreased melioidosis mortality has paralleled increased awareness of
melioidosis amongst urban and rural health staff in the Top End.
Additionally, there has been a more recent policy of using ceftazidime or
meropenem in initial antibiotic treatment regimens in patients admitted to
RDH critically ill with pneumonia, especially in the wet season and in
those with risk factors. Most cases of melioidosis are in fact not
critically unwell and it is appropriate to await definitive diagnosis by
culture before beginning specific B. pseudomallei therapy. This therefore
relies on a high level of clinical suspicion amongst health staff
(especially for diabetics in the wet season) and on the collection of
appropriate samples for culture. Hence the note on this in the CARPA STM
protocol.
Common examples are those with a subacute/chronic pneumonia, who may be
unwell but not critically ill for a few weeks, unrecognised until
appropriate cultures (usually sputum) grow B. pseudomallei, or chronic
unhealing skin sore(s)/abscess(es)/ ulcer(s) which have not responded to
benzathine penicillin or flucloxacillin, and then culture B. pseudomallei
when appropriate swabs are taken. Occasional cases of
acute/subacute/chronic septic arthritis or osteomyelitis, or rarely
cellulitis, are due to B. pseudomallei, making these conditions also worth
considering as possible melioidosis, especially in diabetics, those with
chronic renal impairment and alcohol excess.
Finally, an important syndrome has been increasingly recognised,
especially by medical staff in East Arnhem. This is prostatic/genitourinary
melioidosis in males who are heavy kava and/or alcohol drinkers presenting
with a few days of fever, non-specific abdominal pain, often some diarrhoea
and urinary difficulties (may not be painful, however) culminating in
urinary retention. Drainage of prostatic abscess(es) is almost always
required.
Serology has a limited role in diagnosis as both specificity (for active
infection) and sensitivity (especially in acutely sick patients) are poor.
A positive IHA (titre over 1/40) does need appropriate clinical assessment
for active melioidosis and appropriate microbiology performed. It is now
very rare for true cases of melioidosis in the Top End to be culture
negative, provided the correct samples are taken. Therefore patients are
not treated for melioidosis because of only a positive serology result. In
confirmed cases serology titres may slowly decrease with treatment, but
this is not universal.
Melioidosis needs to be considered in settings of; diabetic foot
infection, osteomyelitis and septic arthritis.

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 Nosebleeds (Epistaxis)

Author: Dr Koen DeDecker

Topic Reviewers: Dr Alam (ENT, ASH); RDH ENT clinic; Kenna Bistani (RAN, Pine
Creek Clinic); Monica Ostigh (RAN, Jabiru Clinic)

Aetiology and definition

Anterior epistaxis
Most commonly (85–95%) nosebleeds originate from an area on the nasal
septum close to the nostrils (Little’s area or Kiesselbach’s area).
Anterior epistaxis is more common in children and young adults and most
often ‘spontaneous’, mild and easy to control.

Aetiological factors
• Environmental factors: cold, dry air1,2 (also associated with posterior
epistaxis) 5
• Local factors: infection1–4, rhinitis, sinusitis
• Trauma: picking the nose1–4, nasal fractures1–4
• Foreign body3,4
• Iatrogenic2,3
• Neoplasia1–4
• Chemicals, including cigarette smoke2
Except with severe facial trauma, such as motor vehicle accident, traumatic
epistaxis is usually from an anterior nasal source and easily treated.2,4

Posterior epistaxis
Less commonly (5–15%) nosebleeds originate from far back in the nose (far
posterior in the inferior meatus).
Posterior epistaxis is more common in elderly patients4,5,16 and often
moderate to severe and may be difficult to control.1,5,16,21
Posterior epistaxis may reflect an underlying condition which needs
further attention:
• Hypertension.2,5–10 It is still controversial whether HT is associated
with adult epistaxis. But it is recommendable to check BP during an
episode of epistaxis and ‘treat it straight away because it may
exacerbate ongoing nasal haemorrhage, as well as after the episode of
epistaxis in order to rule out sustained HT’.6
• Arteriosclerosis.1,2,4,16
• Tumour in paranasal sinus or nasopharynx2–4: (intermittent) epistaxis
can be the only symptom.
• Foreign body3,4: as for a tumour, usually presents with unilateral
symptoms; foul discharge and epistaxis.
• Chronic renal failure2,5: persistent epistaxis may be encountered in CRF
patients.
• Alcohol: patients who have a regular high alcohol consumption have an
increased risk for epistaxis.11
 • Bleeding tendencies associated with liver disease, aplastic anaemia,
leukaemia, thrombocytopenia, hereditary coagulopathies.1–5
• Medications: Warfarin, Aspirin.3,5,10,12,13

The association between non-steroidal anti-inflammatory drugs (NSAIDs) and

epistaxis is unclear.13 Aspirin differs from all other NSAIDs in that it
reproduces irreversible acetylation of cylooxygenase. Hence, its effect is
permanent and lasts for five to seven days, the life of the platelet. In
contrast NSAIDs have a reversible but variable degree of inhibition of this
enzyme.

Management of epistaxis
Acute management
First aid measures should always be performed, independent of the
provisional cause, probable location (anterior versus posterior epistaxis)
and apparent severity of the epistaxis. First aid measures are designed to
stop anterior epistaxis, which is the most common form of epistaxis.
• Calm the patient; sit the patient up, leaning forward.2,15,19 This
position allows gravity to keep blood flowing out of the nostrils,
rather than posteriorly down the throat. Encourage patient to spit out
any blood that trickles down the back of the throat to prevent
swallowing/aspiration4 large amounts of bloods. This allows you to see
if there is ongoing blood loss, and swallowed blood can tend to cause
vomiting.
• Put on gloves and hold the nose firmly between the full surface of the
fingertips of thumb and forefinger (pinch the nasal alae together).1–
4,15,19
Although so simple as to seem obvious, <50% of emergency
department personnel could describe the correct site to apply digital
pressure in a nosebleed.2
• Press for five1,2 to 101,4,15,19 to 154,14 minutes, continuously (without
releasing pressure in the mean time to check for ongoing bleeding).
People tend to check too often without giving natural haemostasis
mechanisms a really good chance. There was nothing in the literature to
recommend one time period over another 10 minutes seems reasonable.
• Giving the patient ice to suck15,19, or holding a cold wet towel over the
upper face (a cold compress on the nasal bridge) is recommended by some
authorities, however no specific evidence of its efficacy could be
found.4,15,19 It was not included in the protocol.
• Check BP, pulse and treat if necessary1,2,4: If BP >180/110 give
Nifedipine 10 mg S/L or oral. [Editor: Fast-acting nifedipine is
unlikely to be available so discuss BP control with a doctor.] If BP
low and pulse high, suspect hypovolaemia, shock and give IV fluids.
• When the bleeding stops, tell the patient not to blow the nose for the
rest of the day. This is simply to preserve the new blood clot.

If bleeding continues
• Apply pressure from within by inserting a cotton pledget (or small
pieces of ribbon gauze) in the nostril(s), impregnated with a
vasoconstrictor14 (to constrict the blood vessels aiming to reduce/ stop
bleeding) and a topical anaesthetic15 (to numb the nasal mucosa,
therefore facilitating further inspection and handling, if
necessary).1,2,4,16
Agents with combined vasoconstrictor-anaesthetic properties are
recommended.

• Commonly used agents with combined vasoconstrictor and anaesthetic

properties: co-phenylcaine forte spray28, cocaine 4%.4,16 Co-phenylcaine
forte spray is widely available, cheap and easily administered.28
However, there are logistical difficulties with storing cocaine-like
substances in many remote clinics.
• Commonly used vasoconstrictors: phenylephrine 0.25%1,2, pseudoephrine2,
adrenaline (1:10 000)2,4,14
• Commonly used anaesthetics: lidocaine solution4 115 -21 -42,16%, lidocaine
gel, xylocaine 10% spray15,19 tetracaine.4
Hold for 10 minutes, then pull pledgets out and look quickly for the
bleeding site (suction away blood 2,4,14).
If a bleeding tendency is suspected (see aetiology), electro-cautery is
not used.1,2,4 Vaseline (petrolatum) gauze is used to apply pressure as
atraumatically as possible to the bleeding point. Note that the Royal
Darwin Hospital ENT clinic does not see any reason to not use cautery in
this situation.
Otherwise, the bleeding point (usually visualised at the anterior nasal
septum, Kieselbach’s or ‘Littles area’) may be cauterised by chemical
cautery: silver nitrate in a 75% applicator bead1,16 or trichloroacetic acid.2
Cautery can be applied to multiple areas in a peripheral to central
direction for four or five seconds4,16: the area immediately around (1 mm
away from) the bleeding area is cauterised first and then cautery is
applied over the bleeding area.28
Up to two or three silver nitrate sticks are needed, but care is
necessary since excessive or bilateral septal cautery may cause septal
perforation.2,4,16 However, the technique most often seems to be effective and
safe (even in inexperienced hands) if one limits cautery to one side of the
septum (only via one nostril). Moreover, chemical cautery is cheap: Graftco
silver nitrate 75% (Sigma) costs A$10–15 for 100 sticks.28
In children, cautery is said to be very effective. A UK study17, however,
claims the application of a nasal antiseptic cream (Naseptin, possibly
similar to Nasalate Nose Cream, a combination of chlorhexidine and
phenylephrine in paraffin listed in MIMS-OTC 2000) is equally effective,
but easier to apply and therefore treatment of choice. This study compares
recurrent epistaxis rate with either option (cautery versus AB cream),
which is only one way at looking at effectiveness. Antibiotic cream
application after cautery is advised by other literature as well.2, 28
If the above is unsuccessful, nasal packing is needed. Classic anterior
nasal packing is performed with narrow gauze1,2,4,15,16,19 (1 cm x 20 cm
length of gauze), soaked with 10% xylocaine spray or 1% lidocaine solution.
Kaltostat as an alternative material for nasal packing showed similar
efficacy and patient acceptance.
The gauze should be impregnated with one of the following three
alternatives:
• Antibiotic2(e.g. Neosporin, Bacitracin, Kenacomb28). The AB aims to
prevent toxic shock syndrome, a rare syndrome that has four major
criteria: fever greater than 38.9?C; an exanthema with erythroderma;
subsequent desquamation; and orthostatic hypotension and shock.18
• BIPP18 (Bismuth Iodine Paraffin Paste), is expensive but seems to be
the most popular in the UK.3,18 This statement seemed to be a general
impression from the authors, shared by Dr Alam (ENT, ASH).18 One study24
 discourages its use in combination with Foley catheter ballooning,
while another study22 recommends its use in combination with Foley
catheter ballooning.
• Vaseline4,16(non-adhering fine mesh gauze impregnated with white
petrolatum) is widely available, cheap, effective and atraumatic (ideal
in case of bleeding tendencies — see above)

The general goal is to place the packing from the back and bottom of the
nose forward.4 Gauze should be inserted with a thin forceps (bayonet or
Tilley’s nasal packing forceps 2,16,19) until sufficient pressure exists to
tamponade the bleeding, leaving 3 cm of the gauze outside the nostril and
taped to the face. The most common error is failure to adequately pack the
posterior aspects of the anterior nasal cavity.2

Merocel nasal packing

A recommended and frequently used alternative to classic anterior nasal
packing is Merocel nasal packing2,18,20 (Xomed). Merocel is a compressed,
dehydrated sponge, which can be slid into the nasal cavity and then, when
rehydrated by blood (or added saline), expands to three times its normal
size partially filling the nasal cavity. A Merocel pack meets nearly all
the criteria for an ideal nasal pack18: it is easy and quick to insert (its
actual insertion takes only a couple of seconds, but is unfortunately not
painless), usually well tolerated when in place and its removal is less
painful than its insertion.
Merocel has minimal risk of aspiration and can be used for anterior (8
cm) and posterior (10 cm) epistaxis as well as for bilateral epistaxis.18
For pragmatic reasons the 10 cm packs could always be used and trimmed with
scissors according to the patient’s internal nasal anatomy.28
Insertion requires minimal teaching and is effective for stopping
epistaxis in over 90% in inexperienced hands.2,18 Merocel packing seem to
inhibit bacterial proliferation and offer some protection against toxic
shock syndrome.18 Moreover, the packs are cheap18 (A$11.00 in 2001)28 for
the 10 cm posterior pack and they have a lengthy shelf life (+/- 10 years).

Insertion18
Merocel is inserted, after lubrication with an antibiotic ointment (e.g.
bacitracin), at an angle of 45? for a distance of 1–2 cm. It is then
brought into the horizontal plane and with firm pressure quickly pushed
straight backwards into the nasal cavity. If the pack doesn’t fully
rehydrate with blood, rehydrate with saline.

Removal18
Using an orange needle, inject the end of the pack and rehydrate with 10 ml
of saline or water. Leave for five minutes. Grab the end of the pack with
forceps and gently withdraw.
• Systemic antibiotics are recommended if a nasal pack has been inserted
to prevent sinusitis.1,2,4 This is important.28
• A nasal pack usually stays in for two days4,28, except for severe cases
where three to four days may be required.2,4,1 In one study5 one of the
factors associated with rebleeding was (posterior) pack removal within
48 hours.

Even when a nasal pack is successfully inserted complications are possible,

hence the recommendation to refer to hospital.
 After anterior packing, the patient’s throat is inspected. If blood is
still visible trickling from the nasopharynx (or patient swallows most of
the blood)19, either the anterior pack is not optimally placed (in which
case one should try to reinsert a nasal pack) or there is a posterior nasal
bleeding source.2,4
Bilateral epistaxis was not helpful in diagnosing posterior epistaxis:
equal numbers of patients presented with unilateral and bilateral bleeding.5

Continued bleeding suggests posterior

bleeding source
Options for controlling a posterior nasal bleed include:
Merocel posterior pack18,20: (Pope Epistaxis Packing #400406, length: 10 cm
pack). Other posterior nasal packs are more difficult to insert.
If a Merocel posterior pack is not available, or failed insertion is
encountered, it might be justified to try tamponade with a catheter balloon
(e.g. Foley catheter). This depends upon one’s experience, confidence and
available equipment — especially in the case of a remote epistaxis-
emergency (a shocked patient or a hypovolaemic patient with significant
ongoing epistaxis) — while awaiting evacuation to hospital.
Posterior bleeds can be very difficult to control and are more likely to
be associated with other diseases needing expert attention, hence the
recommendation to urgently refer any person with a suspected posterior
nasal bleed.
Balloon catheters (Foley catheter, Brighton Balloon, Simpson Balloon)
are an alternative to tamponade by posterior packs inserted in the
nasopharynx via the nostrils and inflated with sterile water or air. The
balloons are secured anteriorly using a clamp (e.g. umbilical cord clamp).
The Foley catheter4,19,21–24 has been used for decades (since 1956).
However, this catheter is not designed and not licensed for arresting
epistaxis; it appears to have higher rates of complications than other
balloon catheters.21
Nevertheless, Foley catheters are frequently successful in arresting
epistaxis, especially in combination with an anterior gauze-based
pack.4,19,21–24 Furthermore, they are cheap and readily available!

Insertion and inflation (of Foley catheter)

The deflated catheter is inserted in the nostril affected by epistaxis
(after the tip is removed because it irritates the posterior pharynx and
causes gagging). Once the catheter and balloon are visualised intra-orally,
the balloon is gradually inflated with air and the catheter is slowly
retracted. When the balloon becomes inflated it catches on the posterior
choana. The recommended inflation method is the one in which half the
required volume is inserted, the balloon is pulled forward to wedge in the
posterior choana and the remainder of the volume is then inserted.22 The
catheter is then clamped (e.g. umbilical cord clamp) anteriorly (just
outside the nostril, with a piece of gauze between the nose and the
clamp)28 in a way that continuous traction is assured.

Catheter size, balloon size, inflation volume, air or liquid

There is lack of consensus. One study recommends size 14 catheters with 30
ml balloon, but doesn’t mention inflation volume. Another study23, using
size 14 catheters, showed complete sealing in 85% of patients at
appropriate inflation volumes and showed that the choana is usually
effectively sealed at 8–15 ml inflation volume.28 Another study22 recommends
to us size 12 Foley catheters with a 30 ml balloon, suggesting liquid
inflation volumes of 6–9 ml (but recommending further studies as to
determine the appropriate volume of inflatant required to occlude the
posterior choana). CRANA19 recommends a size 12 or 14 catheter with a 30 ml
balloon, 10 ml inflation volume with air (which is not recommended by most
of the other studies22,23,24, as spontaneous deflation of air-inflated
balloons is too fast as compared with the liquid-inflated ones). However,
air is safer in remote setting in inexperienced hands, as the liquid-
inflated balloons can be heavy and tend to fall backwards, inducing gagging
and choking.28 Be aware: 3 ml of liquid approximates 4 ml of air in a
catheter.22
A compromise between the different recommendations, and staying
essentially consistent with the CRANA Clinical Procedures Manual, is:
catheter size 14, balloon size 30 ml, inflation volume 10 ml of air.

Hot-water irrigation20,25
Hot-water irrigation (HWI) was introduced as a treatment of epistaxis more
than 100 years ago. It seems to be a less traumatic, less painful and
possibly equally effective alternative to tamponade treatment, requiring
significantly shorter hospital stay.20 However, this study was carried out
by someone with an interest in promoting a device for HWI.
HWI has the risk of aspiration during treatment. This risk may be
minimised with a specially designed catheter 20, which is nevertheless not
widely available.
However, one would think a specially designed catheter could easily be
replaced by the use of two Foley catheters: one 30 ml Foley catheter, size
16, inflated with 10 ml of water could be used to achieve posterior choanal
sealing and a second uninflated Foley could be connected to a 100 ml
syringe to perform the actual HWI. This has not been studied yet.
The actual technique constitutes a simple forceful irrigation of the
nasal cavity with 500 ml of hot water (50?C: narrow thermo-therapeutic
range: 46–52?), with the patient sitting up with the head flexed. The
procedure is repeated once if the bleeding continues.
More evaluation of HWI is needed before it could be recommended.

Further management considerations

There does not appear to be a role for routine coagulation tests (PT, APTT,
platelets) in patients (admitted with) epistaxis.26,27 One study26 admits there
is paucity of scientific information with regard to this aspect of
epistaxis management. Another study27 found that all the abnormal results of
those patients on which coagulation test were performed (8.3% of tested
patients), were found in patients taking warfarin or those on a combination
of warfarin and aspirin. If routine coagulation tests were performed in a
more rational way, appropriate tests would include a more complete
haemostatic work-up, including bleeding time and assays for Factor VIII and
von Willebrand factor, among others. This would significantly increase both
cost and workload if applied in a non-targeted manner.
Our conclusion is that only those patients with recurrent or persistent
bleeding, despite adequate medical therapy, patients on anticoagulant
medication, or those having possible underlying bleeding diatheses based on
either history or examination, should be evaluated further. The
investigations subsequently chosen should also reflect a sound
understanding of haemostatic function.
Approach for habitual nosebleeders7
There does not appear to be a need to have a different approach for
habitual and episodal nosebleeders. Heredity for recurrent nosebleeds was
noted by 42% of the bleeders. The start of the nosebleeds was mostly
spontaneous. Common cold and stress or tiredness were frequently
experienced before the occurrence of nosebleeds. The blood pressure
distribution of the habitual nosebleeders did not differ from that of the
population samples used for comparision.7 Diseases reported by the habitual
bleeders were few, and the routine blood tests revealed only few diseases
that could be related to the recurrent nosebleeds. Persistent recurrent
nosebleeders to be referred to exclude malignancy, especially if epistaxis
is accompanied with foul unilateral nasal discharge.28
There is ongoing controversy whether hypertension is associated with
adult epistaxis.5–10 But it is recommendable to check BP during an episode of
epistaxis and treat it accordingly, as well as after the episode of
epistaxis, in order to rule out sustained HT. In one study HT was
associated with bleeding from the middle meatus, but not with the severity
of the bleeding.9
The use of apirin, epistaxis and untreated hypertension are independent
risk factors for primary intracerebral haemorrhage (ICH) in middle-aged and
elderly people.10,13 (In this study patients were positive for a history of
epistaxis if they had had more than one episode of nosebleed during the
preceding five years or if they had visited an outpatient ENT clinic or had
been hospitalised because of epistaxis.)
Epistaxis is a risk factor for ICH in middle-aged and elderly people,
both independently and combined with the use of aspirin. The history of
epistaxis and use of aspirin constituted a potential and new risk factor
combination, whereas the use of aspirin itself in low dose may not be a
significant risk factor (protective for all types of stroke, even if it
makes haemorragic stroke more common). There is no doubt that daily aspirin
should be continued where it is indicated for high-risk cardiovascular
patients. The conclusion of the author is a careful one, and indeed the
known protective features of aspirin are recognised.10
Other independent risk factors are untreated HT, previous ischaemic
stroke, epilepsy and recent strenuous physical exertion. Epistaxis may be a
warning sign of an increased risk for ICH in subjects using aspirin. Self-
medicating patients on aspirin, especially when presenting with epistaxis,
should be made aware of the significant risk of bleeding. Regular (>once a
week), high alcohol consumption is associated with epistaxis.11 Regular
alcohol consumption reduces platelet aggregation and prolongs the bleeding
time; these effects, coupled with haemodynamic changes such as
vasodilatation and changes in blood pressure, may be important in some
cases of arterial nosebleeds in adults.
Alcohol consumption was defined as follows: one unit = one half pint
(284 ml) of beer = one glass of wine (approx 10 g alcohol).
The patients with nosebleeds drank more alcohol (33 (mean) units a week
versus 7).
Furthermore, the patients with nosebleeds were significantly more likely
than the controls to have drunk alcohol within the 24 hours prior to
admission.
Severe epistaxis and swallowed blood
Severe epistaxis may be caused by liver disease. In this case blood may be
swallowed in large amounts and should be eliminated as promptly as
possible. The GI tract should be sterilised with nonabsorbable antibiotics
(e.g. neomycin 1 g po qid) to prevent the breakdown of blood and the
absorption of ammonia, which in turn can cause hepatic encephalopathy.
Upper gastrointestinal bleeding, which can present as epistaxis, should
be ruled out.

References
1. Section 7. Ear, Nose And Throat Disorders. Chapter 86. Nose and Paranasal Sinuses
In: The Merck Manual of Diagnosis and Therapy. 1995–2001.
2. Tan LKS & Calhoun KH. Epistaxis In: Medical Clinics of North America. Jan 1999;
83(1):43–56.
3. Chopra R. Epistaxis: a review. The Journal of the Royal Society for the promotion
of Health March 2000; 120(1):31–3.
4. Alvi A, Joyner-Triplett N. Acute epistaxis. How to spot the source and stop the
flow. In: Postgraduate Medicine May 1996; 99(5):83–90, 94–6.
5. Viducich RA, Blanda MP, Gerson LW. Posterior epistaxis: clinical features and
acute complications In: Annals of Emergency Medicine Vol 25 No 5 pp 592–6 May 1995.
6. Temmel A F, Quint C, Toth J. Debate about blood pressure and epistaxis will
continue In: BMJ May 2001; 322 (7295):1181.
7. Beran M, Petruson B. Occurrence of epistaxis in habitual nosebleeders and
analysis of some etiological factors. In: ORL Journal of Otorhinolaryngolgy and
Related Specialities, 1986; 48(5):297–303 .
8. Herkner H, Lagner AN, Mullner M, Formanek M, Bur A, Gamper G, Woisetschlager C,
Hirschl MM. Hypertension in patients presenting with epistaxis In: Annals of
Emergency Medicine, Feb 2000; 35(2):126–30.
9. Padgham N. Epistaxis: anatomical and clinical correlates . Journal of Laryngology
and Otology, Apr 1990; 104(4):308–11.
10. Saloheimo P, Juvela S, Hillbom M. Use of Aspirin, epistaxis, and untreated
hypertension as risk factors for primary intracerebral haemorrhage in middle-aged
and elderly people. Stroke Feb 2001; 32(2):399–404.
11. McGarry GW, Gatehouse S, Hinnie J. Relation between alcohol and nosebleeds. BMJ
Sep 1994; 309(6955):640.
12. Denholm SW, Maynard CA, Watson HG. Warfarin and epistaxis: a case controlled
study. Journal of Laryngology and Otology March 1993; 107(3):195–6.
13. Tay HL, Evans JM, McMahon AD, MacDonald TM. Aspirin, nonsteroidal anti-
inflammatory drugs, and epistaxis. A regional record linkage case control study.
Annals of Otology Rhinology Laryngology Aug 1998; 107(8):671–4.
14. Nose and paranasal sinuses. In: The Bobby R Alford Department of
Otorhinolarynology and Communicative Sciences: Core curriculum syllabus, 1996.
15. Nosebleeds. In: Central Australian Rural Practitioners Association Standard
Treatment Manual. CARPA, 1997; 178.
16.Frazee TA & Hauser MS. Nonsurgical Management of Epistaxis. Journal of Oral
Maxillofacial Surgery April 2000; 58(4):419–24.
17. Ghosh A, Jackson R. Towards evidence based emergency medicine: best BETs from the
manchester Royal Infirmary. Cautery or cream for epistaxis in children. Emergency
medicine Journal May 2001; 18(3):210.
18. Pringle MB, Beasley P, Brightwell AP. The use of Merocel nasal packs in the
treatment of epistaxis. Journal of Laryngology and Otology June 1996; 110(6)543–6.
19. Nosebleed: Doing anterior nasal packing: CRANA (Clinical Procedures Manual for
remote and rural practice), 2001; 126–8.
20. Stangerup SE, Dommerby H, Siim C, Kemp L, Stage J. New Modification of Hot-Water
Irrigation in the treatment of posterior epistaxis. Archives of Otolaryngology Head
Neck Surgery June 1999; 125(6):686–90.
21. Holland NJ, Sandhu GS, Ghufoor K, Fosh A. The Foley catheter in the management of
epistaxis. Int J Clin Pract Jan–Feb 2001; 55(1):14–15.
22. Hartley C, Axon PR. The Foley catheter in epistaxis management: a scientific
appraisal. The Journal of Laryngology and Otology May 1994; 108(5):399–402.
23. Wai Chung Lee, FRCS (ORL); Peter Ka Ning Ku, FRCSEd; Charles Andrew van Hasselt,
FRCS. Foley Catheter Action in the Nasopharynx; A Cadaveric Study. Archives of
Otolaryngology Head and Neck Surgery Sep 2000; 126(9):1130.
24. DJ McFerran, FRCS; SE Edmonds, MB, BS. The use of balloon catheters in the
treatment of epistaxis. The Journal of Laryngology and Otology March 1993; 107):197–
200 .
25. MD Seidman. Letters to the Editor. Hot-Water Irrigation in the Treatment of
Posterior Epistaxis. Archives of Otolaryngology Head Neck Surgery Nov 1999;
125(11):686–90.
26. Holland S, Thaha MA, Nilssen EL, White PS. Coagulation studies in patients
admitted with epistaxis: current practice in Scotland. In: Journal of Laryngology
and Otology Dec 1999; 113(12):1086–8.
27. Thaha MA, Nilssen EL, Holland S, Love G, White PS. Routine coagulation screening
in the management of emergency admission for epistaxis: is it necessary? Journal of
Laryngology and Otology Jan 2000; 114(1):38–40.
28. Dr K Alam (ENT specialist at Alice Springs Hospital).
 Painful Scrotum

Author: Stephen Baguley (STI unit, RDH)

Topic Reviewers: Andrew Urquhart, (CAAC); Mutitjulu; Mt Liebig; Janet Knox; and
others

Introduction
Scrotal pain is a common symptom, and when faced with a man with this
complaint the differential diagnosis is diverse. The list of causes can be
broken down into infective and non-infective.

