Textbook Oma 2

NHG Clinical Practice Guidelines
NHG Clinical Practice

Guidelines
M09 Acute Otitis Media (AOM)
M29 Feverish Illness in Childeren
Houten 2011
2011 Bohn Staeu van Loghum, part of Springer Media, the Netherlands
All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, copied or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise without written permission from the publisher.
Any person who does any unauthorized act in relation to this publication may be liable to
criminal prosecution and civil claims for damages.
ISBN 978 90 313 8825 7
NUR 870
Ontwerp omslag: A-Graphics Design, Apeldoorn
Ontwerp binnenwerk: TEFF (www.teff.nl)
Automatische opmaak: Crest Premedia Solutions (P) Ltd, Pune, India
Bohn Staeu van Loghum
Het Spoor 2
Postbus 246
3990 GA Houten
www.bsl.nl
Table of contents
Voorwoord
Preface
M09 NHG Clinical Practice Guideline Acute Otitis Media

(AOM)
M29 NHG Clinical Practice Guideline Feverish illness in

Children
25
Voorwoord
Ruim 20 jaar geleden is de eerste standaard van het Nederlands Huisartsen

Genootschap (NHG) uitgekomen. Daarmee is het richtlijnenproject van het
NHG wereldwijd een van de langst lopende en meest succesvolle programmas voor evidence based richtlijnenontwikkeling. In de loop van de jaren is
de kwaliteit van de standaarden toegenomen. Belangrijke mijlpalen waren
de keus voor een scheiding tussen aanbevelingen en onderbouwing met een
notenapparaat begin jaren negentig en voor de toepassing van systematische
literatuursearches op basis van uitgangsvragen rond de eeuwwisseling. Door
de levensduur van het richtlijnenproject en de vlotte introductie van standaarden als onderwijsmateriaal in de (huis)artsenopleiding, is inmiddels een
groot deel van de zittende huisartsenpopulatie in Nederland opgegroeid met
de standaarden. De meest huisartsen in Nederland gebruiken de standaarden
in de dagelijkse praktijk als leidraad. Over 10 jaar zal het aantal huisartsen
in Nederland dat niet met de standaarden is opgeleid, op de vingers van een
hand zijn te tellen.
Vanwege het grote belang van de NHG-Standaarden voor de huisartsengeneeskunde en de kwaliteit daarvan heeft het NHG gemeend de starten met
het vertalen van standaarden in het Engels. Daarmee komen de in Nederland
geldende evidence based richtlijnen ter beschikking van doelgroepen buiten
Nederland. Als pilot is begonnen met het vertalen van een tweetal standaarden te weten:
M09 Otitis Media Acuta en M29 Kinderen met Koorts.
Afhankelijk van de ontvangst zal worden besloten uit het totale aanbod
van circa 90 NHG-Standaarden meer standaarden te vertalen.
Preface
About 20 years ago, the rst clinical guideline of the Dutch College of General Practitioners (Nederlands Huisartsen Genootschap, NHG) was published.
This makes the NHG guidelines project one of the longest running and most
successful programmes for the development of evidence-based guidelines
in the world. Over the years the quality of the guidelines has improved.
Important milestones were the decisions to distinguish between recommendations and support with footnotes in the early 1990s and to apply systematic
literature searches on the basis of fundamental questions at the turn of the
millennium. Given the long duration of the guidelines project and the rapid
introduction of clinical guidelines as educational material in medical schools,
a large proportion of the current general practitioner population in the
Netherlands has grown up with these clinical guidelines. Most general practitioners in the Netherlands use the clinical guidelines in their daily practice
as reference material. In 10 years time the number of general practitioners in
the Netherlands who have not been trained with the clinical guidelines will
have shrunk to almost none. Given the great importance of the NHG clinical
guidelines for primary care medicine and its quality, the NHG intends to
start translating them into English. This will make evidence-based guidelines applicable in the Netherlands available for target groups outside the Netherlands. As a pilot, the translation of two guidelines has been undertaken,
namely: M09 Acute Otitis Media and M29 Feverish Illness in Children
Depending on their reception a decision will be made to translate more of
the total of 90 NHG clinical guidelines.
M09 NHG Clinical Practice Guideline

Acute Otitis Media (AOM)
Huisarts Wet 2006;49(12):615-21

Damoiseaux RAMJ, Van Balen FAM, Leenheer WAM, Kolnaar BGM
Key messages
In general the natural course of Acute otitis media (AOM)
is mild and the condition has a favourable outcome. The
intervention of GPs can be limited to providing information and prescription of pain relief.

Antibiotic
treatment is indicated in cases of severe or
increasing illness or in the case of risk factors for complications.

Consider
antibiotic treatment in those children who show
no improvement after three days.

Consider
antibiotic treatment in children with an episode
of acute otitis media with otorrhoea at initial presentation
and in children below the age of two with bilateral acute
otitis media.
x
x
x
x
Introduction
The NHG Practice Guideline on Acute otitis media provides guidelines for
the diagnosis and treatment of acute otitis media in children.[1] Acute otitis
media is understood to be an inammation of the middle ear with a maximum duration of three weeks. Acute otitis media is generally associated
with earache, symptoms of general illness, fever and sometimes purulent
discharge (otorrhoea), and is characterised by a bulging tympanic membrane
with change in colour (red or opaque).[2] The characteristics of an acute infection distinguish acute otitis media from otitis media with effusion (OME);
the latter condition is discussed in the NHG Practice Guideline OME.
J. Blijham, M09 Acute Otitis Media (AOM) M29 Feverish Illnes in Childeren
Houten, DOI 10.1007/978-90-313-8872-1_1,
2011 Bohn Stafleu van Loghum, part of Springer Media, the Netherlands
Generally, acute otitis media is a condition that only causes symptoms for a
few days and that rarely leads to complications. In most children only symptomatic treatment is required. The prescription of antibiotics is recommended for only few indications; in a number of other indications prescription
can be considered. GPs are able to treat almost all cases of acute otitis media
themselves. Referral to an ENT specialist is only indicated in the case of
persistent symptoms despite adequate treatment.
Background
Epidemiology
AOM is a common condition: an estimated one-half to three-quarters of the

