Guidelines For Medical Emergencies and Care of Critically Ill Patients

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GUIDELINES FOR MEDICAL EMERGENCIES AND CARE OF CRITICALLY ILL

PATIENTS
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TERTIARY SISTERS OF SAINT FRANCIS
HEALTH BOARD
GUIDELINES FOR MEDICAL EMERGENCIES

AND
CARE OF CRITICALLY ILL PATIENTS
First Edition
2018
I
Published by
Saint Elizabeth Catholic General Hospital and Cardiac Centre, Shisong

P.O. Box 8, Kumbo, Bui Division, North West Region, Cameroon
Tel: (237) 242659959
Email: info@shisonghospital.org
Website: www.shisonghospital.org
Copyright © Tertiary Sisters of Saint Francis (TSSF) Health Board 2018
All rights reserved. No part of this publication may be reproduced, stored in a retrieval
system, or transmitted in any form or by any means: electronically, mechanically,
photocopying, recording or otherwise without the prior permission of the Tertiary
Sisters of Saint Francis Health Board.
i
DISCLAIMER
These guidelines is not a replacement of any existing text books and current national
and international protocols, but a summarized reference to assist in quick decision
making and to help avoid inappropriate management of patients in emergency and
critical conditions. All prescriptions should therefore be in conformity with
manufacturer’s recommendations. We recommend consultation with most recent
editions of drug indices and strict respect of protocols.
ii
FORWARD
Emergency medicine is a specialty within the field of medicine that focuses on the care
of patients that require prompt medical attention and those critically ill in order to
avoid long-term disabilities or death. This guidelines is designed to assist doctors and
nurses in managing certain medical emergencies and in caring for critically ill patients.
Emergency medicine often leads to situations where prompt decisions are needed to
preserve life, prevent danger of further injury and death, and promote quick recovery
of patients, and health professionals need a tool like this for a quick reference when in
doubt of any protocol or prescription. We have therefore tried to respond to problems
encountered in day-to-day practice by health professionals especially in many centres
in sub-Saharan Africa (SSA).
These guidelines is designed to meet the needs of our context in SSA taking to
considerations the limited human and material resources in many hospitals and centres
and the common health conditions in SSA. Although the scope of this edition is still
limited to a few medical emergencies and critical illnesses, many users will still find
the document very useful and a great tool to assist them as a quick reference in daily
practice. This guidelines is divided under 3 sections: section one includes evaluation of
acutely, critically ill patients & first interventions; section two, common medical
emergencies and critical illnesses and section three includes protocols for common
infectious diseases.
Despite the effort put in place to compile this edition, it is possible that many errors
might have been overlooked; we therefore invite you to inform the TSSF Health Board
using the address provided above for improvement of subsequent editions. We remain
open to any recommendations and criticisms to ensure that the guidelines continue to
evolve and remain adapted for use throughout most hospitals and health centres under
TSSF.
Dr Eugene Yeika, MD
St Elizabeth Catholic General Hospital Shisong
Member of the Science and Research Committee, Shisong Hospital Complex
Email: eugenembinglo@gmail.com. Tel: +237 679 934 736
March 2018
iii
ACKNOWLEDGEMENT
On behave of the TSSF Health Board, I wish to acknowledge the following persons for
their recommendations and contributions toward the creation and compilation of these
guidelines. In a special way acknowledge Dr Eugene Yeika for compiling the
guidelines, Dr Cabral Tantchou and Dr Siben Litika for editing the final manuscript.
Contributors
Dr Cabral Tantchou Tchoumi Cardiologist, SECGHS and President of Science

and Research Committee, Shisong Hospital
Complex
Dr Siben Litika Ophthalmologist, Saint Elizabeth Catholic

General Hospital Shisong
Dr Eugene Yeika MD, SECGHS and Member of the Science and

Research Committee of Shisong Hospital
Complex
Dr Bettina Schlemmer MD, Germany
Mr Jonathan Fondzenyuy General Supervisor, Saint Elizabeth Catholic

General Hospital Shisong
Rev Sister Mary Adrine Kinyuy

Director Saint Elizabeth Catholic General Hospital and Cardiac Centre, Shisong
iv
TABLE OF CONTENTS
DISCLAIMER................................................................................................................................ii
FORWARD .................................................................................................................................. iii
ACKNOWLEDGEMENT ............................................................................................................. iv
TABLE OF CONTENTS ............................................................................................................... v
ACRONYMS AND ABBREVIATIONS ................................................................................... viii
LIST OF TABLES ......................................................................................................................... x
FORMULARIES ........................................................................................................................... xi
ALERT/ CALL FOR HELP .........................................................................................................xii
SECTION ONE
EVALUATION OF ACUTELY, CRITICALLY ILL PATIENTS & FIRST
INTERVENTIONS
1.1. RECOGNITION OF CRITICAL ILLNESS: TRIAGE ...................................................... 1
1.2. MODIFIED EARLY WARNING SIGNS SCORE ............................................................ 1
1.3. ASSESSMENT AND INITIAL RESUSCITATION OF AN ACUTELY, CRITICALLY

ILL PATIENTS (ABCDE OF RESUSCITATION) .................................................................. 2
1.4. GLASGOW COMA SCORE ............................................................................................. 3
1.5. CARDIO-PULMONARY RESUSCITATION (CPR) ....................................................... 5
1.6. CONFIRMATION OF DEATH ......................................................................................... 6
SECTION TWO
COMMON MEDICAL EMERGENCIES AND CRITICAL ILLNESSES
2.2. ACUTE FEVER ................................................................................................................. 7
2.2. SEIZURES AND STATUS EPILEPTICUS ....................................................................... 8
2.3. ACUTE PAIN .................................................................................................................. 10
2.3.1. THE MORPHINE DOSES FOR ADULTS WITH SEVERE PAIN .............................. 11
2.3.2. NEUROPATHIC PAIN ................................................................................................. 12
2.3.3. ACUTE ABDOMENAL PAIN ..................................................................................... 13
2.4. SHOCK ............................................................................................................................ 14
2.4.1. VOLUME DEPLETION AND HYPOVOLEMIC SHOCK .......................................... 15
2.4.2. SEPSIS AND SEPTIC SHOCK .................................................................................... 16
2.4.3. ACUTE ANAPHYLAXIS AND ANAPHYLACTIC SHOCK ..................................... 19

v
2.4.4. ACUTE HEART FAILURE, EXACERBATION OF CHRONIC HEART FAILURE
AND CARDIOGENIC SHOCK ............................................................................................. 23
2.5. ACUTE GASTIRTIS AND ACUTE PEPTIC ULCER BLEEDING ............................... 26
2.5.1. HELICOBACTER PYLORI INFECTION ERADICATION REGIMENS ................... 26
2.5.2. ACUTE PEPTIC ULCER BLEEDING ......................................................................... 28
2.5.3. LEWIS MEAL COMPOSITION................................................................................... 29
2.6. HYPERGLYCAEMIC EMERGENCIES ......................................................................... 30
2.6.1. HYPEROSMOLAR HYPERGLYCEMIC STATE AND HYPEROSMOLAR

HYPERGLYCAEMIC NON-KETOTIC COMA .................................................................... 30
2.6.1. DIABETIC KETOACIDOSIS ....................................................................................... 33
2.6.3. HYPOGLYCAEMIA .................................................................................................... 36
2.6.4. INSULIN FORMULARIES AND DOSAGES .............................................................. 37
2.7. HYPERTENSIVE CRISIS ............................................................................................... 38
2.7.1. HYPERTENSIVE URGENCY ..................................................................................... 38
2.7.2. HYPERTENSIVE EMERGENCY OR MALIGNANT HYPERTENSION .................. 38
2.7.2.1. NICARDIPINE (LOXEN®) PROTOCOLS ............................................................... 39
2.8. ASTHMATIC CRISIS ..................................................................................................... 40
2.8.1. ACUTE EXACERBATION OF ASTHMA OR ASTHMA FLARE-UP OR ACUTE

ASTHMA ATTACK ............................................................................................................... 40
2.8.2. SEVERE ASTHMA OR STATUS ASTHMATICUS ................................................... 41
2.9. ACUTE EXACERBATION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE

AND END STAGE COPD...................................................................................................... 44
2.9.1. COPD FLARE-UP/ ACUTE EXACERBATION OF COPD ........................................ 44
2.9.2. END-STAGE COPD ..................................................................................................... 45
2.10. ACUTE GOUT / GOUT FLARE ................................................................................... 48
2.11. SEVERE ANAEMIA AND BLOOD TRANSFUSION ................................................. 50
2.11.1. BLOOD TRANSFUSION ........................................................................................... 51
2.12. ACUTELY RAISED INTRACRANIAL PRESSURE ................................................... 54
2.13. ACUTE AND CHRONIC KIDNEY DISEASES ........................................................... 56
vi
2.13.1. ACUTE KIDNEY DISEASE ...................................................................................... 56
2.13.2. CHRONIC KIDNEY DISEASE .................................................................................. 57
2.13.3. HYPERKALAEMIA AND CORRECTION ............................................................... 59
2.14. BURNS: ASSESSMENT AND TREATMENT ............................................................. 60
2.15. SNAKE BITE AND ENVENOMATION ...................................................................... 64
2.15.1. SNAKE ENVENOMATION ....................................................................................... 66
2.15.2. ANTI-VENOM THERAPY ........................................................................................ 66
2.16. ASSAULT/ BATTERY AND RAPE ............................................................................. 67
2.17. HYSTERIA/ CONVERSION DISORDER .................................................................... 69
2.18. SICKLE CELL CRISES ................................................................................................. 71
2.18.1. VASO-OCCLUSIVE CRISIS OR PAIN CRISIS........................................................ 72
2.19. ACUTE UPPER AIRWAY OBSTRUCTION ................................................................ 74
2.20. ACUTE POISONING .................................................................................................... 75
2.21 PALLIATIVE CARE ...................................................................................................... 78
SECTION THREE
PROTOCOLS FOR COMMON INFECTIOUS DISEASES
3.1. MALARIA FEVER .......................................................................................................... 79
3.2. MENINGITIS .................................................................................................................. 83
3.3. TYPHOID FEVER ........................................................................................................... 85
3.3.1. CHRONIC TYPHOID CARRIER ................................................................................. 86
3.4. VIRAL HEPATITIS ......................................................................................................... 88
3.5. HIV RELATED OPPORTUNISTIC INFECTIONS ........................................................ 90
3.5.1. CNS CRYPTOCOCCOSIS IN HIV .............................................................................. 92
3.5.2. CNS TOXOPLASMOSIS ............................................................................................. 93
3.5.3. DIARRHOEA IN HIV PATIENTS ............................................................................... 94
3.5.4. PNEUMOCYSTIS JIROVECII PNEUMONIA (PJP) ................................................... 97
REFERENCES ............................................................................................................................. 98
vii
ACRONYMS AND ABBREVIATIONS
AC - Ante cibum (before food)
AVPU - Alert, Verbal stimuli response, Painful stimuli response,

Unresponsiveness
ACT - Artemisimin-based combination therapy
AKI - Acute kidney injury
BID - Bi die (12 hourly)
BMI - Body mass index
COPD - Chronic obstructive pulmonary disease
CKD - Chronic kidney disease
CPR - Cardiopulmonary resuscitation
CPP - Cerebral perfusion pressure
CrCl - Creatinine clearance
CSF - Cerebrospinal fluid
DKA - Diabetic ketoacidosis
ED - Emergency department
ESRD - End stage renal disease
ESR - Erythrocyte sedimentation rate
FEV1 - Force expiratory volume at one minute
GCS - Glasgow coma score
GFR - Glomerular filtration rate
HAART - Highly active antiretroviral therapy
HHS - Hyperosmolar hyperglycaemic state
HONK - Hyperosmolar non-ketotic coma
ICU - Intensive care unit
ICP - Intracranial Pressure
IV - Intravenous
viii
IM - Intramuscular
INR - International normalised ratio
KVO - Keep the vein open
MAP - Mean arterial pressure
NRS - Numerical Rating Scale
NPH - Neutral Protamine Hageman
MEWS - Modified early warning signs score
OD - Omni die (daily)
OM - Omni mane (in the morning)
ON - Omni nocte (at night)
PC - Post cibum (after food)
PRN - Pro re nata (when need arises)
PPI - Protein pump inhibitor
PUD - Peptic ulcer disease
PJP - Pneumocystis jirovecii pneumonia
QID - Quarter die sumendus (6 hourly)
RDV - Rendezvous
RRT - Renal replacement therapy
Stat - Statim (as initial dose)
SSI - Sliding scale insulin therapy
SC - Subcutaneous
SCD - Sickle cell disease
Scr - Serum creatinine
TBSA - Total body surface area
TID - Ter die sumendus (8 hourly)
ix
LIST OF TABLES
Table 1: Triage Scale
Table 2: MEWS SCORE
Table 3: Glasgow coma score
Table 4: Stages of hypovolemic shock
Table 5: Clinical criteria for diagnosing anaphylaxis
Table 6: Epinephrine IM Doses
Table 7: NYHA functional classification
Table 8: SC Sliding-Scale Insulin Therapy (SSI) doses
Table 9: Stages of COPD
Table 10: Stages of Chronic Kidney Disease
Table 11: American Burn Association Severity Classification
Table 12: Classification of burns by depth
Table 13: Assessment of severity of envenomation
Table 14: Some Common Poisons and their Antidotes
Table 15: CSF findings in different forms of meningitis
Table 16: Drugs used for the treatments for hepatitis B and C in Cameroon
Table 17: WHO clinical staging of HIV disease in adults, adolescents
Table 18: Ivermectin doses
Table 19: Criteria for HIV treatment failure
x
FORMULARIES
1. Body Mass Index (BMI)
BMI = Weight (kg)/ [Height (m)] 2
2. Total Body Surface Area (TBSA)
TBSA =
3. Mean Arterial Pressure (MAP)
MAP= 1/3(SBP-DBP) + DBP
Where SBP is systolic blood pressure, DBP is the diastolic blood pressure
4. Cerebral Perfusion Pressure (CPP)
CPP = MAP – ICP
Where MAP is the mean arterial pressure, ICP the intracranial pressure.
5. Transfusion volume in adults
Volume = 6 x [Hr – Hp] x Weight (kg)
Where Hr is the required haemoglobin and Hp is the patient’s haemoglobin.
6. Cockcroft-Gault Equation: Use to estimate creatinine clearance (CrCl).
CrCl = [(140 – Age in years) x Weight (kg)] / (Scr x 72) x K
Where Scr is serum creatinine in mg/dl, K is 1 for male patients and 0.85 for
female patients.
7. Parkland Formula: Is used to estimate the amount of replacement fluid

required in the first 24 hours in a burnt patient to ensure hemodynamically
stability.
Volume (ml) = 4 x [Weight (kg)] [Percentage burnt BSA]
8. Percentage Weight Loss (Wp)
Wp = (Initial weight – current weight)/ current weight
xi
ALERT/ CALL FOR HELP
Alert during call: “out of hour period”
Patient requiring urgent

evaluation by a doctor
Call the doctor on call
Not available within 30 minutes
Call back up doctor
Not available within 30 minutes
Call the administrator on call
xii
SECTION ONE
EVALUATION OF ACUTELY, CRITICALLY ILL PATIENTS & FIRST

INTERVENTIONS
1.1. RECOGNITION OF CRITICAL ILLNESS: TRIAGE

Triage is the process of sorting patients into priority groups according to the severity of
their condition and according to the resources available. Triage helps to identifying the
critically ill patients and prioritize medical attention.
5 Steps in triage
Step 1: Registration (name, date of birth, telephone number, residence)
Step 2: Identify main reasons of seeking care (presenting complains, referral)
Step 3: Take vital signs, assess level of consciousness using the AVPU response
Step 4: Determine the modified early warning signs (MEWS) score
Step 5: Orientation - Decide if patient should be treated as an emergency or should

follow the queue.
Table 1: Triage Scale
Level Description Should be seen by provider within
1 Resuscitation 0 minutes
2 Emergency 10 minutes
3 Urgent 30 minutes
4 Semi-Urgent (given priority in queue) 60 minutes
5 Non-urgent (wait their turn in the 120 minutes

queue)
1.2. MODIFIED EARLY WARNING SIGNS SCORE

The MEWS score is a simple score that helps at the emergency department (ED) to
quickly determine the degree of illness and identify critically ill patients. The primary
purpose of this score is to prevent delay in intervention or transfer of critically ill
patients to the intensive care unit (ICU) or reanimation unit. This score is based on the
six cardinal vital parameters (respiratory rate, pulse/heart rate, blood pressure,
temperature, urine output, AVPU response) and one other observation. The scores for
each parameter are recorded at the time that observations are taken.
1
Table 2: MEWS SCORE
Score 3 2 1 0 1 2 3
Respiratory ≤8 9–14 15–20 21–29 > 29

rate (min−1)
Heart rate ≤ 40 41–50 51–100 101–110 111–129 > 129

(min−1)
Systolic BP ≤ 70 71–80 81– 101–199 ≥ 200

(mmHg) 100
Urine output Nil < 0.5

(ml/kg/h)
Temperature ≤ 35 35.1– 36.1–38 38.1–38.5 ≥ 38.6

(°C) 36
Neurological Alert Reacting Reacting Unresponsive

(AVPU) to voice to pain
Interpretation
MEWS >3: Treat as emergency; accompany patient into the observation room /
reanimation unit and call a medical doctor to review urgently.
MEWS ≥5 is statistically linked to increased likelihood of death and patients should be

place in the reanimation unit or ICU until they are stable.
MEWS ≤3: Direct patient to doctor consultation. Tell him/her that he/she will follow
the queue.
1.3. ASSESSMENT AND INITIAL RESUSCITATION OF ACUTELY,

CRITICALLY ILL PATIENTS (ABCDE OF RESUSCITATION)
The ABCDE of resuscitation is used to guide the order of assessing and resuscitating
acutely or critically ill patients.
1. Airway maintenance with cervical spine protection: Maintain patency of

airways. Check for added sound; snoring, gurgling, wheeze, stridor and use of
accessory muscles, see-saw respiratory pattern.
- If the airway is blocked (by blood or vomitus), the fluid must be cleaned out of
the patient's mouth by the help of suctioning instruments.
- In case of obstruction, pass an endotracheal tube.
2. Breathing and ventilation: The aim is to identify and manage six life-threatening
thoracic conditions that result often from trauma: airway obstruction, tension
pneumothorax, massive haemothorax, open pneumothorax, flail chest segment
with pulmonary contusion and cardiac tamponade. Subcutaneous emphysema and
tracheal deviation must be identified if present.
2
- Give concentrated oxygen at 3 – 5 litres/minute.
- Ventilation with a self-inflating bag and mask (AMBU® bag)
3. Circulation with haemorrhage control: Active bleeding (haemorrhage) either

covert or overt should be identified with signs and symptoms of circulatory
collapse. Hypovolemic shock is caused by significant blood loss and can rapidly
result in multi-organ failure (MOF), and death if not address within the first hours
of identification.
- Two large-bore intravenous lines are established and crystalloid solution given.
If the person does not respond to this, cross match and transfuse compatible
whole blood. O-negative can be given to all patients.
- Overt external bleeding is controlled by direct pressure, suturing or cauterisation.
4. Disability/Neurologic assessment: Basic neurological assessment is made with

the help of the mnemonic AVPU (alert, verbal stimuli response, painful stimuli
response, or unresponsive). The Glasgow Coma Scale (GCS) is a quick method to
determine the level of consciousness, and is predictive of patient outcome. An
alteration in the level of consciousness indicates the need for immediate re-
evaluation of the patient's oxygenation, ventilation, and perfusion status.
Hypoglycaemia and drugs, including alcohol, may influence the level of
consciousness. If these are excluded, changes in the level of consciousness should
be considered to be due to brain injury (from meningitis, encephalitis, raised
intracranial pressure) until proven otherwise.
5. Exposure, environmental control and examination: The patient should be

completely undressed, usually by cutting off the garments. It is imperative to cover
the patient with warm blankets to prevent hypothermia. Intravenous fluids should
be warmed and a warm environment maintained. Patient privacy should be
considered. ‘Evidence’ may be gathered from any recent investigations,
prescription or monitoring charts.
1.4. GLASGOW COMA SCORE