Infective causes

Epididymo-orchitis C. trachomatis,
Sexually acquired organism: N. gonorrhoeae,
E. coli (from insertive anal
sex)

Non-sexually acquired E. coli (from a UTI)

organism: Pseudomonas aeruginosa
Mycobacteria tuberculosis
Brucella spp. Epstein-Barr
Virus
Mumps — just orchitis,
after puberty
Scrotal abscess

Non-infective causes
Torsion of testis
Trauma although trauma can also
trigger torsion of testis
Torsion of testicular
appendix
Torsion of epididymal
appendix
Tumour benign
malignant
Strangulated hernia
Varicocoele usually more of a dragging
sensation
Granulomatous a late complication of
epididymo-orchitis vasectomy
Drugs Amiodarone
Referred pain renal tract calculus
leaking aortic aneurysm
Psychological
Behçets disease

This section of the manual is not intended to be a comprehensive algorithm

for diagnosing the cause of scrotal pain. The aim is to offer some tips for
distinguishing between two of the commonest and most acutely serious
conditions: torsion of the testis; and epididymo-orchitis.

The physical findings are schematically shown above. Normally the

epididymis is behind the testis, and the testis hangs with its long axis up
and down. In torsion you may find the twisted testis higher (though one is
usually higher by a small amount) and horizontal. The epididymis may be
rotated to the front

Literature search strategy

Medline 1994–May 2001 was searched using the strategy ((testi* OR spermatic
cord) AND torsion) OR acute scrotum, limit = review. Current national STI
(sexually transmissible infection) guidelines for the management of
epididymo-orchitis/scrotal pain were searched from Australia, United
Kingdom and the United States of America. The Australian Antibiotic
guidelines were searched, as were relevant major textbooks.

Explanation and expansion of the guideline

The start of the section highlights that a painful scrotum should be taken
seriously. This is because of the possibility of testicular torsion, which
can cause infarction (death of the testicle by cutting off its blood
supply) in a matter of hours.1 It is often very difficult to confidently
exclude torsion. This is because the oedema, which quickly occurs with
severe epididymitis or torsion, makes it hard to feel the things inside. If
torsion cannot be confidently excluded the man should be referred
immediately for exploratory surgery, even if it is the middle of the night.
Testicular torsion occurs when the testicle rotates and twists the
spermatic cord (which contains the blood supply to the testicle). Men with
an unusually spacious tunica vaginalis (the pouch which holds the testicle)
are at particular risk of this happening since it allows the testicle to
move around more freely.
Epididymitis is inflammation of the epididymis, if the infection spreads
to the testis it is called epididymo-orchitis. Management and treatment are
the same for both conditions, so the rest of this document just refers to
epididymitis to make it easier to read. Epididymitis is a serious condition
since, if left untreated, it might result in infertility although this is
unlikely if the infection is just on one side.

Age
Torsion can occur at any age but is more common in people aged less than
20. If a pre-pubertal boy has testicular pain he should be considered to
have torsion until exploratory surgery has shown otherwise because
epididymitis is uncommon in this age group.2 In younger sexually active men
epididymitis is usually caused by sexually transmitted organisms, in older
men it is usually caused by gram-negative enteric (i.e. from the gut)
bacteria that cause urinary tract infections. This is more likely if the
man has had urological surgery, urethral instrumentation (such as a
catheter) or if he has an anatomical abnormality.
The UK3 and the USA4 guidelines choose a cut-off age of 35 years to
distinguish between these groups although they acknowledge that there will
be a lot of crossover between them. The Australian STI management
guidelines5 don’t mention enteric organisms as a possible cause and so
don’t mention a likely age. The Australian Therapeutic Guidelines:
Antibiotic6 discuss enteric organisms but again don’t give a cut-off age.
In the population covered by the CARPA manual it is perhaps unrealistic to
recommend a clear age cut-off for deciding whether a man has an STI or an
enteric infection. STIs are common in the CARPA region, and so people
presenting with epididymitis should be treated as if they have one unless
the history and other findings strongly suggest that an enteric organism is
the cause.

How it starts
Half of people with torsion give a history of similar episodes that have
resolved spontaneously. Half report sudden onset pain, peaking in severity
after seconds or a few minutes, which might wake them from sleep. Sometimes
there is a history of trauma prior to the onset of pain; this can cause
confusion, making the examiner think that the pain was directly due to the
injury.
The pain of epididymitis usually starts gradually over hours as the
infection develops but in a study of 92 US servicemen the pain started
suddenly in a third.7

Pain
Torsion doesn’t always cause severe pain and sometimes pain can be felt in
the lower abdomen. Epididymitis can cause inguinal pain and, in severe
cases, flank pain.

Fever
A raised temperature makes epididymitis more likely, but many people with
epididymitis have a normal temperature.

Other symptoms
One of the first symptoms of torsion can be nausea starting at the same
time as the pain.
If the man has symptoms of urethritis, dysuria or a discharge then the
diagnosis is likely to be epididymitis. Often the urethritis is
asymptomatic — perhaps because the scrotal pain gets his attention more
than the urethral symptoms. Don’t forget that he could have torsion and
epididymitis.

Examination
Remember that the left testicle is usually lower than the right and it is
often slightly larger. In torsion the testicle is often so tender that the
man will be very reluctant for you to touch it but you might find that the
torted side is sitting higher in the scrotum and lying horizontally. If the
epididymis is in front of the testis on the unaffected side it is an
indication of a lax tunica vaginalis — the congenital abnormality that
makes torsion possible. This suggests that the cause of the symptoms on the
other side might be torsion as opposed to epididymitis.
When examined early in the course of epididymitis it should be possible
to identify a swollen epididymis — the swelling usually starts at the lower
pole. When the infection spreads, the inflammation and secondary hydrocoele
can make it difficult to determine anatomy.

Lifting the scrotum

Any extra pressure on the testicle will make the pain worse in a case of
torsion. In epididymitis scrotal support can ease the pain; men should
therefore be advised to wear supportive underpants rather than shorts.

Urinalysis
This will be normal in torsion unless there is coexisting urethritis or
testicular infarction has occurred.

Colour Doppler ultrasound

This is available in some centres and can be a useful test for diagnosing
torsion with sensitivity of 82–89% and specificity of 90–99% being
reported.8 False negatives occur, and the test is probably best reserved for
people with an equivocal or low probability of torsion. If torsion is
likely clinically they should have exploratory surgery without waiting for
an ultrasound.

Treatment
It is important to give sufficient analgesia since the pain can be
excruciating. If torsion cannot be confidently excluded, refer for surgery
immediately because the testicle needs to be untwisted as soon as possible.
Manual untwisting is effective at restoring blood supply to the testicle
when immediate surgery is not possible9,10 and can be attempted if the
clinician is familiar with the procedure. The testicle usually needs to be
rotated laterally and may need up to three full turns before it is
untwisted. This will probably be extremely painful so pain relief such as
IV/IM morphine or Entonox (nitrous oxide and oxygen) will be needed. When
fully untwisted the pain improves rapidly. The man still needs to have
surgery to fix the testes in place or else torsion will recur.
There is little consensus on the best treatment for epididymitis.

For epididymitis most likely caused by N. gonorrhoeae or C.

trachomatis.
The Australian STI management guidelines recommend:
 • ceftriaxone 250 mg IM once daily or ciprofloxacin 500 mg orally once
daily PLUS
• doxycycline 100 mg orally twice daily. Patients should take ‘both for
three to five days or until there is clinical improvement. Treatment
can then be continued with doxycycline alone for a total of 21 days.’

The US (Center for Disease Control) guideline recommends:

• ceftriaxone 250 mg IM in a single dose, PLUS
• doxycycline 100 mg orally twice a day for 10 days.

The UK (Medical Society for the Study of Venereal Diseases) guideline

recommends:
• ceftriaxone 250 mg IM single dose or ciprofloxacin 500 mg orally
single dose PLUS
• doxycycline100 mg orally twice daily for 10–14 days

And the Australian Therapeutic Guidelines: Antibiotic recommend (where

penicillin-resistant Neisseria gonorrhoeae is uncommon [prevalence <5%]):

• amoxycillin 500 mg orally, eight-hourly for 10–14 days PLUS

• doxycycline 100 mg orally twice daily for 10–14 days
Otherwise:

• ceftriaxone 250 mg IM single dose OR ciprofloxacin 500 mg orally single

dose PLUS
• doxycycline 100 mg orally twice-daily for 10–14 days (i.e. the same as
the UK guideline)
(If someone is treated as having STI but is later found or suspected to
have an enteric infection then the ceftriaxone or ciprofloxacin should be
continued for 10–14 days.)
This guideline comments that if adherence to two weeks of doxycycline is
likely to be suboptimal there are theoretical grounds to suggest that it
could be replaced by azithromycin 1 g on days one and eight although no
clinical trial has assessed this.
Strangely, the WHO STI11 guidelines recommend treatment as for
uncomplicated N. gonorrhoeae and C. trachomatis. For example, 1 g
Azithromycin and 500 mg Ciprofloxacin.

For epididymitis probably due to enteric organisms.

The US guideline recommends:
• ofloxacin 300 mg orally twice a day for 10 days. (This can also be
used for treating gonorrhoea or chlamydia if the patient is allergic to
cephalosporins and/or tetracyclines). Unfortunately, ofloxacin is not
available under the PBS.

In this situation the UK guideline recommends:

• ofloxacin 200 mg by mouth twice daily for 14 days OR ciprofloxacin 500
mg by mouth twice daily for 10 days

The Australian STI management guidelines do not make a recommendation for

this situation.
The Australian Therapeutic Guidelines: Antibiotic recommend:
Mild to moderate infection:
 • Trimethoprim 300 mg orally daily for 14 days OR amoxycillin +
clavulanate 875/125 mg orally, 12 hourly for 14 days OR cephalexin 500
mg orally, six-hourly for 14 days
If resistance to the above organisms is suspected or proven use:

• Norfloxacin 400 mg orally 12-hourly for 14 days

Severe infection:

• Amoxy/ampicillin 2 g intravenously, six-hourly PLUS

Gentamicin 4–6 mg/kg intravenous daily (tailored to age and renal
function)
Continue until substantial improvement then change to appropriate oral
agent to complete two weeks of treatment.
The CARPA STM guideline recommends 250 mg ceftriaxone intramuscularly as
a one-off dose. This will be enough to treat epididymitis caused by N.
gonorrhoeae and will cover most enteric organisms such as E. coli.
A Medline search (Medline 1994–May 2001 epididymitis AND azithromycin)
failed to find any trials of azithromycin for treating chlamydial
epididymitis but it is known to be very effective at treating uncomplicated
chlamydia infection. Using it with doxycycline will therefore increase the
chance that at least some anti-chlamydial antibiotics will be taken, since
compliance with doxycycline is often poor.
There is no evidence to say how long the course of doxycycline must be
to eradicate C. trachomatis. The available guidelines suggest 10–21 days of
therapy as being sufficient. The CARPA guideline recommends 14 days since
this is convenient to administer.

Follow-up
It is important to follow up men who were not sent for surgery to check
that they’re improving with the antibiotics. A proportion of them will have
torsion or intermittent torsion and could still benefit from referral to a
surgeon for orchidopexy (fixing the testicle in place if it’s still alive)
or orchidectomy (removing it) if it’s dead.
A further review at one week is important. This is an opportunity to
give him the results of the STI check-up and to make sure he’s taken the
doxycycline. If he hasn’t taken sufficient doxycycline, a second dose of
azithromycin should be enough to clear any persisting chlamydial infection.
The results of urine culture should be available within one week. If
there has been a heavy growth of an enteric bacteria, such as E. coli, then
the antibiotics should be changed according to the sensitivity of the
organism.

[Editorial committee comments: Use of ciprofloxicin for men having had

procedures is likely to be fairly rare so no concerns about selection
pressure for resistance and is the recommended best treatment.

In addition, the committee states:

‘In situations when an enteric organism is a likely cause e.g. if there is
a urinary tract abnormality or recent urethral instrumentation in an older
man [who isn’t sexually active] then the doctor with whom the patient is
discussed might suggest using ciprofloxacin. Otherwise the man should be
treated for a sexually transmitted cause in the first instance and
consideration should be given to treating with ciprofloxacin if his
symptoms are slow to resolve or if the results of lab tests indicate it.’

Follow-up
It is important to follow up within 24 hours men who were not sent for
surgery to check that they’re improving with the antibiotics. A proportion
of them will have torsion or intermittent torsion and could still benefit
from referral to a surgeon for orchidopexy (fixing the testicle in place if
it’s still alive) or orchidectomy (removing it) if it’s dead.]

References
1. Dunne PJ et al. Testicular torsion: time is the enemy. Australian and New Zealand
Journal of Surgery 2000; 70:441–2.
2. Berger RE. Acute epididymitis. In KK Holmes et al. (eds). Sexually Transmitted
Diseases. McGraw-Hill, 1999.
3. Clinical Effectiveness Group (Association for Genitourinary Medicine and the
Medical Society for the Study of Venereal Diseases) National guideline for the
management of epididymo-orchitis 2001 http://www.mssvd.org.uk/ceg.htm
4. Centers for Disease Control and Prevention Guidelines for treatment of sexually
transmitted diseases. MMWR 1998; 47 (no. RR-1) pp 86–8.
http://www.cdc.gov/nchstp/dstd/
1998_STD_Guidlines/1998_guidelines_for_the_treatment.htm
5. Venereology society of Victoria National Management Guidelines for Sexually
Transmissible Diseases and Genital Infections 1997; 32–3.
6. Therapeutic Guidelines: Antibiotic. Melbourne, Victoria: Therapeutic Guidelines
Limited, 2000.
7. Blandy J, Fowler C. Testicle: benign swellings. In Urology. Second edition.
Blackwell Science, 1996.
8. Baker LA et al. An analysis of clinical outcomes using color Doppler testicular
ultrasound for testicular torsion. Pediatrics 1997; 105(3)604–7.
9. Sparks JP. Torsion of Testis. Ann R Coll Surg Engl 1971; 49:77–91.
10. Kogan S. Acute and Chronic Scrotal Swellings. In Adult and Pediatric Urology. 2nd
Edn. Gillenwater et al. Mosby year book, 1991.
11. Guidelines for the Management of Sexually Transmitted Infections. World Health
Organization. http://www.who.int/
HIV_AIDS/STIcasemanagement/STIManagemntguidelines/who_hiv_aids_2001.01/index.htm
 Palliative Care

Author: Dr Ofra Fried

Topic Reviewers: Anna Vanderwerf (RAN, Wanarn); Andrew Urquhart (RAN, Beswick
Clinic); Dave Corstorpan (RAN, Nyirripi Clinic)

The World Health Organization has defined palliative care as ‘the active
total care of patients whose disease is not responsive to curative
treatment’ and described the goal of that care as ‘achievement of the best
quality of life for patients and their families’.
Palliative management may be complex and needs to be individualised;
therapeutic doses of many palliative medications can be very variable.1
Palliative medicine is undergoing rapid changes, including developing new
understandings of the causes and treatments of symptoms, and establishing
new uses for old medicines.2 Therapy is guided by standard texts3, shorter
guides to treatment1,4, and a rapidly evolving literature in journals and via
the Internet.5 Existing treatment guidelines probably cannot be condensed
further into the CARPA standard format, however it is possible to summarise
the principles and desirable care standards of palliative care1,6, which can
then be supplemented by specialist advice. This protocol is informed by
policy developed by the Northern Territory Government7 with its emphasis on
providing care appropriate to and accessible by all sectors of the
population.
The holistic nature of palliative practice requires attention to the
physical as well as the psychological, emotional, spiritual and cultural
aspects of care.6 The literature on Indigenous palliative care, and on
specific palliative care issues for Australian Aboriginal clients, is
sparse.8 Indigenous peoples of Canada and North America have described
differences in world views, ethics and decision making processes, and
difficulties in communicating with mainstream health care providers, that
significantly impact on end-of-life care.9,10 This is also true for
Australian Aboriginal peoples.11 Non-Aboriginal health care workers need
guidance on how to deal with Aboriginal clients at this time, both
practically12 and in terms of their care relationships.13 They need to
understand how to work with and take guidance from Aboriginal colleagues
and families.14 Some features of the palliative care of Aboriginal
Australians may differ from that provided to the general population.15,16,17
Many Australian Aboriginal people are uncomfortable within, or in fact
distrust, mainstream health care institutions, and prefer to remain on
their traditional country and to be cared for by their kin.18–21 The wish to
remain on country has been repeatedly documented, not only for sick people,
but also for the elderly.22 This raises practical issues for care including
the training and support of community care workers, and availability of
medications, care equipment, suitable accommodation and transportation.8
With appropriate resources and adequate support of both lay carers and
primary health care providers, most people should be able to be cared for
in the manner they wish, in accordance with contemporary standards of
palliative practice.

References
1. Therapeutic guidelines Palliative Care, Version 1, 2002.
2. Campbell DA, Currow DC. 2002 Palliative Medicine. MJA 176(1):33.
3. Doyle D, Hanks GWC, MacDonald N (eds). Oxford Textbook of Palliative Medicine.
2nd ed. Oxford: Oxford University Press, 1998.
4. Ravenscroft P, Cavenagh J, Regnard CB, Tempest S. Guide to Symptom Control in
Advanced Disease. Sydney: McGraw-Hill, 1995.
5. http://www.palliativedrugs.com
6. [PCA] Palliative Care Australia. Standards for palliative care provision. 3rd Ed.
Canberra: Standards and Quality Committee and Council of Palliative Care Australia,
1999.
7. [THS] Territory Health Services. Palliative Care Policy. Darwin: Territory
Palliative Care, 1998.
8. Fried O. Cross-cultural issues in the medical management and nursing care of
terminally ill Aboriginal people. Unpublished M.Phil Thesis, University of Sydney,
2001.
9. Hepburn K, Reed R. Ethical and clinical issues with Native-American elders: End-
of-life decision making. Clinics in Geriatric Medicine 1995; 11(1):97–111.
10. Kaufert JM, Putsch RW, Lavallee M. End-of-Life Decision Making Among Aboriginal
Canadians: Interpretation, Mediation, and Discord in the Communication of ‘Bad
News’. Journal of Palliative Care 1999; 15(1):31–8.
11. Willis J. Dying in country: implications of culture in the delivery of palliative
care in Indigenous Australian communities. Anthropology and Medicine 1999; 6(3):423–
35.
12. Weeramanthri T. Practice guidelines for health professionals dealing with death
in the Northern Territory Aboriginal Australian population. Mortality 1998;
3(2):161–72.
13. Weeramanthri T. ‘Painting a Leonardo with finger-paint’: medical practitioners
communicating about death with Aboriginal people. Social Science and Medicine 1997;
45(7):1005–15.
14. Fried O. Providing care for Aboriginal patients. Australian Family Physician
2000; 29(11):1035–8.
15. Blackwell N. Cultural Issues in Indigenous Australian People. In: Doyle D, Hanks
GWC, MacDonald N (eds). Oxford Textbook of Palliative Medicine. 2nd ed. Oxford:
Oxford University Press, 1998; 799–801.
16. Prior D. Culturally appropriate palliative care for Indigenous Australian people.
In: Aranda S, O’Connor M (eds). Palliative Care Nursing: A guide to Practice.
Melbourne: Ausmed Publications, 1999; 103–16.
17. Wake D, Martin K, Dineen J. Yarlpuru: on sorrow. Talking to the families of dying
Aboriginal people. Australian Nursing Journal 1999; 6(9):16–18.
18. Aboriginal Research Institute. Developing an Aboriginal palliative care strategy
for South Australia. Adelaide: Aboriginal Research Institute, Faculty of Aboriginal
and Islander Studies, University of South Australia, 1998.
19. Collis-McAnespie C, Dawes A, Hemmings L, Dunn P. The Terminally Ill Koori: Their
Care and Their Carers. Wagga Wagga: Australian Rural Health Research Institute,
Charles Sturt University, 1997.
20. Wagstaff P. Taking care of the dying: a report on the palliative care needs of
Victorian Aboriginal peoples. Victoria: Department of Health and Community
Services, 1997.
21. Williamson P. Let me die in my country: palliative care needs of Aboriginal
people in the Kimberley and Pilbara regions of Western Australia. Perth: Health
Department of Western Australia, 1996.
22. Woenne-Green S. ‘They might have to drag me like a bullock’: The Tjilpi Pampa
Tjutaku Project. Alice Springs: Ngaanyatjarra Pitjantjatjara Yankunytjatjara Women’s
Council Aboriginal Corporation, 1995.
 Paracetamol: An evidence
summary on possible harm from
reducing fever

Author: Dr Peter Silberberg; Dr Dan Ewald

Topic Reviewers: Doctors at Anyinginyi Congress Tennant Creek; Dr Jenny Delima

(Kintore)

Topic
Is the reduction of fever using paracetamol harmful?

Question
Population: All included
Intervention: Fever reduction using paracetamol
Comparison group: No treatment
Outcome: Harmful effects to the patient
Types of studies: Systematic reviews/RCTs/reviews

Rationale for question

There is a fairly entrenched assumption that all fevers should be treated
with regular antipyretics. This is on the basis that fever is a negative
physiological event. Fever may, however, be a useful component of combating
infection.

Inclusion criteria for studies reviewed

Evidence summaries, systematic reviews, randomised controlled trials (RCTs)
and review articles were included.

Search strategy
Cochrane Library, PubMed and EMBASE (June 2002).
Fever (MeSH) AND paracetamol OR acetaminophen (MeSH).

Results
There were 235 studies initially identified. There was one systematic
review (SR) (Cochrane), two randomised controlled trials (RCTs) and two
review articles (RA).

Systematic review
This SR was of high quality and demonstrated excellent representation of
the literature and blinded evaluation of their results. They found 91
relevant publications of which 12 were eligible and included. Their studies
were limited to RCTs only.
This SR evaluated two primary outcomes, one of which was relevant to
this review: comparing paracetamol with placebo or no treatment for fever
clearance time and febrile convulsion. They found only one trial relating
to fever clearance time and there was no statistical significance between
the two groups. Only one trial mentioned febrile convulsions, however, no
convulsions occurred in either group.
The SR had numerous secondary outcomes of which one was relevant to this
review: symptom resolution. They found the mean time to symptom resolution
or healing did not differ significantly between groups when observed over
two to six days. They concluded that the data for the primary outcome was
‘sparse’ and therefore it was not clear whether paracetamol was effective
when compared to placebo or no treatment in reducing duration of fever or
reducing risk of febrile convulsions. They make this conclusion based on
the lack of evidence, rather than due to paracetamol’s ineffectiveness.

Review articles
RA1: This was of good quality, however, it did not outline its literature
review or data analysis process. Studies used for evidence were not limited
to RCTs.
It came to three main conclusions relevant to this review:
1. That the response of a fever to paracetamol in children will not
indicate the severity of the illness and is a bad diagnostic
indicator. They compared six studies (five prospective and one
retrospective) comparing bacteremic to non-bacteremic illness. Only
one study (the retrospective study) showed a significant difference in
fever reduction.
2. No evidence to suggest paracetamol use is effective in suppressing
febrile seizures, even when given prophylactically.
3. While general experience supports the rationale that paracetamol
enhanced patient comfort there have been no carefully controlled
efficacy studies to support this. Further, that there is now evidence
that in some diseases it may have a negative effect:
i. use in chickenpox (see other review in Chickenpox chapter);
ii. increases viral shedding, nasal signs and symptoms and
suppresses serum neutralising antibody response in adults with
rhinovirus infection; and
iii. prolongs parasitaemia in children infected with Plasmodium
falciparum.

RA2 was the same author as RA1 and adds no further information.

RCTs
RCT1: This RCT was of good quality. Its population was of children (aged
six months to six years) but it had a low enrolment rate (225 from 654
eligible), which left it open to potential limitations in its applicability
to other populations. However, its randomisation process was adequate,
which should eliminate biases that would otherwise occur. It had adequate
ascertainment of results and measurement techniques.
The study enrolled 225 children, 123 in the paracetamol arm and 102 in
the placebo arm. Patients were enrolled only if there was no evidence of
bacterial infection. Results were measured using a diary completed by the
parent and via telephone questionnaire until the child was fever free for
24 hours. They found there was no statistically significant difference in
fever clearance time or improvement in mood, comfort, eating or drinking
between the two groups. However, children were statistically significantly
more likely to be active (38% vs 11%, p = 0.05) and alert (33% vs 12%, p =
0.036) after taking paracetamol.
 RCT2 has already been reviewed (effect on chicken-pox: see Chickenpox
chapter).

Conclusion
In general, there appears to be a lack of good evidence in the literature
to answer the question whether using paracetamol to reduce fever is
harmful. Both the SR and RA1 conclude that better designed studies need to
be performed. In contrast, RCT1 concludes that there was no harmful effect
of paracetamol (defined as an increase in severity of symptoms), and that
there was a trend towards a modest benefit in patient comfort. (It is
interesting to note that despite these findings the authors of this article
still conclude that ‘we should treat the child and not the thermometer’).
However, in specific diseases there seems to be mounting evidence that
paracetamol maybe harmful. In the case of chickenpox and viral type
illnesses this would be relevant to our population. The warning that
paracetamol is a poor diagnostic indicator for bacterial illnesses should
be noted. Further, the literature repeatedly states that paracetamol is of
no use in prevention of febrile convulsions.

References
(SR) Meremikwu M, Oyo-Ita A. Paracetamol for treating fever in children. (Cochrane
Review). In: The Cochrane Library, Issue 2, 2002. Oxford.
(RA1) Plaisance KI, Mackowiak PA. Antipyretic therapy: physiologic rationale,
diagnostic implications, and clinical consequences. Arch Intern Med 2000 Feb 28;
160(4):449–56. Review.
(RCT1) Kramer MS, Naimark LE, Roberts-Brauer R, McDougall A, Leduc DG. Risks and
benefits of paracetamol antipyresis in young children with fever of presumed viral
origin. Lancet 1991 Mar 9; 337(8741):591–4.
(RCT2) Doran TF, De Angelis C, Baumgardner RA, Mellits ED. Acetaminophen: more harm
than good for chickenpox? J Pediatr 1989 Jun; 114(6):1045–8.
(RA2) Mackowiak PA. Diagnostic implications and clinical consequences of antipyretic
therapy. Clin Infect Dis 2000 Oct; 31Suppl5:S230–3. Review.
 Rheumatic Fever

Author: Dr Sophie Couzos; Dr Jonathan Carapetis

Topic Reviewer: Dr Dan Ewald

This chapter is made up of edited extracts (by Dr Dan Ewald, with

permission from the authors and publisher) from Couzos S & Carapetis J
2003, ‘Rheumatic Fever’, in Aboriginal Primary Health Care: An evidence-
based approach, 2nd edition, Oxford University Press, Melbourne. Readers
are advised to refer to the full chapter for detailed information on the
prevention and management of rheumatic fever, treatment goals and targets,
case management, program implementation, data collection, and performance
indicators.