general population experiences this condition at least once in their life, generally in early childhood. The incidence of AOM in GP surgeries is approximately 20 per 1,000 patients per year. More than half of these cases are diagnosed
in children below the age of ve. The incidence in this age group is approximately 175 per 1,000 patients per year. AOM becomes a rare condition after
puberty.[3] AOM can recur: 10 to 20% of all children experience at least three
episodes of AOMin the rst year of life.[3] The probability of recurrent AOM is
greater if the rst episode of the condition occurs in the rst year of life.[3]
The condition generally has a favourable natural course: in more than 80%
of children, the most severe symptoms resolve within two to three days.[4]
Children below the age of two with bilateral AOM have a greater chance of
persistent pain and fever. Perforation of the eardrum occurs in approximately
4 to 8% of cases of AOM, causing discharge.[5] Severe complications, including
mastoiditis and meningitis, are very rare.[6] Approximately 50% of children
develop OME four to six weeks after an episode of AOM and approximately
25% still have this condition after three months.
Risk factors for complications are young age (below six months), anatomical ear, nose and throat abnormalities, such as those observed in Downs syndrome and cleft palate and a history of ear surgery or compromised immune
system.[7]
Etiology
Pneumococci are the most common pathogens causing AOM, causing the
condition in 30 to 40% of cases. Haemophilus influenzae and Moraxella catarrhalis are also often cultured. Haemolytic streptococci are found in a very small
percentage of patients only. No bacterial pathogen is found in approximately
40% of middle ear cultures. Episodes of AOM often follow upper respiratory
tract infections. The viruses responsible for these infections can cause AOM
themselves, and it is postulated that bacterial infections often develop following viral preparation of the mucous membranes.[8]
M09 NHG Clinical Practice Guideline Acute Otitis Media (AOM)
Diagnosis
Various signs and symptoms can be a reason to consider a diagnosis of acute

otitis media. Earache and otorrhoea are the primary symptoms, but the GP
should also consider this condition in infants and toddlers presenting with
general symptoms, such as fever, irritability, night-time restlessness or gastrointestinal symptoms (abdominal pain, diarrhoea, vomiting, loss of appetite), even if there is no (indication for) earache or otorrhoea.
History
The GP should query the following:[9]

earache, otorrhoea, hearing impairment; unilateral or bilateral occurrence
of these symptoms;
general symptoms: fever, irritability, night-time restlessness, abdominal
pain, vomiting, diarrhoea, refusal to eat or drink, drowsiness;
symptoms of an upper respiratory tract infection (coughing, nasal
discharge, sore throat);
severity, duration and course of the symptoms;
previous episodes of ear infection in the past twelve months;
presence of grommets.
The GP checks whether there are any risk factors for complications: infants
below the age of six months, anatomical ear, nose and throat abnormalities,
such as those observed in Downs syndrome or cleft palate, a history of ear
surgery or a compromised immune system.
Requests for care for ear symptoms often reach GPs by telephone. Although
physical examination is required to conrm the diagnosis, a tentative diagnosis of AOM is often possible based on the patient history.
Certainty about the diagnosis - i.e. physical examination - is required if one
or more of the following situations apply:
severe or increasing illness;
risk factors for complications;
in all other cases in which the GP considers treatment with an antibacterial
agent.
Telephone advice can be considered adequate in all other cases. The GP can
then limit the intervention to a tentative diagnosis of AOM based on the
patient history, provided that this occurs in concordance with the carers of
the child.
Physical examination
The GP inspects both eardrums, comparing left and right; cotton buds, cerumen loops or a suction device to remove cerumen or debris are used if necessary. Irrigation is not recommended as this can be very painful during an
episode of AOM and because patients may have a hidden perforation of the
eardrum. During otoscopy, the GP should observe:
aspect of the eardrum: colour, vascular injection, opacity;
position of the eardrum: normal, bulging or retracted;
otorrhoea, perforation of the eardrum, presence of grommets.
The GP should be alert to symptoms indicating complicated disease, such
as protrusion of the ear, tenderness in the mastoid area, neck stiffness or
reduced consciousness in children appearing unwell or with risk factors for
complications.
Additional examinations
No additional examinations are required to conrm AOM.[10]

Evaluation
The diagnosis of AOM is based on earache and/or general symptoms of illness, and one or more of the following signs and symptoms:
a red, bulging or opaque eardrum;
a clear difference in redness between the left and right eardrum;
otorrhoea through a perforation of the eardrum or a grommet.
Vascular injection of both eardrums is a symptom that has little specicity for
AOM as this can also occur during a common cold or can be caused by crying.
Management
Information
The GP explains the natural course and the - generally favourable - outcome of AOM. In more than 80% of cases in children aged two or more, the
worst symptoms pass within two to three days and further follow-up is not
required. The symptoms may last longer in younger children: half of the
children below the age of two continue to experience symptoms of earache
and/or crying for longer than eight days.[14] Generally speaking, antibacterial agents do not have a signicant effect on the duration or severity of
symptoms. However, they do work in the case of bilateral otitis media in
children in this age group: the probability of being free of pain or fever within two days increases from approximately 50% to 75% in this age group.
Sometimes, AOM causes the ear to discharge either through a perforation of
the eardrum or through a grommet. This discharge generally clears up spontaneously within a week. However, if otorrhoea occurs soon after the onset
of the middle ear infection, antibacterial agents can reduce the duration of
pain and/or fever: in this instance, the probability increases from approximately 40% to 75%. Patients experiencing otorrhoea are recommended to avoid
swimming with their head underwater; this recommendation also applies to

patients with a perforation without discharge, as irritation of the labyrinth
can cause dizziness to occur. However, showering is allowed, as the probability of water entering the middle ear while showering is minimal.[11] It is not
necessary to advise children with frequently recurring AOM to stop swimming altogether.[11]
Conductive hearing loss or hearing loss caused by uid in the middle ear
can occur during or several weeks after AOM. In most cases the hearing loss
resolves by itself in the course of a few weeks to a few months.
The GP instructs the childs carers to come for a follow-up appointment if
the childs condition deteriorates or if the child fails to improve.
If needed, the GP can support this information by providing the patient
instruction letters about this condition (www.nhg.org, Patient information
section).
Treatment
Symptomatic treatment
The GP starts symptomatic treatment in all cases. The treatment comprises

adequate pain relief with paracetamol as the drug of choice. Orally, paracetamol is administered at a dosage of 10 mg/kg body weight four to six times
daily. Suppositories are administered at a dosage of 20 mg/kg body weight
two to three times daily (see table 1).
Table 1
Paracetamol dosage
age
oral dosage
rectal dosage
children aged 3-12
2.5 ml syrup (24 mg/ml) 4-6 times daily
1 suppository (120 mg) 2-3 times
months
children aged 1-2
daily
5 ml syrup (24 mg/ml) 4-6 times daily
years