The GCS is used to assess the level of consciousness of a patient. It comprises of 3
parameters and values range from 3 – 15. GCS should be assessed and provided in all
acutely critically ill patients presenting at the ED.
Table 3: Glasgow coma score
Eye response (E) – 4 grades
1 No eye opening.
2 Eye opening in response to pain stimulus.
3 Eye opening to speech.
3
4 Eyes opening spontaneously
Verbal response (V) – 5 grades
1 No verbal response
2 Incomprehensible sounds (moaning but no words)
3 Inappropriate words (random or exclamatory articulated speech, but no

conversational exchange. Speaks words but no sentences).
4 Confused (the patient responds to questions coherently but there is some

disorientation and confusion).
5 Oriented (the patient responds coherently and appropriately to questions such as

the patient’s name and age, where they are and why, the year, month and the time
of the day etc.)
Motor response (M) – 6 grades
1 No motor response
2 Extension: Decerebrate posturing accentuated by pain (extensor response:

adduction of arm, internal rotation of shoulder, pronation of forearm and
extension at elbow, flexion of wrist and fingers, leg extension, plantar flexion of
foot)
3 Abnormal flexion: Decorticate posturing accentuated by pain (flexor response:

internal rotation of shoulder, flexion of forearm and wrist with clenched fist, leg
extension, plantar flexion of foot)
4 Withdrawal from pain (absence of abnormal posturing)
5 Localizes pain (purposeful movements towards painful stimuli)
6 Obeys commands (the patient does simple things as asked).
Interpretation
The score is expressed as the sum of the 3 elements in the form E x+Vx+Mx.
GCS of ≤ 8 is definitive of coma. Patients in coma should be intubated and transferred

to the ICU or reanimation unit.
GCS is used to classify head trauma (brain injury):
 Severe, GCS ≤ 8
 Moderate, GCS = 9 – 12
 Minor, GCS ≥ 13
4
NOTE
Tracheal intubation and severe facial/eye swelling or damage make it impossible to test
the verbal and eye responses. In these circumstances, a score of 1 is given with a
modifier attached (e.g. "E1c", where "c" = closed, or "V1t" where t = tube). Often the 1
is left out, so the scale reads Ec or Vt. A composite might be "GCS 5tc". This would
mean, for example, eyes closed because of swelling = 1, intubated = 1, leaving a motor
score of 3 for "abnormal flexion".
1.5. CARDIO-PULMONARY RESUSCITATION (CPR)

CPR is an emergency procedure that combines chest compressions often with artificial
ventilation in an effort to manually preserve brain function until further measures are
taken to restore spontaneous blood circulation and breathing in a person who is in
cardiac arrest. The main objective of CPR is to restore partial flow of oxygenated
blood to the brain and heart hence delaying tissue death and extending a brief window
of opportunity for a successful resuscitation without permanent brain damage.
Indications for CPR
1. Cardiac arrest: Patient is unconscious and the heart sounds are absent
2. Gasping respiration: Breathing only in occasional agonal gasps.
3. Respiratory arrest: Patient still has a pulse but is not breathing. Just ventilations
may be appropriate for resuscitation.
Steps of CPR
Current recommendations place emphasis on early and high-quality chest

compressions over artificial ventilation. The recommended order of interventions is
chest compressions, airway, and breathing. CPR is performed with the person in supine
position by at least 2 trained rescuers.
Ratio of compressions to ventilations: Adults = 30:2, Children = 15:2
1. Chest compressions: Place your hands, one on top of the other, in the middle of
the chest and start with 5 - 6 cm deep chest compressions at a rate of at least 100
per minute. Push hard and fast using your body weight to help you administer
compressions.
2. Artificial ventilation: Done by either exhaling air into the subject's mouth
(mouth-to-mouth resuscitation) or using a device that pushes air into the subject's
lungs (mechanical ventilation with an AMBU® bag). Always lift up the chin
while ventilating.
5
NOTE
Despite the enough well performed CPR will result in few complete recoveries, though
outcome without CPR is almost uniformly fatal.
CPR is continued until the person has a return of spontaneous circulation or is declared
dead.
Children under the age of 5 are more resilient to hypoxic brain injury; therefore, CPR
should be continued in them until normal body temperature is reached.
1.6. CONFIRMATION OF DEATH

Criteria for declaring a patient death
1. Unresponsiveness to verbal stimuli – call the patient by his name aloud.
2. Unresponsiveness to pain – press on fingernail / trapezius squeeze / supraorbital

pressure.
3. Unreactive pupils using pen torch – fixed and dilated pupils indicate brain death.
4. Absence of a central pulse on palpation: Feel for a carotid artery.
5. Absence of heart sounds: Listen for heart sounds for at least 2 minute/ absent.
6. Absence of breath sounds: Listen for respiratory sounds for at least 3 minutes/
absent.
7. Absence of corneal reflexes.
After confirming the patient death
- Document all the clinical findings, the time/date of death, the cause of death (if
available) and sign at the end.
- Inform next of kin.
- Contact the porters to arrange transfer of the body to the morgue/ farewell home.
NOTE
Always check the resuscitation status of the patient before confirmation of death. If
there is uncertainty as to the resuscitation status, CPR should be commenced whilst
this is clarified.
The law does not require the presence of a medical doctor to confirm a patient death.
The doctor's legal duty is to identify the cause of death. There is therefore no legal
obligations on a medical doctor to examine the deceased before signing a death
certificate.
6
SECTION TWO
COMMON MEDICAL EMERGENCIES AND CRITICAL ILLNESSES
2.2. ACUTE FEVER

Fever is usually defined as a core body (rectal) temperature ≥ 38.0°C or 37.5oc when
taken using the axilla.
Acute fever is fever occurring less than 7 days. Acute fever is infectious in most cases,
and of these, most are viral. Acute fever due to septicaemia is a life-threatening
condition and it needs immediate medical attention.
Red flag signs in patients with fever
1. Abnormal vital signs SBP<90 mmHg, HR >120 bpm, RR ≥ 30 min, T > 40° or
< 35 °C
2. Altered mental status
3. Patient unable to walk
4. Purpura fulminans etc
Approach to patients with acute fever
1. Give IV/oral (or rectally for children) antipyretic if temperature ≥ 38.5°C:
- Paracetamol at 15mg/kg/dose q6 – 8 hourly or 1g for adults.
- IV dipyrone or metamizole (NOVALGIN®/ ANALGIN®) in a dose of 10-

15 mg/kg/dose q6 – 8 hourly.
2. Insert IV line and give dextrose 5%/normal saline to keep the vein open (KVO).
3. Investigate and treat the underlying cause. Initial work-up includes full blood
count, malaria parasite, urine analysis and culture, blood sugar in diabetic
patients and chest X-ray if cough or dyspnoea, stool culture if diarrhoea, ESR
and CRP, blood cultures, serum electrolytes / BUN, creatinine and HIV serology.
4. Give antibiotics urgently if meningitis, endocarditis, severe sepsis, purpura

fulminans, peritonitis, necrotizing fasciitis, septic arthritis
NOTE
Peripheral temperature is not clinically accurate and central measurements are the
preferred means of determining temperature. For every 0.55°C increase in temperature,
the heart rate usually increase by 10bpm.
Metamizole is contraindicated to patients with chronic obstructive pulmonary disease

(COPD) and asthma.
7
2.2. SEIZURES AND STATUS EPILEPTICUS
Seizures are hyper-synchronous discharges in the brain that lead to involuntary
movements (stiffness followed by tonic-clonic movements) and sometime urinary
incontinence.
Status epilepticus (SE) is a single seizure lasting more than 5 minutes or two or more
seizures occurring within a 10 minutes without the person regaining consciousness
between the seizures. Status epilepticus is a life-threatening medical emergency. Only
25% of people who experience seizures or status epilepticus have epilepsy.
Aetiology
- Stroke/Haemorrhage
- Hypoglycaemia - Developing a resistance to an

anticonvulsant already being
- Intoxicants or adverse reactions used.
to drugs.
- Gastroenteritis while on an
- Sudden withdrawal of a anticonvulsant, where lower
medication (especially levels of anticonvulsant may
anticonvulsants). exist in the bloodstream due to
vomiting of gastric contents or
- Consumption of alcoholic
reduced absorption due to
beverages while on an
mucosal oedema.
anticonvulsant, or alcohol
withdrawal syndrome. - Developing a new, unrelated
condition in which seizures are
- Fasting while on an
coincidentally also a symptom,
anticonvulsants.
but are not controlled by an
- Starting on a new medication anticonvulsant already used.
that reduces the effectiveness of
- Metabolic disturbances from to
the anticonvulsant or changes
kidney and liver diseases.
drug metabolism, decreasing its
half-life, leading to decreased
blood concentrations.
Approach to patients with seizures/ convulsions
The two priorities are to stop the seizure and determine the cause.
1. Protect patient from trauma (falling), maintain airways and place patient in a
recovery position.
2. Start anti-seizures if generalised seizures last more than 3 minutes.
Diazepam 0.5mg/kg given rectally without exceeding 10mg in children and

10mg given rectally or IV slowly in adults.
8
IN ALL CASES
Repeat dose if convulsions continue after 15 minute.
If convulsions continue after second dose, treat as status epilepticus.
Diazepam is preferably given rectally in children and very elderly patient because
of it effect of suppressing the respiratory system
3. Monitor the vital signs especially for infants and elderly patients.
4. Investigate to look for the cause when the patient is no longer seizing. Urgent
investigations include FBC, blood sugar, serum electrolytes, MP.
5. Keep diazepam and dextrose ready for use in case the patient starts seizing again.
Approach to patients with status epilepticus
1. Maintain the airway and start oxygenation at 5 litres/minute or 2-3 litres/minute

in patients with COPD or asthma.
2. Set an IV line and administer 5ml/kg of dextrose 10% in children and 10ml/kg of
dextrose 50% in adults if blood sugar is ≤ 90mg/dl.
3. Anti-seizures: If the second dose of diazepam has not stopped the seizure,
continue with phenobarbital by IV infusion:
- Children <12years: Give 5-10mg/kg (maximum dose of 1g) in 5mls/kg of

normal saline or 5% dextrose administered over 20 – 30 minute
Or 10mg/kg IV slowly over 15 minutes.
- Adults and children over 12 years: 10mg/kg (maximum dose of 1g) in 100mls
of normal saline or dextrose 5% administered over 20 – 30minutes.
Or 200mg IV slowly
If necessary second dose of phenobarbital should be given 30 minutes after the

first dose. IM route can be an alternative to if IV access is not possible.
Use diazepam as alternative in the absence of IV phenobarbital
Dilute 2 ampoules (20mg) of diazepam in 250mls normal saline or dextrose/saline

and give at a rate of 10 – 20 drops per minute.
NOTE
Monitor for signs of respiratory distress when giving diazepam as it will cause
that.
4. If seizures persist after IV anti-seizures, contact the anaesthetist to provide

general anaesthesia and artificial ventilation.
9
5. If there is fever, administer IV paracetamol at 1g in adults and 15 mg/kg (give
rectally in children).
6. When patient is stable, investigate for the cause.
2.3. ACUTE PAIN

Acute pain is a type of pain that typically lasts less than 3 months, or pain that is
directly related to soft tissue damage such as a sprained ankle or a cut. Acute pain is
relatively more sharp and severe when compared chronic pain. Acute-on-chronic pain
is a pain flare superimposed on underlying chronic pain.
Assessment of pain
Proper assessment of an acute pain helps to make a proper diagnosis and effective
treatment. The mnemonic SOCRATES is used to assess pain.
S = Site of the pain: Is the pain generalized or localized in a particular region
O = Onset of the pain: Gradual or sudden onset…
C = Character of pain: Stabbing or piercing, burning (in gastritis), dull…
R = Radiating/ referral of pain: Where the pain is radiating to (e.g. epigastric pain
radiating to the back, chest region)…
A = Aggravating factors: All the factors that increase the severity of the pain
T = Time: Constant or intermittent pain. If intermittent when does it become worst?

When does the pain come?
E = Elevating factors: All the factors that decrease the severity of the pain.
S = Severity or intensity: Use the Numeric Rating Scale (NRS) to assess the intensity
of pain [NRS involves asking the patient to rate his or her pain from 0 to 10 (11 point
scale) with the understanding that 0 is equal to no pain and 10 is equal to worst pain
imaginable]
Pain Intensity
Pain severity can be broadly categorized as: mild, moderate and severe using the NRS.
This helps to determine the analgesics to use.
- Mild pain (NRS ≤ 3): paracetamol +/- NSAID
- Moderate pain (NRS = 4 - 6): paracetamol +/- NSAID + codeine or tramadol
- Severe acute pain (NRS > 6): paracetamol +/- NSAID + morphine
10
NOTE
Morphine, tramadol or codeine have similar modes of action and should not be given
together. They should be given to patients in respiratory distress.
Approach to patients with severe acute pain
1. Admit patient at the observation ward with acute pain (NRS ≥ 6/10).
2. Insert IV line and give dextrose/normal saline 500 ml KVO.
3. Start analgesia: Tramadol 100 mg IM every 6 hours PLUS paracetamol 1 g q4

hourly.
4. Check any emergencies (ectopic pregnancy, appendicitis, peritonitis, intestinal

obstruction) and address them according.
5. Assess pain severity hourly using the NRS.
6. Monitor vital signs
NOTE
It is not generally advisable to give NSAIDS during management of acute abdominal

pain due to their tendency to trigger acute gastritis or PU bleeding or gastric
perforation.
2.3.1. THE MORPHINE DOSES FOR ADULTS WITH SEVERE PAIN

A. Immediate release
- Tablets for opioid naïve patients: Initial dose = 15 - 30 mg orally every 4

hours as needed.
- Oral solution for opioid naïve: Initial dose = 10 - 20 mg orally every 4 hours
as needed.
- IV for opioid naïve patients: Initial dose = 4 – 10 mg every 4 hours

administered slowly over 5 minutes.
- Suppository: 10 - 20 mg rectally every 4 hours needed.
B. Extended-release oral tabs
- Opioid naïve: Initial dose: 15 – 30 mg orally every 24 hours
- Opioid tolerant patients: Initial dose: 15 – 30 mg orally every 12 hours
Opioid side-effect and management
- Constipation: Regular laxative e.g. Bisacodyl (DULCOLAX®/ CONTALAX®)

5mg q12hrs.
11
- Dry mouth: Frequent sips of iced water, soft white paraffin to lips, chlorhexidine
mouthwashes twice daily, water or saliva sprays.
- Nausea/vomiting: metoclopramide 10 mg 3 times daily or oral domperidone

(MOTLIUM®) 10 mg 3 times daily.
- Sedation: Counselling is very important. Symptoms usually settle in a few days.

Ensure appropriate use of adjuvant analgesics which can have an opioid-sparing
effect.
2.3.2. NEUROPATHIC PAIN

This is pain caused by damage or diseases affecting the somatosensory nervous system
and it resembles electric shocks e.g. post-herpetic neuralgia, trigeminal neuralgia,
diabetic neuropathy, peripheral neuropathy etc.
Characteristics of neuropathic Pain
- Burning, stabbing or pulsing - Pain in response to non-painful

pain stimuli: ‘allodynia’
- Spontaneous pain, without - Increased pain in response to

ongoing tissue damage painful stimuli: ‘hyperalgesia’
- Pain in an area of sensory loss - Unpleasant abnormal

sensations: ‘dysaesthesias’
- Presence of a major
neurological deficit - Poor relief from opioids alone
Treatment of neuropathic pain
a. Anticonvulsants
I. Gabapentin (NEURONTIN®) capsules PO qDay
Day 1 – 5: 300mg
Day 6 – 10: 600mg
Day 11 – 15: 900mg
After day 15, maintenance dose: 1200mg
II. Pregabalin (LYRICA®)
Regular-release capsules
Initial dose: 150mg daily for 1 week OR 50mg 8 hourly
Maintenance dose: 150mg 12 hourly
III. Carbamazepine (TEGRETOL®)
12
Regular-release tablets/capsules
Initial dose: 200mg PO q12hr. Increase qWeek by 200mg/day PO divided q12hr.
b. Tricyclic antidepressant
Amitriptyline (ELAVIL®)
Dose: 50 – 100mg qDay for at least 3 weeks
2.3.3. ACUTE ABDOMENAL PAIN

Acute abdominal pain is the most common acute pain at the ED. Several causes require
urgent and specific diagnosis and subsequent surgical treatment.
Common differential diagnoses of acute abdomen include but are not limited to:
- Acute appendicitis - Ovarian torsion
- Acute peptic ulcer and its - Peritonitis (including hollow

complications viscus perforation)
- Acute cholecystitis - Acute ureteric colic/ Biliary

colic
- Acute pancreatitis
- Bowel obstruction
- Acute intestinal ischemia
- Acute pyelonephritis
- Ectopic pregnancy with tubal
rupture - Sickle cell anaemia
Approach to patients with acute abdomen
1. Identify for the cause of the acute abdomen: through proper history, physical
examination and investigations
2. Insert IV line and set up fluids (Dextrose 5%/normal saline)
3. Start antispasmodics/analgesia:
If pain NRS < 6 - Phloroglucinol (SPASFON®) 40 mg IM every 12 hours or

tiemonium (VISCERALGINE®) IM or hysocine.
If pain NRS ≥ 6 - Tramadol (TRABAR® ) 100 mg IM every 6 hours
4. Insert urinary catheter and monitor urine output. Monitor vital signs 2 - 4 hourly
5. Call the surgeon on call
NOTE
Phloroglucinol, tiemonium and hyoscine are contraindicated in peritonitis, intestinal

obstruction, and acute intestinal ischemia as they can result to paralytic ileus.
13
Guidelines for Medical Emergencies and Care of Critically Ill Patients 2018
2.4. SHOCK
Shock is a critical condition brought on by a sudden drop in blood flow (acute
circulatory collapse), leading to inadequate tissue perfusion (poor tissue oxygen
delivery) throughout the entire body. Unrecognized and untreated shock can lead to
permanent organ damage and death.
Aetiology
a. Hypovolemic shock: Often result from blood loss/ bleeding (incomplete

abortion, ruptured ectopic pregnancy, GIT bleeding, ruptured ovarian cyst,
severe, chronic untreated dysfunctional bleeding, placental abruption, severe
blood loss from trauma) and dehydration (excessive diarrhoea and vomiting).
b. Anaphylactic shock: Results from allergic reaction
c. Septic shock: Results from a systemic infection (sepsis)
d. Cardiogenic shock: Results from pulmonary embolism, or myocardial

infarction/heart failure.
Clinical presentation
- Dizziness, nausea, palpitations, weakness, sweating, agitation and/or confusion.
- Skin: cold clammy extremities, pallor and profuse sweating.
- Cardiac: rapid weak pulse (HR) > 100 bpm or absent peripheral pulses, low
blood pressure (BP) <90/60 mmHg, absent heart beat in some cases, capillary
refill time (CRT >2) seconds.
- Neurological: altered level of consciousness (confused, or somnolence) and

agitation.
- Respiratory: respiratory rate (RR) > 30bpm.
14
2.4.1. VOLUME DEPLETION AND HYPOVOLEMIC SHOCK
Common causes of hypovolemic shock
- Loss of blood (external or internal bleeding)
- Loss of plasma (severe burns and lesions discharging fluid)
- Loss of body sodium and intravascular water e.g. diarrhoea or vomiting
Table 4: Stages of hypovolemic shock
Stage 1 Stage 2 Stage 3 Stage 4
Blood loss Up to 15% 15–30% (750– 30–40% Over 40% (over

(750 mL) 1500 mL) (1500 - 2000 mL)
2000 mL)
Blood Normal Increased Systolic BP < Systolic BP < 70

pressure diastolic BP 100
Heart rate Normal Slight Tachycardia Extreme tachycardia

tachycardia (> (> 120 bpm) (> 140 bpm) with
100 bpm) weak pulse
Respiratory Normal Increased (> 20) Tachypneic Extreme tachypnea

rate (> 30)
Mental status Normal Slight anxiety, Altered, Decreased LOC,

restlessness confused lethargy, coma
Skin Pallor Pale, cool, Increased Extreme diaphoresis;

clammy diaphoresis mottling possible
Capillary Normal Delayed Delayed Absent

refill
Urine output Normal 20–30 mL/h 20 mL/h Negligible
Approach to patients with hypovolemic shock
1. IV resuscitation:
- Insert two large bore cannulae and give 1 litre IV fluid as a bolus (ringers
lactate or normal saline)
- Reassess signs of cardiovascular collapse, if present give a colloid:

Geloplasma 500mls as a bolus.
- Continue with crystalloids at 70ml/kg/24hr for adults and 30 - 50ml/kg/24h

for children.
15
- If you are unable to get IV line access, call the anaesthetist/ anaesthesiologist
for help.
2. Administer oxygen at 5 L/minute unless patient has history of emphysema or

chronic lung disease when the administration rate should be limited to 3-
2L/minute.
3. Insert urinary catheter and monitor urine output.
4. If patient is unresponsive, not breathing and has no pulse, begin CPR.
5. Stop visible bleeding by applying direct pressure or tourniquet to the bleeding

site.
6. Monitor vital signs (oxygen saturation, BP, pulse rate) and LOC.
7. Put the patient in the Trendeleburg position: The patient lie down with feet
higher than the head. Patients in respiratory distress may not tolerate this
position.
8. Keep the patient warm and comfortable. Loosen belt and tightly fitted clothing
and cover the patent with a blanket.
9. Lateral position: Turn the person on his or her side to prevent choking if the
person vomits or bleeds from the mouth. Give nothing by mouth even if the
person complains of thirst.
NOTE
Colloids can cause anaphylaxis. Signs of hypovolemic shock may not become evident
until a 50% loss of blood volume in adults.
2.4.2. SEPSIS AND SEPTIC SHOCK

Sepsis is defined as systemic inflammatory response syndrome (SIRS) secondary to an
infection.
Severe sepsis: This is sepsis with evidence of organ dysfunction and hypotension
(systolic BP < 90 mmHg or > 40 mmHg fall from baseline) that is responsive to fluid
resuscitation.
Septic shock: This is when sepsis is associated with organ failure and hypotension
unresponsive to fluid resuscitation.
Multiple organ dysfunction syndrome (MODS): Sepsis can trigger a cascade of

changes in the body that can cause multiple organ systems failure. Multiple organ
failure (MOF) ensues unless there is prompt treatment of sepsis and appropriate organ
support.
16
Criteria for SIRS
Two or more of these criteria are met with or without evidence of infection is
diagnostic of SIRS.
1. Temperature: T> 38oc or T< 36oc.
2. Respiratory rate > 20 breaths per minutes or an arterial partial pressure of carbon
dioxide (PaCO2) < 4.3 kPa (32 mmHg)
3. Heart rate > 90 beats per minute
4. White blood cell count < 4x109/L (<4000/mm³) or >12x109/L (>12,000/mm³)
Signs and symptoms
- Significantly decreased urine output (Renal failure)
- Abrupt change in mental status (use GCS)
- Decrease in platelet count
- Acute respiratory distress syndrome (ARDS): Difficulty breathing (respiratory

failure)
- Abnormal heart pumping function (heart failure)
- Abdominal pain
Approach to patients in severe sepsis or septic shock
Use the Sepsis Six approach while managing the underlying focus of infection (i.e.
debridement) and multiple organ failure (MOF) (haemodialysis in kidney failure,
mechanical ventilation in lung dysfunction, and transfusion of flesh whole blood).
1. Give 1 litre ringers lactate or normal saline as a bolus and reassess the blood
pressure, if hypotension persist, start vasoconstrictors.
2. Vasoconstrictors
- Give dopamine IV at a constant rate by syringe pump: 10 - 20

micrograms/kg/minute, if not available
- Give IV Epinephrine using a syringe pump at constant rate of

0.1microgram/kg/minute and increase dose progressively until clinical
improvement is seen. (Prepare IV epinephrine by adding 1mg (i.e. 1
ampoule) to 9mls of normal saline to obtain a solution of 0.1mg/ml
(1:1000)).
If the syringe pump is absent
Use the protocol seen below to give epinephrine by IV fluids.