Summary
Rheumatic fever is an autoimmune sequel of infection with group A
streptococcus (GAS), characterised by damage to heart valves, brain,
joints, and/or skin, and less commonly heart muscle, pericardium, or lungs.
The heart valves may be left with permanent damage. This is rheumatic heart
disease (RHD), and its prevention is the main aim of all public health
efforts for rheumatic fever. RHD remains the most common acquired heart
disease of childhood in the world and in Central and Northern Australian
Aboriginal people in particular. It is a classic disease of poverty, as
overcrowding and difficulties in maintaining community and personal hygiene
facilitate transmission of GAS.
Clinicians need to suspect acute rheumatic fever (ARF) to avoid a missed
diagnosis and consequently missed secondary prevention of recurrence and
RHD.
Secondary prophylaxis of rheumatic fever is the single most important
strategy. Benzathine penicillin G is the best prophylactic agent, given
every four weeks. A coordinated control program, with rheumatic fever
registers, is the best way to improve benzathine penicillin G adherence
rates and ensure adequate clinical follow-up, including specialist review
and echocardiography.
There are various relevant national and international policy documents.1,2

Background
Rheumatic fever is now rare in Australia with the exception of Aboriginal
people in Northern and Central Australia. It is a notifiable disease in the
Northern Territory.3
The highest confirmed incidence yet reported was 508 per 100 000
children aged 5–14 years in 12 remote Aboriginal communities in northern
Australia between 1987 and 1996.4 The point prevalence of RHD in all ages
(as of March 1997) was 11.8 per 1000 in the Top End Aboriginal population,
and 22.4 per 1000 in the 12 communities with good ascertainment.5
While the incidence of ARF peaked between five and 14 years of age, the
prevalence of RHD was greatest in those aged between 20 and 34 years.4
Sydenham’s chorea features in 28% of ARF presentations in the Top End.6,7 In
one Central Australian community, the annual incidence of ARF was reported
as high as 815 per 100 000 persons. The point prevalence for RHD was
between 7.9 and 12.3 per 1000 persons.8 These figures are similar to those
observed in the Kimberley region of Western Australia.9,10,11 The prevalence
figures in the north of Australia are over 30 times higher, while the
incidence rate for ARF is over 1000 times higher, than those of
industrialised nations.12
ARF and RHD carry high risks of premature death and considerable
morbidity.13 In the Northern Territory between 1987 and 1996, there were
182 deaths due to ARF or RHD, 94% in Aboriginal people.

Skin or throat infection as the source

There has been a long-held view that rheumatic fever only develops
following GAS throat infection (not skin) and the American Heart
Association restated this in 1992.14 This is difficult to reconcile with the
epidemiology in Aboriginal communities.
The prevalence of throat carriage with GAS is low in Aboriginal children
of Northern Australia15,16, and presentations with sore throat to clinics in
Aboriginal communities may not be common.17 This raises the possibility
that skin infection with GAS may lead to ARF either directly or by skin GAS
infecting the throat.

Case definitions
The Jones criteria14 for diagnosis is applicable only to the initial attack
of ARF. The diagnosis of ARF recurrences requires special interpretation of
the Jones criteria. The diagnosis of chronic RDH is based on clinical
and/or echocardiographic features of typical rheumatic heart valve lesions.

The Jones criteria for guiding the diagnosis of the initial attack of ARF,
updated 1992.

Major manifestations Minor manifestations

Carditis Fever
Polyarthritis Arthralgia
Chorea Elevated acute phase reactan
Subcutaneous nodules Prolonged PR interval
Erythema marginatum
Plus
Supporting evidence of a recent group A
streptococcal infection
– Positive throat culture or rapid antigen test OR
– Elevated or increasing streptococcal antibody titre

The presence of two major or one major and two minor manifestations, plus
evidence of a preceding GAS infection, indicates a high likelihood of ARF.

Two important exceptions to the Jones criteria

Sydenham’s chorea commonly occurs without other manifestations of ARF and
following a prolonged latent period after GAS infection (after serological
markers have returned to normal), so isolated chorea of itself is
sufficient to fulfil the criteria if other causes of chorea have been
excluded.
The finding of a sub-acute or chronic carditis (usually manifest by a
murmur and raised ESR) is also an exception.14
Recurrent attacks can be diagnosed with few of the criteria (one major
or more than one minor), provided there is evidence of a recent GAS
infection,18 and other diagnoses have been excluded.19–22

Making a diagnosis
The diagnosis of rheumatic fever may be easily missed; in the Northern
Territory nearly half of all patients diagnosed with RDH had no recognised
history of ARF.6 It is likely that many cases were missed through low
awareness of the staff, and some were subclinical or mild.

Throat culture for GAS

Many infections would have cleared before ARF developed, and throat culture
can have poor sensitivity.12,23 Of Top End Aboriginal patients with ARF who
had throat swabs, only 4% were positive for GAS.22

Rapid antigen detection kits

Rapid antigen detection kits for GAS diagnosis have been used in the USA
for many years and were found to be cost effective in the primary health
care setting.24 These are not recommended for CARPA regions where rheumatic
fever is still common. (See Sore Throat chapter).

Diagnosing tonsillitis
Making the clinical diagnosis of bacterial tonsillitis or pharyngitis can
be difficult. Clinical prediction rules and screening tests for GAS are not
recommended for Aboriginal children because of the lack of validation for
their use in this group. (See chapter on Sore Throat)

Streptococcal antibody testing

Either the ASOT (anti-streptolysin O titre) or anti-DNase B (anti-
deoxyribonuclease B) titre can be used to confirm a recent GAS infection
for the purposes of rheumatic fever diagnosis. Both the ASOT and anti-DNase
B titres are elevated following GAS pharyngitis but, by contrast, skin
infection with GAS leads to a strong anti-DNase B but a relatively weak
ASOT response.25,26,27
An elevated ASOT occurs in more than 80% of patients after GAS
tonsillitis, and adding the anti-DNase B titre improves the sensitivity of
diagnosis to approximately 95%.14 A twofold rise in ASOT is usually
accepted as confirmation of a recent GAS infection. However, streptococci
other than GAS can cause an elevated ASOT and elevation may not occur if
antibiotics are given early in the infection.28 In many communities, most
children will have had a recent GAS infection and background serology
titres may be high.29 Therefore, a single ASOT result must be interpreted
with caution in the diagnosis of recent GAS infection.28
In a Northern Territory study of 293 cases of confirmed non-chorea ARF,
both titres were elevated in 82% of cases, the ASOT was the only elevated
test in 1% of cases, whereas the anti-DNase B titre was the only elevated
test in 17%.22
Prevention: Primary prevention
Decreasing GAS infections
Acute rheumatic fever is still common in developing countries, probably
because overcrowding and inadequate community sanitation increase the
exposure of susceptible children to GAS.30,31 This is likely to be important
in the Aboriginal health setting.32

Mass antibiotic prophylaxis to prevent initial episodes

There have been numerous outbreaks of rheumatic fever in United States
military training camps. Benzathine penicillin prophylaxis given at the
start of training decreased occurrences, and has been continued since
1953.33 This is partly based on prevented cellulitis and pharyngitis as well
as decreased ARF. This approach (for limited duration) is not recommended
for Aboriginal communities.

Targeted screening and antibiotic prophylaxis

A 1993 Australian primary prevention trial concluded that rheumatic fever
could be prevented.34 However, there are limitations (design) to how this
study can influence policy.
A review of primary prophylaxis did not support the treatment of family
contacts of those with GAS pharyngitis. There was some evidence that
primary prophylaxis could reduce GAS infections but did not prevent non-
suppurative sequelae.35
Asymptomatic GAS carriage is not believed to pose a threat to rheumatic
fever control.

Primary chemoprophylaxis
Treatment of symptomatic bacterial tonsillitis/ pharyngitis (also see
the Sore Throat chapter for more detail).
GAS tonsillitis can be treated with oral, or better with intramuscular
(IM), antibiotics and this strategy prevents development of ARF.36,37,30,38
A systematic review suggested that the routine use of antibiotics for
sore throat when the prevalence of pharyngeal GAS is high (>20%) is
justified, and that there is evidence of a benefit in a reduction of
rheumatic fever.39 Given the high incidence of ARF and difficulty in
confirming GAS infection, there should be a low threshold for antibiotic
treatment of throat infections in Aboriginal children.
The chance of developing rheumatic fever following throat infection is
usually very low (up to 3% in epidemic conditions). In those who have
already suffered an attack, the risk of recurrence is much higher and can
be up to 50% following another streptococcal infection.31 This is because
host susceptibility is an important factor.

Secondary prevention
Regular antibiotics to prevent recurrent episodes
This is the single most cost-effective strategy in rheumatic fever and RDH
control.
In the Northern Territory over the period 1987–96, nearly 40% of episodes
of ARF were recurrences. These cases probably reflect poor adherence to
secondary prophylaxis regimens.5 The incidence of recurrent episodes is
greatest in the first five years after the most recent attack of ARF. The
prevention of recurrent attacks of rheumatic fever in these patients is
crucial and justifies active intervention programs.
 A New Zealand study showed that secondary prophylaxis of rheumatic fever
in those with RDH is cost-effective, with the bulk of the savings in the
management of established RDH.40
Prophylactic benzathine penicillin or oral phenoxymethyl penicillin are
both recommended to prevent recurrences of ARF.41 All patients diagnosed
with ARF with or without carditis should receive subsequent antibiotic
chemoprophylaxis (see ‘Duration of prophylactic therapy’).45,18

Benzathine penicillin
Many randomised controlled trials, prospective studies42 and retrospective
studies43 show that benzathine penicillin is the best choice in
prophylactic therapy for rheumatic fever. The World Health Organization
(WHO) recommends benzathine penicillin as the prophylactic drug of choice,
to be given 4-weekly.18
The current recommended dose for secondary prophylaxis is 2.0 ml (900 mg
or 1.2 million units) given every four weeks, regardless of age or
weight.37,45 The Australian antibiotic guidelines recommends that benzathine
penicillin be administered monthly (rather than four-weekly) for
convenience.44
In those who have a recurrence while on 4-weekly benzathine penicillin,
three-weekly benzathine penicillin may be considered.45 This is supported
by a RCT in Taiwan.45,46
An international prospective study involving 1790 rheumatic fever
patients showed that the rate of allergic reactions with long-term
penicillin was no different from short-term therapy for sexually
transmitted diseases.48
Skin testing for hypoersensitivity is recommended in those with
suspected penicillin allergy.48 Truly penicillin-allergic patients may be
offered penicillin desensitisation.

Oral phenoxymethyl penicillin

The recommended oral phenoxymethyl penicillin dose is 250 mg twice daily
for all ages.37 However, compliance is a significant issue. Erythromycin is
recommended as first-line oral prophylactic therapy in those allergic to
penicillin.37

Duration of prophylactic treatment

Existing guidelines agree on the duration of therapy, which depends on the
age at which the most recent episode of ARF occurred, and the presence and
severity of RDH.37,18 A reasonably simple recommendation for Aboriginal people
is that anyone with ARF or RHD should receive secondary prophylaxis for a
minimum of five years or until age 21 years, whichever is longer. If at
that time there is evidence of persistent cardiac valve damage (usually a
persistent heart murmur with or without evidence of heart failure),
prophylaxis should be continued until age 35 years. Severe cardiac disease
or cardiac surgery warrants lifelong prophylaxis.
People who have had rheumatic fever with carditis should also receive
prophylactic antibiotics (usually clindamycin) for certain invasive
diagnostic or surgical procedures for the prevention of bacterial
endocarditis.37

Reducing failure of secondary prophylaxis

In the Northern Territory, it was shown that nearly 40% of all episodes of
ARF were recurrences.5 The most likely reason for failure of prophylaxis is
that patients did not receive it. This is more likely than failure
secondary to dose or dosing interval.49

Community programs and registers

Coordinated approaches to controlling ARF and RHD should include local
service provision and coordination at a central level. A register of cases
maintains staff awareness of the disease in spite of high staff turnover
and is the best way to ensure timely clinical reviews and chemoprophylaxis.
Education or health promotion strategies for those who are likely to be
non-adherent can also be facilitated.
There are coordinated rheumatic fever and RHD control programs in the
Top End of the Northern Territory and Central Australia. Early reductions
in the incidence of recurrent cases suggest that secondary prophylaxis
delivery may be improving.50,51

Clinical recognition and management of acute cases

The WHO and Northern Territory experts recommend hospital admission for all
patients suspected of having ARF.18,49 This is for clinical assessment,
diagnostic tests, patient’s education and developing a long-term management
plan.

Important clinical aspects of ARF

The clinical features of ARF in the Aboriginal population are similar to
those in classic descriptions.52,53,7,22 However, there are a number of
particular issues of note in this population:

Sydenham’s chorea
‘Purposeless, involuntary, rapid movements of the trunk and/or extremities
often associated with muscle weakness’ are characteristic of Sydenham’s
chorea.14 The movements can be unilateral, making diagnosis difficult.
Sydenham’s chorea is a common manifestation of ARF in Northern Australia
(28% of cases). Almost half of all NT people with chorea will develop RHD.5
Haloperidol, sodium valproate and carbamazepine have been reported to be
effective agents in the treatment of the chorea.54–56 [Editor: See discussion
of the potential long term sequela of haloperidol use in the Psychosis
chapter.]

Arthritis
Polyarthritis of ARF is usually migratory (can be atypical) and does not
result in permanent joint deformity. Improvement with aspirin is so
dramatic that observing this greatly helps confirm or refute the diagnosis.
In Northern Territory Aboriginal people, arthritis affecting only one
joint was present in 17% of non-chorea cases.22 Therefore, although other
causes of mono-arthritis (including septic arthritis) should be excluded,
mono-arthritis should be considered a major manifestation of rheumatic
fever in Aboriginal people.

Fever
Low-grade fevers (>37.5?C) were common in confirmed cases in Northern
Territory Aboriginal people22 and should be considered a minor
manifestation, for diagnostic purposes.
Treatment
There are no interventions in ARF that can alter the likelihood or severity
of long-term valvular disease. Aspirin is only useful for limiting the
symptoms of pain and fever, and should be withheld if the diagnosis is not
clear and pain can be controlled with other medications.

Rheumatic heart disease (RHD)

Carditis associated with ARF is almost always associated with a murmur due
to inflammation of the heart valves. In the absence of a murmur, other
causes of myocarditis or pericarditis should be sought.14 The mitral valve
(incompetence) is most commonly affected, followed by the aortic valve
(incompetence).
Severe or recurrent episodes of valve inflammation leads to scarring,
contracture and stenosis of the valves. Of Aboriginal people in the
Northern Territory with RHD, 48% have two or more valves involved.5
Echocardiography with Doppler is accurate for assessing and managing
suspected carditis and RHD.19 This has become more important with the advent
of valvular repair surgery (rather than valve replacement); a technique
best performed before valve damage becomes severe, and which is associated
with reduced complications due to infection or problems with
anticoagulation.57 Mitral valve repair rather than replacement is the
surgical procedure of choice58,59,60, and early referral for consideration of
this treatment should be in management plans.

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59. Mavioglu I, Dogan OV, et al. Valve repair for rheumatic mitral disease. J Heart
Valve Dis 2001; 10:596–602.
60. Barlow JB. Aspects of active rheumatic carditis. Aust NZ J Med 1992;
22:5(suppl):592–600.
 Septic Arthritis

Topic Reviewers: Robyn Dixson (RAN, Yirrkala Clinic); Dr Ian Dumbrell (Port
Keats)

[Editor:
• Dr Mathew Sharland (RDH orthopaedics) says protocol did not need changing
from third edition. No background offered.
• Dr Gavin Wheaton (ASH Paediatrician) says rheumatic fever has been missed
in ASH and treated as septic arthritis. Presentations can be similar so
RHF needs to be thought of and excluded. This is consistent with the
detailed discussion of rheumatic fever.
• Gary Lum, (clinical microbiologist RDH) offered these additional
comments:
‘If advised give flucloxacillin 50 mg/kg (up to max. of 2 g in adults)
IV/IM every six hours or in a child under five years give ceftriaxone
IV/IM (see doses page).
‘If a child is sent in immediately, the ceftriaxone should hold
staphylococci and haemophili. I would hope the hospital doctors will
consider carefully the value of ampicillin over ceftriaxone in ampicillin
susceptible haemophili.
‘In general the most common cause of adult septic arthritis is
Staphylococcus aureus but gonococcus should be considered in the sexually
active. In children, while Haemophilus influenzae must be considered,
management should be guided by relevant microscopic and culture results.
‘My aim is to minimise the use of third generation cephalosporins and
to avoid the use of two beta-lactams together.
‘With respect to the blood culture bottles, any clinic served by
Western Diagnostic Pathology will probably have bioMérieux VITAL bottles
as opposed to Becton Dickinson BACTEC bottles. The VITAL bottles will not
fit into our (RDH) automated reader. The same is true vice versa. This
leads us to perform blind sub-culture after 48 hours. We have issues of
delayed diagnosis and laboratory contamination of bottles. It is
important the correct bottles are collected for the referring laboratory.
A delay or problem could mean an adverse patient outcome.
‘Getting statistical data is a nightmare particularly for something
like this. Suffice to say gonococcal arthritis is more common here than
anywhere else in Australia. I wouldn't say our septic arthritis due to
all causes is significantly different to other places where I have
worked.’]
 Skin Sores, Abscesses and
Scabies Infections

Author: Dr Christine Connors

Topic Reviewer: Dr Dan Ewald

Skin infections are common health problems, with a higher frequency amongst
children. In the NT, scabies and skin sores are amongst the commonest
presentations in Aboriginal children to community health centres.1 The
bacteria on the skin do not usually cause infection, but the risk increases
with humidity, hot weather, poor hygiene and especially if there is a break
in skin integrity. Scabies is an extremely common factor in the NT, which
underlies secondary impetigo or skin sores.2 Less commonly, skin infections
can lead to septicemia.

Impetigo/skin sores
The commonest causes of skin infections are Staphylococcus aureus, cultured
in 86.7% of impetigo cases, and group A streptococcus (GAS), cultured in
29.2% of cases.3 Other bacteria such as staph epidermis, E. Coli, group B
streptococcus and gram-negatives cause skin infection in less than 5% of
cases. There are very low rates of treatment failure due to these
organisms.3 Local studies have also confirmed the predominance of S. aureus
in impetigo.4 However, it is the GAS that is of greater concern, due to its
potential to cause serious post streptococcal disease. Acute post
streptococcal glomerulonephritis (APSGN) is strongly associated with skin
infection, and NT communities regularly experience epidemics affecting
large numbers of children.5 Recent NT research has demonstrated a six-fold
increased risk for individuals to develop adult renal disease if they have
experienced APSGN as a child.6 Acute rheumatic fever (ARF) and rheumatic
heart disease (RHD) are also due to an abnormal immune response to GAS. The
international literature links ARF/RHD to throat infections from GAS.
However, local experience has shown low rates of throat carriage of GAS,
but up to 70% of children either colonised or infected with GAS. Reducing
GAS skin infections would appear to be an effective public health
intervention to reduce the extremely high rates of ARF/RHD.4,7,8
Antibiotic selection for skin infections should reflect known local
profiles of resistance, and also aim to minimise further development of
antibiotic resistance.9 This is especially important when treating common
infections, and in our setting hyperendemic rates of skin infection.
Inappropriate use of antibiotics can rapidly promote antibiotic resistance.
Other factors which affect choice of antibiotic include the length of time,
dosing frequency, side effects and cost. Unfortunately, there is limited
strong evidence on which to make recommendations for many of the common
childhood infections, including skin infections, but clinical guidelines
show high levels of consensus for specific antibiotics and other
treatments.9
 Staphylococcus is a significant cause of skin infections. Methicillin-
resistant S. aureus (MRSA) has been increasing in both hospital and
community settings for many years. The majority of S. aureus are resistant
to penicillins and, internationally, treatment failure rates with
penicillin vary between 24–47%.3,10 Erythromycin resistance in Australia is
between 30–50%, strongly associated with high rates of use of this
antibiotic. NT hospital studies have shown that MRSA causes 7% of all S.
aureus infections, with 70% of these MRSA infections occurring on the
skin.11 Typing of these MRSA strains has shown increasing rates of WA MRSA
(a strain first detected in the Kimberley). This is more likely to be a
community-acquired, rather than hospital-acquired, infection.12 A study of
patients at Royal Darwin Hospital also demonstrated that Aboriginal
patients had a higher risk of being infected with this strain, as did
people who lived west of Darwin (adjacent to the Kimberley region)
suggesting a spread across the border. This particular strain has also been
associated with very high rates of resistance to mupirocin, a topical
antibiotic.11 Despite earlier studies demonstrating that mupirocin is highly
effective in treating impetigo, it has been associated with rapid
development of staphylococcal resistance.13,14 In the early 1990s mupirocin
was used widely in the Kimberley to treat skin sores in Aboriginal
children, and antibiotic resistance developed within a short period.12
Mupirocin resistance occurs more commonly amongst MRSA strains than
methicillin-sensitive strains. A recent study in a rural Native American
community showed very high rates of MRSA (55% of all S. aureus isolates),
with the majority community-aquired.15 There had been four deaths due to
community-acquired MRSA in previously healthy children in the region which
prompted the study. The authors note that careful antibiotic prescribing is
important to avoid increasing resistance patterns.
Streptococcus pyogenes showed rapid development of resistance to
erythromycin in Japan and Finland, where this antibiotic was widely used.
The data prompted recommendations in Japan for restricted use of
erythromycin for skin infection, and the erythromycin resistance
subsequently decreased. International guidelines commonly recommend
erythromycin or cephalexin for impetigo. The current Australian Therapeutic
Guidelines: Antibiotics recommend penicillin or roxithromycin.10
Despite high use of penicillins for a number of infections amongst
Aboriginal people, GAS remains very sensitive to penicillin.16 Due to this
continuing penicillin sensitivity of GAS, and the requirement to eradicate
GAS to prevent post streptococcal disease, penicillins are the recommended
first choice for impetigo/skin sores in Aboriginal children, despite the
known resistance of S. aureus. Many years of experience by health staff and
families anecdotally confirms the rapid resolution of skin sores following
a single dose of benzathine penicillin. This is the preferred antibiotic as
it is effective in both treating the clinical infection, and in eradicating
the GAS, due to its long action. If oral treatment is preferred by
families, or required due to penicillin allergy, a longer course of an oral
antibiotic for ten days is necessary to achieve effective GAS eradication.
Cellulitis is usually due to streptococci, but can be caused by S.
aureus, similar to skin sores. Recommended treatment is penicillin, usually
procaine penicillin. Elevation of affected area (usually leg or arm) is an
important principle of treatment which reduces swelling.13
Abscess/boils
The principal treatment for abscess (boils) is incision and drainage rather
than antibiotics.3 Antibiotics penetrate the abscess cavity very poorly,
although they will improve surrounding cellulitis. S. aureus is almost
exclusively responsible for causing boils. Flucloxacillin is not currently
recommended due to rare but potentially fatal cholestatic hepatitis.17 This
has occurred mainly in older patients, and those treated with longer
courses (two weeks or more), with the incidence estimated between one in
400 and one in 20 000 courses. The current recommendation is to use
dicloxacillin, which still has a risk of hepatitis, but this risk is
approximately half that seen with fluclocaxillin.18 There is no paediatric
preparation of dicloxacillin, and hepatotoxicity is rare in this age group,
thus flucloxacillin syrup is still recommended for children. Recurrent
boils due to Staphylococcus are seen in a small group of patients. These
patients are carriers of Staphylococcus, usually in the nose and
occasionally in the perineal region. Carriage status should be confirmed
with swabs prior to treatment. Eradication with topical mupirocin has been
successful in a number of trials, and restricting the use of mupirocin for
chronic carriers with recurrent infection may prevent development of
resistance. Treatment is recommended as a single course for between five to
10 days, although one small study showed reduced recurrences amongst people
with frequent infection using prophylactic nasal mupirocin for five days
each month over a one-year period.19,20 In difficult cases with continued
reinfection, oral rifampicin has been successfully trialled.

[Editor: In the Top End wet season, a person with risk factors for
melioidosis, such as diabetes, renal failure, chronic alcohol abuse may
have cellulitis or abscess caused by melioidosis. If suspected, talk to a
doctor. (See the Melioidosis chapter in this book.)]

Scabies
Scabies is caused by an obligate human parasitic mite, Sarcoptes scabiei,
which is transmitted from person to person through close contact. A common
misconception is that dogs are responsible for the high scabies prevalence
in the NT, however genetic typing studies done at Menzies School of Health
Research in the mid 1990s, showed that dog scabies and human scabies are
different subspecies.21,22 The pregnant scabies mite burrows and deposits
about two to three eggs a day in the stratum corneum of the skin. The
nymphs emerge as adults on the surface of the skin after a series of moults
which takes about two weeks. The mature mites mate and reinvade the skin of
the same or another host.