daily
children aged 2-4
6-7 ml syrup (24 mg/ml) or 1 tablet 120 mg 4-6
1 suppository (240 mg) 3 times
years
times daily
daily
children aged 4-6
8 ml syrup (24 mg/ml) or 1.5 tablets 120 mg 4-6
years
times daily
daily
children aged 6-9
10 ml syrup (24 mg/ml) or 0.5 tablet 500 mg 4-6
years
times daily
daily
children aged 9-12
0.75 tablet (500 mg) 4-6 times daily
years
children aged >12
years
daily
1 tablet (500 mg) 4-6 times daily
1 suppository (1000 mg) 2-3

times daily
10
The childs parents or caregivers should be advised to administer the paracetamol at xed times. Oral administration more rapidly leads to an analgesic
effect (from approximately 30 minutes after administration; maximum
plasma level 30 to 90 minutes after administration) than rectal administration does, but the effect resulting from rectal administration is sustained for
longer. Rectal administration is often chosen in children for practical reasons
(see the Dutch College Pharmacotherapeutic Guideline on Pain Relief).
The effect of nose drops or sprays (xylometazoline or physiological saline
solution) on resolving AOM has not been demonstrated. These can be prescribed if there are symptoms of a blocked nose.[12] Topical treatment (e.g.
lidocaine eardrops) is not recommended in the treatment of AOM, as it can
hamper assessment of the eardrum later on. There are also insufcient data
to support the effectiveness.
Antibacterial treatment
Antibacterial agents are not indicated in the majority of children with AOM.
A wait-and-see approach is indicated in children who are not severely ill (aged
over 6 months), in children with unilateral AOM and in children without
otorrhoea. In contrast, antibacterial treatment is recommended:
in severely ill children or when children become more seriously ill;[13]
in the case of risk factors for complications.[14]
In addition, the GP, in consultation with the childs parents or caregivers,
considers starting treatment with oral antibacterial treatment if relief of
fever and pain is important at an earlier stage:
in children below the age of two years with bilateral AOM;[15]
in children with otorrhoea at initial presentation.[15]
This also applies to children that have not shown clinical improvement
within three days.[16]
In all cases, amoxicillin is used as rst-line treatment for a duration of one
week at a daily dosage of 30 mg/kg body weight (see table 2).[17]
Azithromycin or cotrimoxazole is prescribed in children allergic to penicillin: azithromycin for a duration of three days at a daily dosage of 10 mg/kg
body weight, and cotrimoxazole for a duration of ve to seven days at a daily
dosage of 36 mg/kg body weight (see table 2).[17]
When an antibacterial agent is prescribed, the GP advises the childs caregivers to come for a follow-up appointment if the symptoms have not improved within 48 hours of starting the medicine.
Follow-up
Follow-up in children with AOM is generally not necessary, except in the case
of otorrhoea.
If a wait-and-see approach was initially taken for a case of otorrhoea, the
GP prescribes oral antibiotics if the otorrhoea persists for more than one
(not < 6 months)
Cotrimoxazole
Azithromycin
100 mg/ml, 20 ml
Amoxicillin
480 mg tablet
48 mg/ml, 100 ml
250 mg tablet
40 mg/ml, 30 ml
40 mg/ml, 22.5 ml
40 mg/ml, 15 ml
caps. or disp. tab. 250 mg
50 mg/ml, 100 ml
25 mg/ml, 100 ml
preparation
36 mg/kg
10 mg/kg
30 mg/kg
daily dosage
2 daily
3-4 ml
xxx
1 ml 3 daily
2 daily
2 daily
5-6 ml
1 daily
4-5 ml
3-4 ml
1 daily
3 daily
2.5-3 ml
5-6 ml
3 daily
12-15 kg
2-3 years
4-5 ml
10-12 kg
< 10 kg
weight
name
1-2 years
0-1 years
Paediatric dosages of the recommended antibiotic agents
age
Table 2
2 daily
6-7.5 ml
1 daily
daily
7.5-9 ml 2
5-6 ml 1 daily
3 daily
4-5 ml
4-5 ml
3 daily
20-25 kg
5-7 years
3-4 ml
15-20 kg
3-5 years
1-1.5 tablets
2 daily
daily
1 daily
1 daily
1 tablet 2
1.5 tablets
1 tablet
1 daily
8-10 ml
4 daily
6-8 ml 1 daily
250 mg
3 daily
3 daily
6-8 ml
31-42 kg
9-12 years
250 mg
3 daily
5-6 ml
25-31 kg
7-9 years