17
3. Oxygenation: Give oxygen at 5 litres/minute or 2-3 litres/minute in COPD and
asthma patients.
4. Administration of antibiotics. Give empiric broad-spectrum IV antibiotics with

anaerobic coverage after collecting blood and other samples for cultures.
Antibiotics most be given within an hour of recognition of sepsis.
Ceftriaxone 2g q12hrs or 80mg/kg/day in 2 divided doses for children +

Gentamycin 80mg q12hrs.
NOTE
Every hour of delay in the administration of antibiotics is an associated with 6%

rise in mortality.
5. Insert urinary catheter and monitor fluid input and output.
6. Septic screen to look for the origin of infection: At least blood should be
obtained and sent for culture before starting antibiotics. Serum lactate level and
FBC urea creatinine haemoglobin should be determined
Epinephrine protocol for septic shock by infusion
Preparation of solution: Dilute 2 ampoules of 1mg epinephrine (i.e. 2000

micrograms) in 200 ml of dextrose 5% or normal saline to obtain a solution containing
10 micrograms/ ml then:
Adults: Give 10 – 20 drops (5 – 10 micrograms)/ minute and increase by 10 drops after

30 minutes if there is not clinical.
Children: Give 5 – 10 drops (2.5 - 5 micrograms) / minute and increase by 5 drops

after 30minutes if there is no clinical improvement.
Should repeat the dose after one hour if no improvement of symptoms.
18
2.4.3. ACUTE ANAPHYLAXIS AND ANAPHYLACTIC SHOCK
Acute allergic reactions are potentially life-threatening though reversible conditions
that arise after exposure to an allergen. Allergens can affect one or more organ systems
causing a mild to severe allergic reactions.
Mild to moderate allergic reactions: Mild allergy present only with cutaneous
symptoms. Moderate reactions will involve the gastrointestinal tract in addition to the
skin.
Severe allergic reaction anaphylaxis: This involves multiple organ systems with
presence of respiratory compromise with shock inclusive. These may initially appear
minor (e.g., coughing, hoarseness, dizziness, mild wheeze, nausea) but any
involvement of the respiratory tract or circulatory systems has the potential to rapidly
become severe. Death can occurs within minutes, therefore, prompt and effective
treatment is mandatory to save the patient’s life.
Aetiology
a) Medications c) Environmental
- Prescribed medication, - Stings (e.g. bee, wasp, ants).

especially antibiotics,
vaccines. - Pollens, grass, moulds, smoke.
- Illicit or illegal drugs. - Iodinated contrast media.
- Herbal remedies. d) Anaphylaxis can also be

exercise induced or idiopathic.
b) Food
- Tree nuts, peanuts, shellfish

and eggs.
Alarming signs and symptoms indicating Acute Anaphylaxis
- Progressive wheezing - Upper airway swelling

(including lips and tongue)
- Dizziness or fainting
(hypotension) - Laryngeal oedema
- Palpitations - Shock (BP< 90/60mmHg)
- Chest pain - Abdominal pain, nausea,

vomiting and diarrhoea.
- Difficulty breathing
Table 5: Clinical criteria for diagnosing anaphylaxis
Anaphylaxis is highly likely when any one of the following 3 criteria is fulfilled
1. Acute onset of an illness (minutes to several hours) with involvement of the skin,
mucosal tissue, or both (e.g., generalized hives, pruritus or flushing, swollen lips-tongue-
19
uvula) AND AT LEAST ONE OF THE FOLLOWING
a. Respiratory compromise (e.g. dyspnoea, wheeze-bronchospasm, stridor, reduced

peak expiratory flow, hypoxemia)
b. Reduced BP or associated symptoms of end-organ dysfunction (e.g., hypotonia

[collapse], syncope, incontinence)
2. Two or more of the following that occur rapidly after exposure to a likely allergen for
that patient (minutes to several hours):
a. Involvement of the skin-mucosal tissue (e.g., generalized hives, itch-flush, swollen

lips-tongue-uvula)
b. Respiratory compromise (e.g., dyspnoea, wheeze-bronchospasm, stridor, reduced

peak expiratory flow, hypoxemia)
c. Reduced BP or associated symptoms (e.g., hypotonia [collapse], syncope,

incontinence) d. Persistent gastrointestinal symptoms (e.g., crampy abdominal pain,
vomiting)
3. Reduced BP after exposure to known allergen for that patient (minutes to several hours):
a. Children: low systolic BP (age specific) or greater than 30% decrease in systolic BP*
b. Adults: systolic BP of less than 90 mm Hg or greater than 30% decrease from that
person’s baseline
NB:*Low systolic blood pressure for children is defined as less than (70 mm Hg + [2 x age])
from 1 to 10 years, and less than 90 mm Hg from 11 to 17 years.
Approach to patients with mild allergy
1. Give diphenhydramine PO or IM and monitor for 1 hour.
2. Observing the patient for rapid increase in severity of signs and symptoms is
important, as the sequence of itching, cough, dyspnoea and cardiopulmonary
arrest can lead quickly to death.
3. If, after 60 minutes, the patient’s symptoms are still limited to the skin and the
patient is comfortable, then:
- Advise adult patient to take diphenhydramine orally every 6 to 8 hours if

symptoms persist. Advise that if anytime the patient experiences dizziness,
difficulty breathing or chest pain should report back to the hospital.
- Advise parent to give paediatric patient diphenhydramine orally every 4 - 6

hours, if symptoms persist. Advise that if anytime the child experiences
dizziness, difficulty breathing or chest pain to report back to the hospital.
- Inform the patient that he/she has an apparent allergy to the causative agent
and advise that this information should be provided to all healthcare givers in
the future.
20
If the causative agent was a medication being dispensed for additional use at home,
then this plan should be reconsidered and an alternative medication should be used that
is in a different chemical family that is not regarded as having “cross-reactivity” with
the causative agent.
Approach to patients with severe allergic reactions: Anaphylaxis/Anaphylactic

shock
1. Early recognition and early treatment with epinephrine are essential in

preventing rapid progress to death in severe allergy.
Administer epinephrine at the required dose seen below.
- Start with IM and repeat dose in every 10 minutes.
- If anaphylactic shock persist after 3 IM injections, switch to IV.
- Give IV Epinephrine using an electric syringe pump at constant rate of

0.1microgram/kg/minute and increase dose progressively until clinical
improvement is seen.
- Prepare IV epinephrine by adding 1mg (i.e. 1 ampoule) to 9mls of normal

saline to obtain a solution of 0.1mg/ml (1:1000).
- If the syringe pump is absent, use the protocol seen below to give
epinephrine by IV fluids.
2. Give oxygen at 5 L/minute if oxygen saturation is < 90% or at 2 L/minute if

patient has history of chronic lung disease.
3. Give IV hydrocortisone: 200mg q6 – 8 hourly to prevent recurrence of

reactions.
4. If wheezes
- Give salbutamol nebulizer:
Adult: 5mg 6 hourly, Children: 2.5 mg 6 hourly OR
- IV Aminophylline
Adult: 250mg given over 20 minutes and repeat after 30 minutes if necessary.
Children: 5mg/kg over 20minutes as a slow bolus injection or by infusion.
5. Place patient trendeleburg position (supine position with elevated legs) if

tolerated.
6. Begin monitoring vital signs EVERY 5 MINUTES. Monitor for alarming signs
and symptoms: Progressive wheezing, laryngeal oedema, hypotension, shock or
cardiovascular collapse
21
Table 6: Epinephrine IM Doses
Weight / lbs (kg) Epinephrine IM Dose (1mg/ml=1:1,000 wt/volume)
<9 (<4) Weigh baby and calculate appropriate dose
9-15 (4-7) 0.06 mg/0.06 mL
15-24 (7-11) 0.10 mg/0.10 mL
24-31 (11-14) 0.12 mg/0.12 mL
31-37 (14-17) 0.16 mg/0.16 mL
37-42 (17-19) 0.18 mg/0.18 mL
42-51 (19-23) 0.20 mg/0.20 mL
51-77 (23-35) 0.30 mg/0.30 mL
77-99 (35-45) 0.40 mg/0.40 mL
>99 (>45) 0.50 mg/0.50 mL
May repeat every 5 to 15 minutes PRN for a total of 3 doses (<1.5 mL [1.5 mg])
and if anaphylactic shock continues switch to IV. Administration into thigh has
proven more effective at achieving peak blood levels than into deltoid area.
Epinephrine protocol for anaphylactic shock
(If syringe pump is not available, use the following method to give IV epinephrine by
fluids.)
Preparation of solution: Dilute 2 ampoules of 1mg epinephrine (i.e. 2000

micrograms) in 200 ml of dextrose 5% or normal saline to obtain a solution containing
10 micrograms/ ml then:
Adults: Give 10 – 20 drops (5 – 10 micrograms)/ minute and increase by 10 drops after

30 minutes if the BP does not improve.
Children: Give 5 – 10 drops (2.5 - 5 micrograms) / minute and increase by 5 drops

after 30minutes if the BP does not improve.
NOTE
Don’t forget to educate or counsel the patient on the cause of allergy and signs of
severe allergic reactions and place an allergy label on the front cover of the patient’s
medical record before discharging.
22
2.4.4. ACUTE HEART FAILURE, EXACERBATION OF CHRONIC HEART
FAILURE AND CARDIOGENIC SHOCK
Acute heart failure (AHF) is the rapid and life threatening onset of symptoms and
signs of heart failure and occurs with or without previous cardiac diseases. AHF
presents either with acute pulmonary oedema or cardiogenic shock.
Acute exacerbation of CHF: Often referred to a decompensating CHF is a sudden

and prolonged worsening or decompensation of a patient’s CHF symptoms, such as an
increased shortness of breath, mental confusion, legs swelling, fatigue, paroxysmal
nocturnal dyspnoea and weight gain. In severe cases, an exacerbation of CHF can be
complicated by extreme shortness of breath. The patient even may report a feeling of
drowning. The patient may cough up pink frothy sputum or may even become
confused or unconscious.
Cardiogenic shock: Defined as decompensating heart failure with collapsing blood

pressure (BP < 90/60mmHg). Objective of treatment of cardiogenic shock is to restore
efficient cardiac output.
Some causes of CHF exacerbation are:
- Non-compliance to routine heart - Side effects of medications

failure drugs (especially the use of negative
inotropic drugs such as beta-
- Excessive alcohol intake blockers, disopyramide,
verapamil, nifedipine, diltiazem)
- Lung infections
- Increased high blood pressure
- Increased exercise
- Heart valve infections
- Irregular heartbeats (both beats
(endocarditis)
that are too fast and too slow)
- Anaemia
- Coronary artery disease
Table 7: NYHA functional classification
NYHA Class Symptoms
I Cardiac disease, but no symptoms and no limitation in ordinary physical

activity, e.g. no shortness of breath when walking, climbing stairs etc.
II Mild symptoms (mild shortness of breath and/or angina) and slight

limitation during ordinary activity.
III Marked limitation in activity due to symptoms, even during less-than-

ordinary activity, e.g. walking short distances (20–100 m). Comfortable
only at rest.
IV Severe limitations. Experiences symptoms even while at rest. Mostly

bedbound patients.
23
Approach to patient with acute heart failure (blood pressure >90/60 mmHg)
1. Place patient in semi-inclined position with legs lowered.
2. Start oxygenation with 5l/minute or 2l/minute with patients with COPD or

Asthma
3. Reduce pulmonary pressure by combination of furosemide, morphine and rapidly

acting nitrate derivative:
a. IV Lasix (furosemide): 40 – 80mg given 6 – 8 hourly [Monitor blood

pressure and urine output, weight and oxygen saturation]
b. Morphine: 3 – 5mg IV slowly or 5 – 10mg by subcutaneous injection
c. Sublingual glyceryl trinitrate: 0.25 – 0.5mg. (NB: Repeat after 30minutes if

only systemic blood pressure remains >100mmHg.)
4. The patient should be stabilised before therapy with the following medications
initiated:
- ACE inhibitors and ARBs
- Beta-blockers: Beta-blockers are stopped or decreased in people with acutely

decompensated heart failure and a low blood pressure. However,
continuation of beta-blockers may be appropriate if the blood pressure is
adequate.
5. Assess and treat for other comorbidities: e.g. RTI, diabetes, BPH/prostate cancer,
COPD/Asthma.
Approach to patient with decompensating heart failure (blood pressure >90/60

mmHg): cardiogenic shock
1. Place patient in semi-inclined position with legs lowered.
2. Start oxygenation with 5 litres /minute or 2-3 l/minute with patients with cor
pulmonale, COPD or Asthma.
3. Start positive inotropic support:
- Use IV dopamine at a constant rate by syringe pump or electrical syringe (if

available) at 10 - 20 micrograms/kg/minute OR
- Use IV epinephrine: see protocol below
4. Reduce pulmonary pressure by combination of furosemide, morphine and rapidly

acting nitrate derivative:
a. IV furosemide (LASIX®): 40 – 80 mg given 6 – 8 hourly [Monitor blood

pressure and urine output, weight and oxygen saturation]
24
b. Morphine: 3 – 5mg IV slowly or 5 – 10 mg by subcutaneous injection
c. Sublingual glyceryl trinitrate: 0.25 – 0.5 mg. (NB: Repeat after 30 minutes if
only systemic blood pressure remains >100 mmHg.)
5. Consider anticoagulation prophylaxis
- Enoxaparin (CLEXANE® or LEVONOX®) 20mg (2000 IU) / 0.2ml or

40mg (4000 IU) / 0.4ml given daily SC.
- Aspirin or acetylsalicylic acid (ASA) 81mg daily
6. Corticosteroid: They must be given once the patient is stabilised to prevent

recurrence in the short term. I has no effect in acute phase.
Hydrocortisone IV or IM
- Adult: 200mg every 4 hours.
- Children: 1 – 5 mg/kg/day in 2 to 3 doses
Epinephrine protocol for patients with cardiogenic shock
By syringe pump: Dose = 0.1microgram/kg/minute
Preparation: Add 1mg (i.e. 1 ampoule) of epinephrine to 9mls of normal saline (0.9%
sodium chloride) to obtain a solution of 0.1mg/ml (1:1000)
Start with 0.1microgram/kg/minute and increase dose progressively until clinical

improvement is seen
By infusion if no electrical pump is available
Preparation of solution
Dilute 2 ampoules of 1mg epinephrine (i.e. 2000micrograms) in 200mls of Dextrose

5% OR normal saline to obtain a solution containing 10 micrograms/ ml
In adults: Give 10 – 20 drops (5 – 10 micrograms)/ minute and increase by 10 drops

after 30 minutes if the BP does not improve.
In children: Give 5 – 10 drops (2.5 - 5 micrograms) / minute and increase by 5 drops

after 30minutes if the BP does not improve.
NOTE
Do not give IV fluids because nearly all cases of acute heart failure are in a state of
hypervolemia.
Digoxin should not be used for AHF with cardiogenic shock except in rare cases where
supraventricular tachycardia has been diagnosed by ECG.
25
2.5. ACUTE GASTIRTIS AND ACUTE PEPTIC ULCER BLEEDING
Acute gastritis is defined as sudden onset severe epigastric pain often associated with
nausea, vomiting, gnawing and palpitations (awareness of heart beat). Pain may be
improved or worsened with eating. Usually there is history of a noxious agent
(NSAID, chemical, alcohol consumption), stress, starvation, chronic gastritis etc.
Approach to patients with acute gastritis: Protocol
1. Give IV H2 receptor antagonist (cimetidine 400mg 8 hourly or ranitidine 100mg

TID) Or
IV omeprazole 40mg 12 hourly
2. IV antimuscarinics: Hyoscine 20mg 8 hourly or Spasfon 80mg 8 hourly.
3. Antacids: Give magnesium tricilicate or MAALOX® or ROCGEL® 8 hourly
4. Insert IV line with Dextrose 5% / Saline 0.45% solution to KVO.
5. Give an antiemetic if patient is vomiting: IM/IV Metoclopramide 10mg TID or

IV VOLGALENE® (metopimazine)
6. Monitor for signs of PU bleeding or intestinal perforation (peritonitis).
7. Initial investigations should involve helicobacter pylori serology and eradicate if

results are positive.
2.5.1. HELICOBACTER PYLORI INFECTION ERADICATION REGIMENS

A. First-line: Triple therapy
Duration 14 days achieves eradication rate of 81.9%, whereas 7 days attains an

eradication rate of only 72.9%.
1. Proton pump inhibitor (PPI) (omeprazole 20 mg BID, lansoprazole 30 mg

BID, esomeprazole 40 mg QD, pantoprazole 40 mg QD,) plus clarithromycin
250 mg BID and metronidazole 500 mg BID (OR tinidazole 500mg bid)
2. PPI plus amoxicillin 1 g BID and metronidazole 500mg BID
3. PPI plus amoxicillin 1 g BID plus levofloxacin 500 mg QD.
B. Sequential therapy: Superior to standard triple therapy with 14-day eradication

rate of 92.5%.
Start: PPI plus amoxicillin for 5-7 days THEN
Continue: PPI plus 2 other antibiotics for the next 5-7 days (clarithromycin and
metronidazole are the antibiotics usually chosen) but levofloxacin-based
regimens and tetracycline-based regimens are superior.
26
C. Second line therapy: Bismuth-based therapy
PPI or H2 receptor antagonist (e.g. lansoprazole 30 mg BID or ranitidine 150

mg BID) plus bismuth subsalicylate 525 mg QID (or bismuth tripotassium
dicitrate 300 mg QID) plus metronidazole 250 mg QID (or 500 mg TID or
levofloxacin) plus tetracycline 500 mg QID.
NOTE
Bismuth-based therapy is an alternative therapy used when clarithromycin resistance is

suspected.
Symptomatic treatment during eradication
1. Relief of gastrointestinal spasms with use of antimuscarinic medications (e.g.