[Editor: The dog subspecies can still cause an itchy condition (delayed
hypersensitivity) in humans, however it does not reproduce on humans and
was not isolated from humans in the Top End studies mentioned (possibly not
common). It may be unwise to tell people they are wrong in their belief
that dogs are important, as a person who frequently has close contact with
scabies infected dogs (e.g. sleeps with them) may still suffer a chronic
scabies condition. In theory this would be repeated infection with canine
scabies rather than self-sustaining human scabies infection.
There have been a number of successful community scabies control
programs that did not treat dogs. Person to person transmission is the key
aspect of scabies control.]
Initial infestation is asymptomatic. After four to six weeks the host
becomes sensitised to the excreta of the mites and an itch and rash
develops, although in some people the latency period can last for several
months.23 With subsequent reinfestation the host will immediately develop a
hypersensitivity reaction and become symptomatic. Young children have a
poorly developed immune response to the scabies mite and carry greater
numbers of mites. The most common symptom is an itchy rash, which usually
has a classic distribution. In young children, the lesions are usually
widespread, from head to toe, including ‘pustular’ blisters on the palms of
their hands and soles of their feet. These are not infected with bacteria
but are caused by the host immune response to the mite. Older children and
adults usually have lesions at the wrists, in the interdigital space
between fingers and toes, the buttocks and around the ankles. Scabies
lesions may also be found on the head in older children and adults,
although this is much less common. The lesions include vesicles,
excoriation (from scratching), nodules and, less commonly, burrows.24
Investigations are rarely performed for diagnosis because the clinical
picture is usually clear. The diagnosis can be confirmed, if the rash is
atypical, by skin scrapings from the lesions and identification of mites
and eggs using microscopy. Differential diagnosis could include eczema,
mild cases of psoriasis or contact dermatitis. A swab of associated skin
sores will invariably grow Streptococcus and Staphylococcus.
Treatment involves topical application of scabicide ointments, lotions
or creams. Treatment of the affected individual and the close contacts is
recommended, although there are no randomised control trials (RCTs) on
contact treatment.25 A Cochrane review has identified RCTs that have
compared the multiple treatments available for scabies, which have varying
efficacy and ease of application. The clinical cure rates of crotamiton,
lindane, benzyl benzoate and sulphur showed no difference in small RCTs.
Permethrin has similar efficacy to lindane (91.5% cure vs 88%), although
permethrin is more effective in reducing itch. Permethrin was more
effective than crotamiton (89% vs 60%). Oral ivermectin has been trialled
and has similar efficacy to benzyl benzoate and lindane. Ivermectin is not
currently approved for scabies treatment, although may be used ‘off label’
for crusted scabies (see below). There are rare serious adverse effects
from lindane (convulsions, aplastic anemia), permethrin (convulsions) and
ivermectin (apparent increased risk of death in elderly people, although
uncertain association), which have been identified from case reports,
although not from the RCTs.25
Permethin 5% is the currently recommended treatment internationally,
based on small studies and expert opinion. It was introduced in the NT in
1994, and due to low toxicity and ease of application it is the preferred
treatment.26 It is usually prescribed as a single treatment for eight to 12
hours (overnight). People with multiple lesions (usually children) require
a second treatment after two weeks to ensure eradication of newly hatched
mites. People may continue to have itching for two to four weeks after
treatment, although most people experience relief of symptoms within three
days.24
Scabies may be transmitted by fomites (bedding, clothes, linen), and it
is recommended that washing clothing and linen used in recent days is
included as part of the treatment.24 For ordinary cases of scabies
environmental transmission is not as important as person-to-person
transmission. However, for people with crusted scabies who carry millions
of mites it is essential to eradicate the mites from the house.
Crusted scabies
Previously called Norwegian scabies, as it was first described in a
leprosarium in Norway. Crusted scabies is a severe form of scabies
infestation, in which the mite multiplies in the millions. In most studies
people with crusted scabies have some form of immune deficiency, which is
usually well documented, such as HIV infection.27,28 However, in the NT the
underlying immune problems may be more complex and subtle as they are
rarely identified, although there are documented cases of people with HTLV1
and crusted scabies in Central Australia.29,30 In crusted scabies the affected
person cannot immunologically contain the scabies mite and they become
infested with millions of mites, developing a thick, crusted skin in
response. They are highly infectious to others and also highly susceptible
to reinfestation.31
The rash from crusted scabies can vary. Mild cases may have localised
patches on the buttocks, upper thighs, upper arms and occasionally on the
dorsum of the hands and the feet. Severe cases may be covered from head to
toe with thick, elevated crusted lesions, which may also have fissures.
Crusted scabies is often not itchy and it is commonly misdiagnosed as
eczema, psoriasis or other dermatitis.32 Recurrent cases of scabies in
people may be an indicator of contact with a case of crusted scabies. It is
important to confirm the diagnosis with skin scrapings to detect the mite
microscopically, and exclude serious immune deficiency. The NT-CDC
guidelines on community control of scabies and skin infection includes
guidelines on management of crusted scabies.33
Crusted scabies involves both topical treatment with permethrin and a
keratolytic cream to soften the crust as well as oral ivermectin. The
protocol for crusted scabies also includes treatment of the entire
household and environmental health officers working with family members to
clean the house and use insecticide bombs to kill all scabies mites. Severe
cases of crusted scabies usually need treatment in hospital. The main
complication of crusted scabies is septicemia. A study done at Royal Darwin
Hospital showed that people with severe crusted scabies had a five-year
mortality rate of 50% due to septicemia, although improved antibiotic
protocols has reduced this mortality.

[Editor: Given that those with crusted scabies are likely to have an
underlying immune-deficiency or be otherwise debilitated, this high
mortality may not all be attributable to the scabies itself, but scabies
may be important in creating portals of entry for infection or increasing
immune suppression. Prof Bart Currie believes the multiple organisms that
cause the septicemia are directly due to the skin fissures allowing
unimpeded access, not the underlying immunodeficiency see: Currie B, Huffam
S, O’Brien D, Walton S. Ivermectin for scabies. Lancet 1997; vol 350:1551.]
Skin conditions Baseline Follow-up 1 (7 Follow-up 2 (21
screening months) months)
Scabies 56% 28% 48%
Skin sores 14% 35% 41%

Adapted from; Ewald D, Hall G. Housing and Health: Evaluation of the

National Aboriginal Health strategy — Environmental Health program in a
Central Australian Community. Darwin: CRC for Aboriginal and Tropical
Health, 2002.]

Community prevalence and public health programs

There is limited historical documentation about the prevalence of scabies
in the NT. There were reports in 1815 of scabies being problematic on
missions but not amongst tribal people. In Central Australia in 1957 it was
reported to be common, however, in 1960 a scientific expedition in Arnhem
Land demonstrated that scabies was quite rare. This is consistent with the
experience of leprosy nurses who worked throughout the NT and recalled that
scabies and skin sores were rare around that time. Long-term health
professionals in the Top End believe the rates of scabies and skin
infections have been increasing since the 1970s (pers. comm. Joan Fong,
leprosy nurse, CDC).
Currently, community surveys show high but variable prevalence rates
ranging from 30–60% in children under the age of 15. Surveys of adults have
shown similar levels of at least 30% at any one time, although adults
generally have milder clinical manifestations. A successful model to
control high rates of scabies in a community setting has been adapted from
Panama and used effectively in several remote NT communities.15 The Panama
program involved simultaneous supervised treatment of all community members
(the community was on an island), with 5% permethrin cream. This led to a
reduction in prevalence rates of scabies from 33% of the population to very
low levels of 1.5% that were sustained for three years. The pyoderma (skin
sores infection) prevalence rate in children decreased from 32% to 2%
without use of specific antibiotics.
An adapted Panama model was then formally trialled at Minjilang in 1994,
which was successful in maintaining low rates of scabies and skin infection
for up to five years using regular community screening and treatment with
permethrin.7 The scabies rate decreased from 29% to below 10% at two years.
Following the success of this program, guidelines for health staff were
developed with NT Centre for Disease Control.17
A number of communities throughout the NT have subsequently run the
program.34–37 Three communities have successfully maintained low prevalence
rates of scabies and skin infection for at least 12 months (Minjilang,
Wadeye and Kunbarllanjnja). The common element amongst these programs was
ongoing surveillance and community awareness of rates of scabies and skin
infections. In other communities that have available data, the initial
period following the Healthy Skin day has shown a significant reduction in
scabies. The surveillance is important to maintain lower rates and
sustainability of the program. Further research on this issue is currently
occurring through the Cooperative Research Centre for Aboriginal and
Tropical Health.

[Editor: There is some evidence that scabies is not always the major cause
of skin sores in Aboriginal communities. For example, in one series of
surveys and treatment of children under 13 years old, in a Central
Australian community, the prevalence of scabies changed quite differently
to the prevalence of skin sores. This can be seen in the table below.
However, the calculated population attributable risk of skin sores from
scabies was stable at around 34% in each round.]

References
1. Thomas D. Clinical consultations at an Aboriginal community controlled health
service. How are they different to consultations with Australian General
practitioners? Unpublished thesis. Master Medical Science. 1995.
2. Carapetis JR, Connors C, Yarmirr D, Krause V, Currie BJ. Success of a scabies
control program in an Australian aboriginal community. Pediatr Infect Dis J
1997;16:494–9.
3. Darmstadt GL. Oral antibiotic therapy for uncomplicated bacterial skin infections
in children Pediatr Infect Dis J 1997; 16:227–40.
4. Currie BJ, Carapetis JR. Skin infection and infestation in Aboriginal communities
in northern Australia. Australas J Dermatol 2000; 41(3):19–43.
5. Evans C. Acute Post Streptococcal Glomerulonephritis in the Northern Territory
1980–2000. The Northern Territory Disease Control Bulletin 2001; 8:2:1–6.
6. White AV, Hoy WE, McCredie DA. Childhood post-streptococcal glomerulonephritis as
a risk factor for chronic disease in later life. Med J Aust 2001; 174(10):4492–6.
7. Carapetis JR, Wolff DR, Currie BJ. Acute rheumatic fever and rheumatic heart
disease in the top end of Australia’s Northern Territory. Med J Aust 1996; 164:146–
9.
8. Shelby James TM, Leach AJ, Carapetis JR et al. Impact of single dose azitrhomycin
on Group A streptococci in the upper respiratory tract and skin of Aboriginal
children. Pediatr Infect Dis J 2002; 21:5;375–80.
9. Holten KB, Onusko EM. Appropriate Prescribing of Oral Beta-Lactam Antibiotics.
American Family Physician 2000; 62:611–19.
10. Therapeutic Guidelines: Antibiotics Version 11. Therapeutic Guidelines Ltd, 2000.
11. Maguire GP, Arthur AD, Boustead PJ et al. Emerging epidemic of community-
acquired methicillin-resistant Staphylococcus aureus infection in the Northern
Territory. Med J Aust 1996; 17;164 (12):721 –3.
12. Riley TV, Pearman JW, Rouse IL. Changing epidemiology of methicillin-resistant
Staphylococcus aureus in Western Australia. Med J Aust 1995 Oct 16; 163(8):412–14.
13. O’Dell ML. Skin and wound infections: an overview. Am Fam Physician 1998;
57(10):2424–32.
14. Dagan R, Bar-David Y. Double-blind study comparing erythromycin and mupirocin
for treatment of impetigo in children: implications of a high prevalence of
erythromycin-resistant Staphylococcus aureus strains. Antimicrobial Agents and
Chemotherapy 1992; 36:287–90.
15. Groom AV, Wolsey DH, Naimi TS et al. Community-Aquired Methicillin-Resistant
Staphylococcus Aureus in a Rural American Indian Community JAMA 2001; 286:1201–5.
16. Lum G. Antibiograms RDH Microbiology Laboratory. Unpublished data, 2001.
17. Turnbridge J. Editorial: What to use instead of flucloxacillin. Aust Prescr 1995;
18:54–5.
18. NSW Therapeutic Assessment Group. The Flucloxacillin/ Dicloxacillin debate.
NSW TAG. Current Opinion 2000 May.
19 Raz R, Miron D, Colodner R et al. A 1-year trial of nasal mupirocin in the
prevention of recurrent staphylococcal nasal colonisation and skin infection. Arch
Intern Med 1996; 156(10):1109–12.
20. Doebbeling BN, Reagan DR, Pfaller MA et al. Long-term efficacy of intranasal
mupirocin ointment. A prospective cohort study of Staphylococcus aureus carriage.
Arch Intern med 1994; 154(13):1505–8.
21. Walton SF, Currie BJ, Kemp DJ. A DNA fingerprinting system for the
ectoparasite Sarcoptes scabiei. Mol Biochem Parasitol 1997; 85:187–9.
22. Walton S, Bonson A, Low Choy J et al. Dogs are not a reservoir for human
scabies infestations in Northern Australian communities. CARPA Newsletter 1998;
28:4–5.
23. Holness DL, DeKoven JG, Nethercott JR. Scabies in chronic health care
institutions. Arch Dermatol 1992; 128(9):1257–60.
24. Burkhart CG, Burkhart CN, Burkhart KM. An epidemiologic and therapeutic
reassessment of scabies. Cutis 2000; 65 (4):233–40.
25. Walker GJA, Johnstone PW. Interventions for treating scabies (Cochrane
Review). In: The Cochrane Library, Issue 1, Oxford: Updated Software, 2001.
26. Connors CM. Scabies treatment. NT Communicable Disease Bulletin 1994; 2(3):5–
6.
27. Schlesinger I, Oelrich DM, Tyring SK. Crusted (Norwegian) scabies in patients
with AIDS: the range of clinical presentations. South Med J 1994; 87(3):352–6.
28. Kolar KA, Rapini RP. Crusted (Norwegian) scabies. Am Fam Physician 1991;
44(4):1317–21.
29. Mollison L, Lo S, Marning G. HTLV1 and scabies in Aboriginal Australians.
Lancet 1993; 341:1281–2.
30. Gogna NK, Lee KC, Howe DW. Norwegian scabies in Australian Aborigines. Med J
Aust 1985; 142(2):140–2.
31. Huffam SE, Currie BJ. Ivermectin for Sarcoptes Scabiei hyperinfestation. Int
J Inf Dis 2(3):152–4.
32. Gach JE, Heagerty A. Crusted scabies looking like psoriasis. Lancet 2000;
356(9230):650.
33. Communicable Disease Centre. Guidelines for community control of scabies,
skin infection and crusted scabies in the NT. CDC Guidelines, 2002.
34. Dowden M. Scabies eradication day: Galiwinku community. The Chronicle 1999;
2:1,12.
35. Arnold M: Maningrida Healthy skin program. Unpublished report, 2000.
36. Wong LC, Amega B, Barker R, Connors C et al. Factors supporting
sustainability of a community based scabies control program. Australas J Dermatol
2002; 43(4):274–77.
37. Connors C, Leysley L, Benger N, McKinnon M. Kunbarllanjnja ‘Bo Bo Scabies’
program evaluation. Community report. CRCATH unpublished report, 2002.
 Sore Throat

Author: Dr Peter Fletcher (DMO, Top End)

The original protocol is attributed to Dr Jeff Hanna (when he was with CDC in
Alice Springs), reviewed by Dr Christine Lesnikowski (ASRHS) for CARPA(97)

Topic Reviewers: Helen Collinson (RAN, Adelaide River Clinic); Monica Ostigh
(RAN, Jabiru), Dr Penny Roberts-Thomson (Nguiu Clinic), Dr Ian Dumbrell (Port
Keats)

Key questions
What’s the goal of treatment of sore throat
Acute rheumatic fever (ARF) prevention is the key goal in the NT context.
Antibiotic (specifically IM penicillin) treatment of sore throat reduces
ARF as a complication of group A beta haemolytic streptococcal (GABHS) sore
throat to less than one-third of that expected in an untreated group.8 The
Cochrane review states ‘ . . . for Aborigines living in poor socioeconomic
conditions, antibiotics (for the treatment of sore throat) may be justified
to reduce the complication of ARF in this setting.’8 Whether preventing ARF
requires eradication of GABHS from the throat, rather than just treatment
with penicillin per se, is controversial.14 vs 8
Symptom reduction? Antibiotic treatment has a relatively small effect on
reducing symptom duration and severity.7,8 However, most of the studies
included in the Cochrane review were in adults, and many were not specific
for group A strep-positive sore throat, thus the real benefit of
antibiotics in symptom reduction in GABHS pharyngitis in children is likely
to be substantially higher than reported by the Cochrane review.16 Most GABHS
pharyngitis patients improve in three to four days even without treatment.
Prevent suppurative complications? Antibiotic treatment does reduce these
(e.g. quinsy), thought to be infrequent, complications.8 Being so rare, they
do not constitute a great burden of disease.
Reduce community load of GABHS? Given the already low (NT) throat carriage
rates, anecdotal low GABHS pharyngitis rate, and high skin sore rates, this
goal seems unlikely to be met.
Reduce infectivity? Patients are non-infective 24 hours after commencing
antibiotic treatment.14,9
Minimise potential adverse effects of inappropriate antibiotic therapy.

Can streptococcal sore throat be diagnosed clinically

Most sore throats are of viral aetiology. Clinical prediction rules
attempting to identify which sore throats are caused by GABHS have poor
sensitivity and specificity6, and are promoted in contexts of low ARF
incidence (such as North America) to reduce antibiotic use. Rapid antigen
tests have reasonable specificity10, but poor sensitivity (see throat
culture below), and detect only GABHS, not Streptococcus groups C or G.7 The
delay in ‘diagnosis’ and treatment inherent in the use of throat cultures
would negate potential symptom improvement benefits of antibiotics, but
would not affect ARF prevention (up to nine days post-onset of illness).
However, Del Mar reports ‘throat cultures probably only have a sensitivity
of <30%, and a specificity of 70–80% for GABHS’11, using a ‘gold standard’
of a rise in specific antibody titre, and allowing for a throat swab’s
inability to differentiate carrier status from disease. Thus, current
clinical prediction rules, rapid antigen tests, and throat cultures are
mostly inappropriate for use in the NT, and not recommended in this
protocol.

What is appropriate treatment for GABHS sore throat?

All treatment guidelines recommend penicillin, either benzathine penicillin
IM single dose, or phenoxymethyl penicillin (penV) oral two to three times
daily for 10 days.4,14 For those penicillin allergic the options are oral
erythromycin14 or oral roxithromycin.4 The addition of one to three days of
procaine penicillin IM recommended in CARPA third edition is said to lead
to more rapidly achieved higher serum concentrations of penicillin, in turn
thought to lead to a quicker clinical resolution.15 I could not find any
published evidence on this. One published guideline offers the option of a
single dose of procaine in addition to the benzathine7, presumably because a
commercial combination was available, while addition of procaine to
benzathine makes the injection less painful. So the use of procaine is
really on the recommendation of experienced clinicians, and the current
CARPA manual. The weight of literature would support using only bicillin.
Compliance concerns have precluded the recommendation of 10 days oral
penicillin in this guideline. If included, bd dosing is as good at ‘cure’
as tds or qid.18
Only IM penicillin has ‘level 1’ evidence supporting its role in
prevention of ARF. Other newer agents have been shown to have equivalent
GABHS throat clearance rates, and thus are proffered as alternatives,
including daily amoxycillin for 10 days, and daily azithromycin for five
days2, but concerns including the rapid development of resistance of GABHS
to macrolides7, side effect profiles, cost, the ‘broad spectrum’ of some
alternatives, and the decision to ‘save’ azithromycin for STDs and trachoma
in the NT15, all preclude the use of these agents in the current guideline.
The ‘new’ recommendation that antibiotic treatment of ‘simple’ sore
throat be limited to those aged two to 25 years or with a history of
ARF/rheumatic heart disease (RHD) brings CARPA in line with the Therapeutic
Guidelines4, and follows the observations that GABHS pharyngitis is rare in
those under three years of age, and initial episodes of ARF rare outside
the ages of five to 25 years.15
The use of ‘symptomatic’ treatment (antipyretics, oral fluids, rest, and
aspirin or warm saltwater gargles) is widely recommended4,7, though the
evidence base could not be located.

Other issues in the NT context

Is GABHS pharyngitis the most significant precursor of ARF in the NT?
There are low pharyngeal carriage rates of GABHS in Aboriginal communities
in the NT, but high pharyngeal carriage rates of group C and G
streptococcus.1 While there is no supporting evidence, this has raised
conjecture as to whether strep C or G infection might lead to ARF.1
The incidence of sore throat and GABHS pharyngitis in Aboriginal
children is unknown, but only 2–4% of ARF cases are preceded by sore throat
in this group.16,17 There is anecdotal evidence that only GABHS sore throat is
uncommon in Aboriginal children. Thus, the significance of the treatment of
sore throat in primary prevention of ARF is not clear.16
The very high rates of group A streptococcal skin infections have
implicated these in the epidemiology of ARF 3,5 but this ‘requires further
study’.5

The differential diagnosis

The protocol does not currently mention the differential diagnosis,
especially URTI, EBV, gonococcal infection, herpes, and diphtheria. The
editorial committee might consider inclusion of an opening statement such
as: ‘Most sore throats are caused by viruses, as part of an URTI. Clinical
findings that make this more likely are: rhinorrhoea, cough, absence of
large tonsils, absence of pus on the tonsils, and absence of tender
cervical lymphadenopathy.’4,6 The ‘danger’ of this would be undertreatment of
GABHS pharyngitis. Also consider a closing statement such as: ‘Also
consider the possibility of other causes of sore throat, including URTI
(the most common cause), glandular fever, gonococcal infection, herpes, and
diphtheria.’
No data on the percentage of NT sore throats that are caused by GABHS,
or other causes, or reinfection rates after treatment could be found.

Other issues of concern in the literature

Some studies suggest that immediate antibiotic treatment, while shortening
the duration of symptoms and contagion, increases re-infection rates and
decreases eradication, compared to a two to three day delay in treatment
(in USA context).12 Furthermore, recurrences are often milder illnesses,
therefore may lead to less ‘presentations’ with GABHS pharyngitis, though
the risk of sequelae is still real. It’s possible that a more liberal use
of penicillin may increase streptococcal carriage rates, with perhaps
implications for ARF.
There is also a recent report of reduced microbiological efficacy of
penicillin in eradicating GABHS after pharyngitis (>1/3 patients GABHS
positive swabs at 10–14, or 29–31 days post treatment)13, raising questions
as to a possible need for increased doses of penicillin, and the role of
re-infection, and family and close contacts.

Summary statement
Although antibiotic treatment of group A streptococcal pharyngitis may have
some benefit in reducing severity and/or duration of symptoms, in
Aboriginal patients the main aim is to prevent rheumatic fever and also to
prevent the spread of disease-causing bacteria to others. Because of
concerns about the timely availability of throat culture results and the
limited sensitivity of throat culture when not performed by experienced
staff, and because of the importance of not missing group A streptococcal
pharyngitis in this population, it is recommended that all sore throats (in
Aboriginal people aged two to 25 years, and in all patients with a history
of ARF/RHD) be treated with antibiotics. Health staff should not attempt to
use clinical features to distinguish likely group A streptococcal infection
from other bacterial or viral pharyngitis, as clinical diagnosis is
unreliable. Although most cases of rheumatic fever in the Aboriginal
population do not follow a sore throat, and therefore will not be prevented
using this guideline, some cases of rheumatic fever may be prevented by
antibiotic treatment.

[Editor: Given that the evidence for the benefit of giving additional high
dose penicillin is anecdotal, we felt it was better to use wording that
reflected this. Otherwise the management of severe tonsillitis is the same
as any other pharyngitis, and the differentiation is not clear, so the
separate protocol for severe cases was removed.
The option for refused benzathine was included partly because we are
aware that many staff object to giving up their autonomy to make an
assessment about someone being able to take a full 10 days of oral
penicillin. This option, worded for those that refuse, should guide towards
Pen V rather than roxithro.]

Medline key words: sore throat, streptococcus, rheumatic fever

References
1. Haidan A, Talay SR, Rohde M, et al. Pharyngeal carriage of group C and group G
streptococci and acute rheumatic fever in an Aboriginal population. Lancet 2000 Sep
30; 356(9236):1167–9.
2. Tarlow MJ. Macrolides in the management of streptococcal pharyngitis/tonsillitis.
Pediatr Infect Dis J 1997 Apr; 16(4):444–8.
3. Carapetis JR, Currie BJ. Group A streptococcus, pyoderma, and rheumatic fever.
Lancet 1996 May 4; 347(9010):1271–2.
4. Therapeutic Guidelines: Antibiotics. version 11. North Melbourne, 2000; 129–130.
5. Carapetis JR, Currie BJ. Skin infections and infestations in Aboriginal
communities in northern Australia. Australas J Dermatol. 2000 Aug; 41(3):139–43.
6. Ebell MH, Smith MA, et al. Does This Patient Have Sore Throat? JAMA Dec 13, 2000;
284(22).
7. Bisno A. Acute Pharyngitis. NEJM Jan 18, 2001; 344(3).
8. Antibiotics for sore throat. Del Mar CB, Glasziou PP, Spinks AB. Cochrane
Database Syst Rev. 2000; (2):CD000023.
9. Pichichero, ME. Group A beta-haemolytic streptococcal infections. Pediatr-Rev
1998.
10. Johnson DR, Kaplan EL. False positive rapid antigen detection tests. J Infect
Dis 2001 Apr 1; 183(7):1135–7.
11. Del Mar CB, Glasziou PP. Antibiotics for sore throats? J Paediatr Child
Health 1998; 34:498–9.
12. Pichichero M. Cost-effective Management of Sore Throat. Arch Ped Adolesc Med
July 1999; 153.
13. Kaplan EL, Johnson DR. Unexplained reduced microbiological efficacy of
penicillin in eradication of GAS. Pediatrics 2001 Nov; 108(5):1180–6.
14. Dajani A et al. Treatment of Acute Streptococcal Pharyngitis and Prevention
of Rheumatic Fever. Pediatrics. Oct 1995; 96(4):758–64.
15. Currie B. Personal communication.
16. Carapetis J. Personal communication.
17. Carapetis JR, Currie BJ. Rheumatic fever in a high incidence population: the
importance of monoarthritis and low grade fever. Arch Dis Child 2001 Sep; 85(3):223–
7.
18. Lan AJ et al. The impact of dosing frequency on the efficacy of 10 day
penicillin or amoxycillin treatment for streptococcal tonsillo-pharyngitis: a meta-
analysis. Pediatrics 2000 Feb; 105:E19.
 Strongyloidiasis
[Editor: This document is a synthesis of the evidence relating to diagnosis
and management of strongyloidiasis, and commentary on this evidence from
individuals with particular expertise or interest. Strongyloidiasis has
proven to be a controversial topic, and there is not necessarily consensus
between all the contributors, particularly about the application and
interpretation of the serology test for strongyloides. We provide here the
rationale and thinking behind the strongyloides component of the ‘worms’
protocols.
Other aspects of the ‘worms’ protocol have only been partially covered.
The key differences between this protocol and the earlier edition of the
CARPA manual are:
• Encouraging a higher index of suspicion for strongyloides, based on
broader range of clinical symptoms that may be due to strongyloides
infection
• Stressing the importance of excluding strongyloidiasis in people who
will be given immunosuppressive treatments and may have occult
strongyloides infection
• Treatment with ivermectin for people over the age of five years

Population screening has been advocated by two of the major contributors

(WP and RS), however, other advisers and the editorial committee believe
there are significant unresolved problems with the interpretation of the
serology result when used as a screening tool.
WP and RS also recommend using serology to monitor effectiveness of
treatment. We believe this is not warranted without a good understanding of
the likelihood of reinfection and the natural decay rate of sero-
positivity. However, if there is clinical suspicion of re-infection or
persisting infection, then repeated serology may clearly be warranted.
Sources used for this document were
• Direct searching and appraising of the available literature
• Evidence summaries from 2002 Darwin Evidence Based Medicine workshop
(prepared by Drs Johnston and Morris)
• Discussion paper for the CARPA manual prepared by Drs Page and Van
Ingen Schenau and Ms Karen Dempsey
• Community newsletter about Strongyloidiasis in Aboriginal Australia by
Assoc Prof Speare
• Contributions and commentary on the above documents provided to the
CARPA editor by
Prof Bart Currie, Dr Fay Johnston,
Prof David Brewster, Dr James McCarthy,
Assoc Prof Rick Speare, Dr Wendy Page,
Dr Christine Connors, Dr Dan Ewald
Issues are discussed under the following headings:

• Prevalence
• Aetiology and life cycle
• Clinical picture
• Diagnosis
• Treatment
• Community control strategies.]
Prevalence
An estimated 50 to 100 million people are infected worldwide1,2 and community
prevalence rates of above 5% are considered hyperendemic.3 In Australia,
infection with strongyloides is common in northern Aboriginal communities
and individual cases are also seen among immigrants from tropical countries
and returned travellers, including military veterans.4
Selected groups in the NT have had faecal or serological testing,
however information about the proportion of people sampled, how they were
selected and which segments of the population they were drawn from is not
readily available. In general these have demonstrated relatively high and
widely varying rates of positivity. See table 1.
A well-designed long-term prevalence study of parasites in children from
five Aboriginal communities in the Kimberly region of Western Australia
found a prevalence in stools of only 0.26%.5 Other studies from communities
in the Kimberleys and north Queensland have reported rates of around 30%.6
The Alice Springs Hospital laboratory reports finding strongyloides (and
the other worms covered in the CARPA protocol, except that hookworm is not
common in children that have not been living in the Top End) in stool
specimens from Central Australian children, but no analysis of the relative
frequency of different gut parasites has been performed (pers. comm. Fran
Morey ASH micro lab).