11
12
week.[18] When the otorrhoea has resolved - spontaneously or after the use of
antibacterial agents - a follow-up visit is recommended after one month to
assess whether the perforation of the eardrum has closed.
Consultation or referral
Refer any child with clinical signs and symptoms of mastoiditis or meningitis
to an ENT specialist or a paediatrician respectively.[19]
Consult an ENT specialist or refer the patient to this specialist in the following cases:[20]
failure to improve within 48 hours of starting antibacterial treatment;
persistence of otorrhoea following a course of an antibacterial agent;[21]
persistent perforation of the eardrum one month after the onset of otorrhoea;[22]
children with frequently recurring AOM (three or more episodes per six
months or four episodes per year).[23]
Establishment
A working group started the revision of the NHG Standard on Acute otitis
media in March 2005. The working group was composed of Dr R.A.M.J.
Damoiseaux, Dr F.A.M. van Balen and W.A.M. Leenheer, all General Practitioners. In May 2006, the concept text was submitted for comments to a number of reviewers. The working group received comments from the following
reviewers: Dr C.L.M. Appelman, Dr E.H. van de Lisdonk and Dr H. van Weert,
all General Practitioners, Dr J.Q.P.J. Claessen and Dr A.G.M. Schilder on behalf
of the Dutch Association of Otorhinolaryngology and Head & Neck Surgery,
A.C. van Loenen, Hospital Pharmacist/Clinical Pharmacologist and Chief
Editor of the Pharmacotherapeutic Compass, on behalf of the Health Care
Insurance Board and M.J. Swart-Zuijderduijn, Pharmacist, on behalf of the
Scientic Institute of Dutch Pharmacists. Mention of the reviewers names in
this standard does not necessarily mean that the reviewers endorse all details
of the standard.
The NHG Authorisation Committee commented on and authorised the
standard in July 2006. Dr B.G.M. Kolnaar, General Practitioner and Scientic
Staff Member of the Department of Standard Development and Science of the
NHG, provided the working group and the editors of this standard with support
and guidance.
Dutch College of General Practitioners
Notes
Note 1 Acute otitis media in adults As was the case with previous editions of
this standard, insufcient usable research on acute otitis media in adults
was found for this revision. Others encountered the same lack of data when
generating a literature overview [Anonymous 2003]. Data collected from an
international registration network of GP surgeries in 1986 showed that the
symptoms and signs and the treatment administered in adults was essentially the same as that in children [Froom 1990, Culpepper 1993]. However,
the working group is of the opinion that the lack of scientic data about the
course, risk factors, diagnosis and treatment effects in adult cases of acute
otitis media mean that the guidelines in children cannot be applied in adults
per se.
Note 2 Diagnostic criteria There is international agreement on the denition
of acute otitis media [Gates 2002]. However, there is no agreement on the
clinical criteria that should be met to make this diagnosis. An important difference between international guidelines is the criterion of effusion in the
middle ear. Doctors in the United States especially take the view that the
presence of uid in the middle ear should be demonstrated in order to diagnose the condition with sufcient condence. This is the case when patients
present with otorrhoea (following tympanocentesis or otherwise), or decreased tympanic membrane mobility, preferably demonstrated by pneumatic
otoscopy or - as a second choice - by tympanometry or acoustic reectometry
[Marcy 2001]. However, the latter examinations are hardly ever carried out
in GP surgeries in the Netherlands or in other Western European countries.
The criteria described in this standard are in line with the opinions of the
Dutch Association of Otorhinolaryngology and Head & Neck Surgery and the
procedures followed by GPs [Grote 1988]. According to the ICPC-2, one of the
following ve criteria should be met: recent perforation of the eardrum with
pus-like discharge, inamed and bulging eardrum, one eardrum redder than
the other, red eardrum with earache, blister formation on the eardrum [Gebel
2000].
Note 3 Data on the incidence of acute otitis media Based on their overview of
studies in rst-line populations, Casselbrant and Mandel concluded that 19
to 62% of all children have at least one episode of acute otitis media before
the second year of life, and that 50 to 84% have at least one episode before the
fourth year of life. Most studies show the incidence to peak in the second half
of the rst year of life and the incidence to decrease afterwards [Casselbrant
2003].
The incidence rate of acute otitis media in GP surgeries is particularly high
in the youngest children: the incidence in children decreases from 193 per
1,000 patients per year in children below the age of one and 139 in children
aged one to four, to 52 in children aged ve to nine and 14 in children aged
ten to fourteen. The condition is far less prevalent in later life: from 7 per
1,000 patients per year in young adults to 2 in old age [Van der Linden 2004].
13
14
According to the literature overview mentioned above, 10 to 20% off all

children have at least three episodes of acute otitis media in the rst year of
life [Casselbrant 2003]. An American cohort study showed that 39% of children aged seven had had at least six episodes of acute otitis media [Teele 1989].
Appelman found that 5.4% of all children in a Dutch rst-line population of
684 children (from birth to age thirteen) in whom a GP had diagnosed acute
otitis media were otitis prone, meaning to say that they had four or more
episodes of acute otitis media in the subsequent year [Appelman 1992]. The
probability of the condition recurring is greater if the rst episode of acute
otitis media occurred in the rst year of life [Teele 1989, Kvaerner 1997].
It may be expected that the incidence of acute otitis media will decrease
in the Netherlands after the introduction of pneumococcal vaccination in
infants on 1 April 2006. However, the extent of the decrease in the long term
cannot be predicted (also see note 23).
Note 4 The course of acute otitis media Adequate research of the early natural
course of acute otitis media (including the rst days) in an open population
or in a GP practice was not found. The course in placebo groups in randomised intervention studies may provide some information. A meta-analysis
of data from eleven placebo groups shows that the symptoms of 61% (95%
CI 50-72%) of children subside within one day of the diagnosis, and that
the symptoms of 80% (95% CI, 49-92%) of children subside within two to
three days [Rosenfeld 2003]. Complete clinical recovery occurs after seven to
fourteen days in 70% of children (95% CI, 49-92%); any residual otitis media
with effusion has not been included in the analysis. The latter condition is
still present after four to six weeks in approximately 50% of children and
after three months in approximately 25% of children. Complications (mastoiditis, meningitis) are rare. These results are in line with those of other systematic overviews of intervention studies in which the course in the placebo
groups was also summarised [Marcy, 2001, Glasziou 2003]. However, it should
be noted that severely ill children are very poorly represented in intervention
studies and therefore in these systematic overviews, so that these results
cannot simply be reapplied to this group [Bain 2001]. Recovery after acute
otitis media seems to take longer in very young children: Dutch research in
children between the ages of six months and two years shows that half still
have symptoms of earache or crying after eight days [Damoiseaux 2000b]. A
meta-analysis of individual data of 824 children in the placebo groups of six
randomised studies shows that children below the age of two with bilateral
acute otitis media have double the risk of a longer disease course (pain and/or
fever persisting beyond three days; absolute risk 55%) than children aged two
or over with unilateral acute otitis media (absolute risk 25%) [Rovers, 2006].
With regards to the required clinical policy, the working group nds this sufcient reason to regard this age group as a separate category in addition to
infants from birth to six months and children over the age of two.
Note 5 The incidence and course of otorrhoea In the course of one year, GPs
diagnosed 2,254 cases of acute otitis media in a Finnish population of 14,200
children below the age of 16. Otorrhoea through a spontaneous perforation of