hyoscine or scopolamine (BUSCOPAN®) 20mg TID or flouroglucinol
(SPASFON®) 80mg TID.
2. Antacids (Magnosium tricilicate 2 tabs TID for 5-10days or alluminiun

hydroxide 2 tabs TID for 5-10days or MAALOX® /ROCGEL® /GESTID® /
SUPRALUX® syrup TID for 5-10days).
3. In patients presenting with palpitations or anxiety: Propranolol 40mg QD or

bisoprolol 2.5mg QD should be given for 15-20 days.
Follow-up: PPI should be continued after eradication for 1 – 2 months and monthly
RDV given to patients. Some patients need to be placed on long-term PPIs for ulcers to
heal completely.
27
2.5.2. ACUTE PEPTIC ULCER BLEEDING
Acute PU bleeding is a frequent complication of peptic ulcer disease (PUD) and is
often associated with a high mortality especially when poorly managed.
Cardinal features of acute PU bleeding
- Hematemesis: Vomiting of red blood.
- Coffee ground vomitus (action of gastric acid on blood).
- Melena: Passage of black tarry stools (blood altered by passage through the gut).
- Hematochezia: Passage of red or maroon-coloured stool per rectum if massive

bleeding.
- Hypovolemia or hypovolemic shock.
Approach to patients with acute PU bleeding
1. Establish IV access with 2 large bore cannulae. Insert a central line if brisk bleed.
Give colloid or transfuse if necessary.
Indications for transfusion in acute PU bleeding
- Haemoglobin < 10 g/dl in patients with recent or active bleeding
- Presence of SHOCK
2. Take blood for URGENT haemoglobin or FBC, grouping and cross matching.
3. Start Intravenous PPI: Give omeprazole 80 mg as a start dose followed by

infusion 8 mg/hour for 72 hours.
This significantly reduces re-bleeding rates and the need for surgery. H2-receptor
antagonists (ranitidine, cimetidine) are of no value in PU bleeding.
4. Oxygen therapy: Give oxygen at 5 litre / minute or 2- 3 L/ minutes for patients

with COPD/Asthma.
5. IV Tranexalic acid (EXACYL®) 10 – 15 mg over 20minutes THEN

1mg/kg/hour and place on 500ml of dextrose saline and continuously infuse for 6
- 10 hours.
Or
IV/IM Etamsylate (DICYNONE®) 500 – 720 mg given 8 hourly
6. Give Lewis Meal: 1 glass 6 hourly
7. Monitor for persistence of bleeding: Monitor the pulse and blood pressure half-
hourly.
28
8. Surgery is needed if bleeding persists.
2.5.3. LEWIS MEAL COMPOSITION

Mix the following items and keep in the fridge for 10 minutes.
1. One litre of water
2. One ampoule of adrenaline
3. Four sachets of MAALOX® or PHOSPHALUGEL® or ROCGEL® (or any

other antacid)
4. Four ampoules of etamsylate (DICYNONE®)
5. Four ampoules of tranexalic acid (EXACYL®)
6. Two sachets of DUPHALAC® or other bulk laxative
29
2.6. HYPERGLYCAEMIC EMERGENCIES
Hyperglycaemic emergencies continue to be important causes of morbidity and
mortality among patients with diabetes in spite of major advances in the understanding
of their pathogenesis and more uniform agreement about their diagnosis and treatment.
They are often referred to as hyperglycaemic crisis. Two main types exist:
hyperosmolar hyperglycaemic state (HHS)/ hyperosmolar non-ketotic coma (HONK)
and diabetic ketoacidosis (DKA).
NOTE
Aggressive fluid resuscitation is the key in the management of hyperglycaemic

emergencies.
2.6.1. HYPEROSMOLAR HYPERGLYCEMIC STATE AND

HYPEROSMOLAR HYPERGLYCAEMIC NON-KETOTIC COMA
HHS also called Non-ketotic Hyperosmolar Syndrome is a triad of hyperglycaemia
with plasma glucose ≥ 600 mg/dl (>30 mmol/L) PLUS altered level of consciousness
PLUS profound dehydration (averaging 9 litres). HHS is characterized by
hyperglycaemia, hyperosmolarity, and dehydration (triad) without significant
ketoacidosis (urinalysis reveals no acetone or traces of acetone +). HONK defined as
HHS occurring in the context of coma. HHS/HONK mainly occurs in type II diabetes
mellitus.
Symptoms of HHS
- Altered level of consciousness seizures, myoclonic jerking,

reversible paralysis
- Nausea, vomiting, and
abdominal pain - Motor abnormalities including
flaccidity, depressed reflexes,
- Dehydration (poor skin turgor, tremors or fasciculation
dry mucous membrane, sunken
eyes, anuria) - Hyperviscosity with increased
risk of blood clot formation/
- Profound weight loss stroke
- Neurologic signs: blurred - Shock: Low blood pressure with
vision, headaches, focal standing
Approach to patients with HHS/ HONK
1. IV volume replacement: Ensure IV access and give normal saline rapidly and
aggressively.
First hour: Give fluids rate of 20 ml/kg as a bolus (i.e. 1 – 2 L in an average-size

person).
Next four hours: Give 50 ml/kg (i.e. 1 L/hour in an average-size person)
30
4 - 24 hour: Give 15 ml/kg (1 litre 4 hourly in an average size person)
NOTE
- Patients with HHS can respond to fluids alone if they are well hydrated.
- It is compulsory to always check the blood glucose prior to serving insulin.
- Isotonic sodium chloride is the fluid of choice for initial treatment.
- Rapid fluid resuscitation is contraindicated only in patients with renal or

cardiac insufficiency.
2. Insulin therapy: Give soluble (ACTRAPID®) or regular insulin IV/IM after

infusion of 1 – 2 L of fluid.
- Dose: 0.5 units/ kg/ day in 4 divided doses until HHS resolves
(If electric insulin pump is available: Give 0.1 unit/kg/hour as continuous

infusion)
- Switch to SC insulin after resolution of HHS/HONK (regain normal mental

status + blood sugar< 250mg/dl) and change infusion to dextrose/saline.
Continue insulin given SC until the patient becomes more alert and
hyperosmolarity has resolved then switch from short acting regular insulin to
intermediate acting NPH insulin or MIXTARD and the dose adjusted
accordingly in relation to meals.
NOTE
It is preferable to give NPH or MIXTARD after IV fluid resuscitation if patient is

conscious and eating.
3. Potassium replacement: All patients with DKA have depleted potassium. K+

ions should be added to fluids after the first two litres of fluids have been infused
if the patient is voiding
- 2 ampoules (27 mEq) of KCl should be added to every litre of IV fluid.
NOTE
It is important to replenish potassium before starting insulin infusion, especially

when levels are below 3.5 mEq, to avoid cardiovascular compromise.
Check potassium at 4 - 6 hourly until blood glucose concentration is stabilized.
4. Open blood sugar monitoring chart and monitor blood sugar every hour until
blood sugar levels are stable for 3 hours and then continue monitoring 4 hourly
thereafter. If the blood sugar goes below 250mg/dl, switch from IV to SC insulin
and set up dextrose/saline.
31
NOTE
The golden range of blood sugar is 200 – 300mg/dl
5. Identify and treat the underlying diseases: Usually missing a dose of oral anti-
diabetic or an infection.
FBC (helps to identify sepsis), urea/creatinine, serum electrolytes, serum pH, and
urinalysis
6. Monitor vital signs and open fluid input and output.
7. Once HHS has resolved, provide dietary counselling to all patients.
NOTE
Starting insulin therapy before fluid replacement may precipitate dehydration and
increases risk of shock, hypokalaemia and cerebral oedema. The osmotic pressure that
glucose exerts within the vascular space contributes to the maintenance of circulating
volume in these severely dehydrated patients. Institution of insulin therapy drives
glucose, potassium, and water into cells. This results in circulatory collapse if fluid has
not been vigorously replaced first.
Although many patients with HHS respond to fluids alone, IV insulin in dosages
similar to those used in DKA can facilitate correction of hyperglycaemia.
If the patient is new to insulin or a newly diagnosed diabetic, total subcutaneous

insulin dosages should not exceed 1 unit/kg/day.
Changing from normal saline to dextrose/saline will prevent a precipitous fall in

glucose, which may be associated with cerebral oedema.
32
2.6.1. DIABETIC KETOACIDOSIS
DKA is characterised by hyperglycaemia (> 250 mg/dl) plus ketonuria (ketones are
seen urinalysis – i.e. acetone ++) plus profound dehydration (triad). DKA is more
difficult to handle compared HHS and HONK. Commonly occurs in type 1 diabetes
mellitus and may be seen in some cases of type II diabetes mellitus.
Symptoms
- The most common early symptoms of DKA are the insidious increase in
polydipsia and polyuria
- Malaise, generalized weakness, and fatigability
- Nausea and vomiting; may be associated with diffuse abdominal pain, decreased
appetite, and anorexia
- Rapid weight loss in patients newly diagnosed with type 1 diabetes
- History of failure to comply with insulin therapy or missed insulin injections due
to vomiting or psychological reasons or history of mechanical failure of insulin
infusion pump
- Decreased perspiration
- Altered consciousness (mild disorientation, confusion); frank coma is uncommon

but may occur when the condition is neglected or with severe
dehydration/acidosis
Signs
- Ill appearance - Characteristic acetone (ketotic)

breath odour
- Dry skin
- Tachycardia
- Laboured respiration
- Hypotension
- Dry mucous membranes
- Tachypnoea
- Decreased skin turgor
- Hypothermia
- Decreased reflexes
Approach to patients with DKA
1. IV volume replacement: 7 litres of normal saline should be given in 24 hours
- 0 – 1 hour: 1 litre of normal saline
- 1 – 3 hours: 2 litres (500 ml / h of normal saline)
- Next 20 hours: 4 litres
33
NOTE:
- There is profound dehydration averaging 7 – 9 L in most patients.
- Encourage oral hydration on demand if patient is conscious.
2. Insulin therapy: IV/IM soluble or regular insulin should be given after infusing
1-2 litres fluids.
- Dose: 0.5 IU/ kg/day (children - 0.1 unit/kg/day) given in 4 divided doses
until resolution of DKA
- Switch to SC insulin (same doses) with the resolution of DKA (i.e. plasma
glucose < 250mg/dl) and set up dextrose 5% to keep blood glucose around
200 mg/dl (11 mmol/l).
- When the blood glucose stabilises such the patient can commerce oral
feeding, switch from short acting regular insulin to intermediate acting NPH
insulin and the dose of the later adjusted accordingly in relation to meals.
3. Potassium replacement: All patients with DKA have depleted potassium. K+

should be added to fluids after the first two litres of fluids have been infused and
the patient is voiding
2 ampoules (27 mEq) of KCl should be added to 1litre of all IV fluids.
NOTE
Check potassium at 4 hourly until blood glucose concentration is stabilized.
4. Correction of severe metabolic acidosis. Add 2 ampoules of NaHCO3 to 1 litre

of dextrose/saline and infuse over 1-2 hours.
5. Monitor blood glucose hourly: If levels are stable for 3 hours, decrease
frequency of testing to 2 hourly. Change fluids to Dextrose/saline (i.e. dextrose
5% / saline 0.45%) when blood sugar decreases to < 250 mg/dl. And switch from
IV/IM insulin to SC.
6. Look for the precipitating factor: Give broad spectrum antibiotics with
anaerobic coverage to febrile patients.
- IV Ceftriaxone 1 given 12 hourly + IV Metronidazole 500mg given 8 hourly.
7. Monitor the level of consciousness and vital signs hourly.
8. Open input and output chart.
9. Urgent work-up : FBC, urea/creatinine, serum sodium and potassium and

urinalysis
34
Table 8: SC Sliding-Scale Insulin Therapy (SSI) doses
Glucose Regular Insulin Scale
140 – 199 mg/dl 6 units SC
≥ 300 mg/dl Resume IV or IM Insulin
NOTE
- SSI must be given 6 hourly prior to every meal
- Measure always the blood sugar level prior to SSI
- SSI can result in the ROLLER COASTER EFFECT
ROLLER COASTER EFFECT
When not given the proper dosages, SSI often cause blood sugar levels to dip too low
(hypoglycemia), this condition is known as the Roller Coaster Effect. This is because
SSI does not take into consideration the weight of the patient and therefore may over
estimate or under estimate the amount of insulin received. The sliding-scale insulin
also fails to individualize insulin requirements and bases insulin doses on glucose
levels prior to meals without regard to a patient’s basal metabolic needs, the types and
amounts of food to be consumed, a patient’s weight, or other factors influencing
insulin demands such as previous insulin needs, insulin sensitivity, or resistance. For
example, a patient weighing 80 kg would receive the same insulin dose as a patient
weighing 65 kg if their blood glucose levels are within the same range. Subsequently,
the 80kg patient may not receive sufficient insulin, placing him or her at increased
hyperglycemia risk, and the 65kg patient may receive a potentially excessive dose that
could result in hypoglycemia.
35
2.6.3. HYPOGLYCAEMIA
One of the most frequently encountered complications of diabetes that often result
from anti-diabetic treatment.
Clinical presentation: Blood sugar < 80mg/dl plus the following symptoms and signs
Autonomous symptoms: sweating, trembling, pounding heart, anxiety, hunger, nausea
Neurologic symptoms: weakness, visual disturbance, difficulty speaking, tingling,

dizziness, difficulty concentrating, tiredness, convulsion, drowsiness, confusion
Approach to patient with hypoglycaemia
A. Conscious patient
1. Oral glucose: 0.3-0.5 g/kg of body weight or 2-3 cubes of sugar
2. Control finger stick glucose after 10 minutes, if no improvements, give 50 ml

of 50% dextrose.
3. Allow oral feeding immediately: give fruits or a meal.
B. Unconscious patient
1. Insert IV line and commence 250 ml 10% dextrose over 5 min or 50 ml of 50%
dextrose.
2. When consciousness returns, allow oral feeding immediately: give fruits or a

meal.
3. Counselling on the cause, identifying symptoms and management by patient.
C. Search for the causes in diabetic patient (e.g. drugs like glibenclamide
(DAONIL®) causes hypoglycaemia, diet, and high doses of insulin).
36
2.6.4. INSULIN FORMULARIES AND DOSAGES
A. MIXTARD®
MIXTARD® contains both fast-acting (soluble) and long-acting (isophane) insulin in

3 forms.
- MIXTARD® 30: soluble insulin 30% and isophane insulin 70%.
Dose: 0.3-1.0 IU/kg/day. MIXTARD® is given 30 minutes before a meal. It is usually

given once or twice a day when a rapid initial effect together with a more long-lasting
effect is needed.
B. Regular insulin
Administer U-100 insulin subcutaneously 3 - 5 times a day approximately 30 minutes

before meals. Administer U-500 insulin subcutaneously 2 - 4 times a day
approximately 30 minutes prior to start of a meal.
Dose: - 0.5 – 1.0 unit / kg/day of U-100 regular insulin given SC in 4 divided doses
C. Soluble Insulin (ACTRAPID®, INSULINARD®)
Soluble insulin is a fast-acting insulin and may be used with intermediate or long-
acting insulin to control blood glucose levels.
Dose: 0.5 - 1.0 unit/kg/day given in 4 divided doses
D. NPH (Neutral Protamine Hagedorn)
This is an intermediate–acting insulin called isophane. NPH is preferred during

pregnancy and is relatively safe for the baby.
Dose: 0.4-1.0 IU/kg/day in two divided doses
NOTE
Soluble and regular insulin can also be given IV or IM in situation like HHS or DKA
SC insulin is given by injection under the skin, in the thigh, the abdominal wall (at the
front of the waist), the gluteal region (buttocks) or the deltoid region (shoulder). The
injection site should be changed for each injection. The patient's blood glucose (sugar)
should be tested regularly to find the lowest effective dose.
37
2.7. HYPERTENSIVE CRISIS
Hypertensive crisis is an umbrella term for hypertensive urgency and hypertensive
emergency. These two conditions occur when blood pressure becomes very high,
possibly causing organ damage.
2.7.1. HYPERTENSIVE URGENCY

Hypertensive urgency occurs when blood pressure readings is ≥ 180/110 with no
evidence of damage to the body's organs. Hypertensive urgency is often discovered
when a patient comes to the hospital with other medical problems. After the diagnosis
of hypertensive urgency, blood pressure must be immediately controlled to prevent
imminent organ damage. This can be done using oral antihypertensive medications.
Approach to patients with hypertensive urgency
1. Admit patient for observation of the BP and signs of eminent organ damage.
2. Give oral antihypertensive
 If patient is non-compliant to medications restart antihypertensive

medications and include:
- Nicardipine 20 mg every 8 hours (or Nifedipine 20 mg every 12 hours)

plus hydrochlorothiazide 25mg daily plus captopril 25mg 12hourly
- If patient is compliant to medications
- Add another antihypertensive to routine medication: e.g. nicardipine or

nifedipine.
- Doses of existing antihypertensive medications should be increased.
3. Reassurance and counselling: Hypertensive urgency is often because the

patients misses doses of antihypertensive or stressed up.
4. Urgent work-up: Urea/ creatinine, urinalysis
2.7.2. HYPERTENSIVE EMERGENCY OR MALIGNANT HYPERTENSION

Hypertensive emergency occurs when blood pressure readings are ≥ 180/110 and there
is evidence of damage to the body's organs. E.g.
- Changes in mental status such - Worsening chest pain (unstable

as confusion, headache, blurred angina)
vision, seizures
- Fluid in the lungs (pulmonary
- Focal signs/ neurologic deficits oedema)
- Acute heart failure (increasing - Acute chest pain (aortic

shortness of breath, swelling or dissection)
oedema)
38
- Eclampsia (occurs during pregnancy)
Approach to patients with Hypertensive Emergency/malignant hypertension
1. Determine the initial MAP. Open BP monitoring chart and monitor blood
pressure. Bring down MAP by of 25% of the initial value.
2. Start the LOXEN® protocol: This rapidly brings down the blood pressure and
prevents further organ damage. When the blood pressure goes down by 25%,
stop the IV nicardipine and switch to oral medications.
- Nicardipine 20 mg every 8 hours or Nifedipine 20mg every 12 hourly
3. Treat the organ that is damaged with specific therapies.
4. Urgent work-up: urea/creatinine, urinalysis, serum electrolytes.
5. Patient should be reviewed by cardiologist and ophthalmologist (to examine the

eyes for swelling and bleeding)
6. Counsel patients to be compliant to medication.
2.7.2.1. NICARDIPINE (LOXEN®) PROTOCOLS

Aim: To lower mean arterial pressure (MAP) by 25% of pre-treatment values in 2
hours.
Protocol 1
Preparation: 210 ml of dextrose 5% + 4 ampoules of LOXEN® (40mg)
1. Start with 10 – 15 drops/ minute. The initial infusion rate of IV nicardipine of 10

drops/minute gives 5 mg/h.
2. Monitor BP at 10 minutes intervals and increase the flow rate by 5 drops every
10 minutes to a maximum of 30 drops/min until target MAP is reached (25% of
the initial value) then switch to oral treatment.
Protocol 2:
1. Give 2.5 mg IV slowly over 10 min with maximum dose 10 mg and repeat after
30 minutes if target MAP is not reached.
2. Monitor BP at 10 min interval. When 25% decrease in MAP is attained, switch

to oral medications.
39
2.8. ASTHMATIC CRISIS
Asthma is defined as chronic inflammatory disorder of the airways leading to recurrent
episodes of wheezing, breathlessness, chest tightness/pains and coughing associated
with airflow obstruction often reversible, either spontaneously or with treatment.
Asthmatic crisis is common amongst patients with chronic asthma.
2.8.1. ACUTE EXACERBATION OF ASTHMA OR ASTHMA FLARE-UP OR

ACUTE ASTHMA ATTACK
This is the sudden worsening of asthma symptoms in a known asthmatic patient, but
responds to standard treatments. It can be triggered by a variety of things. Some of the
more common triggers are: upper respiratory infections, colds, pollens, moulds, dust
mites, pets, tobacco smoke, dry air, exercise and gastro-oesophageal reflux disease.
Symptoms of acute asthma attack
- Shortness of breath: Use of - Bluish tint to your lips

accessory muscle
- Feel agitated, confused, or can’t
- Can’t speak in full sentences concentrate
- Difficulty to talk or cough - Hunched shoulders, strained

abdominal and neck muscles
- Paradoxical thoraco-abdominal
movement - Feel that you need to sit or stand
up to breathe more easily
- Feel breathless even when you
lie down - Agitation, anxiety
- Chest feels tight -

Silent lungs or RR >40/min,
HR> 120 bpm, bradycardia,
- Altered mental status SBP < 90 mmHg or
hypertension
Approach to patient with acute asthma attack: Protocol
1. Place patient in semi-recumbent position.
2. Give beta-2 agonists:
- Salbutamol/ albuterol (VENTOLINE ® 100 µg) using metered dose inhaler 4

puffs one at time every 20 min for one hour (ask the patient to breath in and
out 4 times after each puff).
Use bottle spacers (500 ml plastic bottle) to increase effectiveness OR
- Give salbutamol/albuterol (VENTOLINE ® 0.5 mg/ml amp) SC
3. Give steroids: Dexamethasone 8mg IV start dose or 0.5mg/kg IV start dose for
paediatric patients <16kg
40
4. Observe the patient for 2 – 3 hours when the attack completely resolves and
discharge with:
- Salbutamol 4 puffs every 6 hours for 24 hours &
- Oral prednisone 1 mg (adult: 40-50mg) once daily for 7 days and the taper by
10mg every 5days.
5. If symptoms worsen or do not improve, treat as status asthmaticus/ severe

asthma.
NOTE
Always observe the patient using the inhaler. Explain and demonstrate the appropriate
use if incorrect technique.
Avoid bolus IV injections of aminophylline in patients who have been on theophylline,

for risk of cardiac arrhythmias, seizures due to toxic blood levels. Rather give
aminophylline 250 mg as slow infusion over 6-8 hours
2.8.2. SEVERE ASTHMA OR STATUS ASTHMATICUS