Prevalence: Comment/conclusion
In spite of the limitations of studies to date and the limitations of
interpreting serology in endemic populations (see section on diagnosis
below), it is reasonable to conclude that there is a very high prevalence
of strongyloides infection in northern Australian Aboriginal communities.
The high prevalence is of clinical importance because of the risk of
precipitating severe disseminated disease in asymptomatic individuals, with
immunosuppressant therapies (see section on clinical picture below).
Table 1: Summary of studies of indices of infection with strongyloides in
Aboriginal patients in the Top End of the NT

Group Year Method Percent Reference

positive
East Arnhem community 1996 Single stool 15% positive Aland7
1 specimens
using the
Harada-Mori
technique
East Arnhem community 1993 Single stool 41% of 29 Flannery8
2 specimens people tested
East Arnhem community 1993 Serology 59.6% Flannery8
3
Royal Darwin Hospital 2002 Stool 7.2% (12 Kurkuruzovic9
study of children examination cases in
under five admitted total)
with diarrhoea.

Cases diagnosed in 1993 Stool 37 cases Fisher10

under five-year-olds examination
admitted to RDH over
a one-year period
Patients with 2001 Serology 56% positive Page11
incidentally
identified
eosinophilia.
(Clinical audit by GP 32% of 143
members of the Top End patients with
Division of General eosinophilia
Practice) were tested

Table 2: Symptoms possibly associated with S. stercoralis infection in

children before and 24 days following treatment with either albendazole or
ivermectin (N = 333)15

Symptom Before 24 days after X2 p

treatment treatment
Cough, 59 (18%) 22 (6%) 19.2 p<0.001
without
evidence of a
cold
Abdominal 35 (11%) 10 (3%) 14.9 p<0.001
distension
Diffuse 17 (5%) 8 (2%) 3.4
itching
Visible 11 (3%) 2 (0.6%) 6.4 p<0.050
urticaria
Larva migrans 9 (3%) 0 9.1 p<0.010
Aetiology and life cycle
The usual mode of infection is penetration of skin by infective larvae from
the soil or direct contact with faeces. The larvae are then carried in the
bloodstream to the right side of the heart. They enter the alveolar spaces
in the lungs, ascend the bronchial tree and are swallowed. In the small
intestine the larvae mature into adult female worms and penetrate the
mucosa of the proximal small bowel where they lay eggs. This occurs 17 to
28 days after the initial infection. The eggs hatch in the intestinal
mucosa to release rhabditiform larvae that migrate to the lumen of the
bowel.
Three cycles are possible.
1. Direct host-soil-host cycle: The rhabditiform larvae in the faeces
become infective filariform larvae that can then infect a host. This
is direct transmission from faeces to new host. This direct cycle is
not seen in other common helminths such as hookworm and Trichuris,
which require maturation of eggs in the soil before becoming
infective. Thus, faeces is a direct source of contamination.
2. Indirect cycle: The rhabditiform larvae in the faeces enter the soil
and develop into free-living male and female adults, which reside and
reproduce in the soil, thus creating a reservoir of infection
independent of the human host. Current thinking is that there is only
one free-living cycle and it is thought that faecal contaminated soil
is infective for about three weeks (pers. comm. Assoc Prof Rick
Speare).
3. Autoinfection or hyperinfection cycle: The rhabditiform larvae
develop into infective filariform larvae before they are passed in the
stool. The filariform larvae can penetrate the colonic wall or
perianal skin and enter the circulation to repeat the migration that
establishes ongoing internal reinfection. Replication occurs through a
process called parthenogenesis. Migratory routes involving organs
other than the lungs may predominate.12 This cycle allows
strongyloidiasis to persist for decades after the host has left an
endemic area.

Aetiology: Comments/conclusions
Infection, which may or may not be symptomatic, can persist in an
individual for decades.

Clinical picture
Acute infections in children
A study of 333 children in Zanzibar, found to be stool-positive for
strongyloides infection, reviewed symptoms before and after treatment with
either albendazole or ivermectin. The results are summarised in table 2.
This gives an indication of what the more common manifestations of acute
infection in children may be.
Both Australian and international studies9,13 including a systematic
review14 demonstrate that:
• Malnutrition predisposes children to infection with strongyloides
 • Infestation with helminths, including strongyloides, are unlikely to
be an important contributor to poor growth in children

Children with infestation with strongyloides are more likely to be

hypokalaemic and wasted than children with diarrhoea caused by other
pathogens.9

Potential symptoms in children and adults with chronic infection

Textbooks1,16 report that infection is usually asymptomatic but may affect
any organ of the body including:
• Skin: larva currens (migratory, changing hour to hour), raised itchy
patches, lesions over lower back and buttocks, recurrent urticaria
• Respiratory: dyspnoea, bronchospasm, gross haemoptysis, pneumonia,
lung abscess
• GIT: subacute obstruction or segmental ileus, ulcerative colitis with
intestinal perforation and peritonitis, vague abdominal complaints,
epigastric pain and tenderness
• Urinary tract infections, granulomata and/or abscesses occur in liver
and kidney17
• CNS signs or symptoms
• Systemic: gram-negative bacteraemia or meningitis, disseminated
strongyloidiasis
• Blood: eosinophilia is present in 10–50% of people with positive tests
for strongyloidiasis.
• Abnormal chest X-rays18
• MRI is able to detect CNS changes that a CAT scan shows as negative2

Disseminated strongyloidiasis
Asymptomatic infection can persist for decades and not be recognised. There
have been many reported deaths in patients commenced on high dose
immunosuppressive therapy in whom asymptomatic infection was not
identified, and disseminated disease was precipitated.19,20,21

Clinical picture: Comments/conclusions

In the Top End there are three important clinical manifestations of
infection with S. stercoralis in Aboriginal communities.
1. Acute gastrointestinal infection in children. The more common symptoms
appear to be diarrhoea, abdominal distension, urticaria, larva migrans and
possibly cough. The diarrhoeal stools have a distinctive odour. Pseudo
intestinal obstruction can occur. While strongyloides infection is
associated with wasting and hypokalaemia in children, it is not an
important contributor to malnutrition. However, malnutrition is a risk
factor for acquiring strongyloides.
2. Gram-negative meningitis or septicaemia secondary to intestinal
parasites facilitating the entry of gut organisms into the blood stream.
This may occur in otherwise asymptomatic adults.
3. Disseminated strongyloidiasis in patients on immunosuppressive therapy.
There have been several deaths in the Top End over the last 15 years in
patients on high dose immunosuppressive therapy in whom asymptomatic
infection was not identified. Protocols for excluding latent infections
with organisms such as tuberculosis, strongyloides and melioidosis, prior
to immunosuppressive therapy are in place in the Top End.
Diagnosis of Strongyloidiasis
Microscopy
Microscopy is the gold standard for diagnosis. This is usually from faeces.
However, other body fluids such as duodenal aspirate and sputum in
hyperinfective cases may show the parasite.

Faecal Microscopy
Specificity is high but sensitivity is low (0–50%)32 and multiple specimens
are required.

Cultures
Agar plate is presently considered the most sensitive culture technique
(78–100%).32
Its limitation is that it relies on detection of viable larvae, and this
becomes increasingly difficult as the time from collection to examination
of the specimen increases.
The Baermann stool concentration technique (as with the Agar plate)
requires viable larvae.22 The formalin-ether stool concentration techniques
has a reported 13–55% sensitivity.32 Harada Mori culture is reported to
have a sensitivity of ~26%.

Microscopy and culture: Conclusion/comments

In acute strongyloidiasis and in disseminated strongyloidiasis (high
excretors) sensitivity is improved. This is particularly true in hospital
settings where the faecal specimens can be examined on the same day.
However, for adults who are more likely to be chronic carriers and low
excretors, microscopy and culture may be less useful.
Multiple specimens should be sent to improve the sensitivity.
 Table 3: A summary of studies of strongyloides ELISA

Publication Year Sensitivity Specificity Positive Negative Faecal test

predictive predictive
value value
Schaffel24 2001 68% 89% 48% 95% Three stool
Brazil: examinations
tertiary
hospital
Gyorkos25 1990 95% 29% 30% 95% Stool
Population- examination
based study: (not
SE Asian described)
refugees in
Canada
Genta26 1988 88% 99% Charcoal
culture
Bailey27 1989 97% 99% Culture
Lindo28 1994 80 and 85% 94 and 97% Agar plate
(two
techniques
used)
Mangali29 1991 95% 96.6% Tube culture

Gam30 1987 96.6% 98%

Muhiudden31 1995 92.8% 100%
Uparanukraw32 1999 63.6% 95.4% Agar plate

Serology
The strongyloides ELISA test detects serum IgG antibodies to Strongyloides
stercoralis. The ELISA uses an arbitrary cut-off optical density point to
determine positive and negative cases. A high cut-off point will have a
lower sensitivity, higher specificity and therefore more false negatives. A
low cut-off point will have a higher sensitivity and many false positives.
The period from infection to seroconversion is unknown and acute cases may
be stool positive but seronegative.9 The proportion of people who remain
seropositive after successful treatment is not known.6 Filariasis and
ascariasis can cause cross-reactivity in the ELISA test.16 However, in
remote communities in the Northern Territory where these parasites are
uncommon, they are unlikely to contribute to false positives.23 A summary of
serological studies is presented in table 3.
Few of the studies calculated the predictive value of the test for the
particular population that was studied. This information is important for
the interpretation of the test and needs to be calculated for different
population groups as it is greatly affected by the prevalence of the
infection in each population. A large recent study of serology among
Brazilian in-patients (Schaffel24 — see table below) calculated a positive
predictive value (PPV) of 48% and a negative predictive (NPV) value of 95%
for the strongyloides ELISA. This PPV means that only about half of those
individuals with positive serology actually had strongyloides infection.
The NPV means that 95% of those with negative serology did not have
infection with strongyloides. Another population-based study of SE Asian
refugees in Canada found the test had a predictive value of 30%.
Statistical techniques have been developed to try to overcome these
limitations of available tests for strongyloides and other parasites where
results from stool examinations generally underestimate the prevalence, and
serology generally results in overestimation. Using a Bayesian approach,
simultaneous inferences about the population prevalence and the
sensitivity, specificity, and positive and negative predictive values of
each diagnostic test are possible.33 These may be adaptable to the setting
of Aboriginal communities in northern Australia.
In non-endemic communities serology has been used to monitor the
effectiveness of treatment34,35 in a manner analogous to the use of
treponemal serology to monitor treatment for syphilis. These studies have
shown variability in rate of decline of IgG ELISA following treatment.
Anecdotally, some practitioners in northern Australia believe that with
adequate treatment, serology should become negative within six months.
Studies are needed to validate these observations.

Comments/conclusions: Strongyloides serology

Serology is useful, particularly for excluding infection in adults. It is
also useful for diagnosing the condition in patients with symptoms, or
those at particular risk, such as those about to commence immunosuppressive
therapy. Positive tests need to be interpreted in the light of the clinical
picture and the original reason the test was done.
The role of serology in the follow-up of individual patients after
treatment is strongly advocated by some practitioners. Some clinicians have
found it to be useful in patients in non-endemic communities. However, the
meaning of positive and negative results requires further study in endemic
populations. Until there is better evidence, and better consensus among
those with expertise, it is not appropriate that CARPA protocols include
follow-up serology. In our view testing prior to immunosuppressive therapy
is a more practical way to prevent disseminated disease in individuals than
using resources to chase people at six and 12 monthly intervals to ‘ensure
cure’ especially when those individuals live in endemic communities and are
still at risk of re-acquiring the infection at a future time. Though
disseminated strongyloidiasis can occur in people without apparent immuno-
suppressing disease or treatment, we believe to be relatively rare and a
case management approach rather than a population approach is appropriate.
An incomplete review of known cases at the Royal Darwin Hospital and
discussions with relevant physicians suggests that, from anecdotal
experience, it is anticipated that there will be up to two cases per year
of disseminated strongyloides, almost invariably in people with clear
immunosuppressive treatment. There are likely to be a number of cases that
are not recognised.
As the predictive value of the test will vary with the prevalence of the
infection in the population, more studies in Aboriginal communities are
needed to guide the interpretation of the test in these settings. It is
particularly important that the PPV and NPV of the test are known before
its use can be considered for screening and treatment programmes. In our
view it would be better to put resources into facilitating community
development, with improved living conditions, which would have a positive
impact on many diseases, than to put resources in to programs of mass
screening and individual treatment for this one condition where the
predictive value of a positive screening test is not known.
The interpretation of serology results in the equivocal range
(borderline positive) is especially difficult. It may represent variance
due to the testing technique, occult infection, treatment failure or
persistent antibodies following successful treatment or spontaneous cure.
Interpretation should be in the light of the clinical setting. Further
study is needed.

Drug Treatment
Treatment of individuals has relied upon the use of antihelminthic drugs.
The main two drugs in use at present are albendazole and ivermectin.
Albendazole belongs to the benzimadole group of drugs which include
mebendazole and thiabendazole. It also has activity against hookworm, while
ivermectin does not. Nitazoxanide is a newer agent currently undergoing
trials. It may prove to be effective against trichuris, giardia,
cryptosporidium, hymenolepsis and strongyloides.36
Evidence summaries about the effectiveness of albendazole and ivermectin
against strongyloides infection are presented below.

Albendazole
Search question
Among people with strongyloides infection, does albendazole treatment
(compared to no treatment) reduce persistent infection as determined by
faecal tests?

Types of evidence reviewed

Evidence summaries, systematic reviews and randomised controlled trials
(identified from Clinical Evidence, Cochrane Library, PubMed).

Results
We identified no evidence summaries or systematic reviews. We did not
identify any trials that randomised participants with symptoms. We
identified two randomised trials that compared treatment with no treatment
in individuals with a range of helminthic infections. The first study37
found a cure rate of 38/47 (81%) with a single dose of 400 mg albendazole
vs 17/53 (32%) in the control group. The second study38 described cure rates
of 12/25 (48%) after albendazole daily for three days, versus 0/29 (0%) for
particpants who received placebo.

Albendazole: Comments/conclusions
Treatment with albendazole is clearly superior to no treatment. In these
two studies you would only need to treat two people before one would
benefit. However, these treatment regimes were less intensive than that
currently recommended in the CARPA STM third edition (three days without a
repeat course).

Ivermectin
Search question
Does treatment with ivermectin reduce persistent symptoms or signs of
strongyloides infection to a greater extent than the benzimidazole group of
antibiotics (albendazole, thiabendazole or mebendazole)?
Types of evidence reviewed
Evidence summaries, systematic reviews and randomised controlled trial
identified from Clinical Evidence, Cochrane Library and PubMed.

Results
We identified no evidence summaries or systematic reviews. We identified
three trials comparing treatment with ivermectin with treatment with
albendazole. A fourth study compared treatment with ivermectin to treatment
with thiabendazole. The studies are summarised in table 4 (below).

Estimated cure rates

Ivermectin 83–97%
Albendazole 38–77%
(Thiabendazole 95% cf 100% with 95% having short-term adverse effects)

Cure ratios (alb/iver) Difference in cure NNT

rates
0.54 38% 2.6
0.79 20% 5.0(randomisation not
stated)
0.46 45% 2.2 (small study)

Ivermectin: Comments/conclusions
All comparative studies demonstrated higher cure rates for ivermectin
compared with albendazole. You would need to treat between two and five
people with ivermectin instead of albendazole before one person would
benefit. All studies were conducted in high risk groups for strongyloides
infection. Only the first study (Zanzibar) was conducted in an area in
which S. stercoralis infection is endemic. The treatment regimen of the
largest study was similar to that recommended in CARPA STM third edition
for albendazole, except that the CARPA STM recommends repeating treatment
with albendazole after one week. The CARPA STM third edition does not
currently recommend ivermectin.
All experts agree that the CARPA STM fourth edition should recommend
ivermectin as the drug of first choice for adults at a dose of 200 μg/kg
for individual patients diagnosed with strongyloides. There is a diversity
of opinion about whether patients should receive a single dose as
recommended in the antibiotic guidelines, two doses (a week to 10 days
apart) or even three doses at monthly intervals. The effectiveness of
differing regimens has not been subjected to any trials. Those that argue
for three doses do so because of (1) the desire to eradicate larvae that
are extra-intestinal for transit periods of approximately one month and (2)
concern about promoting resistance to ivermectin, if a single dose is not
curative.
For the CARPA STM fourth edition, recommending multiple dosing in
patients who are immunosuppressed, or have other reasons for clinical
concern is certainly reasonable. Alternatively, two doses a week apart as a
general recommendation for all cases may not be unreasonable to keep the
guidelines simple, and address some of the worries about single dose
therapy.
As the drug is not licensed for use in children the recommendation for
albendazole should remain unchanged as the treatment regimen in children
under five years. However, ivermectin may be recommended for two- to five-
year-olds in individual children after specialist review.
Table 4: Comparative studies of the effectiveness of ivermectin

Population Treatment Blinding Random Therapy Time of Parasitological

repeated final cure rates
follow-up
(No. of
specimens
examined
for‘cure’)
301 Ivermectin Not Y N 24 days Ivermectin 83%
children in 200 mg/kg vs stated
Zanzibar 39

endemic
Albendazole
400mg daily (2 specs)
for 3 days Albendazole
45%

211 Ivermectin 6 Not Not Y 12 months Ivermectin 97%

Japanese mg stat vs stated stated
adults40 Albendazole 2 weeks
400 mg/day later (2 specs) Albendazole 77%
area for 3 days vs
previously Pyrvinium
endemic pamoate
5 mg/kg for 3 Pyrvinium 23%
days
53 Ivermectin N Y N 90 days Ivermectin 83%
residents 150–200 mg/kg (‘open (3 specs)
of France41 vs study’)
Albendazole
non-endemic 400mg daily Albendazole 38%
for 3 days

54 Ivermectin Y Y N 22 months Ivermectin

residents 200 mg/kg (single spec single dose 100%
of USA42 stat only)
vs
non-endemic Ivermectin Ivermectin two
200 mg/kg on consecutive
days one and doses 100%
two
vs
Thiabendazole Thiabendazole
(50 95%
mg/kg/day)
twice daily
for 3
consecutive
days
Community control strategies
Infection is likely to disappear from a community with improving
socioeconomic status as the environmental reservoir diminishes and the
infected population ages and dies.43 Screening and treatment of adults has
been tried in Japan — where living conditions had improved markedly and
people were no longer being infected from the environment — and at least
10% of the adult population continued to harbour the parasite. A five-year
program in which 20% of the adult population were screened with faecal
examination each year, and offered treatment if positive, resulted in a
slow decline in prevalence rates.44 Chemotherapy directed at groups
particularly at risk of infection has been suggested.43 This would require
knowledge of prevalence rates, the value of screening tests used and the
costs and benefits and the resources required. This information would need
to be balanced against the costs and benefits of alternative approaches
before a reasonable recommendation could be made.

Community control: Comments/conclusions

There is insufficient information available to determine the value of
community-wide screening and treatment programs. In the light of the many
other major public health issues facing Aboriginal communities, and
difficulties with interpreting serology, CARPA should not recommend
community screening and treatment of strongyloides.

References
1. Grove DI. Human Strongyloidiasis. Advances in Parasitology1996; 38:281-309.
2. Lahn MM, Staub-Schmidt T, Him R et al. Strongyloides stercoralis infection in a
non-immunosuppressed tourist with involvement of the central nervous system.
Tropical and Geographical Medicine 1994; 46(6):368–70.
3. Grove DI. Strongyloidiasis. A major roundworm of man. UK & USA: Taylor & Francis
Ltd, 1989.
4. Hanson HJ. Strongyloidiasis in veterans. Med J Aust 2001; 175:503.
5. Meloni BP, Thompson RC, Hopkins RM, Reynoldson JA & Grcey M. The prevalence of
Giardia and other intestinal parasites in children, dogs and cats from aboriginal
communties in the Kimberley. Med J Aust 1993 Feb 1; 158(3):157–9.
6. Speare R & White S. Strongyloidiasis: a social determinant of heath? Outback
Flyer Nov/Dec 2001; 50;4–5.
7. Aland K. Worm Project at Galiwin’ku. Working Together 1996; 6(6):10.
8. Flannery G, White N. Immunological parameters in northeast Arnhem Land
Aborigines: consequences of changing settlement and lifestyles. Urban Ecology and
Health in the Third World. Schell LM Smith MT Bilsborogh A. Cambridge University
Press, 1993.
9. Kukuruzovic RH, Robins Browne RM, Anstey N,Brewster DR. Enteric pathogens,
intestinal permeability and nitric oxide production in childhood diarrheal diseases.
Paediatric Infectious Disease Journal In Press, August 2002.
10. Fisher D, McCarry F & Currie B. Strongyloidiasis in the Northern Territory.
‘Under-recognised and under-treated?’ Med J Aust 1993: 159:88–90.
11. Page W. Strongyloidiasis Clinical Audit Report. Darwin: Top End Division of
General Practice, 2002.
12. Markell EK, Voge M, John DT. Medical Parsitology. USA: WB Saunders Company, 1992.
13. Stettler N, Schutz Y, Jequier E. Effect of low-level pathogenic helminth
infection on energy metabolism in Gambian children. Am J Trop Med Hyg 1998 Apr;
58(4):476–9.
14. Dickson R, Awasthi S, Williamson P, Demelweek C, Garner P. Effects of treatment
for intestinal Helminth infection on growth and cognitive performance in children:
systematic review of randomised trials. British Medical Journal 2000; 320:1697–701.
15. Marti H, Haji HJ, Savioli L, Chwaya HM, Mgeni AF, Ameir JS, Hatz C. A comparative
trial of a single-dose ivermectin versus three days of albendazole for treatment of
Strongyloides stercoralis and other soil-transmitted Helminth infections in
children. Am J Trop Med Hyg 1996 Nov; 55(5):477–81.
16. Wilson JD et al. Harrison’s Principles of Internal Medicine. USA: McGraw Hill,
1991.
17. Eddleston M and Pierini S. Oxford Handbook of Tropical Medicine. Oxford
University Press, 2000: 158.
18. Mukerjee CM, Walker J. Pulmonary Strongyloidiasis Mimicking Cavitary Pulmonary
Tuberculosis. TB into the New Millennium. 14–18 July 2000: 90.
19. Lim L, Biggs B. Fatal disseminated strongyloidiasis in a previously treated
patient. Med J Aust 2001; 174:355–6.
20. Hansman D. Public Health Information. A Rapidly Progressive Fatal Illness
Associated with Strongyloidiasis. Communicable Disease Report. Adelaide: Women’s and
Children’s Hospital, 1995.
21. Byard R W, et al. Pulmonary strongyloidiasis in a child diagnosed on open lung
biopsy. Surgical Pathology 1993; 5(1):55–62.
22. Pelletier LL, Baker CB, Gam AA, Nutman TB, Neva FA. Diagnosis and Evaluation of
Treatment of Chronic Strongyloidiasis in Ex-Prisoners of War. Journal of Infectious
Diseases March 1988; 157(3).
23. Lynch NR et al. Specificity of Toxocara Elisa in tropical populations. Parasite
Immunology 1988; 10:323–37.
24. Schaffel et al. The value of an immunoenzymatic test (enzyme-linked immunosorbent
assay) for the diagnosis of strongyloidiasis in patients immunosuppressed by
hematologic malignancies. American Journal of Tropical Medicine and Hygiene 2001;
65:346–50.
25. Gyorkos TW, Genta RM, Viens P, MacLean JD. Seroepidemiology of Strongyloides
infection in the Southeast Asian refugee population in Canada. Am J Epidemiol 1990
Aug; 132(2):257–64.
26. Genta RM. Predictive value of an enzyme-linked immunosorbent assay (ELISA) for
the serodiagnosis of strongyloidiasis. American Journal of Clinical Pathology 1988;
89:391–4.
27. Bailey JW. A serological test for the diagnosis of Strongyloides antibody in ex-
Far East prisoners of war. Annals of Tropical Medicine and Parasitology 1989;
83:241–7.
28. Lindo JF, Conway DJ, Atkins NS, Bianco AE, Robinson RD, Bundy DA. Prospective
evaluation of enzyme-linked immunosorbent assay and immunoblot methods for the
diagnosis of endemic Strongyloides stercoralis infection. Am J Trop Med Hyg 1994
Aug; 51(2):175–9.
29. Mangali et al. Southeast Asian Journal of Tropical Medicine and PublicHealth
1991; 22:89–92.
30. Gam et al American Journal of Tropical Medicine and Hygiene 1987; 37:157–61.
31. Muhiudden et al. Journal of the Egyptian Society of Parasitology 1995; 25:491–8.
32. Uparanukraw P et al. 1999.Fluctuation of larval excretion in Strongyloides
stercoralis infection. Am J Trop Med Hygiene; 60(6):967–73.
33. Joseph L, Gyorkos TW, Coupal L. Bayesian estimation of disease prevalence and
the parameters of diagnostic tests in the absence of a gold standard. Am J Epidemiol
1995 Feb 1; 141(3):263–72.
34. Kobayashi J, Sato Y, Toma H, Takara M, Shiroma Y. Application of enzyme
immunoassay for postchemotherapy evaluation of human strongyloidiasis. Diagn Microl
Infectn Dis 1994 Jan; 18:19–23.
35. Braun TI et al Strongyloidiasis in an Institution for Mentally Retarded Adults.
Arch Intern Med 1988; 148:634–6.
36. Ortiz JJ, Chegne NL, Gargala G, Favennec L. Comparative clinical studies of
nitazoxanide, albendazole and praziquantel in the treatment of ascaris, trichuriasis
and hymenolepiasis in children from Peru. Trans R Soc Trop Med Hyg 2002; 320:1697–
701.
37. Pene P, Mojon M, Garin JP, Coulaud JP, Rossignol JF. Albendazole: a new broad
spectrum anthelmintic. Double-blind multicenter clinical trial. Am J Trop Med Hyg
1982; 31(2):263–6.
38. Rossignol JF, Maisonneuve H. Albendazole: placebo-controlled study in 870
patients with intestinal helminthiasis. Trans R Soc Trop Med Hyg 1983; 77(5):707–11.
39. Marti H, Haji HJ, Savioli L, Chwaya HM, Mgeni AF, Ameir JS, Hatz C. A comparative
trial of a single-dose ivermectin versus three days of albendazole for treatment of
Strongyloides stercoralis and other soil-transmitted Helminth infections in
children. Am J Trop Med Hyg 1996 Nov; 55(5):477–81.
40. Toma H, Sato Y, Shiroma Y, Kobayashi J, Shimabukuro I, Takara M. Comparative
studies on the efficacy of three anthelminthics on treatment of human
strongyloidiasis in Okinawa, Japan. Southeast Asian J Trop Med Public Health 2000
Mar; 31(1):147–51.
41. Datry A, Hilmarsdottir I, Mayorga-Sagastume R, Lyagoubi M, Gaxotte P, Biligui S,
Chodakewitz J, Neu D, Danis M, Gentilini M. Treatment of Strongyloides stercoralis
infection with ivermectin compared with albendazole: results of an open study of 60
cases. Trans R Soc Trop Med Hyg 1994 May–Jun; 88(3):344–5.
42. Gann PH, Neva FA, Gam AA. A randomized trial of single- and two-dose ivermectin
versus thiabendazole for treatment of strongyloidiasis. J Infect Dis 1994 May;
169(5):1076–9.
43. Conway DJ, Lindo JF, Robinson RD and Bundy DAP. Towards Effective control of
Strongyloides stercoralis. Parasitology Today 1995; 11(11):421–4.
44. Toma H, Shimabukura I, Kobayashi J, Tasaki T, Takara M, Sato Y. Community control
studies on Strongyloides infection in a model island of Okinawa, Japan. Southeast
Asian J Trop Med Public Health 2000 Jun; 31(2):383–7.
 Tetanus Immunisation

The protocol is adapted directly from the Australian Immunisation Handbook,

seventh edition. The table has been redesigned in a way that we believe is
clearer and essentially the same as practitioners would be used to from the
previous edition of the CARPA Standard Treatment Manual.
Note: Tetanus toxoid is only recommended in instances where there is a
contra-indication to the diphtheria component of the ADT or DTPa. This will
be rare.
Using the combination vaccines (ADT and DTPa) will have additional benefits
of boosting immunity for diphtheria and (for children) pertussis as well.
For more details on tetanus immunisation, see the latest edition of the
Australian Immunisation Handbook.
 Tinea of Skin and Nails

Author: Dr Karen Koh (RDH, MSHR)

Topic Reviewers: Peter Wordsworth (RAN, Burunga Clinic); Janet Fletcher (RAN,
Ngukurr Clinic); Mt Liebig Clinic; Kaz Knudsen (RAN, WA)

Synonyms: Ringworm, ‘jock itch’ (groin), athlete’s foot (feet).