the eardrum occurred in 4.6% of these cases [Pukander 1983].
A Dutch study in children below the age of two with acute otitis media
(n=204) showed that 8% of patients developed a perforation of the eardrum
with otorrhoea within ten days of the visit to the GP. The median duration of
the otorrhoea was one day only. The median duration of the otorrhoea was
four days in the 36 children that already had a perforation of the eardrum
with otorrhoea caused by acute otitis media at initial presentation [Damoiseaux 2000b].
Note 6 The incidence of mastoiditis The incidence rate of mastoiditis has decreased drastically over the last decades due to both the use of antibiotics and
the now milder clinical picture of the condition [Van Buchem 1989]. Based
on the diagnoses in children below the age of 15 at the time of the discharge
from hospital, Van Zuijlen et al assumed an incidence of mastoiditis of 3.8 per
100,000 patient years [Van Zuijlen 2001].
Note 7 Risk groups for complications It is assumed that children with acute
otitis media that are either below the age of six months, have anatomical ear,
nose and throat abnormalities, such as those observed in Downs syndrome
and cleft palate, or have a history of ear surgery or a compromised immune
system have an increased risk of complications [Grote 1988]. However, adequate research into this has not been found.
Note 8 Etiology In all studies, the micro-organisms most frequently found
in ear drainage cultures in cases of acute otitis media are pneumococci (30 to
40%). In addition, Haemophilus influenzae (20 to 30%) and Moraxella catarrhalis
(10 to 20%) are often found. However, 40% of all middle ear cultures are found
to be negative [Bluestone 2001]. All respiratory viruses can cause otitis media
[Heikkinen 1999]. There are also indications that the immune response triggered by viruses enhances the sensitivity of the middle ear to bacterial invasion [Ruuskanen 1994]. A study in children below the age of 16 (n=2,254) with
acute otitis media showed that 60% of patients had an upper respiratory tract
infection in the two weeks before [Pukander 1983]. It is hypothesised that bacterial or viral infections cause abnormal Eustachian tube drainage or abnormal ciliary activity. At a young age, the Eustachian tube is shorter and wider
and has a more horizontal course than in later life and it is therefore postulated that it provides bacteria with easier passage from the nasopharynx to
the middle ear. Alongside adenoid hypertrophy, early age, male sex, winter
season, the use of dummies and childcare attendance are risk factors for the
development of acute otitis media. Passive smoking is a risk factor for the
development of upper respiratory tract infections in general and therefore
also for the occurrence of acute otitis media [Casselbrant 2003, Uhari 1996].
Note 9 The diagnostic value of the history and physical examination There is
insufcient data available about the diagnostic value of the history and physical examination for acute otitis media. Research into this is hampered by the
15
16
lack of a valid and usable gold standard. Pus drainage following tympanocentesis is considered as such, but tympanocentesis in patients in whom there is
insufcient certainty about the presence of acute otitis media - necessary for
valid diagnostic research - is not ethically acceptable. In their systematic overview, Rothman et al found only ve studies usable to some extent (four about
historical ndings, one about otoscopic ndings) [Rothman 2003]. They drew
the following conclusions: from the historical ndings researched (earache,
children pulling or rubbing the ear, fever, coughing, nasal discharge, excessive crying, loss of appetite, vomiting, throat ache, headache, disturbed
sleep and carers suspicion of acute otitis media), earache seemed to have the
highest diagnostic value (positive LR 3.0 to 7.3; however, negative LR only 0.6
to 4.0). In addition, children pulling the ear and the carers suspicion of acute
otitis media also seemed to have some value (positive LR 3.3 and 3.4 respectively; however, negative LR 0.7 and 0.4 respectively). From the otoscopic ndings, a bulging or opaque eardrum make acute otitis media very likely (positive LR 51 and 34 respectively), but clear redness also contributes somewhat to
the diagnosis (positive LR 8.4).
Otoscopy only has a diagnostic value if the ndings from this examination are sufciently reliable. Appelman et al performed research into this by
comparing the otoscopic ndings of the eardrums of children with (a clinical
suspicion of) acute otitis media made by GPs with those made by ENT specialists. The ndings were similar in children aged two and over, but moderate
in younger children [Appelman 1993].
Note 10 Additional examinations Pneumatic otoscopy and tympanometry aim
to demonstrate middle ear effusion. Fluid is also present in the middle ear
in most cases of acute otitis media. Both examinations are valuable if it is
important to demonstrate the presence of uid. For more details, please refer
to the NHG Standard on Otitis Media with Effusion.
Palmu et al conducted a study in a cohort of 329 children to determine the
value of tympanometry to predict the course of acute otitis media [Palmu
2002]. It was not possible to use the tympanogram curves to predict the
course.
The working group therefore does not consider it necessary to perform
additional examinations to diagnose acute otitis media.
Note 11 Swimming Swimming with the head underwater can lead to irritation of the labyrinth in patients with a perforation of the eardrum. Water is
thought to enter the middle ear through the perforation. The recommendation in children with a perforation of the eardrum is different to the recommendation in children with grommets, as the probability of water passing
through the narrow lumen of the grommet into the middle ear is only small.
Please refer to the NHG Standard on Otitis Media with Effusion for recommendations concerning grommets.
Usable research about the once postulated relationship between regular
swimming and recurrent acute otitis media was not found. Based on consen-
sus, the working group therefore recommends GPs not to advise children
with recurrent otitis media to stop swimming altogether.
Note 12 Decongestants The postulated mechanism of decongestant nose drops
is a reduction of the swelling of the nasopharyngeal mucous membrane,
causing improved drainage of the middle ear. A Cochrane review about this
topic showed hardly any effect of decongestants (nor of antihistamines)
[Flynn 2004]. However, most of the included studies used oral medication, in
contrast to the nose drops commonly used in the Netherlands. Some patients
positively appreciate the improved (temporary or otherwise) nasal patency. As
temporary use is not found to lead to disadvantages, the use of decongestants
is included in the standard as optional.
Note 13 Antibiotic agents in the treatment of severe illness Severely ill children
are often excluded from studies into the effect of antibiotics on acute otitis
media [Bain 2001, Damoiseaux 2000a, Le Saux 2005]. As a result, there is
neither proof that these medicines have an effect in this group of children,
nor proof that they do not.
Based on consensus, the working group recommends that GPs prescribe
antibiotics to children who are severely ill when they visit the GP or who
become more ill during the course, despite the fact that there is neither proof
that these medicines have an effect, nor proof that they do not.
Note 14 Antibiotic agents in risk groups for complications The working group
subscribes to the recommendations from the Dutch Association of Otorhinolaryngology and Head & Neck Surgery to prescribe antibiotic agents in cases
of acute otitis media in patients in the risk groups for complications (see note
7) [Grote 1988]. However, adequate research into the effect of these medicines
in these patients has not been found.
Note 15 Antibiotic agents (general) A Cochrane review of the effectiveness
of antibiotic treatment of acute otitis media in children (ten studies; 2,287
children) investigated the following outcome measures: pain after 24 hours,
pain on the second to the seventh day, perforation, vomiting, diarrhoea, rash,
deafness and recurrent acute otitis media [Glasziou 2003]. It was found that
there was no effect on the pain in the rst 24 hours, a moderate reduction
of pain on the second to the seventh day, no effect on recurrent acute otitis
media and no effect on deafness. Vomiting, diarrhoea and rash were clearly
more common after the use of antibiotics. In summary, this review suggests
that an early start of these medicines in cases of acute otitis media has a limited effect; it takes 15 children to be treated with these medicines to prevent
one child from still having some earache after two to seven days.
A meta-analysis based on individual patient data of 1,643 children showed
that antibiotic agents have very different effects on pain reduction and/or
disappearance of fever in the treatment of acute otitis media in certain
subgroups [Rovers, 2006]. The effect (on pain or fever after two to seven days)
in the entire group was an absolute risk reduction of 13% (95% CI 9-17%),
17
18
which corresponds to an NNT of 8. This effect, and smaller effects still, are
seen in children aged over two (NNT 10), in children with unilateral acute
otitis media (NNT 17) and in children without aural discharge (NNT 8). The
effects are so small that a wait-and-see approach in these groups is most certainly justied. However, the effect on pain or fever after two to seven days
was considerably greater in children below the age of two with bilateral acute
otitis media and in children with aural discharge at initial presentation (NNT
4 and 3 respectively), although the effect of the antibiotic agent was no longer
signicant in either group after seven to ten days.
Conclusion It has been demonstrated that antibiotic agents do not have a
relevant effect on acute otitis media, at least in children who are not severely
ill and who are not part of a risk group. However, such medicines increase
the probability that children below the age of two with bilateral acute otitis
media and children with aural discharge at initial presentation are free of
fever and pain after two days. This is the reason why GPs should consider (in
consultation with the childs carers) prescribing antibiotics in these children,
at least if this effect is considered important in the individual case.
Note 16 Antibiotic agents when patients fail to improve Only one study was
found into the effect of antibiotic agents in children with acute otitis media
who fail to improve sufciently after three to four days of symptomatic treatment (Van Buchem 1985). In this study, GPs initially gave all 4,900 children
aged between 2 and 12 years symptomatic treatment. In children who still
had fever and/or pain after three to four days (3% of the total group), antibiotic agents proved to be more effective than myringotomy.
It is not clear whether this nding also holds for younger children. As
remarked before (see note 4), children below the age of 2 often take longer to
recover (50% still have symptoms of crying or earache after eight days) and
antibiotic agents have only been shown to have a relevant effect in subgroups
and only if the medicine was administered from the beginning of the episode
(see note 15).
While there is insufcient evidence to substantiate this, the working group
recommends that treatment with antibiotics is still started when children fail
to improve after three to four days of symptomatic treatment (in consultation
with the parents).
Note 17 Recommended antibiotics Hardly any comparative research has been
conducted on different antibiotic medicines for the indications formulated in
the standard. Differences in effectiveness between narrow-spectrum penicillin and amoxicillin or amoxicillin-clavulanic acid in the treatment of acute
otitis media could not be demonstrated in a meta-analysis [Rosenfeld 1994].
Most Western countries also prefer broad-spectrum antibiotics (amoxicillin
or amoxicillin-clavulanic acid with possibly cotrimoxazole as an alternative)
on the basis of pathophysiological considerations (better penetration into the
middle ear) [Froom 1997]. There have been good experiences with amoxicillin
in the Netherlands for some time now.
Azithromycin and cotrimoxazole can be prescribed if there is a contraindication for amoxicillin [Pharmaceutic Aid Committee 2006]. Azithromycin
can be administered less frequently and has a similar effect [Ioannidis 2001].
Note 18 Eardrops In practice, antibiotic eardrops are frequently prescribed
(especially by ENT specialists) in case of persistent aural discharge through
a grommet or through a perforation of the eardrum caused by acute otitis
media. Please refer to the NHG Standard on Otitis Media with Effusion for
the guidelines on the treatment of aural discharge through a grommet.
The authors of a systematic overview of studies into the effect of local antibiotics (drops) compared with systemic antibiotics in the treatment of chronic otorrhoea (persisting for more than two weeks) found only few usable
studies [Madfadyen 2006]. Two studies showed that quinolone drops were
more effective than systemically administered antibiotics. However, most of
the patients included in these studies were adults. Whether these results are
also relevant in children and for eardrops containing other antibiotics is not
known.
Based on the above, the working group is of the opinion that eardrops for
persistent aural discharge through a perforation of the eardrum caused by
acute otitis media have no place in the GP surgery.
Note 19 Acute mastoiditis The clinical picture of an acute mastoiditis comprises one or more of the following symptoms: general symptoms of illness,
protrusion of the ear, prolapse of the posterior superior wall of the ear canal,
increasing temperature and pain (spontaneous and during palpation of the
mastoid area). CT scans conrm the diagnosis. The treatment consists of tympanocentesis, antibiotics (intravenous) and possibly mastoidectomy [Huizing
2003].
Note 20 Tympanocentesis Tympanocentesis is now only rarely carried out
in patients with otitis media, as current views suggest that there is hardly
any indication for this. There are views that tympanocentesis can still be
benecial to relieve severe pain caused by a bulging eardrum (only effective
in the early phase). Tympanocentesis is otherwise conducted to conrm the
diagnosis of acute otitis media in infants and to collect material for culturing.
However, these indications are part of specialist medical care.
Note 21 Persistent otorrhoea Prolonged otorrhoea can indicate mastoid involvement or a chronic inammation of the middle ear with or without cholesteatoma formation [Huizing 2003].
Note 22 Persistent perforation of the eardrum Perforations of the eardrum
exceeding 25% of the area of the eardrum lead to a clear loss of hearing,
though generally less than 35 dB. Perforations of the eardrum sometimes
rapidly cause the ear to discharge after exposure to water. If perforations are
persistent, then myringoplasty is indicated for disturbing loss of hearing or if
the patient wants to swim [Huizing 2003].
19
20
Note 23 Recurrent acute otitis media In studies and international guidelines,