Severe asthma is an acute exacerbation of asthma or asthma flare-up that does not
respond to standard treatments of bronchodilators (inhalers) and corticosteroids. It
occurs in over 5% of asthma patients. Severe asthma can result in hypoxemia,
hypercarbia, and secondary respiratory failure posing a life-threatening medical
emergency. Severe asthma can complicate leading to a chronic lung condition called
COPD (chronic obstructive pulmonary disease) or asthma-COPD overlap.
Approach to patients with severe asthma: Protocol
1. Place patient in semi recumbent position and start oxygenation at 2 - 3 litres /

minutes and continuous positive airway pressure (CPAP) can also be used.
2. Give short acting beta agonists (SABA) by nebulization:
- Salbutamol nebulizer:
Start with: 2.5 - 5mg q20 minutes x 3 doses over period of 1 hour.
Continue with: 2.5 – 5mg q4hourly PRN
NOTE
There is no advantage of IV over inhaled salbutamol/albuterol even in severe

asthma.
If patient is not able to use inhalator i.e. cannot move enough air to take full
advantage of nebulisation, give SC terbutaline.
41
- SC terbutaline (BRICANYL®) 0.25 - 0.5 mg q20-30 minutes X 3 doses PRN
(not to exceed 0.5mg/4hours) given in the deltoid muscle.
3. Give anticholinergic: They are as effective as beta agonists during acute crisis
and synergistically improve symptoms when co-administered with
albuterol/salbutamol
Ipratropium inhaler: 2 actuations (34mcg) q6 hourly, then additional actuations

PRN not to exceed 12 actuations/day
Ipratropium nebulizer: 2.5ml (500mcg) q6-8 hourly.
4. Intravenous steroids:
- IV/IM methylprednisolone (SOLU-MEDROL®) 1 mg/kg once daily for 1

week OR
- IV hydrocortisone at 2 – 5 mg/kg (Adult: 250mg) start dose or 8 hourly if

crisis persist
5. Give methylxanthines: They are adjunctive agents (i.e. can be added to

treatment if the patient is not responding to beta agonist treatment).
IV aminophylline
Loading dose: 6 -7mg/kg infuse over 20 minutes
Maintenance dose: 0.5mg/kg/hour set in dextrose/saline solution
NOTE
- IV aminophylline has a propensity to cause arrhythmias. It interacts with

cimetidine, ciprofloxacin and macrolides (erythromycin).
- Do not give a loading dose to patients already on oral

aminophylline/theophylline.
6. Identify and address the precipitating factors: Chest infections are often a
common factor in COPD. Give empiric broad spectrum antibiotics with coverage
against pneumococcus, H. influenza and gram negative enterics while awaiting
sputum cultures.
NOTE
In cases of severe acute exacerbation of chronic bronchitis, guidelines suggest

using fluoroquinolones (gatifloxacin, ciprofloxacin, levofloxacin) as first line
therapy as resistance to these agents is still low.
7. Work-up: Spirometry, chest x-ray, sputum culture and analysis for AFB (do
Xpert RIF or gene Xpert), ESR and FBC
42
8. Indications for Intubation: The need for intubation can be established quickly
at the bedside by asking the patient to hold the nebulizer in his or her hand. If the
patient becomes sleepy that the nebulizer starts to fall away, the patient should be
intubated. Call the anaesthetist or anaesthesiologist.
9. Physiotherapy: Can be very helpful for patients with severe asthma.
NOTE
Multiple therapies should be used simultaneously to rapidly reverse the effects of

status asthmaticus and reduce permanent damage of the airways. Patients with severe
asthma should be managed with at least four different types of asthma medicines at
once.
43
2.9. ACUTE EXACERBATION OF CHRONIC OBSTRUCTIVE PULMONARY
DISEASE AND END STAGE COPD
COPD is defined as chronic inflammation of the bronchial mucosa due to irritation
(tobacco, pollution), allergy (asthma), and infective (repetitive acute bronchitis)
usually characterised by productive cough for 3 consecutive months per year for 2
successive years, gradual onset persistent dyspnoea and persistent bronchial wheezes.
The classic triad of COPD includes chronic bronchitis, emphysema and to a lesser
extend asthma. COPD leads to irreversible airflow limitation during force expiration.
Chronic bronchitis is defined as excessive mucus production with airway obstruction

and notably hyperplasia of mucus producing glands. Emphysema is defined as the
destruction of airways distal to the terminal bronchioles.
Table 9: Stages of COPD
Mild COPD or Stage 1 Mild COPD with a FEV1 about 80 percent or more of normal.
Moderate COPD or Stage 2 Moderate COPD with a FEV1 between 50 and 80 percent of
normal.
Severe COPD or Stage 3 Severe emphysema with a FEV1 between 30 and 50 percent of
normal.
Very Severe COPD or Stage Very severe or End-Stage COPD with a lower FEV1 than
4 Stage 3, or people with low blood oxygen levels and a Stage 3
FEV1.
2.9.1. COPD FLARE-UP/ ACUTE EXACERBATION OF COPD

COPD flare-up or acute exacerbation of COPD is the sudden worsening or
deterioration of already existing signs and symptoms of COPD. These includes:
- Severe worsening dyspnoea
- Severe worsening wheezing suggestive of mucus or pus blocking the airway.

Gurgling or rattling could mean fluid in the lungs.
- Irregular breathing and use of accessory muscles of respiration.
- Worsening cough with increased volume of purulent sputum. It could be dry or

bring up yellow, green, or bloody phlegm.
- Changes in skin or nail colour. Bluish tint around your lips and nails seem blue
or purple. Skin looks yellow or gray.
- Trouble sleeping and eating. Symptoms get worst when lying down. Patient
don’t feel like eating.
- Difficulty to speak: This is a late and dangerous sign of worsening breathing.
44
- Early-morning headaches: Throbbing head worst in the morning because of a
build-up of carbon dioxide in blood.
- Swollen ankles or legs or abdominal pain.
- Fever. A higher temperature could be a sign of infection and an oncoming flare-

up
2.9.2. END-STAGE COPD

Patients with end-stage COPD or very severe COPD will present as emergencies with
flare-ups that are not normally controlled by the basic management with
bronchodilators (inhalers) and corticosteroids.
Characteristics of end-stage COPD
- Severe shortness of breath - Having extreme difficulty

(dyspnoea) at rest or stage IV “catching your breath” or
dyspnoea. talking
- Failure of routine medications to - Having a very rapid heartbeat

control symptoms
- Having very rapid breathing
- Onset of cor pulmonale (right
heart failure) - Being confused
- Accelerated resting heart rate - Not being mentally alert, or

(tachycardia) of more than 100 having slower mental
beats per minute. functioning
- Progressive weight loss - Feeling excessively sleepy or

drowsy
- Profound decrease I quality of
life - Onset respiratory failure.
Approach to patient with exacerbated COPD
1. Place patient in semi recumbent position and start oxygenation at 2 - 3 litres /

minutes and continuous positive airway pressure (CPAP) can also be used.
2. Give short acting beta agonists (SABA) by nebulization:
Salbutamol nebulizer
Start with: 2.5 - 5mg q20 minutes x 3 doses over period of 1 hour.
Continue with: 2.5 – 5mg q4hourly PRN
NOTE
There is no advantage of IV over inhaled salbutamol/albuterol even in severe

asthma.
45
If patient is not able to use inhalator i.e. cannot move enough air to take full
advantage of nebulisation, give SC terbutaline
- SC Terbutaline (BRICANYL®): 0.25 - 0.5 mg q20-30 minutes X 3 doses

PRN (not to exceed 0.5mg/4hours) given in the deltoid muscle.
3. Give anticholinergic: They are as effective as beta agonists during acute crises
and synergistically improve symptoms when co-administered with
albuterol/salbutamol
Ipratropium inhaler: 2 actuations (34mcg) q6 hourly, then additional actuations

PRN not to exceed 12 actuations/day
Ipratropium nebulizer: 2.5ml (500mcg) q6-8 hourly.
4. Intravenous steroids:
- IV/IM methylprednisolone (SOLU-MEDROL®) 1 mg/kg once daily for 1

week OR
- IV hydrocortisone at 2 – 5 mg/kg (Adult: 250mg) start dose or 8 hourly if

crisis persist
5. Give methylxanthines: They are adjunctive agents (i.e. can be added to

treatment if the patient is not responding to beta agonist treatment).
- IV aminophylline
Loading dose: 6 -7mg/kg infuse over 20 minutes
Maintenance dose: 0.5mg/kg/hour set in dextrose/saline solution
NOTE
- IV aminophylline has a propensity to cause arrhythmias.
- Interacts with cimetidine, ciprofloxacin and macrolides (erythromycin).
- Do not give a loading dose to patients already on oral theophylline.
6. Identify and address the precipitating factors: Chest infections are often a
common factor in COPD
- Give empiric broad spectrum antibiotics with coverage against

pneumococcus, H. influenza and gram negative enterics while awaiting
sputum cultures.
NOTE
46
In cases of severe acute exacerbation of chronic bronchitis, guidelines suggest
using fluoroquinolones (gatifloxacin, ciprofloxacin, levofloxacin) as first line
therapy as resistance to these agents is still low.
7. Indications for Intubation: The need for intubation can be established quickly
at the bedside by asking the patient to hold the nebulizer in his or her hand. If the
patient becomes sleepy that the nebulizer starts to fall away, the patient should be
intubated. Call the anaesthetist or anaesthesiologist.
8. IV Magnesium sulphate: Added as last therapy by infusion in 0.9% sodium

chloride over 20 minutes, while monitoring blood pressure.
Adults: 1 - 2 g
Children over 2 years: 40 mg/kg
9. Work-up: Spirometry, chest x-ray, sputum culture and analysis for AFB (do
Xpert RIF or gene Xpert), ESR and FBC
10. Physiotherapy: Can be very helpful for patients with end-stage COPD.
47
2.10. ACUTE GOUT / GOUT FLARE
Acute gout (or a gout flare) is an intensely painful and disabling inflammatory arthritis,
usually involving a single joint but occasionally involving two or more joints. The pain
is severe, and patients often cannot wear socks or touch bed sheets during flare-ups
Even without treatment, acute attacks typically subside or resolve within five to seven
days.
Differential diagnosis:
- Acute septic arthritis
- Acute gout sometimes resembles cellulitis and can lead to skin desquamation
over the inflamed area.
- Acute gout can also cause acute bursitis or tenosynovitis of periarticular

structures
- Acute gout can cause a high fever and leukocytosis
The goal of therapy in an acute gout attack is prompt and safe termination of pain and
disability. Without therapy, acute gouty arthritis usually resolves completely within a
few days to several weeks, particularly in early disease. However, symptoms improve
more quickly with administration of any of a broad array of anti- inflammatory drugs.
Approach to patients with Acute Gout
1. Colchicine protocol: Used to prevent or treat gout attacks. Colchicine is an

alternative for those unable to tolerate NSAIDs in gout because of its anti-
inflammatory effect.
Posology 1 (COLCRYS® posology) (standard): 1.2mg PO at first sign of flare,

then 0.6mg 1hour later not to exceed 1.8mg in 1 hour period.
Posology 2: Give 1mg at first sign of flare, then 0.5mg 1 hour later and continue
with prophylaxis doses.
Prophylaxis
Day 1: Colchicine 1mg TID
Day 2-5: Colchicine 1mg BID.
2. Allopurinol (ZYLORIC®) usage: Used mainly to prevent further episode of

gout flare. It is not recommended to start allopurinol during an acute attack of
gout, but should always be prescribed after the flare.
Posology:
Initial dose: Allopurinol 100 - 150mg once daily for 10 days
48
Maintenance dose: 200 - 300 mg (mild gout) orally once daily or 400 - 600
mg/day (moderate - severe tophaceous gout) in 2 divided doses.
3. NSAID (Indomethacin, Diclofenac, Ibuprofen)
- Indomethacin 50 mg given 8 hourly for 4 - 10 days.
- Diclofenac 50 mg given 8 hourly for 5 – 10 days.
4. Steroids: Are as effective as NSAIDS. Used in cases of contraindications to

NSAIDs (e.g. renal failure, PUD)
- IM methylprednisolone, single 80 - 120mg dose
- Intra-articular methylprednisolone (DEPO-MEDROL®, SOLU-MEDROL®)

as single 20 - 40mg dose
- Prednisone tabs 20 - 40 mg daily for two or three days, then taper over 10 -
14 day
NOTE
- The diagnosis of acute gout attack should not be excluded in the presence of
normal serum uric acid levels if the clinical manifestations or the positive
response at colchicine are suggestive of gout.
- Don’t give colchicine in long-term treatment of gout, to patients with chronic

kidney disease or chronic liver disease or to children less than 16years.
49
2.11. SEVERE ANAEMIA AND BLOOD TRANSFUSION
Anaemia is defined as a decrease in the total amount of red blood cells or haemoglobin
in the blood, or a lowered ability of the blood to carry oxygen.
Cut up values for haemoglobin in anaemia vary with age and sex.
- <13g/dl in adult males - <11g/dl in children 6 months to

11 years
- <12g/dl in adult females (non-
pregnant) - <12g/dl in children 12 – 15
years
- <10g/dl in pregnant women
- <13g/dl in the first week if life
Causes of anaemia
1. Decreased production of normal red blood cells
- Nutritional deficiencies due to - Lead poisoning

insufficient intake or absorption
(iron, B12, folate) - Chronic renal disease
- HIV infection - Neoplastic diseases (leukaemia,

neoplasms invading bone
- Chronic diseases or marrow)
inflammation
2. Increased destruction of red blood cells
- Malaria - Rh D or ABO incompatibility in

the neonate
- Haemoglobinopathies (sickle
cell disease, thalassemia) - Autoimmune disorders
- G6PD deficiency - Spherocytosis
3. Loss of red blood cells
- Hookworm infection - Surgery
- Acute trauma
Causes of decompensating anaemia
Many factors can precipitate decompensation in an anaemic patient and lead to life-
threatening hypoxia of tissues and organs. Usually acute shortage of oxygen carrying-
capacity
- Increased demand for oxygen: (infection, pain, fever, exercise)
- Further reduction in oxygen supply (active bleeding or haemolysis)
50
- Acute blood loss
- Pneumonia etc
Signs of decompensating anaemia
- Laboured, rapid breathing with - Mental status changes

intercostal, subcostal and
suprasternal retraction/recession - Diminished peripheral pulses
(respiratory distress)
- Congestive cardiac failure
- Forced expiration (‘grunting’)
- Hepatomegaly
- Flaring of nostrils
- Poor peripheral perfusion
- Difficulty with feeding (capillary refill greater than 2
seconds)
Approach to patients with decompensating anaemia
1. Cross-match and transfuse the required volume of blood (see quantity under
transfusion).
2. Oxygenation: Give oxygen at 2- 3 litres/ minute especially to children

presenting with respiratory distress.
3. Give furosemide 1 mg/kg by mouth or 0.5 mg/kg by slow IV injection to a

maximum dose of 20 mg/kg if child is likely to develop/ or show signs of cardiac
failure and pulmonary oedema from fluid overload.
Infants and children require small volumes of fluid and can easily suffer
circulatory overload if the infusion is not well-controlled.
4. Monitor vital signs and watch out for signs of transfusion reaction.
5. Re-evaluate the patient’s haemoglobin or haematocrit and clinical condition after

transfusion. If the patient is still anaemic with clinical signs of hypoxia or a
critically low haemoglobin level (< 5g/dl), give a second transfusion of 10-15
ml/kg of whole blood.
6. Identify and treat the underlying cause of the anaemia to help haematological
recovery.
2.11.1. BLOOD TRANSFUSION

This is the ultimate treatment of severe decompensating anaemia. The decision to
transfuse should not be based on the haemoglobin level alone, but also on a careful
assessment of the patient’s clinical condition. In our setting, whole blood is transfused
but modern medical practice commonly uses only components of the blood such as red
blood cells, white blood cells, plasma, clotting factors, and platelets.
Absolute indications for blood transfusion

51
1. Haemoglobin concentration of 4 g/dl or less (or haematocrit 12%), whatever the
clinical condition of the patient.
2. Haemoglobin concentration of 4-6 g/dl (or haematocrit 13-18%) if any the

following clinical features are present:
- Clinical features of hypoxia: Acidosis (usually causes dyspnoea), Impaired

consciousness
- Hyperparasitemia (>20% or ) in malaria patients
3. Haemoglobin of 10g/dl or less with evidence of active bleeding: e.g. in Upper GI

bleeding from PUD or RTA.
Infections that can be gotten through Blood Transfusions
- Human immunodeficiency virus - Human herpes virus 8
- Hepatitis B virus - Malaria and babesiosis
- Hepatitis C virus - Pandemic influenza
- Treponema pallidum (syphilis) - West Nile virus
- Human T-lymphotropic virus 1 - Trypanosoma cruzi (Chagas

or 2 disease)
- Creutzfeldt-Jakob disease
Signs and symptoms of allergic reaction during transfusion
You may have a mild allergic reaction even if you get the correct blood type.
- Fever. - A fast heart rate.
- Hives. - Chills.
- Shortness of breath. - Low blood pressure.
- Pain.
Estimated volume of whole blood to be transfused
For Paediatrics: Give 10 ml/kg whole blood over an hour. (This will increase
haemoglobin concentration by approximately 2-3 g/dl unless there is continues
bleeding or haemolysis). (Transfusion rate: 1ml of whole blood = 15 drops)
For Adults: Is estimated by the formula
Volume= 6 x [Hr – Hp] x Weight (kg)
Where Hr is the required haemoglobin and Hp is the patients’ haemoglobin.

52
NOTE
It is generally advice to transfuse 1 unit (450mls) of whole blood over a period of

90minutes. 1 unit of whole blood increases the haemoglobin level in an adult by 1.
There are some patients with moderate-to-severe anaemia but are well compensated or
tolerated (i.e. very low haemoglobin levels can be tolerated with few or no symptoms,
provided anaemia develops slowly over weeks or months. Do not transfuse cases of
tolerated anaemia). The decision to transfuse should not be based on the haemoglobin
level alone, but also on a careful assessment of the child’s clinical condition.
The empty blood bag could be kept beside the patient for about 1-2 hours before
discarding it in case of any legal concern in relation to the blood transfused. Never use
an adult unit of blood (450mls) for paediatric patients because of the risk of bacteria
entering the pack during the first transfusion and proliferating while the blood is out of
the refrigerator. (i.e. always transfuse the blood as a single donation unit. This reduces
the risk of infection).
53
2.12. ACUTELY RAISED INTRACRANIAL PRESSURE
Intracranial pressure (ICP) is the pressure inside the skull and thus in the brain tissue
and cerebrospinal fluid (CSF) and is normally 7–15 mmHg for a supine adult. Raised
ICP or intracranial hypertension is elevation of the pressure in the cranium to above
20mm Hg.
The Monro-Kellie hypothesis: states that the cranial compartment is incompressible

and the volume inside the cranium is fixed. The cranium and its constituents (blood,
CSF, and brain tissue) create a state of volume equilibrium, such that any increase in
volume of one of the cranial constituents must be compensated by a decrease in
volume of another
Cerebral perfusion pressure (CPP) depends on mean systemic arterial pressure (MAP)
and ICP by the following relationship:
CPP = MAP – ICP, where MAP =1/3 (SBP - DBP) + DBP.
Implies that a raise in ICB must results in a rise in MAP in order to maintain CPP
within normal range.
Causes of acutely raised ICP
- Mass lesion / Intracerebral - Cerebral oedema

haemorrhage or hematoma
(epidural and subdural - Hydrocephalus
hematoma, cerebral contusions),
depressed skull fractures - Idiopathic or benign intracranial
hypertension
- Ischemic stroke
Clinical presentation of acutely raised ICP
- Severe progressive headache - Ocular palsies
- Altered level of consciousness: - Back pain

ranges confusion about time to
coma - increased blood pressure
- decreased mental abilities - Pupils that don’t respond to

changes in light
- Double vision
- Shallow breathing
- Projectile vomiting without
nausea - Seizures
Cushing's triad: sign of increased intracranial pressure
Physical exam may reveal the Cushing triad and unequal pupils with one pupil dilated
and not reactive to light or Cushing reflex (Cushing effect or Cushing reaction or
54
Cushing phenomenon or Cushing response) is a physiological response to increased
ICP indicated by a triad.
1. Hypertension (progressively increasing systolic blood pressure)
2. Bradycardia or irregular respirations
3. Widening pulse pressure (an increase in the difference between systolic and
diastolic pressure over time)
NOTE
Cushing's triad suggests terminal stages in the setting acute head injury of trauma or a
space occupying lesion (e.g. brain tumour) that is growing and a possible impending
fatal herniation of the brain.
Approach to patients with acutely raised ICP
1. Start oxygenation immediately at 5 l/minute
2. Give IV mannitol 20 – 25 %: Dose - 1.5 – 2 g/kg infused over 30 – 60 minutes.
Adults: 250mls/ day (30 – 40 drops/minute)
Children: 5ml/kg/day (5 – 10 drops/minute)
3. Refer urgently for CT scan of the brain and further management.
NOTE
The nearest CT scan can be done at the Mbingo Baptist Hospital/ Bamenda Regional
Hospital. Steroids have demonstrated no benefit in the treatment of acute head injury.
55
2.13. ACUTE AND CHRONIC KIDNEY DISEASES
2.13.1. ACUTE KIDNEY DISEASE
Acute kidney injury (AKI) or acute renal failure (ARF) is the sudden / abrupt loss of
kidney function or reversible damage kidney that happens within a few hours or a few
days. AKI is characterised by anuria or Oliguria (urine output of less than 400mls in 24
hours (< 0.5ml/kg/h)) + elevated blood urea nitrogen and creatinine + electrolyte
imbalances + signs and symptoms below
Signs and symptoms of AKI
- Too little urine leaving the body - Confusion
- Swelling in legs, ankles, and - Nausea

around the eyes
- Seizures or coma in severe cases
- Fatigue or tiredness
- Chest pain
- Shortness of breath
- Hypotension
- Abdominal distension/ ascites
Aetiology
1. Prerenal AKI (>70%): Result from decrease effective blood flow to the kidney
and cause a decrease in the glomerular filtration rate (GFR)
- Low blood pressure ( e.g. dehydration from profuse vomiting and diarrhoea,
excessive bleeding from trauma/ GI bleeding, shock)
- Organ failure (e.g. liver cirrhosis, heart failure, heart attack,
- Local changes to the blood vessels supplying the kidney (renal artery
stenosis or renal vein thrombosis)
- Severe allergic reactions
- Life-threatening infection e.g. severe sepsis
- Major surgery
2. Intrinsic AKI: Intrinsic AKI refers to disease processes which directly damage
the kidney itself.
- Glomerulonephritis, acute - Certain medication classes

tubular necrosis such as calcineurin
inhibitors (e.g., tacrolimus)
- Acute interstitial nephritis
- Overuse of pain medicines
- Rhabdomyolysis from burns (NSAIDs)
- Tumour lysis syndrome
56
3. Post renal AKI: Results from urinary tract obstruction.
- Benign prostatic hyperplasia - Obstructed urinary catheter
- Kidney and bladder stones - Cancer of the bladder,

ureters, or prostate.
- Urethral stricture
Approach to patients with AKI: Protocol
1. Insert urinary catheter and monitor urine output.
2. Fluid resuscitation if low blood pressure or shock, IV access with preferably

normal saline or dextrose/saline. Give a colloid if the is patient in shock
(Geloplasma 500mls bolus) or blood if acute decompensating anaemia from
bleeding
3. Start empiric broad spectrum IV antibiotics if SEPSIS.
4. Place a cardiac monitor if available.
5. Identification and treatment of the underlying cause.
NOTE
Furosemide (LASILIX®) do not treat ARF, but can be useful if fluid overload or
hyperkalaemia. The use of furosemide is not associated with higher mortality nor with
any reduced mortality.
2.13.2. CHRONIC KIDNEY DISEASE