Tinea of the skin and nails is a major problem in remote communities of the
Top End. Green3 estimates that point prevalence in classes of school
children may reach up to 15%. The condition is of concern to the affected
person due to its appearance cosmetically. However, tinea of nails and skin
also predisposes to streptococcal and other skin infections. Serious
complications from streptococcal infections include acute rheumatic fever
and post-streptococcal glomerulonephritis.1 Skin infections and its
complications are of special concern in diabetic patients who are more
predisposed to infections in general. Anthropophilic tinea is transmitted
between people who live together in a household2, and this is an important
factor in communities where overcrowding is a major problem. This has
implications for re-infection of successfully treated patients. Little data
has been collected on the epidemiology of tinea in the Top End. The last
extensive studies characterising tinea in the NT were in the 1970s.4,8

Tinea corporis
This predominantly affects trunk, limbs and groin. Less commonly the face
is involved (tinea faciei). Often tinea occurs as asymmetrical, solitary
lesions (60%), but can be bilateral and multiple.
Typically tinea begins under the posterior beltline with scaling the
earliest sign. Frequently it then extends above the beltline, and often
down onto buttocks. Tinea can be itchy, especially in areas of increased
sweating such as the groin (tinea cruris).
Clinically tinea is a scaly plaque with a spreading edge. There is
increased pigmentation and often increased skin markings (lichenification
from scratching). There may be thickened darker papules. Scaling may be
marked or minimal.
Inflammation with blisters and weeping is uncommon in Aboriginal
populations unless there is secondary bacterial infection. Tinea can be
more inflammatory in Caucasians2, though this may be because you can see it
more clearly on fair skin.
Tinea tends to be chronic, with the incidence of secondary bacterial
infection often underestimated.2
Tinea is endemic in tropical regions including the Top End of the NT.
Children, adolescents and adults are all commonly affected.2 Transmission is
usually person-to-person (anthropophilic).2
Usually anthropophilic fungi cause tinea corporis.
• Trichophyton rubrum is the most common type in northern Australia2,4
 • Trichophyton violaceum and T. tonsurans are more commonly found on
culture in central and southern Australia2,4
• Epidermophyton floccosum often affects skin folds (e.g. groin) and
between toes (tinea pedis)2

The high prevalence of anthropophilic infection in Aboriginal populations

probably relates to poor living conditions and overcrowding in communities.2

Tinea pedis/tinea manuum

This usually presents as an asymmetrical (but sometimes bilateral) scaling
on the feet. Scaling and maceration also may occur between the toes. Often
tinea pedis is asymptomatic but may be itchy, blistering and inflammatory.
Tinea from the feet may spread to other parts of the body. Involvement of
the palms (tinea manuum) is less common, but presents in a similar fashion.
In Aboriginal populations anthropophilic dermatophytes such as
Epidermophyton floccosum are the commonest cause.2

Diagnosing tinea of the skin

When practical, patients should be told not to use any antifungal topical
treatment for at least two to seven days before any skin scrapings are
taken.

Skin scrapings for microscopy and fungal culture

Using a disposable scalpel; scrape the raised edge of the scaly plaque to
collect as much scale as possible. This is where hyphae are likely to be
numerous. This can be collected in a folded black cardboard (pathology
companies usually make these up, with stickers on the side to seal them;
much easier to use than plastic jar as skin doesn’t stick to the side) or a
plastic specimen jar.
Generally, scraping should not produce bleeding. If more than one site
is affected separate specimens should be taken using a new scalpel blade.
Dermatophytes in skin will remain viable for about 30 days, however,
delay between specimen collection and processing increase the chance of
possible deterioration and contamination. Specimens should be kept in a
cool dark place, i.e. less than 30?C, not refrigerated.

Tinea unguium/onychomycosis
This presents as thickening or irregularity of the nails (fingers and
toes). The nails are white and lift up from the underlying nail bed
(onycholysis) with marked amounts of chalky material under the nail
(subungual hyperkeratosis). Usually nail tinea is associated with tinea
elsewhere on the skin. Nail involvement can be unilateral or bilateral and
toenails are more commonly affected than fingernails. Nail tinea is usually
caused by anthropophilic dermatophytes such as Trichophyton rubrum and T.
tonsurans in Aboriginal populations.2

Diagnosing tinea of nails

Taking specimens from affected nails that are thickened and dystrophic can
be difficult. The nail should be clipped back until the crumbling portion
of the nail is reached. Chalky debris from under the nail should be scraped
and collected.
Tinea capitis
This usually presents as areas of poorly defined scale on the scalp with
varying degrees of hair loss. Scale may be defined or diffuse, fine
(dandruff-like) or thick and adherent. Kerion of the scalp (inflammatory
boggy folliculitis) is rare in Aboriginal populations.2
Tinea capitis can be secondarily infected with bacteria. Tinea capitis
is caused by:2

Anthropophilic fungi Trichophyton violaceum,

T. tonsurans
T. rubrum is an unusual
cause of tinea capitis
Zoophilic fungi Microsporum canis, (from cats,
(from animals) dogs; common in children.)
T. verrucosum (cattle: less
common)
T. mentagrophytes (kangaroos)
Geophilic fungi M. gypseum
(from soil)

Diagnosing scalp tinea

Using a Wood’s lamp (black light) Microsporum canis infection fluoresces
green/yellow.
Skin scrapings and pulled hair specimens for fungal microscopy and
culture should be collected.
Hair microscopy can help with diagnosis.

M. canis small spores, ectothrix (spores

form sheath around surface of hair
shaft)
T. tonsurans, large spores, endothrix (hyphae
T violaceum penetrate the inside of the hair
shaft and break up into parallel
chains
T. rubrum ecto-endothrix (spores occur both
on the outside and inside of the
hair shaft)

Treatment of tinea
Griseofulvin has been the mainstay of oral antifungal treatment in the
past. Griseofulvin is fungistatic (fungus is inactivated but not killed)
and therefore necessitates long treatment schedules for control of disease.
This long duration of treatment is particularly of concern in the treatment
of tinea nail infection (onychomycosis) where treatment is longer due to
the natural slow growth of new nails (3mths for fingernails, 6mths for
toenails to fully grow out).
The newer antifungal agents itraconazole, terbinafine and fluconazole
are now used to treat onychomycosis. In the last 10 years these agents have
superseded griseofulvin as the agent of choice for onychomycosis. Unlike
griseofulvin, the new agents have a broad spectrum of action that includes
dermatophytes, Candida species and nondermatophyte moulds. These agents are
generally well tolerated with drug interactions that are usually
predictable.6
Itraconazole and fluconazole are not PBS listed for treating
onychomycosis and therefore are very expensive. Fluconazole can be obtained
on Section 100 prescription. Terbinafine can be obtained on authority
prescription if positive microscopy or fungal culture is determined by a
recognised laboratory.
Daily oral terbinafine (Lamisil) has been increasingly used in remote
communities for the treatment of extensive tinea. Although more expensive,
duration of treatment with terbinafine is shorter compared to older
treatments such as griseofulvin. This enhances compliance and is therefore
potentially more cost-effective. Terbinafine is fungicidal (fungus is
killed), especially with Trichophyton species that cause tinea in the Top
End. There are no formal studies in the NT regarding griseofulvin use, but
anecdotally it is reported to be poorly tolerated in extended treatment
regimes, and compliance is therefore poor. Studies in the UK show higher
success rates with terbinafine compared to griseofulvin in treating
fingernail and toenail onychomycosis (terbinafine 78% versus griseofulvin
18% for toenails, 95% terbinafine versus griseofulvin 60% for fingernails)
with total days of therapy being fewer for terbinafine (102 days versus 211
for griseofulvin).7
Comparative studies have shown that terbinafine is more effective than
griseofulvin, fluconazole or itraconazole in the treatment of
onychomycosis, providing a cure rate of 70–80% and an excellent
tolerability profile. Terbinafine is also the most cost-effective agent. In
cases where there is treatment failure, nail debridement may need to
precede drug therapy in order to maximise the prospects of cure.10
I am conducting a prospective study looking at the efficacy of oral
terbinafine in managing skin and nail tinea in remote Aboriginal
communities in 2001.
Topical terbinafine is also effective in treating skin tinea. One study
showed 84.6% of patients in a terbinafine-treated group were culture
negative after one week, compared with only 55.8% in the clotrimazole
(Canestan) group. The study showed that terbinafine achieves mycological
cure more rapidly than clotrimazole.9

Other Treatments
Itraconazole: pulse therapy with the oral drug being administered for one
week with three weeks off treatment between successive pulses (200 mg twice
daily for one week per month x three pulses).
Fluconazole: once-weekly treatment. 150 mg/wk until the abnormal-
appearing nail plate has grown out, typically over a period of nine to 18
months.
Sequential pulse treatment with itraconazole and terbinafine: one study
proposed sequential pulse therapy (IIT) with two pulses of itraconazole
followed by one or two pulses of terbinafine (itraconazole pulse is 200 mg
twice daily for one week and terbinafine pulse is 250 mg twice daily for
one week) versus three or four pulses of terbinafine (TTT). At week 72, in
the IIT versus TTT groups, the mycologic cure rate was 54 of 75 (72.0%)
versus 44 of 90 (48.9%), clinical cure rate was 42 of 75 (56.0%) versus 35
of 90 (38.9%), effective therapy 49 of 75 (65.3%) versus 41 of 90 (45.6%),
and complete cure 39 of 75 (52.0%) versus 29 of 90 (32.2%), respectively.
This protocol was well tolerated.4
 I recommend daily oral terbinafine for extensive tinea corporis or tinea
unguium. It is well tolerated and serious side effects are few and
uncommon.7,10
Some practitioners prefer pulse treatment, others prefer continuous
treatment. Finding a medication regimen with a dosing schedule which
increases compliance depends on the individual.

References
1. Currie BJ, Carapetis JR. Skin infections and infestations in Aboriginal
communities in northern Australia, Australas J Dermatol, August 2000; 41(3):139–43
quiz 144–5.
2. Green A. A handbook of skin conditions in Aboriginal populations of Australia:
2001 Blackwell Science Asia Pty Ltd pp 20–24, 54–57, 80–82, 130–132.
3. Green, A. Australian Aborigines and ringworm (tinea) Australas J Dermatol 1998;
59:192–194.
4. Green A, Kaminski G. Australian Aborigines and their dermatophytes Australas J
Dermatol Dec 1977; 18(3):132–6.
5. Gupta AK, Lynde CW, Konnikov N. Single-blind, randomized, prospective study of
sequential itraconazole and terbinafine pulse compared with terbinafine pulse for
the treatment of toenail onychomycosis. JAAD Mar 2001; 44:485–91.
6. Gupta AK. Shear NH A risk-benefit assessment of the newer oral antifungal agents
used to treat onychomycosis Drug Saf 2000 Jan; 22(1):33–52.
7. Humphrey KM, Cork, MJ, Haycox A. A retrospective cost-effectiveness analysis
of the treatment of onychomycosis in general practice; Br J Derm 1998; 139:660–4.
8. Kaminski G, Green A. Tinea Capitis in Aboriginal children at Maningrida, NT,
Australia; Australas J Dermatol Aug 1977; 18(2):88–97.
9. Patel A, Brookman SD, Bullen MU, Marley J, Ellis DH, Williams T, Barnetson RS.
Topical treatment of interdigital tinea pedis: terbinafine compared with
clotrimazole. Australas J Dermatol 1999 Nov; 40(4):197–200.
10. Roberts DT. Onychomycosis: current treatment and future challenges Br J Derm
1999 Nov; 141(Suppl)56:1–4.
 Tuberculosis (TB)

Author: Dr Craig Boutlis (Infectious Disease physician, MSHR)

Topic Reviewers: Dr Vicki Krause; Dr Ral Antic; Dr Justin Waring; Liz

Stephensen (RAN, Nhulunbuy CDC); Peter Wordsworth (RAN, Burunga Clinic);
Bernard Egan (RAN, Bulman Clinic)

Introduction
Mycobacterium tuberculosis (MTB) is a bacterium which is estimated to
currently infect over one third of the world’s six billion people, causing
over eight million new cases of disease annually.1 Infection is much less
common in populations with good access to health care and where overcrowded
living conditions are uncommon. Most people infected with MTB will never
realise it, as the immunity they develop contains the infection, but around
10–20% will at some stage become sick with active TB, a serious but curable
disease.2 Pulmonary TB is by far the most frequent presentation of disease
and is the form primarily involved in the transmission of infection. Extra-
pulmonary TB is rarely infectious and may affect the linings of the lungs
or heart (causing pleural effusions or pericarditis), lymph nodes, bone and
joints, genitourinary tract, brain (causing meningitis or space-occupying
lesions), peritoneum or any other part of the body. All forms of active TB
may present with systemic symptoms including fevers, weight loss, night
sweats, and loss of appetite.

Transmission of Mycobacterium tuberculosis

Infection is transmitted from one person to another by invisible droplets
that are expelled into the air when coughing, sneezing, laughing or
talking. These droplets can stay suspended in the air for a number of hours
but are rapidly inactivated by sunlight. Those patients with the highest
concentration of MTB in their lungs (smear-positive cases on sputum
microscopy) are the most infectious.3 Transmission is relatively
inefficient, therefore the more time someone spends with an infectious
case, the more chance they will become infected. The chance of infection
will also be increased if the contact is close or occurs in rooms without
good ventilation.4

Epidemiology of TB in the Northern Territory

Each year there are between 30 and 60 new cases of active TB notified in
the NT.5 Approximately 60% of these occur in Aboriginal persons, 30% in
migrants and 10% in the remainder of the community. Over the last 10 years,
TB notification rates have averaged around 22 per 100 000 per annum in the
NT compared to six per 100 000 in the wider Australian community in 1999.1
The rate in NT Aboriginal and migrant communities has been approximately 40
per 100 000 per annum which is approximately 10 times the rate of four per
100 000 per year in the remainder of the NT population. About half of the
NT cases occurred in people aged 15–44 years. The spectrum of disease in
the NT is similar to that in other populations, with approximately 70% of
new cases due to pulmonary TB, and the most common cause of extra-pulmonary
disease being lymphadenitis.6 Control of TB throughout the NT requires a
coordinated effort involving health staff from remote communities working
in partnership with their patients and Department of Health and Community
Services TB Control Units.

Priorities for the control of TB in the

Northern Territory
• To rapidly identify and provide effective treatment and support to
infectious cases with active TB, so the chance of transmission to
others and the consequences of disease for the patient are reduced.
• To protect contacts of an infectious case with infection control
measures instituted from the time active TB is first suspected until
the case is no longer infectious.
• To identify and treat people with latent (asymptomatic) infection
who are most at risk of developing active TB. At highest risk are
recent contacts of infectious cases, especially young children and
people who are immunosuppressed.
• To prevent severe disease in those at highest risk with BCG
vaccination (i.e., very young children who are most susceptible to
disseminated TB and tuberculous meningitis).
• To promote effective communication between urban and remote-area
health staff and specialist TB units.

Review
Key questions for the control and management of TB within the CARPA manual
use area:
• How can active TB be recognised quickly?
• What infection control measures can be instituted to prevent
transmission once a suspected active case is identified?
• What treatment should be given to people with active TB?
• How can people with latent TB infection (LTBI) at highest risk of
active disease be identified?
• How should people identified to have LTBI be managed?
• What are the indications for the appropriate use of BCG vaccination?
• How can effective communication between health staff and TB Control
Units be facilitated?

Prompt recognition of active TB

Symptoms and signs of active TB
An important clue to the recognition and diagnosis of active TB is that it
occurs with increased frequency in populations known to be at higher risk
for transmission and/or progression of infection.7 This includes Aboriginal
people, migrants from high prevalence countries and people with chronic
diseases such as HIV, diabetes, renal failure and malnutrition. Very few
symptoms are specific to TB but persistence of symptoms is a very important
feature of all forms of the disease. Pulmonary TB should be suspected if a
cough lasts for longer than three weeks or is associated with blood-stained
sputum. Unexplained weight loss, night sweats, fevers, tiredness and loss
of appetite are also common features of pulmonary TB.
These non-specific symptoms may be the only feature of extra-pulmonary
TB but symptoms and signs specific to the organs of involvement may also be
present. These may include chest pain secondary to infection of the pleura
or pericardium, bone pain (the spine is most commonly involved), or
abdominal swelling in the case of peritoneal disease. Persistent painless
enlargement of lymph nodes, usually without systemic symptoms, is the most
common presentation of tuberculous lymphadenitis and can also represent
infection with non-tuberculous (‘atypical’) mycobacteria, especially in
children.8 Patients with tuberculous lymphadenitis may have been
unsuccessfully treated with standard antibiotics previously. Alteration of
conscious state or focal neurological signs in someone with fever or other
systemic symptoms, especially in children, should prompt urgent in-hospital
investigation that includes tests for tuberculous meningitis or tuberculous
brain lesions.

Laboratory diagnosis of active TB

Sputum collection
A diagnosis of pulmonary TB can usually be made by collecting three early-
morning sputum specimens and requesting laboratory examination by smear and
culture for TB or ‘AFBs’ (acid fast bacilli).9 Routine microscopy and
culture should also be performed, including (in the Top End) selective
tests for melioidosis.10,11 Cytology should be ordered if lung cancer is part
of the differential diagnosis (e.g., in smokers or older people with blood-
stained sputum). It is desirable to collect these three specimens over
three mornings in a row, as morning specimens give the best results.7
However, it may be necessary to collect the first specimen immediately when
the patient is first seen or to collect the other two on the same day if
the person is highly mobile or likely to be difficult to follow up. Sputum
specimens should be protected from light (as UV light kills MTB) by first
sealing the containers in a plastic BioHazard bag and then placing the
BioHazard bag into a brown paper bag. If the specimen cannot be transported
to the laboratory within one hour of collection, then it should be
refrigerated prior to and during transport.
Patients with pulmonary TB are infectious to other people and special
care must be taken to prevent transmission of infection to contacts and
health personnel (see below). Patients should be given a specimen container
and asked to go outside into the fresh air away from other people to
produce their sputum specimen. It may help the patient to cough if they
have had a drink of water beforehand. A good sputum specimen is one which
covers the bottom of the specimen container and contains very little saliva
(it should stick to the bottom of the container when tipped upside down).
Patients with suspected pulmonary TB who are unable to cough may be able to
produce an induced sputum specimen with the help of a physiotherapist, or
may require bronchoscopy for accurate diagnosis.2

Collection of gastric aspirates and tissue specimens

Gastric aspirates, which contain sputum that has been swallowed overnight,
may need to be collected to diagnose pulmonary TB in children and in adults
who cannot produce sputum. The sensitivity of gastric aspirates for the
diagnosis of pulmonary TB varies from 30–50% in those aged two to 12 years
to up to 70% in infants less than two years of age.12 As the best gastric
aspirate specimens are those collected prior to waking, and the acid in the
aspirate needs to be neutralised soon after collection, these are best
collected in a hospital environment.13 Patients with extra-pulmonary TB will
usually require a fine needle aspirate or biopsy for microscopic
examination and culture to confirm the diagnosis. Specimens collected in
this way should be sent to an appropriate laboratory without delay in a
small amount of normal saline. Biopsy specimens must not go into formalin
as this will kill any MTB organisms present.

Role of tuberculin skin testing (Mantoux) in diagnosis of active TB

The Mantoux test is not a good test to diagnose active TB14, especially in
adults. Negative Mantoux tests will be observed in approximately 10–25% of
patients with active TB15,16, therefore the Mantoux test cannot be used to
eliminate the possibility of active TB.2 Because active TB is more frequent
in risk groups with a high prevalence of latent TB infection, Mantoux tests
will often be positive even when disease is not present — i.e. the
predictive value of a positive test is very low.17 Therefore, in adults, the
focus of investigation should be to obtain relevant sputum and tissue
specimens for microscopy and culture as this decision will not be
influenced either way by a Mantoux result. A positive Mantoux test in
association with a compatible clinical picture is more suggestive of
disease in children where the likelihood of false-negative reactions is
approximately 10% and the background prevalence of infection is expected to
be low.18 Its use in this context should be discussed with an expert in the
management of TB.

HIV testing
The highest rate of reactivation of latent TB infection occurs in patients
with human immunodeficiency virus (HIV) infection — roughly 10% per year as
opposed to 10% per lifetime if HIV-negativ.19 Active TB may present early on
in the course of HIV infection, before patients become significantly
immunosuppressed.20 Because treatment is now available that will
significantly improve the prognosis of patients with HIV21, all patients
with active TB should be counselled and advised to undergo HIV testing. It
is hoped that this strategy will identify people earlier in the course of
their HIV infection at a time when treatment may provide the most long-term
benefit.

Infection control measures

Prevention of airborne transmission
The risk of transmission of MTB to others can be minimised by instituting
sensible infection control procedures once a case of suspected pulmonary TB
has been recognised. Because MTB is spread by airborne droplet nuclei,
transmission to contacts may be reduced by asking the patient to cover
their mouth and nose with a handful of tissues or a handkerchief when
coughing and sneezing.22 Facemasks designed to filter fine particles have
also been suggested for patients and health staff to decrease expulsion of
bacilli and inhalation of droplet nuclei. A recommended particulate filter
mask is one which provides face-seal leakage of less than 10% and that has
greater than 95% efficiency in filtering 0.3 micron particles (e.g., ‘duck-
bill’ masks).23

Travel and hospitalisation of patients with suspected active TB

People with suspected active TB should only travel by air on commercial
aircraft if known to be smear-negative on three separate sputum smears.24
Patients who are smear-positive or whose sputum smears have not been
examined should wear a mask during transport and only travel by air with an
air medical service, preferably without other patients on board. Road
travel should be undertaken with masks on and windows down to promote
maximum ventilation. Suspected TB cases should be housed in hospital in
single rooms with negative pressure ventilation and respiratory isolation
precautions until three separate early morning sputum smears are negative.

Treatment of active TB
Drug therapy
Treatment of TB typically requires at least six months of multi-drug
therapy and is extremely effective for most forms of disease.25 Some forms
of extrapulmonary disease may require longer therapy up to and in excess of
12 months on occasions (e.g., disseminated TB, bone and joint disease and
cerebral tuberculomas). Treatment may need to be started in hospital if
infection control measures are required for smear-positive patients, but
may sometimes be started as an outpatient if the risk of transmission to
others is judged to be very low. Patients who were smear-positive on sputum
microscopy will usually be non-infectious after two weeks of effective
treatment.26 Patients with more advanced cavitatory disease may take longer,
sometimes months, to become smear-negative.
Four anti-TB drugs (rifampicin, isoniazid, pyrazinamide and ethambutol)
should be given initially to rapidly decrease the burden of tuberculous
bacilli and to cover the possibility of drug resistance. Pyrazinamide may
be poorly tolerated by elderly people and ethambutol should not be used in
people who might have difficulty in reporting visual loss, e.g., those with
large cataracts or children under six years of age. Pyrazinamide and
ethambutol can usually be ceased after two months if susceptibility tests
confirm no drug resistance. Rifampicin and isoniazid are continued for the
duration of therapy. Different combinations may be required depending on
whether the patient’s MTB isolate is resistant to first line drugs or if
side effects occur on standard therapy. Pyridoxine (vitamin B6) is given at
the same time to minimise the risk of isoniazid-induced peripheral
neuropathy.19 Drug dosages can be found in standard treatment guidelines27,28
and may require adjustment during therapy for changes in body weight.
Monthly clinical monitoring for side effects is necessary for all patients
and monthly liver function tests will be necessary for people at increased
risk of liver toxicity.27

Helping patients complete their treatment

Completing a full course of treatment for active TB or latent TB infection
can be difficult because of the complexity of multi-drug regimens and the
length of therapy. However, it is extremely important that the patient is
supported and able to take all of their prescribed therapy, as
interruptions or early cessation of the treatment regimen can lead to the
serious problem of emergence of drug resistance, which can make re-
treatment more difficult in both the index case and any secondary cases in
contacts. Patients may be more motivated if they and their families have
received education about the disease and its treatment in their primary
language.29 This should be done with the help of visual aids and through an
interpreter whenever one is available. It should be explained that it will
usually be possible to simplify the drug regimen after two months of
therapy. Providing feedback to patients during therapy may also help to
enhance adherence to the drug regimen. Showing patients how chest X-ray
changes improve with treatment can be very useful in this regard.
Patients should be warned that their urine will turn a pink to orange
colour while taking rifampicin but that this is not at all harmful, in fact
it can be a good sign that the drug is being absorbed and doing its work.
It is extremely important that patients are told to look out for common
(e.g., skin itch, difficulty sleeping or concentrating) and potentially
serious side effects. The latter includes symptoms of liver toxicity such
as nausea; loss of appetite; abdominal pain and tenderness; darkening of
the urine (jaundice). Pyrazinamide may also cause gout and ethambutol can
result in loss of visual acuity. Patients should be advised not to drink
alcohol while on therapy as it may enhance the risk of liver toxicity.30
Nothing is more important than telling all patients on TB therapy of any
kind to stop their medication and seek help immediately if they develop any
new symptoms, as these may represent drug toxicity.
The most effective way of ensuring that a patient can adhere to their
treatment regimen is to administer their therapy under direct supervision.31
This is called Directly Observed Therapy (DOT).32 DOT works best when the
patient has easy access to their medication either by having the medicine
brought out to them or being able to access their medicine from a clinic
without having to wait. To facilitate DOT, most anti-TB drug regimens can
be given two to three times weekly at doses higher than the usual daily
dose. DOT is given three times weekly in the NT. Any missed doses should be
added to the end of the treatment regimen so that all the intended doses
get taken, even though this means extending treatment. Management of
patients who have a prolonged break from therapy will need to take into
consideration issues of possible disease relapse or drug resistance and
should be done with the consultation of regional TB Control Units.