recurrent acute otitis media is often dened as having three or more episodes
per six months or four episodes per year [Dowell 1998]. Patients with frequent acute otitis media are tested for infectious foci (adenoid and nasal sinuses) that can be cleansed or removed (e.g. by adenotomy). An American study
showed that adenotomy (optionally combined with tonsillectomy) only had a
limited, short-term effect [Paradise 1999]. A Finnish study showed no effect of
adenotomy on recurrent acute otitis media [Koivunen 2004]. Grommets and
a maintenance treatment with antibiotic medicines are also therapeutic options for the prevention of frequent episodes of acute otitis media. Williams et
al conducted a meta-analysis of the effectiveness of a maintenance treatment
with antibiotic medicines for frequent episodes of acute otitis media (at least
three episodes in the previous twelve months) [Williams 1993]. The outcome
measure was the number of episodes of acute otitis media per patient month.
Pooling showed that there was approximately one fewer episode of acute
otitis media per patient per year in the group treated with antibiotics (n=490)
than in the placebo group (n=468) (antibiotic group versus placebo group
0.08 and 0.19 episodes of acute otitis media respectively per patient month,
difference of 0.11; 95% CI 0.03-0.19). Casselbrant et al conducted a randomised placebo-controlled study in children aged between seven and thirty-ve
months (n=264), in which the value of prophylactic maintenance treatment
with amoxicillin, the placement of grommets and a placebo treatment for the
prevention of recurrent episodes of acute otitis media were compared successively for a period of two years [Casselbrant 1992]. Recurrent acute otitis
media was dened as three episodes in six months or four or more episodes in
twelve months. The average number of recurrent episodes in one year was 0.6
in the group treated with amoxicillin (signicant difference versus placebo),
1.02 in the group in which grommets were placed (not signicant versus placebo) and 1.08 in the placebo group. The authors concluded that prophylactic
antibiotic treatment led to fewer recurrent episodes, while grommets did not
have this effect. In contrast, the placement of grommets did lead to episodes
of acute otitis media with fewer symptoms (less pain).
Vaccination against pneumococci is also mentioned as a preventative
measure against frequent acute otitis media. However, a Dutch study and a
systematic literature overview showed that this vaccination does not have an
effect in children that already have recurrent otitis [Veenhoven 2003, Straetemans 2004]. Vaccination with a conjugated pneumococcal vaccine in all children from birth resulted in the number of episodes of acute otitis media to
decrease by 6% (randomised controlled research; n=1,662) [Eskola 2001]. The
number of children with frequent acute otitis media also reduced as a result
[Black 2000]. However, the negative effects of such an approach are as yet
unclear. The long-term consequences of the serotype replacement observed
in various studies are as yet unknown [Veenhoven 2003, Damoiseaux 2002].
In conclusion, the placement of grommets, optionally combined with
adenotomy, is an alternative for the prevention of recurrent episodes of acute
otitis media when prophylactic treatment with antibiotic agents delivers
insufcient effect or when carers reject these medicines. However, both have
a limited effect.
As recommended by the Health Council of the Netherlands, the vaccination against pneumococci in all children from birth was introduced nationwide from 1 April 2006. With this vaccination, the Health Council aims to
reduce the number of cases of severe invasive conditions caused by pneumococci (meningitis, sepsis, pneumonia) [Health Council of the Netherlands
2005].
Literature
In case of references to NHG products: see www.nhg.org
Anonymus. Acute otitis media in adults: many unknown. Prescrire Int 2003;12:108-9.
Appelman CLM, Claessen JQPJ. Recurrent otitis media [dissertation]. Utrecht: Univer-
Appelman CLM, Claessen JQPJ, Touw-Otten FW, Hordijk GJ, De Melker RA. Severity of
siteit Utrecht, 1992.