CKD is defined as progressive and irreversible decline in kidney functions that persists
for ≥ 3 months resulting from structural or functional kidney damage with or without
alteration of GFR. It is necessary to verify chronicity in every suspected case of acute
renal failure.
Criteria for of CKD
GFR < 60 for ≥ 3 months with or without kidney damage + any of the below criteria
a. Anamnestic criteria
- Past history of renal disease
- Previously high creatinine concentration = major confirmatory argument
b. Morphological criteria
- Decreased size of the kidneys = major confirmatory argument
- Ultrasound: < 10cm
- Abdominal X ray: < 3 verterbrae

57
- Ostitis fibrosa (hyperparathyroidism)
c. Biological criteria
- Normochromic normocytic anaemia (HB level < 10g/dl with
- Hypocalcaemia indicating active vitamin D deficiency (calcium level < 8.5

mg/dl) + high parathyroid hormone level
The most commonly used biochemical parameter to estimate GFR is the serum by
using the Cockcroft-Gault equation (See formulary). GFR is then used to stage CKD.
Table 10: Stages of Chronic Kidney Disease
Stage GFR Description

(ml/min/1,73m2)
1 ≥ 90 Kidney damage with normal or increase GFR
2 60 – 89 Kidney damage with mild GFR
3 30 – 59 Moderate GFR
4 15 – 29 Severe GFR
5 < 15 End stage renal disease (ESRD) – Send patient for

dialysis
Indications for renal replacement therapy (RRT) - dialysis
1. When complications arise
- Uremic manifestations (uremic syndrome, encephalopathy, pericarditis, uremic

thrombopathy.
- Severe hyperkalaemia resistant to medical treatment (K > 6 mmol/L).
- Acute pulmonary oedema (sudden decrease in oxygen saturation).
- Severe metabolic acidosis (pH < 7.1).
- Hyponatremia (Na < 120 mEq/l) or hypernatremia (Na > 155mEq/l) resistant
to medical treatment.
2. Anuria (urine < 50 ml/12h).
3. Drug poisoning.
4. Evidence of stage 4 or 5 CKD (ESRD).
58
2.13.3. HYPERKALAEMIA AND CORRECTION
Hyperkalaemia is defined as an elevated level of potassium (K+) in the blood serum >
5.5 mmol/L. High levels of potassium (> 5.5 mmol/L) have been associated with
cardiovascular events (cardiac arrhythmia or sudden cardiac death). It id a common
life-threatening complication of AKI or CKD. Hyperkalaemia can be classified as mild
(5.5-5.9 mmol/L), moderate (6.0-6.4 mmol/L), and severe (>6.5 mmol/L).
Correction of hyperkalaemia
A. Temporal reduction in serum K+ levels
1. Calcium (calcium chloride or calcium gluconate): 10 mL of 10% calcium

chloride or 30 mL of 10% calcium gluconate given IV slowly for over 10
minutes.
NOTE
10 ml of 10% calcium chloride contains 6.8 mmol of calcium while 10 ml of

10% calcium gluconate has only 2.26 mmol of calcium.
2. Insulin / Dextrose combination: Give IV 10-15 units of regular insulin along

with 50 ml of 50% dextrose to prevent the blood sugar from dropping too low.
This drives potassium ions into cells.
3. Salbutamol (albuterol): β2-selective catecholamine administered by nebulizer

(e.g. 10–20 mg)
B. Prolonged reduction in in serum K+ levels
1. Furosemide (LASILIX®): Give 40-80mg of furosemide or 0.5mg/kg in children.
2. Using cation exchange resins. Place a cardiac monitor if available before

beginning administration of a cation exchange resin soon after the other drugs
have been administered.
3. Dialysis
NOTE
Measure potassium levels at 1, 2, 4, 6, and 24 hours after identification and treatment

of hyperkalaemia.
Patient should be referred immediately for haemodialysis if moderate to severe ensue

hyperkalaemia after starting medical treatment.
59
2.14. BURNS: ASSESSMENT AND TREATMENT
A burn is defined as destruction of the human skin due to the effect of a number of
physical or chemical agents; the most common of these agents is temperature. Some
recent analysis have demonstrated that more than 90% of burns are preventable by
simple common sense measures; thus, as a public health issue, the management of burn
injury must comprise education about simple measures that can help prevent this type
of injury.
Classification of burns: Burns are classified by severity, depth and size.
1. SEVERITY
Table 11: American Burn Association Severity Classification
Minor Moderate Major
Adult <10% TBSA Adult 10–20% TBSA Adult >20% TBSA
Young or old < 5% Young or old 5–10% Young or old >10% TBSA
TBSA TBSA
<2% full thickness 2–5% full thickness burn >5% full thickness burn
burn
High voltage injury High voltage burn
Possible inhalation injury Known inhalation injury
Circumferential burn Significant burn to face, joints, hands or
feet
Other health problems Associated injuries
2. DEPTH
Table 12: Classification of burns by depth
Degree of burn Description
First degree burn - Involves only the epidermis
- No blisters are formed
- Very painful
- Healing in 1 week e.g. sunburn
Second degree burn - Includes the superficial layer of the dermis
- superficial - Painful
dermal
- It typically forms blisters
- Healing within 3 weeks
- Deep dermal - Includes the reticular layers of the dermis
- It also forms blisters, but when removed, the wound is white,
60
indicating little or no blood flow
- Wound still heals spontaneously in 3 to 9 weeks
Third degree burns (full - It involves the whole dermis

thickness)
- Heals by retraction or by skin grafting
- May display blisters
- There is little pain
- There is eschar formation
Fourth degree - It destroys all the skin layers and involves the sub-cutaneous
fat and other underlying structures
- There is carbonization.
3. SIZE
The total burned surface area is usually estimated using the WALLACE RULE OF
NINE: where each upper extremity accounts for 9% of TBSA; each lower extremity
accounts for 18%; the anterior and posterior trunk each account for 18%; the head and
neck account for 9% and the perineum for 1%. Treatment plans and the need for
referral to a burn centre are based on the percentage of burned body surface.
NOTE
The palm size represents over 1% of TBSA.
61
Determination of the volume IV fluid to be given in a burn case: The Parkland

formula
The Parkland formula is used to estimate the amount of replacement fluid required for
the first 24 hours in a burn patient so as to ensure they remain hemodynamically stable.
Volume (ml) = 4 x [Weight in kg] [percentage burnt BSA]
The first half of this amount is delivered within 8 hours from the burn incident, and the
remaining fluid is delivered in the next 16 hours.
Approach to patients with burns
1. Determine the severity (size and depth).
2. Start IV fluids resuscitation with Ringers Lactate solution and encourage patient
to drink lots of fluids.
Determine the amount of fluid to give in 24 hours using the Parkland formula.
Cross match and transfuse whole blood in patients with severe anaemia.
3. Give high concentration oxygen (100%) at 5L/minute where inhalation of smoke

has occurred.
4. Pain control:
For mild to moderate burns give paracetamol at 15mg/kg
For severe burns use Morphine
- Adults: 10mg start dose IV, IM, SC
- Paediatric: <2 years : 100 – 200micrograms/kg SC or IM
>2years: 200micrograms/kg SC or IM OR
- Pethidine IM at 100mg 4 hourly, Children: 2mg/kg 4 hourly

62
5. Start antibiotics therapy if signs of super-infection.
6. Give tetanus prophylaxis at ATS 1500 IU SC
7. Clean and irrigate wounds with normal saline and cover with petroleum jelly
(VASELINE®) gauze. Apply ointments such as VASELINE® to soften eschars
and debride.
8. Escharotomy is done in circumferential burns to avoid compartment syndrome.
Criteria for transfer/referral to a burn centre
1. Any partial thickness burn larger than 20% of TBSA in a patient of any age or
larger than 10% of TBSA in children younger than 10 years or adults older than
50 years.
2. Third degree burns covering more than 5% TBSA.
3. Second or third degree burns involving critical areas (e.g. hands, feet, face,
perineum, genitalia, and major joints).
4. Burns with associated inhalation injury.
5. Electrical or lightening burns.
6. Severe burns complicated by coexisting trauma – if traumatic injuries pose high

risk to the patient than the burn injuries, the trauma should be handled with
priority.
7. Chemical burns with threat of cosmetic or functional compromise.
8. Circumferential burns on the extremities or the chest.
NOTE
Do not break blisters. All burns due to hot liquids or steam should be washes with
clean tap water immediately they happened ad left under for 10 – 15 minutes.
Do not give NSAIDS to burnt patients.
63
2.15. SNAKE BITE AND ENVENOMATION
Snake-bite is an important medical emergency, and a well-known occupational hazard
amongst farmers, plantation workers, and other outdoor workers that results in much
morbidity and mortality throughout the world. Early recognition and treatment of
snake bites prior to development of complications generally results in very good
outcomes with most patients being discharged from hospital within 12-48 hours.
Initial evaluation of patients with snake bite
- Begin with the assessment of the airway, breathing, circulatory status, and
consciousness.
- Evaluate for signs of systemic and local envenomation. The bite site should be
examined for signs of local envenomation (oedema, petechiae, bullae, oozing
from the wound, etc) and for the extent of swelling.
- The circumference of the bitten limb should be measured every 15 min

thereafter, until the swelling is no longer progressing. Serial measurement of
circumference helps in estimating spread of venom and effect of anti-venom.
- The extremity should be placed in a well-padded splint for at least 24 hours.
- Lymph nodes draining the limb should be palpated and the presence of
lymphangitic lines noted.
- Distal pulses should be checked and monitored if there is presence of gross

swelling. This will help identify a compartment syndrome.
Laboratory work-up
Although lab tests are of little value in the diagnosis of snake envenomation, they are
useful for prognosticating and for making decisions about specific interventions
- 20-min whole blood clotting test (20 WBCT): The 20 WBCT is a simple bedside
test of coagulopathy to diagnose viper envenomation and rule out elapid bite.
Cobras or kraits do not cause antihemostatic symptoms.
- Serum creatinine: This is necessary to rule out renal failure after viper and sea
snake bite.
- Serum amylase and creatinine phosphokinase: Elevated levels of these markers

suggests muscle damage.
- Prothrombin time (PT) or INR and activated partial thromboplastin time (aPTT):
Prolongation may be present in viper bite.
- Urine examination: Can reveal haematuria, proteinuria, haemoglobinuria, or

myoglobinuria.
64
- Electrocardiogram (ECG): Nonspecific ECG changes such as bradycardia and
atrioventricular block with ST-T changes may be seen.
Approach to a patient beaten by a snake
1. Urgent resuscitation will be needed in those in shock (anaphylaxis or

cardiovascular toxicity), those with respiratory failure (neurotoxin), and in those
who have had cardiac arrest (due to hypoxia, cardiac toxicity, or hyperkalaemia
from rhabdomyolysis). Use the ABCDE of resuscitation.
2. Determine if there is envenomation and the severity of envenomation and

administer anti-venom if there is envenomation. Oxygen should be administered
to every envenomed patient.
3. A large-bore IV catheter should be inserted and bolus of normal saline or

Ringer's lactate should be given to all patients with suspected envenomation.
4. The first blood drawn from the patient should be typed and cross-matched, as the
effects of both venom and anti-venom can interfere with later cross-matching.
5. Monitor: Measure circumference of the affected limb below and 12 cm above

bite site every 20 min until oedema subsides mark the advancing edge, WBCT 2
hours after the end of infusion then every 4 hours
6. Tetanus prophylaxis should be given, ATS 1500IU.
7. Reassure the victim (Immobilize the affected limb by bandage or clothes to hold
splint, but tight arterial compression is not recommended)
NOTE
Observation in the emergency department for 8-10 hours may be needed for dry bites
to ensure no of progression of symptoms. The use of black stone has no effective
control of poison.
65
2.15.1. SNAKE ENVENOMATION
This is the process by which venom is injected into the body following snake bite.
Diagnosing snake envenomation is a crucial step in determining if anti-venom is to be
administered. Over 70% of all snake bites are by non-venomous snakes and 50% of
bites by venomous species are dry bites (no envenomation or venom not injected into
the system).
Table 13: Assessment of severity of envenomation
No envenomation Absence of local or systemic reactions; fang marks present or absent (+/−)
Mild Fang marks (+), moderate pain, minimal local oedema (0–15 cm), erythema
envenomation (+), ecchymosis (+/−), no systemic reactions
Fang marks (+), severe pain, moderate local oedema (15–30 cm), erythema and
Moderate
ecchymosis (+), systemic weakness, sweating, syncope, nausea, vomiting,
envenomation
anaemia, or thrombocytopenia
Fang marks (+), severe pain, severe local oedema (>30 cm), erythema and
Severe
ecchymosis (+), hypotension, paraesthesia, coma, pulmonary oedema,
envenomation
respiratory failure
Clues for severe snake envenomation
- Snake identified is a very venomous species (cobra, python, mamba, water

snake, etc.).
- Rapid early extension of local swelling from the site of the bite.
- Early tender enlargement of local lymph nodes, indicating spread of venom in

the lymphatic system.
- Early systemic symptoms (dyspnoea, altered level of consciousness, coma,

hypotension).
- Early spontaneous systemic bleeding (especially bleeding from the gums).

Passage of dark brown urine.
2.15.2. ANTI-VENOM THERAPY

Give immunotherapy/anti-venom if envenomation or abnormal WBCT
- FAV®-Afrique over 1 hour (2 amp in 500 ml of normal saline) if edema,

abnormal coagulation test and no bleeding
- FAV®-Afrique over 5 minutes (2 amp) if trismus, ptosis, dyspnea, persistent

local bleeding, spontaneous bleeding
- In both cases: repeat if persistent clinical abnormalities or coagulation test after 2

hours and 6 hours
66
2.16. ASSAULT/ BATTERY AND RAPE
An assault is defined as the attempt to initiate harmful or offensive contact with a
person, or a threat to do so.
Battery refers to the actual achievement of such contact. It is both a crime and a tort
and, therefore, may result in either criminal and/or civil liability. Corporal punishment
administered to children by their parent or legal guardian is not legally considered to
be assault unless it is deemed to be excessive or unreasonable.
Sexual assault or rape is defined as having sexual intercourse or other forms of sexual
penetration with a person without that person's consent. The act may be carried out by
physical force, coercion, abuse of authority, or against a person who is incapable of
giving valid consent, such as one who is unconscious, incapacitated, has an intellectual
disability or is below the legal age of consent (<16 years). Rape is a crime and requires
a medico-legal certificate after hospital discharge for patients who want to pursue
justice.
Complications of sexual assault
- Patient can acquire infections - Addiction to sexual intercourse

(HIV, hepatitis B/C etc.)
- Battery
- Patient can become pregnant
- Major depressive disorder,
- Posttraumatic stress disorder contemplate suicide and other
psychopathologies
Approach to rape victims
1. Prevention of unwanted pregnancy: Emergency contraceptive medications are

offered to women raped by men because about 5% of such rapes result in
pregnancy.
Dose: Levonorgestrel 1.5mg taken as soon as possible within 48 hours of

exposure.
NOTE
The TSSF as part of the catholic faith do not accept interception of procreation
for whatever reason, therefore this method is not permitted in their health system.
2. Prevention of HIV: Post Exposure Prophylaxis to HIV most be initiated as soon

as possible within 48 hours after exposure. PEP is given for 30days.
NOTE
Victim most be tested for HIV prior to commencing PEP. PEP is not effective in
victims presenting after 72 hours.
67
3. Work-up: Blood serum is collected to test for STIs (such as HIV, hepatitis B and
syphilis). A high vaginal swab and examination may indicate spermatozoa
confirming a doubted rape case. After collecting HVS, the vagina can be washed
with antiseptics.
4. Preventative medication against sexually transmitted infections are given to all

victims of all types of sexual assault (especially for the most common diseases
like chlamydia, gonorrhoea, trichomoniasis and bacterial vaginosis).
5. Any survivor with abrasions are immunized for tetanus if 5 years have elapsed
since the last immunization. Human tetanus immunoglobulin (Anti-Tetanus
Serum) 1500 IU given SC.
6. Short-term treatment with a benzodiazepine may help with acute anxiety and
antidepressants may be helpful for symptoms of posttraumatic stress disorder,
depression and panic attacks.
7. Counselling: this includes trauma counselling, crisis prevention, HIV pre and
post-counselling and PEP adherence counselling.
68
2.17. HYSTERIA/ CONVERSION DISORDER
Hysteria is a common medical diagnosis reserved exclusively for women. Hysteria is
no longer recognized by many medical authorities as a medical condition.
Conversion Hysteria: One type is the conversion disorder, in which a patient usually
complains of a physical illness that has no medical cause. The other type is the
dissociative disorder, in which the patient experiences interruptions in his memory,
consciousness, and his awareness of his surroundings. Both types are said to have a
common cause: a repressed or suppressed psychological or emotional experience that
manifests itself in a physical manner
Symptoms: anxiety, shortness of breath, fainting, insomnia, irritability, nervousness,

as well as sexually forward behaviour.
Some of the common symptoms are mentioned below:
- Partial paralysis - Palpitations
- Temporary blindness or tunnel - Feeling of a foreign body

vision. lodged in the throat
- Sensory disturbances like - Swelling of the neck

heightened sense of sight, smell,
touch and taste. - Suffocation
- Involuntary movements like - Headache

eyeball rolling inwards
- Clenched teeth
contracted facial muscles.
- Generalized and voluntary
- Abnormal muscle contractions
tensing of muscles of
causing person to have
locomotion
unnatural positions, for e.g. the
leg may be folded backwards. - Loss of consciousness
Heaviness in the limbs
- Violent and tumultuous
- Severe cramps heartbeats
- Strong feeling of ascending - Weakness
abdominal constriction
- No willpower
- Continual sighing
- Tendency towards emotional
- Difficulty in breathing instability
- Constriction in the chest
69
Approach to patients with hysteria
1. Psychotherapy: Identifying the psychological challenge that prompted the

patient to manifest physical and counselling the patient is the main stay of
treatment. Psychotherapy is useful in encouraging the person to go through life’s
challenges with a positive attitude. It helps the patient understand what helps
them feel positive, as well as accepting their strong and weak points.
2. Antidepressants or anxiolytics should be given if depression or anxiety co-exists.
3. Analgesia: Give to relieve backache, body ache and headache. Conversion

disorder often co-exist with stress induced gastritis, so patient may need to take
PPI and antimuscarinics.
4. Exclude other medical conditions: Routine investigations like blood, urine and
stool tests as well as X-rays etc.
5. Ideally, patient needs to try to get walking to help stimulate blood flow, improve
breathing, and create natural distractions that come from the sensations of
walking.
70
2.18. SICKLE CELL CRISES
Sickle cell disease may present either in steady state crises or with complications.
Irreversibly sickled cells have a shortened survival and plug vessels in the
microcirculation resulting in a number of acute syndromes, termed ‘crises’, and
chronic organ damages.
These syndromes include:
- Painful vaso-occlusive crisis - Sequestration crisis
- Acute chest syndrome - Aplastic crisis
Factors that precipitate/trigger sickle cell crises
- Infection (e.g. malaria, - Acidosis

pneumonia, cellulitis, sepsis,
osteomyelitis) - Exposure to extremes of
weather.
- Hypoxia
- Dehydration
Causes of acute severe anemia in sickle cell patients
- Malaria will cause massive hemolysis: fever, haemoglobinuria, and jaundice
- Splenic sequestration (trapping of blood cells in the spleen) mostly in children 1