Diagnosis of latent TB infection (LTBI) in people at high risk

Identification of people with LTBI is an essential component of TB control
programs in developed countries. Treatment of LTBI will substantially
reduce an individual’s risk of developing active TB and also potentially
decrease transmission within a community.19 The most efficient use of this
control strategy is to target individuals at highest risk of being infected
or developing disease. This includes recent contacts of infectious cases
(whose risk of infection may be as high as 50%3), people with LTBI who have
reduced immunity to MTB (e.g., because of immunosuppressive drugs like
high-dose or prolonged steroids; or chronic diseases including HIV,
diabetes, renal failure and malnourishment) and people with fibrotic chest
X-ray changes of TB.33 Children are at particularly high risk.

Contact tracing
Contact tracing of people exposed to an infectious (index) case of TB is
vitally important to prevent more people getting sick and to interrupt
transmission within a community. To be effective, contact tracing
necessarily involves a lot of time and must begin as soon as possible after
a presumptive diagnosis of active TB has been made. The efficiency of
contact tracing will be enhanced when local health staff work together in
partnership with the index case, their family (with the index case’s
consent) and the regional TB Control Unit whose responsibility it is to
coordinate the process. The risk of transmission to contacts will be
highest when the index case is smear-positive for AFBs on sputum smear and
when the degree of contact is close.7 Household contacts and school or
workplace contacts who work alongside the index case are the highest
priorities in contact tracing. If evidence of transmission is found within
these groups, then lower-risk contacts will also need to be followed up.
 Contact tracing should begin by providing the index case with an
understanding of the contact tracing process and educating them about the
benefits of early diagnosis and treatment for their friends and families.
If the patient is agreeable, this is often best explained in the company of
their family. Contact lists should be drawn up of all contacts going back
at least three months (longer if the patient’s symptoms began before this),
identifying each according to their level of exposure. The highest priority
will be given to close contacts (as above), especially young children and
adolescents. It is extremely important to screen contacts for symptoms and
signs of active TB as these may have developed recently. Details of prior
Mantoux tests, treatment of latent or active TB and chest X-ray results
should be checked for each contact with the regional TB Control Unit.
Further decision making with regard to Mantoux testing, chest X-ray, and
treatment of latent or active TB (below) needs to be made in consultation
with the regional TB Control Unit.
Contact tracing for lower-risk cases of active TB (including smear-
negative pulmonary TB and extra-pulmonary disease) is also important, as
friends and family are likely to have shared similar exposure to the person
from whom their friend or relative has acquired their infection. This will
also be true for children who are discovered on school screening to have a
positive Mantoux test without symptoms of active TB, as they are likely to
have been infected with TB relatively recently and other members of the
family may also be at risk.

Mantoux testing
The Mantoux method of tuberculin skin testing remains the most reliable and
widely validated means of assessing whether an individual has been infected
with MTB. In vitro assays of the cellular immune response to tuberculous
proteins (such as the QuantiFERON™ test) currently offer few advantages
over Mantoux testing, as false-positive results occur in BCG-vaccinated
subjects34 and there has been far less experience with their use. This
situation may change as assays are developed that measure the immune
response to MTB-specific PPD subunit proteins that are not present in BCG
vaccine strains of M. bovis.35
Assessment of an individual’s cutaneous reaction to tuberculin must take
account of the size of the reaction, the predictive value of the test based
on possible causes of false-negative and false-positive reactions and the
risk of development of active TB. Readers are referred to the most recent
Centre for Disease Control Guidelines for the Control of TB in the Northern
Territory for the interpretation of Mantoux tests. Note that repeat testing
of contacts 10 weeks after their last exposure to an infective case is
often required as it can take that long for a person to develop an immune
response to MTB that is detectable by Mantoux testing.16
Because of the difficulty in interpretation of Mantoux tests in people
at low risk for TB, there has been a trend towards targeting testing toward
people at higher risk who will benefit the most from treatment of LTBI.19
This includes contacts of a case of active TB (as defined above) but also
people at increased risk of progression of LTBI to active TB. The latter
group includes people with chest X-ray changes that could be consistent
with previous TB infection, recent migrants (assumed to have been exposed
up to the time of departure) and patients who are immunosuppressed because
of disease (e.g., HIV, diabetes, renal failure, malnutrition) or drugs
(e.g., oral steroid therapy). A baseline Mantoux test should also be done
for staff who will be working in settings with evidence of increased TB
transmission (e.g., Aboriginal health centres, drug and alcohol
rehabilitation centres, prisons and hospitals).
Mantoux tests should not be done in people with prior Mantoux results of
15 mm or greater or previous known TB, therefore an inquiry should be made
to the regional TB Control Unit as to a person’s prior Mantoux and TB
history before testing.

Treatment of latent TB infection

Benefits of treatment
With few exceptions, in people targeted for Mantoux testing because of an
increased risk of infection or disease the decision to test can be regarded
as the decision to treat.19 This statement reflects the view that the
benefits of treating LTBI will outweigh the risks in patients of all ages
if they are selected on the basis of being in an at-risk group without
significant contra-indications to treatment.36 Recent evidence indicates
that the risks of isoniazid toxicity, particularly liver toxicity, are
lower than previously assumed, especially if treatment is monitored
appropriately.37–40 Isoniazid alone can be expected to reduce an individual’s
risk of developing active TB by between 65–75%, depending on the length of
therapy.41 With good adherence to therapy (>80% of doses taken), this
benefit may rise to 69–93%.33

Drug regimens used for treatment

The standard six month isoniazid recommendation (either daily or 2–3 times
weekly) for the treatment of LTBI has recently been revised and updated.19
This followed a review42 of older studies demonstrating longer regimens to
be more efficacious33,43,44 and newer studies showing decreased liver toxicity
in patients on isoniazid who were appropriately monitored.38 The American
Thoracic Society (ATS) and US Centers for Disease Control (CDC) and
Prevention have firmly recommended nine months of isoniazid as preferred
therapy for the treatment of LTBI in children under 18 years of age,
persons with HIV infection and persons with chest X-ray changes consistent
with prior TB. Six month regimens of isoniazid are considered an acceptable
alternative for other groups of adults where the risks of active TB and
advantages of longer therapy may be lower, however, nine months is still
preferred. Daily isoniazid can be provided to adults in dosette boxes that
are filled weekly if they are not likely to experience problems with
adherence to therapy. In children <15 years and adults who may have
difficulty with adherence to the daily regimen, isoniazid should only be
given as directly observed therapy 2–3 times weekly.
A number of new regimens for the treatment of LTBI have recently been
recommended for HIV-positive and HIV-negative adults on the basis of
clinical studies in HIV-positive populations.45–47 In general, these regimens
have been shown to be as effective as isoniazid with the advantage of being
significantly shorter. They may be of use where adherence to therapy is
expected to be difficult or where limited time or resources make short-
course therapy more feasible than with longer regimens. An example of such
a regimen is rifampicin plus pyrazinamide given by DOT twice weekly for two
months. The higher costs of the drugs in these regimens may be offset by
decreased administration costs and opportunity costs related to a decrease
in active TB rates. However, there have been recent reports of toxicity
(including deaths) associated with rifampicin plus pyrazinamide therapy.48
This has lead to a revision of the recent ATS and US CDC guidelines with an
emphasis on restricted patient selection and frequent clinical and
laboratory monitoring.49

Monitoring of treatment
Careful monitoring of patients taking treatment for LTBI should consist of
regular monthly clinical reviews and instructions to stop treatment and
report immediately any symptoms that may be due to drug toxicity. This is
especially important for symptoms of possible liver toxicity such as
nausea, loss of appetite, abdominal tenderness and jaundice. Liver function
tests should be done at baseline and every month in patients at increased
risk of liver toxicity, including all patients over 35 years, those with
increased risk of chronic hepatitis (e.g. due to hepatitis B, C or alcohol)
and special subgroups such as HIV-positive and pregnant women. Similarly,
LFTs and full blood examinations need to be done fortnightly in all
patients taking regimens containing rifampicin and pyrazinamide.

Indications for BCG vaccination

Recommendations regarding the use of BCG vaccination vary from country to
country and within different population groups.50,51 Two recent meta-analyses
have concluded that the protective efficacy of BCG vaccination for
preventing serious manifestations of TB, such as meningitis in children, is
high (>80%).52,53 However, the efficacy of BCG vaccination in preventing
pulmonary TB in adolescents and adults remains uncertain despite years of
experience with its use. Furthermore, BCG vaccination in low-risk
populations makes assessment of tuberculin skin tests difficult due to the
high incidence of false-positive reactions. BCG vaccination is therefore
not currently recommended for Australians older than five years.
It is generally accepted that selective use of BCG vaccination is
warranted for vulnerable young children from high-risk populations.54 It is
recommended that Aboriginal babies be vaccinated at birth in the NT.
Children under five years who will be living overseas in countries with
high TB prevalence or in Aboriginal communities for longer than three
months should also be vaccinated with BCG. BCG vaccine may cause local
reactions in children previously infected with TB; therefore should be
preceded by Mantoux testing in children over six months of age or in
infants less than six months of age with a history of exposure to an index
case with active TB. There are other contraindications and side effects
related to the use of BCG vaccination54, therefore it should only be given
by people skilled in its administration.

Communication between health staff and TB control units

TB Control Units are divisions of the Centre for Disease Control, which in
turn is governed by the NT Department of Health and Community Services. The
central TB Control Unit is located in Darwin and there are regional TB
Control Units located in Nhulunbuy, Katherine and Alice Springs. These
units maintain primary responsibility for coordinating aspects of TB
control in Northern Territory including:
• Recording notification of all cases of active TB and results of all
Mantoux tests on a database accessible by remote area health staff.
• Production of evidence-based standard treatment guidelines (last
edition Guidelines for the Control of TB in the Northern Territory,
1997, under revision 2002).
 • Coordination and help with contact tracing.
• Provision of resources such as educational material, standard data
collection, treatment and information forms, tuberculin (PPD) for
Mantoux testing, BCG vaccine and anti-TB medications (free for all
patients who require it).
• School screening and screening of other high-risk groups (such as
migrants and prisoners).
• Providing advice to health staff throughout the NT on all aspects of
control and management of TB at all levels from public health through
to individual patient management.
• Outpatient TB clinics are held at each of the CDC centres. Bookings
can be made on the phone numbers below.
Out-of-hours advice for information about TB can be obtained through the
medical registrar on call at Royal Darwin Hospital and from Darwin CDC on-
call personnel who may be contacted through the Royal Darwin Hospital
switchboard (phone (08) 8922 8888).
Contact details for each of the TB Control Units are as follows:

Darwin region
Centre for Disease Control
PO Box 40596
Casuarina NT 0811
Phone: (08) 8922 8804 switch, (08) 8922 8522 direct
Fax: (08) 8922 8310

Central and Barkly regions

Centre for Disease Control
PO Box 721
Alice Springs NT 0871
Phone: (08) 8951 7548 direct
Fax: (08) 8951 7900

East Arnhem region

Centre for Disease Control
PO Box 421
Nhulunbuy NT 0881
Phone: (08) 8987 0282 switch, (08) 8987 0359 direct
Fax: (08) 8987 0355

Tennant Creek and Barkly region

Centre for Disease Control
PO Box 346
Tennant Creek NT 0861
Phone: (08) 8962 4399, (08) 8962 4259, (08) 8962 4420

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45. Halsey NA, Coberly JS, Desormeaux J, Losikoff P, Atkinson J, Moulton LH et
al. Randomised trial of isoniazid versus rifampicin and pyrazinamide for prevention
of tuberculosis in HIV-1 infection. Lancet 1998; 351(9105):786–92.
46. Mwinga A, Hosp M, Godfrey-Faussett P, Quigley M, Mwaba P, Mugala BN et al.
Twice weekly tuberculosis preventive therapy in HIV infection in Zambia. AIDS 1998;
12(18):2447–57.
47. Gordin F, Chaisson RE, Matts JP, Miller C, de Lourdes GM, Hafner R et al.
Rifampin and pyrazinamide vs isoniazid for prevention of tuberculosis in HIV-
infected persons: an international randomized trial. Terry Beirn Community Programs
for Clinical Research on AIDS, the Adult AIDS Clinical Trials Group, the Pan
American Health Organization, and the Centers for Disease Control and Prevention
Study Group. JAMA 2000; 283(11):1445–50.
48. Centers for Disease Control and Prevention. Fatal and severe hepatitis
associated with rifampin and pyrazinamide for the treatment of latent tuberculosis
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49. Centers for Disease Control and Prevention. Update: Fatal and severe liver
injuries associated with rifampin and pyrazinamide for latent tuberculosis
infection, and revisions in American Thoracic Society / CDC recommendations — United
States, 2001. MMWR Morb Mortal Wkly Rep 2001; 50(34):733–5.
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prevention and control of tuberculosis in the United States. A joint statement by
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 Urinary Tract Infection (UTI)
and Pyelonephritis

Author: Dr Nina Kilfoyle

Topic Reviewers: Editorial committee

Introduction
The topic ‘renal tract infections’, with all its subtopics, is huge. There
is a lot of information published each year related to renal tract
infections and their diagnosis and treatment. Unfortunately, there is a
paucity of good quality trials and research. Much of the literature is in
the form of reviews, and a lot of recommendations are not backed up with
reasonable evidence. Standard practice seems to be historically based.
This document is a reasonable review of the literature and reasonably
represents current evidence and views. It is by no means comprehensive:
this topic itself has many Cochrane review topics in it.
Urinary tract infections affect 10–20% of women at some stage in their
lifetime. The incidence of symptomatic urinary infection in men is quite
low. This difference is explained by the anatomic differences between the
sexes.
I have chosen the following areas for discussion.

Specimen collection
The third edition of the CARPA Standard Treatment Manual recommends
perineal cleansing before collection of first pass urine (FPU) and mid-
stream urine (MSU) specimens. This practice is accepted as the gold
standard in specimen collection by many people and aims to increase the
validity of subsequent testing by minimizing perineal contamination. In
clinical practice this is rarely how specimens are collected (personal
observation).49
A review of the available literature reveals only a few studies in this
area. Baerheim et al.1 studied 864 morning urine samples from 110 female
students. Each morning a different collection technique was used (holding
labia apart, soap, disinfectant and saline). Only holding the labia apart
decreased the contamination rate and the number of colony-forming units at
culture. (Previous studies by the same authors came to similar
conclusions). Morris et al.2 compared specimen collection without
instruction, to collection after perineal cleansing with sterile water. The
results between the two groups were virtually identical. Schlaeger et al.3
studied asymptomatic pregnant adolescents, comparing MSU collection before
and after perineal cleansing. The results were similar for both groups.
Schlaeger cites other studies that have similar conclusions. The results of
a study by Winkens et al.49 concludes that in practice few specimens are
actually MSU, but this has no effect on urinalysis or MCS anyway.
This information suggests not only that perineal cleansing is not
indicated, but perhaps also that instruction on mid-stream is not important
as it is not often adhered to. Further study needs to be done to ascertain
if holding the labia apart yields better results.
Dr Lum, microbiologist with NT Department of Health and Community
Services (pers. comm.), has observed that the normal flora in Indigenous
women seems to vary from the non-Indigenous population. He suggests that
even though perineal cleansing and mid-stream collection is not often
performed, it should still be recommended until studies like the above are
performed on the Indigenous population.
It would be interesting to know if contamination increased the yield of
PCR testing for STI on urine samples.

Processing of urine specimens

Ideally the urine needs to be plated onto the dipslide within 20 minutes of
collection or be placed in the refrigerator until this can be done.52 The
quicker the urine is plated the more accurate the colony counts of
pathogen, and the less the overgrowth of contaminants.
Microscopy is also more accurate if done within one to two hours. Cells
tend to lyse if left in urine for periods longer than this, underestimating
actual urine cell counts.
I did not look into whether delay in plating/cell counting has an impact
on clinical decision making.

Urine dipstick analysis

Leukocytes, nitrites, protein, blood and ketones can be present in UTI. Of
these, leukocytes and nitrites are usually helpful diagnostically. Protein
is positive usually because of increased cell counts. Blood on dipstick can
be related to inflammation or false-positive. Ketones indicate starvation
and an increased catabolic state from being unwell [Editor: Or marked lack
of insulin].

Leukocytes
The reaction reveals the presence of esterases that occur in granulocytes.
False-positives can occur (vitamin C, high levels of
protein/glucose/ketones).7 With respect to UTI, the leukocyte esterase test
has a reported sensitivity of 75–96% and specificity of 94–98%8 for
detecting significant pyuria. Hooten and Stamm8 state that there is some
evidence that this test does not perform this well in daily practice.
Note: Skov64 found that the leukocyte esterase test was positive (>trace) in
50% of screening (STI) urine samples from Central Australian women, and 40%
of Central Australian men. In these groups 75–87% had STI. On discussion of
this issue with Knox6, she states that Tristate sexual health program and
other audit information suggests that Leukocyte positivity in symptomatic
individuals is a very poor discriminator in this population and should be
omitted from treatment algorithms. In a female, the symptom of dysuria
indicates UTI, although in the 15–40 year age group they may also have an
asymptomatic STI. In a male, the symptom of dysuria is more consistent with
STI, with or without leukocytes.

Nitrites
The reaction reveals the presence of nitrite and therefore nitrite-forming
bacteria (E. coli, Klebsiella, Proteus, Staphylococcus and Pseudomonas).
Accuracy improves with prolonged retention of urine in the bladder (four to
eight hours).7 Antibiotics should not have been taken within the preceding
three days.7 False-positives are seen in contaminated specimens, and false-
negatives in very dilute or very concentrated urine specimens, ascorbic
acid, high bacterial count, pH<6, high urobilinogen, and high specific
gravity.10
There are many trials looking at sensitivity and specificity of the
nitrite test for UTI. In the literature I reviewed11,12,13, sensitivity ranged
from 27–39.5% and specificity from 92.9–99%. Bachellor14 cites sensitivity
35–85% and specificity 92–100%. So, if the nitrite is positive, it’s very
likely a UTI is present, but if it is negative, the chances of UTI are
still quite reasonable.

Diagnosis of UTI
Kass and colleagues (1957, cited by Rubin43) did a lot of research into UTI
and MSU and bacterial counts. The presence of >105 cfu/ml of urine is widely
accepted as the traditional standard for defining significant bacteriuria
(sensitivity 99% and specificity 51%). Kass also noted that in a minority
of patients a true bacteriuria was present with <105 cfu/ml.
Stamm (1980, as cited by Rubin43) found that approximately 30% of women
with symptoms of UTI, positive urinalysis and good response to
antimicrobial treatment have true infection with 102–105 cfu/ml. If the
definition of significant bacteriuria was extended to include most of this
group (i.e. ≥103), sensitivity would decrease to 90% but specificity would
increase to 80%.
It is worth noting that S. saprophyticus is usually found in smaller
numbers (102 –104) when it is found to be the cause of UTI (Rubin43 citing
Hovelius 1979).
Bacterial counts can vary with any circumstance that alters the
concentration of bladder urine, and as discussed above, with delay to
plating on culture medium.

UTI versus STI

The differential diagnosis of dysuria is UTI, STI and vaginitis/vulvitis.
UTI and pelvic inflammatory disease (PID) can also both be associated with
lower abdominal pain. In a standard population, history-taking can help
identify vaginal/pelvic symptoms that make STI and vaginitis/vulvitis more
likely, and UTI less likely. In the NT Aboriginal population it is my
personal experience that accurate and detailed history-taking to the degree
that is necessary to help differentiate between these diagnoses is mostly
not possible.
Generally, the best predictor of STI risk is based on age (15–40 years
old, but especially 15–25 years old).6,64 According to Knox6, chlamydia and
gonorrhoea may present with dysuria, but it is still more likely that a
patient with dysuria has a UTI than a symptomatic STI. Hence, the best
predictor of UTI in a female is dysuria, and although in the age groups
above STI should be tested for (concomitant asymptomatic infection),
empiric treatment should be for UTI. In a male, dysuria is predictive of
STI, and should be treated as such.
Examination is limited in distinguishing between these clinical
syndromes. Mild PID causes suprapubic pain, as does cystitis in at least
10% of women. Often, in remote clinics, it is impracticable (workforce
issues, staff gender issues, lack of privacy in clinic examination rooms)
or unacceptable (patient refusal) to perform a full women’s check-up with
every presentation, to try and ascertain if cervicitis/pain on balloting
the uterus is present.

In summary
In the Aboriginal population, dysuria in women indicates UTI, and this is
confirmed by a positive nitrite test. Negative nitrites means that the
diagnosis is still UTI, but there is a small chance it could be STI. Treat
for UTI, but test for STI if in the at-risk age groups. In men, dysuria
indicates STI regardless of urinalysis. A UTI should be expected only if
symptoms do not resolve with adequate treatment of the person and contacts.
Aside from difficulties distinguishing between STI/vaginitis and UTI,
there is the added problem that they often co-exist. UTI is a common
infection in any population, and seems to at least be as common in
Aboriginal people. The STI rates in this population are extremely high. It
is conceivable then that a patient with a symptomatic UTI may also have an
asymptomatic STI.
I could find few studies (and none of significant quality) looking at
UTI versus STI in causing dysuria, let alone studies in a similar patient
population (with respect to disease rates and cultural aspects). Wong4
performed a small study on a population of women with UTI, and compared
their clinical presentation to those with gonorrhoea, chlamydia, and
vaginitis. It was found that UTI was significantly associated with
suprapubic tenderness (as with PID), and that there was considerable
overlap between symptoms and signs in all groups. Accurate differentiation
required pelvic examination, examination of vaginal fluid, and urine
analysis.
Berg5 similarly found no difference between the symptoms and signs of
patients with STI and UTI. In this study it was also found that in those
diagnosed with a UTI who had a full pelvic examination and STI screen, 53%
were found to have STI when microbiological results were available. It was
not clear what proportion had both UTI and STI.
Knox6 (unpublished audit from Central Australia) looked at investigation
and microbiological results for women presenting with abdominal pain and/or
dysuria. She suggests that lower abdominal pain without dysuria is more
indicative of an STI. Conclusions regarding dysuria are found above. The
audit involved small numbers and was by no means comprehensive, but the
most striking result was inadequate work-up of more than 50% of women
presenting with genitourinary symptoms.
As noted above, Skov64 found high rates of leukocyte positivity on
screening urinalysis in asymptomatic individuals, with subsequent high STI
rates in this group. However, as far as I am aware, there is no data
relating to the predictive value of leukocytes with negative nitrites on
urinalysis for STI vs UTI in symptomatic individuals (i.e. dysuria).

Sending MSU samples

It is worth considering whether to recommend sending an MSU in young women
with a single uncomplicated UTI where the clinical diagnosis is certain
(nitrite positive on UA). The general rule is that a test should be ordered
if it changes management.
Komaroff52 cites a cost-effectiveness analysis showing that the small
benefit of sending an MSU in this situation (that is, reduces duration of
symptoms by 10%), does not warrant the increased cost (40%) of laboratory
confirmation. A large proportion of practitioners using this manual will be
working remotely, and results of MSU are unlikely to have any impact on
duration of symptoms as results arrive well after the fact. Even patients
who fail to respond to first-line therapy are likely to re-present before
results are available, and treatment with a second-line agent is likely to
have been started empirically. Also, I suspect that the cost of remote
collection of MSU gives less reliable results and incurs a greater cost
than seen in the above study.
On the other hand, results of MSU are important in surveillance of
organism prevalence and antibiotic sensitivity. Also, in a population where
there is a high prevalence of STI, MSU processing is important for
gonorrhoea isolates and sensitivities, to confirm dysuria is indeed from
UTI rather than STI or other causes of dysuria, and also the specimen can
be used for PCR testing to diagnose STI (either symptomatic or
asymptomatic). It also helps in clinical audits such as the one performed
by Knox6 where, if investigation were complete for each patient, conclusions
could be drawn on predictive value of symptoms, signs and UA. Sending an
MSU on all patients presenting with dysuria would also mean a more
straightforward protocol for the manual. It is also my own personal
observation that MSU in symptomatic individuals are often not requested,
which becomes difficult when working out who really gets recurrent UTI and
should receive further attention. Perhaps the greater cost of sending an
MSU on each person with symptoms could be balanced out by more clearly
stating that only a pregnant asymtomtomatic woman should have and MSU for
MCS and be treated if there is indeed evidence of infection.
For the current protocol I have recommended that an uncomplicated UTI
(see below) does not need an MSU, but all others do. [Editor: This position
is supported by the editorial committee for the above reasons.] This could
be changed in future if there was evidence that this resulted in
compromised patient care.