inammation of tympanic membrane as predictor of clinical course of recurrent acute
otitis media. BMJ 1993;306:895.
5
Bain J. Treatment of acute otitis media: Are children entered into clinical trials representative? Br J Gen Pract 2001;51:132-3.
Black S, Shineeld H, Fireman B, Lewis E, Ray P, Hansen JR, et al. Efcacy, safety and
immunogenicity of heptavalent pneumococcal conjugate vaccine in children. Northern California Kaiser Permanente Vaccine Study Center Group. Pediatr Infect Dis J
2000;19:187-95.
Bluestone CD, Klein J.O. Otitis media in infants and children. Philadelphia: WB Saun-
Casselbrant ML, Kaleida PH, Rockette HE, Paradise JL, Bluestone CD, Kurs-Lasky M, et
ders, 2001.
al. Efcacy of antimicrobial prophylaxis and of tympanostomy tube insertion for prevention of recurrent acute otitis media: Results of a randomized clinical trial. Pediatr
Infect Dis J 1992;11:278-86.
9
Casselbrant ML, Mandel EM. Epidemiology. In: Rosenfeld RM, Bluestone CD, editors.
Evidence-based otitis media. Hamilton: BC Decker, 2003.
10 Commissie Farmaceutische Hulp. Farmacotherapeutisch Kompas 2006. Amstelveen:

College voor Zorgverzekeringen, 2006.
11 Culpepper L, Froom J, Bartelds AI, Bowers P, Bridges-Webb C, Grob P, et al. Acute otitis
media in adults: A report from the International Primary Care Network. J Am Board
Fam Pract 1993;6:333-9.
12 Damoiseaux RA, Van Balen FA, Hoes AW, Verheij TJ, De Melker RA. Primary care based
randomised, double blind trial of amoxicillin versus placebo for acute otitis media in
children aged under 2 years. BMJ 2000a;320:350-4.
13 Damoiseaux RAMJ, Van Balen FAM. Duration of clinical symptoms in children under
two years of age with acute otitis media. Eur Gen Pract 2000b;6:48-51.
14 Damoiseaux RA. De angst regeert: Impact van pneumokokkenconjugaatvaccin overschat. Huisarts Wet 2002;45:510-1.
21
22