– 4 years: Presents with sudden enlargement of the spleen, left upper quadrant
pain, thrombocytopenia and circulatory collapse. Recurrent sickling in the spleen
in childhood results in infarction and adults may have no functional spleen. In
adults, the liver may undergo sequestration with severe pain due to capsular
stretching.
- Aplastic crisis: transient suspension of RBC production by the bone marrow
Follow-up of patients with SCD
1. Use daily oral prophylactic penicillin for children below the age of 5 years.
Begin at 2months with 125mg BID of penicillin V or G and at 3 years, increase
dose to 250mg BID. Prompt treatment of all infections in adult patients using
broad spectrum antibiotics.
2. Give oral folic acid supplement daily at the following doses
- 0 – 6 months: 0.1mg/day
- 6 months – 1 years: 0.25mg/day
- 1 – 2 years: 0.5mg/day
- >2 years: 1mg/day
71
NOTE
There may be a co-existing iron deficiency, in case of anemia in SCD.
3. Counselling of the family and education on the care of patients with SCD.
4. Education of the patient on identifying trigger factors. Patient should generally

avoid vigorous activities.
5. Frequency of visits in the hospital may depend greatly on the patient’s clinical
status. Follow-up should be every 3 months for patients with normal symptoms.
6. Vaccination against S. pneumoniae, meningococcus, haemophilus influenzae B,

hepatitis B and seasonal influenza.
2.18.1. VASO-OCCLUSIVE CRISIS OR PAIN CRISIS

This is the most common manifestation of sickle cell disease. It results from plugging
of small vessels in the bone producing acute severe bone pain. This affects areas of
active marrow: the hands and feet in children under 2 years (so-called dactylitis) or the
femora, humeri, ribs, pelvis and vertebrae in adults.
Severity
- Fever > 39° C - Acute abdominal pain
- Shock - Respiratory signs: chest pain,

dyspnea, cough,
- Limb weakness or alteration of
consciousness - Symptomatic anemia
Approach to patients with vaso-occlusive crisis
1. Analgesic: Manage as severe pain using paracetamol + NSAIDs + opioids
- Paracetamol 1g IV given 6 – 8 hourly or 15mg/kg
- NSAIDs
 IM or oral diclofenac 3mg/kg/day in 3 divided doses
 Ibuprofen 7.5 mg/kg every 6-8 hours
 Ketoprofen (PROFENID®) 100 mg IM q12 hours (if no abdominal

pain, if no infection or dehydration)
- Opioids
 Tramadol 100 mg IM/IV 12 hourly
 Morphine (oral or rectal)
72
6-12 months: 200micrograms/kg/4hours
1-12 years: 300micrograms/kg/4 hours
>12 years: 5 – 10 mg/ 4 hours
NOTE
- Tramadol is contraindicated to children below 12 years.
- Do not underestimate the patient’s pain. Failure to treat acute pain aggressively
and promptly will lead to chronic pain syndrome.
- Control of acute pain is best achieved with opioids. Morphine is the drug of
choice.
2. Vigorous hydration
- Ringers lactate or dextrose-saline or normal saline: 100 – 150ml/kg/day in

children and 50ml/kg/day in adults (i.e. 4 liters daily for an average size adult)
3. Anxiety
- Hydroxyzine (ATARAX®) 25 mg BID OR
- Mexazolam (MELEX®, TEMESTA®) 0.5 - 1mg BID or TID (For elderly

patients maximum dose is 0.5mg)
4. Transfuse patient if hemoglobin < 5g/dl or fall > 2 g/dl under patient’s baseline
level.
5. Oxygenation if oxygen saturation falls below 90%.
6. Identify the precipitating/trigger factors and treat.
7. Urgent work-up: Full blood count, CRP, MP, urinalysis.
8. Counsel the patient and family. Complications are prevented by appropriate

education of patient and family.
NOTE
All patients with sickle-cell disease should receive prophylaxis with daily folic acid,
and penicillin V to protect against pneumococcal infection, which may be lethal in the
presence of hyposplenism. Splenectomy is contraindicated in sickle cell patients.
73
2.19. ACUTE UPPER AIRWAY OBSTRUCTION
Complete upper airway obstruction is a rapidly deathly condition and warrants
emergency interventions.
Causes
- Foreign body aspiration - Burns
- Trauma - Infections (croup, epiglottitis,

tracheitis)
- Anaphylaxis
Management of foreign body aspiration
 Children over 1 year and adults: Perform the Heimlich manoeuvre.
Heimlich manoeuvre is includes abdominal thrusts provided by a rescuer

standing behind the patient and using his hands to exert pressure on the bottom
of the diaphragm. This compresses the lungs and exerts pressure on any object
lodged in the trachea, and hopefully expelling it.
 Children under 1 year: Place the infant face down across the forearm, support
the infant’s head with the hand. With heel of the other hand, perform one to five
slaps on the back, between shoulder plates. If unsuccessful, turn the infant on
their back. Perform five forceful sternal compressions as in cardiopulmonary
resuscitation: use 2 or 3 fingers in the centre of the chest just below the nipples.
Press down approximately one third the depth of the chest.
 Refer the patient to an ENT surgeon if the Heimlich manoeuvre fails to expel the
foreign body for bronchoscopy.
NOTE
Perform manoeuvres to relieve obstruction only if the patient cannot speak or cough or
emit any sound. Foreign body aspiration is most frequently seen in a children from 6
months to 5 years of age playing with a small objects or during eating.
74
2.20. ACUTE POISONING
The following are possible causes for acute poisoning
- Accidental ingestion of household products (household cleaners). The

following are neurotoxic chemicals are commonly found in household cleaners:
chlorine (dishwasher detergents), ammonia (antibacterial cleaning agents),
petroleum (dish soaps, laundry detergents, floor waxes).
- Medication errors or mix-ups. This happens most often to elderly people.

Sometimes it is hospital staff that makes the error; at other times, it is the patient
who gets confused about the identity or dosage of the drugs. Medicines are one
of the most common causes of accidental and intentional (suicide) poisonings.
Drugs most commonly involved are aspirins, acetaminophen, sedatives, any
psychoactive drug where a patient is more prone to impulsive, suicidal action
(e.g. antidepressants), anti-seizure drugs, iron pills, vitamins/mineral
supplements containing iron, and cardiac drugs, such as digoxin and quinidine.
- Excessive alcohol or drug abuse.
- Traditional medicines can also be a source of poisoning.
Assessing poisoned cases
- Obtain full details on the amount ingested and time the poison was ingested.
- Identify exact agents involved.
- Check for signs of burns in or around the mouth or of stridor which suggest
ingestion of corrosives. Corrosives can cause oesophageal burns, which may not
be immediately apparent.
- Petroleum products, if aspirated into the lungs, can cause pulmonary oedema,
which may take some hours to develop.
Approach to patients with acute chemical poisoning
Treatment is most effective if given as quickly as possible after the poisoning event,
ideally within 1 hour.
1. Primary resuscitation: airway, breathing, circulation and level of

consciousness. Some poisons depress breathing, cause shock or induce coma.
Administer oxygen if respiratory distress, cyanosed or saturation ≤ 90%. Set a
cardiac monitor.
2. Identity of the poison and give a specific antidote if this is indicated: If is

known to the patient or the parents of the affected child. The role of the
physician is to determine what treatment (if any) is necessary based on the
amount of toxic substance ingested, the identity of the chemical and patient's
signs and symptoms.
75
(See table for antidotes)
3. Gastric decontamination: Ingested poisons must be removed from the stomach

by gastric lavage. This is most effective within 1 h of ingestion. After this time,
usually little benefit, except for agents that delay gastric emptying or in patients
who are deeply unconscious. Gastric lavage does not guarantee that all the
substance has been removed, so the patient may still be in danger.
4. IV access and hydration with diuresis: This helps to eliminate the toxins that
have been absorbed already into the system through the kidney. This is only
effective provided the poison is not nephrotoxic.
5. Give activated charcoal: It helps to reduce the absorption of the toxic substance.
Doses
 <1 year = 1g/kg
 1 – 12 years = 25 -50g
 Adolescents and adults = 100g
6. Give a cocktail of antacid, milk and water: This will help to dilute corrosive
agents.
7. Identify and treat severe depression, suicidal attempts: This will include
psychotherapy and use of antidepressants.
8. Urgent work-up: Blood sugar, urea/creatinine, serum electrolytes,
9. Keep the patient under observation for at least 24 hours.
10. Sent for haemodialysis if patients is not responding to medical treatment or the
poison has no available antidote.
NOTE
Never provoke vomiting if the patient has swallowed kerosene, petrol or petrol-based
products; if the patient’s mouth and throat have been burnt or if the patient is drowsy.
This may cause further damage to the mouth, throat, airway, lungs, oesophagus and
stomach. If the patient swallowed bleach or another corrosive, give milk or water to
drink as soon as possible.
Table 14: Some Common Poisons and their Antidotes
Poison Antidote
Paracetamol Oral methionine or IV acetylcysteine
every 4 h for four doses
76
Carbon monoxide 100% Oxygenation
Aspirin and other salicylates IV sodium bicarbonate at 1 mmol/kg over 4 h to correct

acidosis
Vitamin K at 10 mg IM or IV
Iron Give deferoxamine by slow IV infusion: initially 15 mg/kg

per hour. Reduce after 4–6 h so that the total dose does not
exceed 80 mg/kg in 24 h. Maximum dose, 6 g/day.
If deferoxamine is given IM: 50 mg/kg every 6 h.

Maximum dose 6 g/day.
Morphine and other opiates Naloxone IV 10 μg/kg; if no response, give another dose
of 10 μg/kg
If IV route is not feasible, give IM, but action will be

slower
Tricyclic antidepressants: Sodium bicarbonate

amitriptyline
Organophosphates (GAMALIN) Anticholinergic (Atropine)
Digoxin Fab fragments
Beta blockers ( propranolol, Glucagon IV followed by insulin in drip.

atenolol)
Cyanide Nitrites
Sulfuric acid Antacids
Alkali: Sodium hypochlorite (La

Croix®,…), hydrogen peroxide
77
2.21 PALLIATIVE CARE
Palliative care is a multidisciplinary approach provided by a team of physicians,
nurses, physiotherapists, occupational therapists and other health professionals for
people with life-limiting illnesses. It focuses on providing relief from the symptoms,
pain, physical stress, and mental stress of a terminal diagnosis. Palliative care increases
comfort by lessening pain, controlling symptoms, and lessening stress for the patient
and family, and should not be delayed when it is indicated. Palliative care is not
reserved for people in end-of-life care and can improve quality of life for both the
person and their family, decrease depressive symptoms, and increase survival time.
Although it is an important part of end-of-life care, it is not limited to that stage.

Palliative care can be provided across multiple settings including in hospitals, at home,
as part of community palliative care programs, and in skilled nursing facilities.
Medications and treatments are said to have a palliative effect if they relieve symptoms
without having a curative effect on the underlying disease or cause.
Some indications for palliative care
1. Terminal diseases
- End-stage cancers - Advance liver cirrhosis/

chronic liver disease
- End-stage CKD
- AIDS
- End-stage COPD
- Alzheimer's,
2. People with limited ability to care for themselves
- Very elderly people with senile dementia
- Paralysis from trauma, complete spinal cord injury, surgery,
78
SECTION THREE
PROTOCOLS FOR COMMON INFECTIOUS DISEASES
3.1. MALARIA FEVER

Malaria fever present either as simple or severe (complicated). Severe malaria is a
medical emergency which can be identified by the following WHO criteria.
WHO criteria for severe malaria
1. Impaired consciousness: Altered level of consciousness ranging from lethargy to

confusion and delirium to coma not attributable to any other causes.
2. Repeated generalized seizures/convulsions: ≥ 3 convulsions observed within 24

hours.
3. Prostration: Generalized weakness with patient is unable to sit, stand or walk

unsupported.
4. Repeated vomiting.
5. Hyperpyrexia: Core body temperature >40°C.
6. Severe anaemia: Haematocrit <15% or haemoglobin < 50 g/l in the presence of

parasite count >10 000/μl
7. Acute renal failure: Presenting as oliguria or anuria (urine output <400 ml/24
hours in adults or <12 ml/kg/24 hours in children) and/or a serum creatinine>265
μmol/l (> 3.0 mg/dl) despite adequate volume repletion.
8. Macroscopic haemoglobinuria: This results from haemolysis and often referred

to as black water fever (seen clinically by coca-cola urine).
9. Hypoglycaemia: Whole blood glucose concentration <2.2 mmol/l (<40 mg/dl).
10. Hyperbilirubinemia: Total bilirubin >43 μmol/l (> 2.5 mg/dl) seen clinically by
jaundice.
11. Abnormal bleeding and/or disseminated intravascular coagulation: Spontaneous

bleeding from gums, nose, gastrointestinal tract, or laboratory evidence of
disseminated intravascular coagulation.
12. Pulmonary oedema and acute respiratory distress syndrome (ARDS): The acute
lung injury score is calculated on the basis of radiographic densities, severity of
hypoxemia, and positive end-expiratory pressure.
13. Circulatory collapse (algid malaria): Systolic blood pressure <70 mmHg in
patients > 5 years of age (< 50 mmHg in children aged 1–5 years), with cold
clammy skin or a core-skin temperature difference >10°C.
79
14. Academia/acidosis: Arterial pH <7.25 or acidosis (plasma bicarbonate < 15
mmol/l).
15. Hyperparasitemia: ≥ 5% parasitized erythrocytes or ≥ 250 000 trophozoites/μl (in

non-immune individuals).
Management for severe malaria
The treatment of severe malaria is put in place in one of the following situations:
1. Existence of one or several signs of severity
2. Worsening symptoms in a patient on oral treatment
3. Malaria in pregnancy
Treatment Protocols
A. Artesunate protocol (MALACEF®) (ampoule = 60 mg)
First day: Artesunate 2.4 mg/kg IV or IM given on admission at 0h, 12 h, 24 h
Subsequent days: then continue with daily 2.4mg/kg dose for a maximum of 7
days or until the patient is able to take oral medication, then continue with 3 days
ACT.
B. Quinine Protocol (ampoule = 300mg)
Loading dose: 20mg/kg given IV in 250 – 500ml of glucose 5% or 10% and

electrolytes to be given in 4 hours.
Maintenance dose: 10 mg/kg hours every 8 hours
Switch to oral quinine when the patient is able to take drugs orally to make up
treatment duration of 7 days.
C. Artemether protocol (PALUTHER®) (ampoule = 80mg)
First day: Adult: 160mg, children: 3.2 mg/kg given IM as a single dose or in two
divided doses
Subsequent days: Adult: 80mg, Children 1.6 mg/kg daily for four days
Switch to ACT for additional 3 days.
Symptomatic treatment
3. Antipyretics: As per protocol under management of acute fever.
4. Antiemetics: Metopimazine or metoclopramide 10 mg IM/IV q12 hourly or PRN

if patient is vomiting.
80
5. Anticonvulsants: Diazepam 0.2 mg/kg intravenously (if ongoing seizure) or as
per protocol under seizures and status epilepticus.
6. Give a bolus of normal saline or Ringer’s lactate 1 litre IV if SBP < 90 mmHg
Management uncomplicated (simple) malaria
1. Artimisimin based combination therapy (ACT) should be used for 3 days or oral
quinine for 7days.
2. Paracetamol 1g 8 hourly or 15mg/kg 8hourly.
NOTE
- Do not administer the loading dose if the patient is a pregnant woman or has
taken quinine within the last 24hrs or mefloquine within the past 7 days or is a
failure patient.
- Arthemeter and artesunate are not use for treatment of malaria in the first
trimester of pregnancy.
81
82
3.2. MENINGITIS
Meningitis is an acute infection and inflammation of the protective membranes
covering the brain and spinal cord, known collectively meninges. It is a medical
emergency.
Symptoms
- Fever, headache, and meningism (neck stiffness, inability to tolerate light

(photophobia) or loud noises (phonophobia)). This is called the triad of
meningitis and occurs in over 90% of all cases.
- Altered level of consciousness ranging from confusion to coma
- Seizures
- Vomiting
- Young children often exhibit only nonspecific symptoms, such as irritability,

drowsiness, or poor feeding
Signs
- Nuchal rigidity occurs in 70%
- Presence of Kernig's sign: Kernig's sign is assessed with the person lying supine,
with the hip and knee flexed to 90 degrees. In a person with a positive Kernig's
sign, pain limits passive extension of the knee.
- Brudziński sign. A positive Brudzinski's sign occurs when flexion of the neck
causes involuntary flexion of the knee and hip
Work-up
- FBC
- Cerebrospinal fluid (CSF) analysis and culture
- Thick and thin blood film for MP
Table 15: CSF findings in different forms of meningitis

Type of Glucose Protein Cells
meningitis
Acute bacterial Low high PMNs,
often > 300/mm³
Acute viral normal normal or high mononuclear,
< 300/mm³
Tuberculous Low high mononuclear and
PMNs, < 300/mm³
Fungal Low high < 300/mm³
Malignant Low high usually
83
mononuclear
Management
1. Antibiotics:
- Ceftriaxone IV or deep IM
Adults: 2 mg given twice daily for 7 – 10 days
Children < 12years: 80 – 100mg/kg twice daily for 10 – 14 days
Neonates: 100mg/kg daily for 14days
Alternatively
- Ampicillin IV
Adults: 1 – 2 g given 6 hourly for 14days
Children: 200mg/kg/day in 3-4 divided doses
PLUS
- Chloramphenicol IV
Adult: 1g 6 hourly for 14days
Children: 25mg/kg given 6 hourly for 14days
2. IV steroids: Dexamethasone 4 -10 mg given 6 hourly for 5 days.
Children: 0.15 mg/kg 4 times daily for 5 days NB:
NOTE
Dexamethasone started together or before antibiotics reduces the sequelae of

hearing loss and death from meningitis.
3. Insert IV line and urinary catheter and monitor fluid input and output.
4. Control symptoms like fever, headache with IV paracetamol.
84
3.3. TYPHOID FEVER
Typhoid or enteric fever, also known simply as typhoid, is a bacterial infection due to
Salmonella typhi or S. paratyphi. Humans are the only known reservoirs of Salmonella
typhosa.
Signs and symptoms
Classically, the course of untreated typhoid fever is divided into four distinct stages,
each lasting over weeks.
First week
- Slow rise in body temperature
- Faget sign (temperature pulse dissociation): Fever fluctuations are seen with
relative bradycardia
- Malaise, headache
- Epistaxis
- Abdominal pain
Second week
- Prostration
- High fever in plateau around 40 °C and bradycardia (sphygmothermic

dissociation or Faget sign), classically with a dicrotic pulse wave
- Delirium is frequent, often calm, but sometimes agitated. This delirium gives to
typhoid the nickname of "nervous fever"
- Rose spots. (Not easily seen in dark skin people)
- Diarrhoea can occur in this stage: pea soup stool with a characteristic smell
- Hepatosplenomegaly
(The major symptom of this fever is that the fever usually rises in the afternoon up to
the first and second week.)
Third week (week of complications)
- Intestinal haemorrhage due to bleeding in congested Peyer's patches
- Intestinal perforation in the distal ileum
- Encephalitis
- Metastatic abscesses, cholecystitis, endocarditis, and osteitis
85
- Neuropsychiatric symptoms (described as "muttering delirium" or "coma vigil"),
with picking at bedclothes or imaginary objects.
- Platelet count goes down slowly and risk of bleeding rises.
- Dehydration ensues, and the patient is delirious (typhoid state)
- One-third of affected individuals develop a macular rash on the trunk.
Workup
1. Cultures: stool, blood and urine
2. Typhidot ELISA test (detects IgM and IgG antibodies)
3. Widal serological test. Due to the poor sensitivity and specificity of Widal test, it
is no longer used in TSST-HB.
Treatment
1. Antibiotics
- Flouroquinolones: Adult: 2 – 4 g daily in two