Complicated versus uncomplicated UTI

Patients with UTI can be divided into two broad groups. There are those who
are more likely to respond poorly to standard treatment regimens and have a
higher incidence of severe complications (the complicated UTI), and those
that are more likely to respond quickly to treatment with a very low risk
of complications (the uncomplicated UTI).
There are several host factors that have been identified as markers of
complicated UTI:8
• Anatomic abnormalities of the renal tract: obstruction, urolithiasis,
polycystic kidney disease etc.
• Neurological disorders affecting bladder function
• Pregnancy
• Male gender
• Instrumentation: stents, indwelling urinary catheters
• Unusual or multi-resistant organisms (including hospital acquired
infections)
• Chronic renal failure
• Immunosuppressive therapy or disease
• Childhood
There is some debate regarding the following groups:
 • Diabetics
• Elderly women
• Postmenopausal women
• Duration of symptoms

Diabetics
Some of the literature I viewed included diabetes as a host factor
associated with complicated UTI. Patterson15 reviewed the literature and
found that bacteriuria and UTI are more common (up to threefold) in
diabetic women. Pyelonephritis was also more common (up to fivefold). Hence
their recommendation that people with diabetes should be included in the
definition of uncomplicated UTI.
Ronald16 agrees that there is an increased incidence of all renal tract
infections in diabetic patients. However, he concludes that, because of the
poor quality of data and the lack of trials with alternate treatment
durations, most diabetics should be classified as uncomplicated UTI. He
follows this recommendation with a call for more research.
Nicolle et al.17 looked at hospitalisation rates for pyelonephritis in
Manitoba over a three year period and found that rates among Native
American women with treaty status was five to 20 times greater that those
among other women, and that this difference was partially attributable to a
greater frequency of pregnancy and diabetes. This study was flawed but
indicates that further study needs to be done in this subpopulation.
Subsequent study may be easily extrapolated to our patient population.
Data regarding hospitalisation rates for Aboriginal women in the
Northern Territory was not looked at for the purpose of this document.
Analysis of hospital separation data is problematic as there are multiple
variables in addition to diabetes that could influence outcomes (delay to
presentation, access to health care, diabetes, diabetic control, antibiotic
compliance, renal disease and other co-morbidities).
The third edition of CARPA and the eleventh edition of Australian
Therapeutic Guidelines: Antibiotic33 don’t distinguish between complicated
and uncomplicated, let alone diabetic versus non-diabetic patients.
Due to the lack of good evidence, it is my recommendation that diabetics
with UTI are uncomplicated unless they qualify for complicated status on
other grounds. This will result in an easier protocol to follow and better
compliance.

Elderly women
Being elderly is often quoted as an independent risk for complicated UTI.8
‘Elderly’ is not defined in most articles, but Beier18 implies elderly is
over 65 years of age. He cites a review article by Nicolle (1992) that
concludes elderly women have lower rates of eradication of UTI with any
duration of therapy, and tend to fare poorly after short-course therapy.
The Cochrane review19 on this topic defines elderly as over 60 years of
age, and states ‘Many Authors do not recommend single dose treatments in
elderly women because these seem to be less effective . . . This attitude
is based on either previous review articles or on results from three trials
which did not specifically assess the efficacy in women over 60 years with
symptomatic uncomplicated UTI’.
Institutionalised women and those with debilitating disease tend to have
increased rates of UTI (Nicolle 1992, cited by Hatton et al.23). Beier
points out that there are many factors that lead to nursing home residents
as being classified as complicated; stroke, prior antibiotic use, bladder
catheterisation, incontinence, residual urine, decreased functional status.
There may be a case for classifying nursing home residents as complicated
in an effort to make CARPA guidelines more straightforward.

Postmenopausal women
Hormonally induced changes in the vaginal flora associated with menopause
may play a role in UTI in older women (increased pH and decreased
Lactobacilli).20 This has been linked to recurrent UTI. Postmenopausal women
may have a cystocoele or ureterocoele, which by definition constitutes a
structural abnormality of the renal tract and hence indicates complicated
UTI.
There is no evidence that menopausal status alone should influence
duration of antibiotic treatment. However, Naber32 cites a recommendation by
Raz that, in postmenopausal women with recurrent UTI (>3 episodes per
year), the acute episode should be treated with a conventional treatment
course.

Recent UTI or recent antibiotic treatment

‘Recent’ is not qualified in any of the literature.8,21,22 Relapse UTI is
defined as recurrence of symptoms within two weeks of finishing
antibiotics. Hence ‘recent antibiotic use’ could also be defined as two
weeks, as I assume the implications are the same (resistant infection and
treatment failure). Fihn et al.55 noted a UTI in the preceeding six weeks
was more often associated with treatment failure, possibly indicating a
period as long as six weeks where more resistant infection is selected for.

Duration of symptoms
The longer the duration of symptoms, the greater the possibility of occult
upper tract infection/invasive tissue infection (this is not a variable
that has been studied well on its own). Hooten and Stamm8 suggest symptoms
longer than seven days identifies patients at higher risk of
complication/treatment failure. They use this cut-off in their own
randomised trial of three-day antimicrobial treatment in uncomplicated
cystitis in women.58 Caron and Humbert24 suggest infection longer than four
days indicates complicated UTI (based on Nicolle). Bump30 sits between,
recommending that infection longer than five to seven days be regarded as
complicated infections (five references cited). Komaroff52 recommends
greater than seven to ten days be regarded as complicated UTI.
Rubin et al.54 used antibody-coated bacteria (ACB) as an indicator of
occult upper tract infection when comparing short-course versus
conventional-course antibiotics. Those positive for ACB were excluded from
the study but it was noted that ACB-positive patients had a significantly
longer duration of symptoms, had less access to medical care and more
severe symptoms at presentation. However, I did not look at the validity of
ACB in diagnosing occult upper tract infect

Temperature
With respect to pyelonephritis, Hoang and Pollack48 use a temperature above
38.8?C as an indicator of severe pyelonephritis. There was no other
discussion about this issue in the literature reviewed.
Infecting organisms
A report in the Australian Family Physician25 based on data from 1993
National Antimicrobial Resistance Surveillance Program (28 laboratories
from around Australia) found:

Uncomplicated UTI (% of total)

E. coli 80–90%
S. saprophyticus 5–15%
Other Klebsiella, Enterobacter, Proteus

Complicated UTI (no percentages available)

E. coli, Proteus, Pseudomonas, Klebsiella, Enterobacteria, Serratia.
Enterococci and Staphylococcus are more likely multi-resistent
Pyelonephritis
E. coli

Note 1: Central Australian Children/Adult data 2001 from THS26 found E. coli
85%, S. saprophyticus 5.2%, Klebsiella 1.3%, Enterobacteria 3.9%, Proteus
2.6%.

Note 2: Western Diagnostic Pathology MSU Isolates from an Alice Springs

Aboriginal Medical Service (CAAC) in 200127 found: E. coli 85%, S.
saprophyticus 4.7%, Klebsiella 2.2%, Enterobacteria 2.2%, Proteus 2.2%

Sensitivity to antibiotics of the infecting organisms

The antibiograms presented are from DHCS laboratory data for Central
Australia28, DHCS NT-wide data for 2000, and Western Pathology data for CAAC
2001.27 It is worth noting that it is not routine practice for MSU to be
sent on all patients with potential UTI, and an MSU is more likely to be
sent in the cases of a recurrent or resistant infection. Also, the DHCS
2000 NT-wide data predominantly includes urine samples from hospital in-
patients. Hence these results are an indication only of what is seen in the
primary care setting and should be interpreted cautiously.
It should also be noted that even organisms seen to be resistant on
Kirby-Bauer disk testing in vitro, can still be sensitive to the very high
urinary concentrations of antibiotic in vivo.52

Resistance (per cent)

E. coli Ampi/amoxycillin 53–70%
Trimethoprim 23–41%
Cephalexin 1.0–1.5%
Amoxicillin/clavulanate 1.0–1.5%
Gentamycin 4.0–5.5%
S. saprophyticus Trimethoprim 85%
Klebsiella Ampi/amoxycillin 100%
Proteus Nitrofurantoin 100%
Enterococci Cephalexin 100%

Natural history of UTI

There is evidence of spontaneous resolution of UTI in up to 40% of cases
(20–40 year old age group).23 Naber32 discusses the few placebo-controlled
studies and concludes that 20–50% of patients become asymptomatic within
one week. Hooten and Stamm8 suggest that 50–70% of lower UTI clear
spontaneously, although symptoms may persist for several months. This
conclusion was based on information from two studies (1972, 1984). They
also cite a placebo-controlled study by Asbach (1991) that showed 26% of
women on placebo treatment cleared their bacteriuria at two weeks (nil
information on symptoms, complications, further follow-up).

Which antibiotic to use: Pyelonephritis

In contrast to lower urinary tract infection there has been less study of
treatment options for pyelonephritis.31,45,34,47,8
The ideal antibiotic is bacteriocidal with high penetration and
concentration in both urine and renal tissue.45 The choices therefore are
aminoglycosides, penicillins/clavulanate, monobactams (aztreonam),
carbapenums (imipenum), cephalosporins (third generation, although second
generation is acceptable in areas where resistance is low38),
flouroquinolones, trimethoprim/sulphamethoxazole. Nitrofurantoin does not
satisfy these criteria.
Tolkoff-Rubin and Rubin34 recommend that empiric therapy for
pyelonephritis must cover >95% of possible infecting organisms. Hence,
ampicillin alone is not appropriate. All the other agents listed above
fulfill this criterion. It is worth noting that in acute uncomplicated
community-acquired pyelonephritis, Enterococcus is very uncommon.50
As far as the length of therapy goes, most clinicians continue IV
therapy until afebrile then switch to oral therapy. Up to 12% of patients
are bacteraemic — bacteraemia does not attribute a worse prognosis, and
blood cultures rarely change treatment and are therefore not routinely
recommended.8 There is no evidence to guide optimal IV treatment lengths.
The duration of therapy in total is usually two weeks. Again, there is
little evidence upon which to recommend an appropriate total treatment time
so it stands that, until research is done, two weeks is standard practice.
It has been noted that in severe cases of pyelonephritis, two-week therapy
is associated with up to 50% relapse. Four to six weeks of therapy is
associated with >95% cure rates but with higher side effects.34
Warren et al.47 made recommendations on behalf of the Infectious Diseases
Society of America. Based on available evidence they recommend:

Two weeks’ treatment appears to be adequate for most women (A,I)

1. Mild cases can be managed with oral treatment — Flouroquinolone
(A,II), co-trimoxozole (B,II) or amoxicillin/clavulanate if organism
is gram positive (B,III).

2. Severe cases should be admitted to hospital (A,II) for parenteral

therapy — flouroquinolone, aminoglycoside +/– ampicillin, third
generation cephalosporin +/– aminoglycoside (B,III).

It should be noted that, in Australia, first-line treatment with a

flouroquinolone is unacceptable due to concerns regarding emerging
resistance with widespread use, and cost.
The eleventh edition of the Australian Therapeutic Guidelines:
Antibiotic33 recommends:
1. For mild to moderate infection, oral treatment with cephalexin,
amoxycillin/clavulanate or trimethoprim (duration: two weeks).
 2. For severe infection, parenteral therapy with ampicillin and
gentamycin, or ceftriaxone.

In view of the resistance patterns detailed above, trimethoprim is not a

valid choice. For severe pyelonephritis diagnosed remotely it would be
quite acceptable to give IV or IM either gentamycin or ceftriaxone stat
while awaiting transfer. Ceftriaxone is a little more expensive, and needs
to be mixed with lignocaine for intramuscular administration, but is
acceptable and effective as a first-line option, with the advantage over
other cephalosporins being its longer half-life. Dr Lum, Microbiologist for
DHCS (pers. comm.), notes that a lot of ceftriaxone is used in the NT and
perhaps cephazolin is a better choice. A drawback of cephazolin is the need
for eight-hourly dosing, which may compromise treatment if the patient is
delayed in getting to hospital. Perhaps this is an issue better addressed
in the hospital setting.

UTI in men
A UTI in a male is by definition a complicated infection. Most infections
are associated with urological abnormalities, bladder outlet obstruction or
instrumentation. Anatomical features of the male urinary tract protect from
UTI (that is, a long urethra). There are a small number of 15–50-year-old
men who suffer acute uncomplicated UTI. Factors associated with this
include homosexuality, intercourse with an infected partner, and lack of
circumcision (as cited in Hooten and Stamm8).
Due to the low frequency of UTI in men, good quality treatment trials
are non-existent.8 Hence, most reviews recommend empiric use of antibiotics
as for complicated UTI or pyelonephritis. Nitrofurantoin should not be used
in men as it doesn’t achieve reliable tissue concentration and hence is not
useful in occult proststitis or pyelonephritis.
Recommendations regarding length of therapy vary. Hooten and Stamm8
suggest an initial seven days of treatment. Other authors14,23,33 suggest
between seven and 14 days. All agree that relapse needs investigation for
pyelonephritis/prostatitis/epididymitis and treatment for four to six weeks
(or up to three months in the case of chronic prostatitis14).

Further investigation in a male

All men, after proven UTI, should be investigated for renal tract
abnormalities or occult tissue infection (e.g. rectal examination for
prostatic hypertrophy, culture of prostatic secretions, renal tract imaging
US/IVP).14 Hooten and Stamm8 suggest this is not necessary in those with no
obvious complicating factors with single uncomplicated UTI. Lipsky (cited
by Stamm31) notes that urological evaluation in young men who respond to
therapy is usually unrewarding.
Proteus UTI is associated with infected stones. All cases with a proteus
UTI should receive appropriate treatment and subsequent imaging of the
renal tract for stones.

Further investigation in a female

Most women with recurrent uncomplicated UTI have no anatomic abnormality of
the renal tract and therefore do not need an evaluation of their urinary
tract.8,12 Clinical suspicion of a complicating factor increases the yield of
further investigation.
 Similarly, further investigation of a young female with acute
uncomplicated pyelonephritis is not cost-effective and has a low diagnostic
yield (Johnson 1992, as cited by8). It is rare to find urological
abnormalities in those who respond promptly to antimicrobial therapy
(personal observation8). Some practitioners recommend a follow up MSU two
weeks after antibiotic cessation50, but this doesn’t seem to be based on any
evidence. It would also be reasonable to image the urinary tract if
pyelonephritis became a recurrent problem.
Proteus UTI is associated with infection stones. All cases with a
proteus UTI should receive appropriate treatment and subsequent imaging of
the renal tract for stones.

Other therapies
Hydration35
Theoretically, dilution of microbes and frequent micturition should aid in
recovery from UTI. However, antimicrobial concentrations and host bacterial
response may also be diluted. There is limited trial information on this
issue.

Urine acidification35,23
Acidification is antibacterial. Urine acidification is difficult to achieve
and maintain and is therefore rarely attempted. It should be noted that
high-dose ascorbic acid is associated with the formation of urate stones.

Urinary alkalinisation
Urinary alkalinisation is used widely for ‘symptom relief’. There is little
trial evidence to support its use. Brumfitt et al.36 found no correlation
between pH and the incidence of symptoms of UTI, number of symptoms,
symptomatic vs asymptomatic bacteriuria, and significant vs insignificant
bacteriuria. This information casts doubt on the place of urinary
alkalinisation in the treatment of UTI.

Asymptomatic bacteriuria
Asymptomatic bacteriuria is the presence of >105 CFU of a bacterial species
on mid-stream urine, without symptoms or pyuria. The incidence of
asymptomatic bacteriuria varies with age and sex. The incidence in
schoolgirls is 1–2%, sexually active females 2–4%, over 60-year-old women
6–8%, over 80-year-old women >20%, institutionalised women 30–50%. For
males, childhood to middle age <1%, over 60 year old men 1–3%, over 80-
year-old men >10%, institionalised men 20–40%.21
Approaches to asymptomatic bacteriuria are varied. The concern with
asymptomatic bacteriuria is progression pyelonephritis. The concerns with
treatment are lack of evidence of benefits with respect to morbidity and
mortality, the transient results, and emergence of resistance. The only
population where treatment has decreased the incidence of complications is
in pregnant women27 — there is widespread agreement that in pregnancy
asymptomatic bacteriuria should be screened for and treated if found.
Another population where there seems to be widespread agreement on
management is to not treat the institutionalised elderly.19 Treatment of
this group is associated with no change in mortality and treatment
failures, and recurrences are common.35,38
 Opinions otherwise vary. Bachellor14 recommends treatment in those with
structural abnormalities of the renal tract, renal impairment, mechanical
heart valves or joint prostheses, immunosuppressed patients and prior to
instrumentation of the urinary tract. Korman and Grayson25 suggest that
pregnant women and men <50 years old should definitely be treated, but not
the elderly. Auchenthaler21 recommends not looking for it, and not treating
it (the exception being pregnancy). Lutters and Vogt19 state in the
introduction to a Cochrane review on treatment of UTI in elderly women that
‘. . . there is consensus in the medical literature that elderly patients
without symptoms should not be treated’. Nicolle37 feels that there is not
sufficient evidence to make recommendations either way regarding screening
for, or treatment of, asymptomatic bacteriuria.

Recurrent UTI
Recurrent UTI is defined as three or more infections per year.
Approximately 20% of young women with their first UTI will have a recurrent
infection.31 Only rarely do patients have an underlying renal tract
abnormality (see above). The ongoing use of diaphragm with spermicide is
associated with recurrences, possibly because spermicide promotes E.coli
colonisation of the vagina. Other risk factors include39 more than four
episodes of sexual intercourse per month, a new sexual partner within the
preceding 12 months, maternal history of recurrent UTI, first UTI at <15
years old, and shorter distance between urethra and anus. Of note, voiding
patterns (e.g. after intercourse), bacterial vaginosis, STIs, douching,
wiping patterns, tub bathing, types of underwear worn and lifetime sexual
partners were not associated with recurrent UTI.
Raz et al. (as cited by31,39) found that in postmenopausal women anatomical
differences are important. The presence of incontinence, residual urine and
history of UTI before menopause were identified as risk factors. Also, in
postmenopausal women, the lack of oestrogen results in a change in the
vaginal normal flora with loss of lactobacilli and colonisation by E.
coli.20
The management of recurrent UTI can take several forms.35,25,41,39
• Intermittent (self) treatment of the acute infection (antibiotics
according to the patient’s individual status as complicated or
uncomplicated)
• Continuous low-dose antibiotic prophylaxis e.g. trimethoprim 150 mg
daily, cephalexin 250–500 mg daily, nitrofurantoin 50–100 mg daily
• Post-coital prophylaxis (stat dose of antibiotic e.g. trimethoprim 300
mg)
• Hormonal support (vaginal oestrogen)20

It should be noted that antibiotic prophylaxis is safe for periods of up to

over five years. Once prophylaxis has ceased, most women revert back to
experiencing recurrent infections.

A note on cranberries
A Cochrane review exists regarding the place of cranberry products in the
prophylaxis of recurrent UTI.44 The authors conclude ‘. . . the small number
of poor quality trials gives no reliable evidence of the effectiveness of
cranberry juice and other cranberry products. The large number of
dropouts/withdrawals indicates that cranberry juice may not be acceptable
over long periods of time . . . Cranberry juice cannot be recommended for
the prevention of UTI . . . Further properly designed trials with relevant
outcomes are needed’.

Which antibiotic regimen?

When choosing an antibiotic regimen, the following questions need to be
addressed:
Which antibiotic?
This is mostly covered above because it is primarily decided by sensitivity
data from Kirby-Bauer disc testing in the laboratory on MSU specimens from
a representative population. As discussed above, in vivo and in vitro
sensitivities vary in lower UTI because the antibiotics used achieve
extremely high urinary concentrations. The general rule is that once
resistance to an antibiotic by an organism is greater than 20%, treatment
failure rates become too high for further use to be acceptable. Hence it
seems that trimethoprim’s days are over! Bump30 reviewed single-dose
treatment trials and found that many trials excluded patients with
resistant organisms. Of the studies that didn’t, some showed lower cure
rates and others no significant difference (it should be noted, however,
that there seems to be general agreement that most studies of single-dose
therapy lacked sufficient power to draw accurate conclusions61). Hence, in
the absence of specific trials that test the effectiveness of an antibiotic
regardless of laboratory sensitivity, or until a new method of testing
urinary pathogens for antibiotic sensitivity that takes into account this
discrepancy is developed, these rules should be adhered to.
Antibiotic cost and the possibility of emerging resistance is also
considered when choosing an antibiotic. This is especially the case where
the flouroquinolones are involved.

What dose?
The main issue here is whether a lower overall dose and/or decreased
frequency of daily dosing can be used to minimize side effects and improve
treatment compliance. These changes can be made because of the fact that
the antibiotics used achieve extremely high urinary concentrations. An
example is twice-daily dosing of cephalexin60, nitrofurantoin 50 mg three
times per day.57

What duration?
Single dose, short course (three days), conventional (five to seven days)
or long (two weeks)? The duration has to be sufficient to have high cure
rates and low relapse rates but also not so long that compliance and side
effects are an issue. For high cure rates and low relapse rates, the
duration must be sufficient to cover occult upper tract infection and
vaginal/rectal colonisation by the pathogenic organism.22 Up to 30% of
patients with a clinical lower UTI are thought to have subclinical upper
tract involvement.31,34,54 Laboratory techniques for the non-invasive
evaluation of anatomic site of infection have not proved sensitive enough
to be useful in clinical practice34, so it remains impossible to identify
this group of patients at the outset. Of the common antibiotics used in
lower UTIs, it is worth noting that nitrofurantoin achieves poor tissue
levels and performs poorly in upper tract/invasive tissue infections (e.g.
prostatitis). However, it has performed well in clinical trials and remains
a valid first-line option.
 Stamm22 discusses antibiotic performance with respect to elimination of
pathogenic organisms from the vaginal/rectal reservoir. Further study needs
to be done but it appears that trimethoprim and the flouroquinolones are
concentrated in vaginal secretions. Some trials have evaluated vaginal and
fecal carriage (as cited by Stamm22) and show that trimethoprim,
trimethoprim/sulphamethoxazole and flouroquinolones effectively eradicate
pathogenic organisms from these areas after three to 10 days’ treatment.
Beta-lactams and nitrofurantoin do not. Also, the former group of
antibiotics has little impact on normal flora (anaerobes and lactobacilli),
whereas the latter group can eradicate normal flora. Further study needs to
be done to look at the significance of these points.
Compliance remains an issue and it is observed that particularly in the
setting of UTI, patients often discontinue medication after symptoms
subside (average three to four days). Compliance is approximately 75% for
seven day treatment59 (author states similar results in other studies).

A note on single-dose therapy

The advantages of single-dose therapy are cost, compliance and lower side
effect profile. Single-dose therapy was widely evaluated in the 1970s and
80s with promising results. Amoxycillin and amoxicillin/clavulanate overall
fared poorly, but trimethoprim, trimethoprim/ sulfamethoxazole and the
flouroquinolones showed very promising results. Note that in the 1970s and
80s resistance to trimethoprim was extremely low.60 Subsequently, reviewers
have concluded that a majority of studies were of insufficient power due to
small numbers and, to a certain degree, poor methodology.61,22,53 When the few
reasonable trials are compared with trials of longer duration, it seems
that single-dose therapy is generally less effective than the same
antibiotic used for longer duration.60,61 This difference was less pronounced
for trimethoprim. When patients have proven lower tract disease (patients
selected with invasive or non-invasive localisation techniques), cure rates
are >90–95%.63 However, in clinical practice localisation isn’t practical
(see above). When relapse rates are significant, cost increases, because of
the management of the relapse. Some authors have proposed single-dose
therapy as a diagnostic tool for occult upper tract infection54,22, thereby
identifying those that need treatment for mild pyelonephritis. This
approach has not been integrated into clinical practice!
Past trials of single-dose therapy have focused mainly on trimethoprim,
beta-lactams, nitrofurantoin and some study of flouroquinolones. There may
still be a place for single-dose therapy in the future when
flouroquinolones are indicated as first-line agents (e.g. increasing
resistance levels to other agents), or with other poorly studied agents
such as gentamycin or fosfomycin trometerol.

A note on short-course therapy (three days)

Again, short-course therapy has advantages of lower cost, better compliance
and lower side effects compared to conventional course, with better results
than single-dose therapy. Trimethoprim performs particularly well with
three-day treatment having equivalent cure rates to seven-day treatment
(1989)59, and it being superior (six-week cure rate 82%) to three-day
treatments with amoxycillin, first generation cephalosporin, and
nitrofurantoin (six-week cure rates 61–68%, 1991).58 However, as noted
above, sensitivities have changed since 1989–91 and trimethoprim may not
perform so well overall today.
Notes on individual antibiotics
Amoxycillin. Small trials in the 1970s showed great promise for single dose
amoxycillin, but larger trials in the 1980s were less convincing with cure
rates 60–80%. Longer durations of treatment improved cure rates but the
rates remained inferior to trimethoprim.8 Resistance since that time has
been steadily climbing. Stamm22 concludes that the lesser therapeutic
effectiveness of amoxycillin is only partly explained by resistance, and
proposes that the short urinary half-life (18 hours) may also be a factor.
There is also the effect of this antibiotic on normal flora and the
vaginal/rectal reservoir as discussed above. The precise role of each of
these factors in the poor performance of amoxycillin is unknown.
Amoxycillin is no longer recommended for first-line use in UTI due to
its failure rate and increasing resistance, and is not recommended in this
protocol.

Amoxicillin/clavualnate. I ended up with little data on

amoxicillin/clavulanate. Johnson and Stamm50 reviewed two studies (details
unknown) that had favorable cure outcomes but high frequency of side
effects. Also, there was evidence for selection of resistant organisms in
subsequent episodes of UTI. They conclude that the side effects and cost
preclude it as a first-line agent. The paucity of trials indicates that
further investigation into the exact place of amoxicillin/clavulanate in
UTIs needs to be further evaluated, especially in the face of increasing
resistance to trimethoprim. The Australian Therapeutic Guidelines:
Antibiotic (TGA) recommends amoxicillin/clavulanate as first-line treatment
as a five-day course.33 In view of cost, side effects, availability of other
agents and the remaining uncertainty about efficacy, I have recommend
amoxicillin/clavulanate only for complicated UTI in the full-length course.

Cephalosporins. Cephalosporins have similar urinary half-lives, urinary

concentrations and modes of action to amoxycillin. In the past they have
not performed nearly so well as trimethoprim in treatment of any duration.
Also, the longer the treatment course, the better the cure rates.60 The
current CARPA manual recommends three-day treatment with twice-daily
cephalexin. The current TGA recommend five-day treatment with twice-daily
cephalexin33, but fails to distinguish between complicated and uncomplicated
infection. Cephalexin is pregnancy category A. Trials have been performed
using multiple different dosing regimens, and twice-daily dosing for three
days achieves reasonable cure rates. Hence, for uncomplicated UTI, I have
not changed the recommendation of cephalexin from the previous CARPA
manual.

Trimethoprim. Unfortunately trimethoprim is no longer a first-line agent

because of decreasing sensitivity.

Nitrofurantoin. Nitrofurantoin does not achieve adequate urinary levels

when the creatinine clearance is <40 ml/min, and serum concentrations
increase causing problems in toxicity.23 Hence, it should not be used in
renal impairment/failure. It also achieves poor tissue levels and should
not be used in upper tract infections and invasive disease (see above).
Warren et al.47 predict that nitrofurantoin will become an important agent
with increasing resistance to trimethoprim, and I agree. Bailey57 cites
studies that have shown that lower doses of the macrocrystalline form of
nitrofurantoin are as effective as higher doses, with less side effects
(that is, 50 mg three times daily compared with 100 mg four times daily).
Nitrofurantoin performs reasonably well in short-course, but a five- to
seven-day course is superior.32

Norfloxacin/Flouroquinolones. Personal feedback from microbiologists and

infectious disease physicians, and also TGA recommendations33, supports the
recommendation that these agents not be used as first-line agents in the
treatment of UTI.

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