Ciprofloxacin divided doses
Orally: 500mg given 12 hourly Children: 100mg/kg per day

for 10days
Alternatively
IV: 200mg 12 hourly in
critically ill patients. - Azithromycin
- Third generation Adult: 500mg daily for 7 days

cephalosporins: Ceftriaxone
Children: 10 – 20 mg/kg daily x
7days
3.3.1. CHRONIC TYPHOID CARRIER

Over 3% of patients infected with typhoid fever become chronic carriers. This chronic,
asymptomatic carrier state is thought to be a key feature of continued maintenance of
the bacterium within human populations. Humans carries S. typhi in the gall bladder or
the biliary tree. The Typhoid Mary is the term used to describe an asymptomatic
chronic carrier who moves around infecting others. Chronic typhoid carriage state is
detected through serial stool and urine cultures.
Eradication of the carrier stage: May require treatment with one or two antibiotics
for over period of 4 – 6 weeks.
Adult: Amoxicillin 1g 8hourly
Children: Amoxicillin 250 – 500mg 8 hourly
86
NOTE
When antibiotics fail to eradicate hepatobiliary carriage, the gallbladder should be

resected, although cholecystectomy is not also always successful in eradicating the
carrier state.
87
3.4. VIRAL HEPATITIS
(World Hepatitis Day, observed July 28, aims to raise global awareness of hepatitis B
and hepatitis C and encourage prevention, diagnosis, and treatment)
Most commonly encountered will be the chronic forms: Hepatitis B and C viral
infections.
Hepatitis B infection
Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that affects
the liver. It can cause both acute and chronic infections. In those who get infected
around the time of birth 90% develop chronic hepatitis B while less than 10% of those
infected after the age of five do.
Many people have no symptoms during the initial infection. Some develop a rapid
onset of sickness with vomiting, yellowish skin, tiredness, dark urine and abdominal
pain
Most of those with chronic disease have no symptoms; however, cirrhosis and liver
cancer may eventually develop. These complications result in the death of 15 to 25%
of those with chronic disease. Hepatitis B virus DNA persists in the body after
infection, and in some people the disease recurs. Although rare, reactivation is seen
most often following alcohol or drug use or reactivation can occur spontaneously.
Approximately 50% of overt carriers experience acute reactivation. The risk of
reactivation varies depending on the serological profile; those with detectable HBsAg
in their blood are at the greatest risk, but those with only antibodies to the core antigen
are also at risk. Treatment with prophylactic antiviral drugs can prevent the serious
morbidity associated with HBV disease reactivation.
Complications of chronic hepatitis
- Acute liver failure
- Liver cirrhosis
- Hepatocellular carcinoma
Management of hepatitis B and C in Cameroon
Acute hepatitis B infection does not usually require treatment and in most adults, the
infection clears up spontaneously. However, over 10% will require to be referred to a
treatment centre for proper treatment by a HEPATO-GASTRO-ENTEROLOGIST.
Because of the high cost and rarity of treatment for hepatitis B and C, the Cameroon
government have created 5 treatment centres with subsidized treatment: Douala
General Hospital, Yaoundé General Hospital, Yaoundé Central Hospital, Centre
Hospitalier Universitaire de Yaoundé (CHU) and Hopital Laquintinie de Douala.
Patients should be well counselled on the treatment modalities including the cost of
treatment before referral to the treatment centre. The treatment protocols and duration
88
of treatment depends on the state of the patient and the viral genotype isolated and can
last for more than 6 months. The drugs used have been heavily subsidised by the
government and the cost still ranges from 384,000 – 760,000 FCFA even with the
subsidized rate. This cost excludes the cost of pre-therapeutic work-up which can be as
high a 350,000 FCFA.
Table 16: Drugs used for the treatments for hepatitis B and C in Cameroon and their
recent costs
Drugs for hepatitis C for a month
Sofosbuvir 400mg + Ledipasvir 90mg ( 28caps) 120.000 FCFA
Sofosbuvir 400mg (28caps) + Ribavirine 200mg (168 caps) 100.00 FCFA
Ribavirine 200mg (168 caps) 20.000 FCFA
Drugs for hepatitis B and D
Tenofovir 300mg + Emtricitabine 200mg (30caps) 3.500 FCFA
Tenofovir 300mg (30caps) 3.000 FCFA
Lamivudine 150mg (30caps) 2.500 FCFA
Interferon alpha 180 micrograms (one ampoule injectable) 50.000 FCFA
89
3.5. HIV RELATED OPPORTUNISTIC INFECTIONS
Table 17: WHO clinical staging of HIV disease in adults, adolescents
Clinical stage 1
- Asymptomatic
- Persistent generalized lymphadenopathy
Clinical stage 2
- Moderate unexplained weight loss (<10% of presumed or measured body weight)
- Recurrent respiratory tract infections (sinusitis, tonsillitis, otitis media, pharyngitis)
- Herpes zoster
- Angular cheilitis
- Recurrent oral ulceration
- Papular pruritic eruption
- Fungal nail infections
- Seborrhoeic dermatitis
Clinical stage 3
- Unexplained severe weight loss (>10% of presumed or measured body weight)
- Unexplained chronic diarrhoea for longer than 1 month
- Unexplained persistent fever (intermittent or constant for longer than 1 month)
- Persistent oral candidiasis
- Oral hairy leukoplakia
- Pulmonary tuberculosis
- Severe bacterial infections (such as pneumonia, empyema, pyomyositis, bone or joint

infection, meningitis, bacteraemia)
- Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis
- Unexplained anaemia (<8 g/dl), neutropaenia (<0.5 × 109/L) and/or chronic

thrombocytopaenia (<50 × 109/L)
Clinical stage 4
- HIV wasting syndrome
- Pneumocystis (jirovecii) pneumonia
90
- Recurrent severe bacterial pneumonia
- Chronic herpes simplex infection (orolabial, genital or anorectal of more than one
month in duration or visceral at any site)
- Oesophageal candidiasis (or candidiasis of trachea, bronchi or lungs)
- Extrapulmonary tuberculosis
- Kaposi sarcoma
- Cytomegalovirus infection (retinitis or infection of other organs)
- Central nervous system toxoplasmosis
- HIV encephalopathy
- Extrapulmonary cryptococcosis, including meningitis
- Disseminated non-tuberculous mycobacterial infection
- Progressive multifocal leukoencephalopathy
- Chronic cryptosporidiosis
- Chronic isosporiasis
- Disseminated mycosis (extrapulmonary histoplasmosis, coccidioidomycosis)
- Lymphoma (cerebral or B-cell non-Hodgkin)
- Symptomatic HIV-associated nephropathy or cardiomyopathy
- Recurrent septicaemia (including nontyphoidal Salmonella)
- Invasive cervical carcinoma
- Atypical disseminated leishmaniasis
91
3.5.1. CNS CRYPTOCOCCOSIS IN HIV
Cryptococcosis is the most common fungal infection of the central nervous system in
HIV patients and often presents as meningitis, meningoencephalitis or as a space
occupying lesion.
Investigations
CSF analysis with Indian ink stain will reveal the fungus Cryptococcus neoformans.
Management
1. Fluconazole 1200mg/day in 4 divided doses for 2 weeks
Then
Fluconazole 400mg daily for 8 weeks (2 months)
Then
Fluconazole 200mg daily until sustained immune reconstitution
2. Dexamethasone:
Initial dose: 10mg given IV
Maintenance dose: 4mg q6hrs until clinical improvement.
May reduce after 5 days and gradually discontinue.
3. Symptomatic management of fever, severe headache…
NOTE
If patient is unconscious, insert a nasogastric tube and pass drugs using it.
92
3.5.2. CNS TOXOPLASMOSIS
Typical presentation is that of a patient suffering from HIV/AIDS with a low CD4
count presenting with seizures and headache to the ED, where he/she had a computed
tomography (CT) scan of the head showing characteristic ring enhancing lesions.
Clinical manifestations
- Low grade fever, headache - Lethargy
- Seizures - Focal neurological deficits
- Confusion - Chorio-retinitis: altered vision,

moving objects
- Ataxia
Investigations
- CT scan of the brain with contrast will reveal ring enhanced lesions
- Tissue biopsy reveals toxoplasma gondi
NOTE
Toxoplasma serology has a low sensitivity for the diagnosis of cerebral toxoplasmosis.
Treat only if patient is severely immonocompromised and symptomatic.
Management
1. Standard regimen: Treatment duration of 6 weeks
a) Pyrimethamine: 200mg single loading dose, followed by 50-75mg daily
b) Sulfadiazine given 100mg/kg/day in 4 divided doses with maximal dose of

6g/day (i.e. 1 -1.5g given 6 hourly)
c) Folinic acid 25mg daily
NOTE
If patient is hypersensitive to the sulphonamides, replace sulfadiazine with

clindamycin 2.4g/day in 4 divided doses
2. Alternative regimen
- Cotrimoxazole double strength (960mg): 2 tabs 8 hourly for 6 weeks
- Children: 75/15mg/kg/day given 8 hourly for 6 weeks
NOTE
Preferable to start with IV route.
93
3. Prevention of recurrence given after treatment: Cotrimoxazole 960mg daily
4. Supportive treatment: Physiotherapy if focal deficits, counselling when

depressed and use of antidepressants.
5. Corticosteroids: often used in patients with intracranial hypertension
6. Anti-seizure medications: used if form of presentation was seizures or status

epilepticus.
3.5.3. DIARRHOEA IN HIV PATIENTS

Refractory diarrhoea is a complex problem among patients with HIV/AIDS. In
evaluating an AIDS patient with diarrhoea, the differential diagnosis broadens further
to include opportunistic pathogens. Diarrhoea is perhaps the most common complaint
of AIDS patients worldwide; in developing countries, nearly 100% of patients with
AIDS report diarrhoea.
Diarrhoea is usually defined as the production of more than 200 g of faecal matter per
day, but this definition will miss 20% of cases in which stools are frequent but the
amount is scant. Acute diarrhoea often lasts for 2 to 4 weeks and can be caused by an
infection with a virus, bacterium, or parasite.
Aetiology of diarrhoea in HIV patients
1. Common pathogens: salmonellosis, shigellosis, giardia, entamoeba histolytica,

campylobacter, clostridium difficile
2. Opportunistic neoplasm
- Lymphoma
- Kaposi sarcoma
3. Opportunistic infections
A. Bacteria:
- Mycobacterium avium or Mycobacterium avium-intracellulare constitute the

group of nontuberculous mycobacteria known as Mycobacterium avium
complex (MAC)
B. Protozoa
- Cryptosporidium
- Microsporidia (Enterocytozoon bieneusi, Encephalitozoon intestinalis) the

former accounting for 80% of microsporidial diarrhoea and being refractory
to treatment
94
- Isosporiasis, also known as cystoisosporiasis, is a human intestinal disease
caused by the parasite Isospora belli
- Strongyloidiasis is a human parasitic disease caused by the nematode called

Strongyloides stercoralis
C. Viruses
- Cytomegalovirus (CMV)
D. Fungal: Candida
4. Idiopathic HIV/AIDS enteropathy: HIV itself may be a pathogen that causes

diarrhoea. HIV enteropathy is diagnosed in an HIV patient who has diarrhoea for
more than a month when no other cause is found. AIDS enteropathy has emerged
and evolved over the years and reflects an idiopathic, pathogen-negative
diarrhoea whose underlying cause might involve undiscovered infectious
pathogen(s), inflammatory changes within the GI tract caused by HIV or other
environmental/infectious agents, HIV itself, or a complex interplay among any
one of these aetiologies
Treatment
Non-pharmacological
Treatment includes prolonged therapy with 2 or more agents, although once again, the
use of an effective antiretroviral regimen can lead to resolution of the illness and
discontinuation of treatment. People with chronic HIV who are malnourished may
experience worsened diarrhoea. This issue is more common in developing nations
where malnutrition is a problem for people with and without HIV. Treatment should
therefore include adequate hydration and good nutrition. Adequate sugar and
electrolyte-rich fluids and, if necessary, an elemental diet or nutrient formula
containing medium chain triglycerides.
Diarrhoea may also be treated with home remedies and lifestyle changes. You may try
to drink more clear liquids, avoid caffeine, refrain from consuming milk products, eat
20 grams or more of soluble fibre per day, and avoid greasy, spicy foods.
Pharmacological
1. Microsporidiosis and gnathostomiasis can be effectively treated with:
Albendazole 400mg or 25 mg/kg (Children) given 12 hourly for 21 days
2. Isosporiasis or cystoisosporiasis can be effectively treated with:
Cotrimoxazole 960mg give 12 hourly for 14 days Or Pyrimethamine given 50mg

daily + folinic acid given 25mg daily for 2- 4 weeks
3. Strongyloidiasis can be effectively treated with:
95
Albendazole 25 mg/kg twice daily for 5 days—400 mg maximum (generally) OR
Single dose of Ivermectin
Table 18: Ivermectin doses
Weight Dose
15 – 24 mg 3 mg
25 – 35mg 6 mg (2 tabs)
36 – 50mg 9 mg (3 tabs)
51 – 65mg 12 mg (4 tabs)
66 – 79mg 15mg (5tabs)
>80 kg 200 mcg/kg
4. Idiopathic HIV or AIDS enteropathy
i. Loperamide (IMODIUM®)
Acute diarrhoea: 4mg initially, then 2mg after each loose stool not to exceed
16mg/day. Discontinue if no improvement seen within 48 hours.
Chronic diarrhoea: 4mg initially, then 2mg after each loose stool until
controlled, and then 4 – 8 mg/day in divided doses.
ii. Octreotide 500 mg subcutaneously every 8 hours
iii. Oral rehydration solution.
iv. In case of HIV wasting syndrome add parenteral nutrition: ASTYMIN –

SN®
Adults: 200 – 800 ml I.V. /day
Children: 10 – 20 /kg/day
Drip Rate: 15 – 20 drops/minute initially followed by 30 – 40 drops per

minute
NOTE
ASTYMIN-SN® is contraindicated in cardiac insufficiency and irreversible liver

damage.
96
3.5.4. PNEUMOCYSTIS JIROVECII PNEUMONIA (PJP)
Characterised by sudden onset cough, fever and severe dyspnoea
Investigations
- Chest x-ray: Bilateral opacities characteristic of military TB
- Broncho-alveolar lavage revealing pneumocystis cysts
Management
1. IV Cotrimoxazole 960mg: 2 tabs 8 hourly for 3 weeks
Then continue with
Cotrimoxazole 960mg daily until immune reconstitution
2. Start steroids within 24 hours of initiation of cotrimoxazole.
- Methylprednisolone
30mg IVq12hr for 5 days then 30mg IV q24hr for 5 days, then 15mg q24hr for
5days. OR
- Prednisolone
40mg q12hr for 5 days then 40mg q24hr for 5 days then 20mg q24hr for 5 days
NOTE
In case of allergy to cotrimoxazole, give atovaquone 1500mg/day or dapsone 50-

100mg/day
Table 19: Criteria for HIV treatment failure
Clinical
- Occurrence of a knew infection classified in WHO clinical stage IV after 6months of

effective treatment (i.e. patient is compliant to treatment)
Immunological
- CD4 count falls to the baseline (or below) and after 6 months of well observed and
effective HAART
- Persistent CD4 levels < 100cells/ mm3 after 6 months of well observed and effective
HAART
Virological
- Viral load > 1000 copies/ml after 6months (or 12months depending on the time of follow-
up result) of well observed and effective HAART.
97
REFERENCES
1. Médecins Sans Frontières Clinical Guidelines - Diagnosis and treatment manual.

2016 edition – using the recommendations of World Health Organization
(WHO).
2. Prevention and Control of Non-communicable Diseases: Guidelines for primary

health care in low resource settings 2016
3. Guidelines from American Diabetes Association 2017.
4. MEDSCAPE 2017
5. WHO Guidelines 2017
6. Government of Western Australia. Department of Health. Remote Area Nursing

Emergencies guidelines. Fourth Edition 2005.
7. Betalli P et al. Update on management of caustic and foreign body ingestion in

children. Diagnostic and therapeutic endoscopy 2009
98
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GUIDELINES FOR MEDICAL EMERGENCIES AND CARE OF CRITICALLY ILL

Book · November 2018

Eugene Vernyuy Yeika Tantchou Cabral

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GUIDELINES FOR MEDICAL EMERGENCIES

Saint Elizabeth Catholic General Hospital and Cardiac Centre, Shisong

Copyright © Tertiary Sisters of Saint Francis (TSSF) Health Board 2018

Dr Cabral Tantchou Tchoumi Cardiologist, SECGHS and President of Science

Dr Siben Litika Ophthalmologist, Saint Elizabeth Catholic

Dr Eugene Yeika MD, SECGHS and Member of the Science and

Dr Bettina Schlemmer MD, Germany

Mr Jonathan Fondzenyuy General Supervisor, Saint Elizabeth Catholic

Rev Sister Mary Adrine Kinyuy

1.2. MODIFIED EARLY WARNING SIGNS SCORE ............................................................ 1

1.3. ASSESSMENT AND INITIAL RESUSCITATION OF AN ACUTELY, CRITICALLY

1.4. GLASGOW COMA SCORE ............................................................................................. 3

1.5. CARDIO-PULMONARY RESUSCITATION (CPR) ....................................................... 5

1.6. CONFIRMATION OF DEATH ......................................................................................... 6

2.2. SEIZURES AND STATUS EPILEPTICUS ....................................................................... 8

2.3. ACUTE PAIN .................................................................................................................. 10

2.3.2. NEUROPATHIC PAIN ................................................................................................. 12

2.3.3. ACUTE ABDOMENAL PAIN ..................................................................................... 13

2.4. SHOCK ............................................................................................................................ 14

2.4.1. VOLUME DEPLETION AND HYPOVOLEMIC SHOCK .......................................... 15

2.4.2. SEPSIS AND SEPTIC SHOCK .................................................................................... 16

2.4.3. ACUTE ANAPHYLAXIS AND ANAPHYLACTIC SHOCK ..................................... 19

2.5. ACUTE GASTIRTIS AND ACUTE PEPTIC ULCER BLEEDING ............................... 26

2.5.1. HELICOBACTER PYLORI INFECTION ERADICATION REGIMENS ................... 26

2.5.2. ACUTE PEPTIC ULCER BLEEDING ......................................................................... 28

2.5.3. LEWIS MEAL COMPOSITION................................................................................... 29

2.6. HYPERGLYCAEMIC EMERGENCIES ......................................................................... 30

2.6.1. HYPEROSMOLAR HYPERGLYCEMIC STATE AND HYPEROSMOLAR

2.6.1. DIABETIC KETOACIDOSIS ....................................................................................... 33

2.6.3. HYPOGLYCAEMIA .................................................................................................... 36

2.6.4. INSULIN FORMULARIES AND DOSAGES .............................................................. 37

2.7. HYPERTENSIVE CRISIS ............................................................................................... 38

2.7.1. HYPERTENSIVE URGENCY ..................................................................................... 38

2.7.2. HYPERTENSIVE EMERGENCY OR MALIGNANT HYPERTENSION .................. 38

2.7.2.1. NICARDIPINE (LOXEN®) PROTOCOLS ............................................................... 39

2.8. ASTHMATIC CRISIS ..................................................................................................... 40

2.8.1. ACUTE EXACERBATION OF ASTHMA OR ASTHMA FLARE-UP OR ACUTE

2.8.2. SEVERE ASTHMA OR STATUS ASTHMATICUS ................................................... 41

2.9. ACUTE EXACERBATION OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE

2.9.1. COPD FLARE-UP/ ACUTE EXACERBATION OF COPD ........................................ 44

2.9.2. END-STAGE COPD ..................................................................................................... 45

2.10. ACUTE GOUT / GOUT FLARE ................................................................................... 48

2.11. SEVERE ANAEMIA AND BLOOD TRANSFUSION ................................................. 50

2.11.1. BLOOD TRANSFUSION ........................................................................................... 51

2.12. ACUTELY RAISED INTRACRANIAL PRESSURE ................................................... 54

2.13. ACUTE AND CHRONIC KIDNEY DISEASES ........................................................... 56

2.13.2. CHRONIC KIDNEY DISEASE .................................................................................. 57

2.13.3. HYPERKALAEMIA AND CORRECTION ............................................................... 59

2.14. BURNS: ASSESSMENT AND TREATMENT ............................................................. 60

2.15. SNAKE BITE AND ENVENOMATION ...................................................................... 64

2.15.1. SNAKE ENVENOMATION ....................................................................................... 66

2.15.2. ANTI-VENOM THERAPY ........................................................................................ 66

2.16. ASSAULT/ BATTERY AND RAPE ............................................................................. 67

2.17. HYSTERIA/ CONVERSION DISORDER .................................................................... 69

2.18. SICKLE CELL CRISES ................................................................................................. 71