15 Dowell SF, Marcy SM, Philips WR, Gerber MA, Schwartz B. Otitis media: Principles of
judicious use of antimicrobial agents. Pediatrics 1998;101 Suppl:165-91.
16 Eskola J, Kilpi T, Palmu A, Jokinen J, Haapakoski J, Herva E, et al. Efcacy of a pneumococcal conjugate vaccine against acute otitis media. N Engl J Med 2001;344:403-9.
17 Flynn CA, Grifn GH, Schultz JK. Decongestants and antihistamines for acute otitis
media in children. Cochrane Database Syst Rev 2004;CD001727.
18 Froom J, Culpepper L, Grob P, Bartelds A, Bowers P, Bridges-Webb C, et al. Diagnosis
and antibiotic treatment of acute otitis media: Report from International Primary Care
Network. BMJ 1990;300:582-6.
19 Froom J, Culpepper L, Jacobs M, De Melker RA, Green LA, Van Buchem L, et al. Antimicrobials for acute otitis media? A review from the International Primary Care Network.
BMJ 1997;315:98-102.
20 Gates GA, Klein JO, Lim DJ, Mogi G, Ogra PL, Pararella MM, et al. Recent advances in
otitis media. 1. Denitions, terminology, and classication of otitis media. Ann Otol
Rhinol Laryngol Suppl 2002;188:8-18.
21 Gebel RS, Okkes IM, editors. ICPC-2-NL: International Classication of Primary Care.
Utrecht: Nederlands Huisartsen Genootschap, 2000. Gezondheidsraad. Vaccinatie van
zuigelingen tegen pneumokokkeninfecties. Den Haag: Gezondheidsraad, 2005.
22 Glasziou PP, Del Mar CB, Sanders SL, Hayem M. Antibiotics for acute otitis media in
children. Cochrane Database Syst Rev 2003;CD000219.
23 Grote JJ, Van Buchem FL, editors. Otitis media bij kinderen: Rapport uitgebracht aan
de Ned Ver voor KNO-heelkunde en Heelkunde van het Hoofd-halsgebied. Leiderdorp:
De Medicus, 1988.
24 Heikkinen T, Thint M, Chonmaitree T. Prevalence of various respiratory viruses in the
middle ear during acute otitis media. NEngl J Med 1999;340:260-4.
25 Huizing EH, Snow GB, editors. Leerboek keel-, neus- en oorheelkunde. Houten: Bohn
Staeu Van Loghum, 2003.
26 Ioannidis JP, Contopoulos-Ioannidis DG, Chew P, Lau J. Meta-analysis of randomized
controlled trials on the comparative efcacy and safety of azithromycin against other
antibiotics for upper respiratory tract infections. J Antimicrob Chemother 2001;48:67789.
27 Koivunen P, Uhari M, Luotonen J, Kristo A, Raski R, Pokka T, et al. Adenoidectomy
versus chemoprophylaxis and placebo for recurrent acute otitis media in children aged
under 2 years: Randomised controlled trial. BMJ 2004;328:487-90.
28 Kvaerner KJ, Nafstad P, Hagen JA, Mair IW, Jaakkola JJ. Recurrent acute otitis media:
The signicance of age at onset. Acta Otolaryngol 1997;117:578-84.
29 Le Saux SN, Gaboury I, Baird M, Klassen TP, MacCormick J, Blanchard C, et al. A randomized, double-blind, placebo-controlled noninferiority trial of amoxicillin for
clinically diagnosed acute otitis media in children 6 months to 5 years of age. CMAJ
2005;172:335-41.
30 Macfadyen CA, Acuin JM, Gamble C. Systemic antibiotics versus topical treatments for
chronically discharging ears with underlying eardrum perforations. Cochrane Database
Syst Rev 2006;CD005608.
31 Marcy M, Takata G, Chan LS, Shekelle P, Mason W, Wachsman L, et al. Management
of acute otitis media. AHQR Evidence report/technology assessment. Rockville (MD):
Agency for Healthcare Research and Quality, 2001.

32 Palmu A, Puhakka H, Rahko T, Takala A, Kilpi T. Predicting the development and outcome of otitis media by tympanometry. Int J Pediatr Otorhinolaryngol 2002;62:135-42.
33 Paradise JL, Bluestone CD, Colborn DK, Bernard BS, Smith CG, Rockette HE, et al.
Adenoidectomy and adenotonsillectomy for recurrent acute otitis media: Parallel randomized clinical trials in children not previously treated with tympanostomy tubes.
JAMA 1999;282:945-53.
34 Pukander J. Clinical features of acute otitis media among children. Acta Otolaryngol
1983;95:117-22.
35 Rosenfeld RM, Vertrees JE, Carr J, Cipolle RJ, Uden DL, Giebink GS, et al. Clinical efcacy of antimicrobial drugs for acute otitis media: Metaanalysis of 5400 children from
thirty-three randomized trials. J Pediatr 1994;124:355-67.
36 Rosenfeld RM, Kay D. Natural history of untreated otitis media. Laryngoscope
2003;113:1645-57.
37 Rothman R, Owens T, Simel DL. Does this child have acute otitis media? JAMA
2003;290:1633-40.
38 Rovers MM, Glasziou P, Appelman CL, Burke P, McCormick DP, Damoiseaux RA, et
al. Antibiotics for acute otitis media: An individual patient data meta-analysis. Lancet
2006;368:1429-35.
39 Ruuskanen O, Heikkinen T. Viral-bacterial interaction in acute otitis media. Pediatr
Infect Dis J 1994;13:1047-9.
40 Straetemans M, Sanders EA, Veenhoven RH, Schilder AG, Damoiseaux RA, Zielhuis
GA. Pneumococcal vaccines for preventing otitis media. Cochrane Database Syst Rev
2004;CD001480.
41 Teele DW, Klein JO, Rosner B. Epidemiology of otitis media during the rst seven
years of life in children in greater Boston: A prospective, cohort study. J Infect Dis
1989;160:83-94.
42 Uhari M, Mantysaari K, Niemela M. A meta-analytic review of the risk factors for acute
otitis media. Clin Infect Dis 1996;22:1079-83.
43 Van Buchem FL, Peeters MF, t Hof MA. Acute otitis media: A new treatment strategy.
BMJ 1985;290:1033-7.
44 Van Buchem FL. De behandeling van otitis media acuta. Ned Tijdschr Geneeskd
1989;133:290-2.
45 Van der Linden MW, Westert GP, De Bakker D, Schellevis FG. Tweede Nationale Studie
naar ziekten en verrichtingen in de huisartsenpraktijk: Klachten en aandoeningen in
de bevolking en in de huisartspraktijk. Utrecht/Bilthoven: NIVEL/RIVM, 2004.
46 Van Zuijlen DA, Schilder AG, Van Balen FA, Hoes AW. National differences in incidence
of acute mastoiditis: Relationship to prescribing patterns of antibiotics for acute otitis
media? Pediatr Infect Dis J 2001;20:140-4.
47 Veenhoven R, Bogaert D, Uiterwaal C, Brouwer C, Kiezebrink H, Bruin J, et al. Effect of
conjugate pneumococcal vaccine followed by polysaccharide pneumococcal vaccine on
recurrent acute otitis media: A randomised study. Lancet 2003;361:2189-95.
48 Williams RL, Chalmers TC, Stange KC, Chalmers FT, Bowlin SJ. Use of antibiotics in
preventing recurrent acute otitis media and in treating otitis media with effusion: A
meta-analytic attempt to resolve the brouhaha. JAMA 1993;270:1344-51.
23
M29 NHG Clinical Practice Guideline

Feverish illness in Children
Huisarts Wet 2008:51 (6):287-96

Berger MY, Boomsma LJ, Albeda FW, Dijkstra RH, Graafmans TA, Van der Laan
JR, Lemmen WH, Oteman N
Key messages
Fever is usually caused by a viral infection. Recognising
children with a serious underlying disease in time is
important.

Warning
symptoms are more important than the height of
the fever.
Children under the age of 3 months are at higher risk of a
serious underlying disease.

Temperature
measurements in children under the age of
3 months must be veried rectally.
distinction is made between observations by parents
A
and assessment by the GP. The parents/caregivers need
to watch out for alarm symptoms; the GP assesses
whether there are warning symptoms that can be objectied.

Information
about the childs past medical history is
requested during telephone triage.

In
children under the age of 2 with fever without apparent
source, after history-taking and physical examination,
urine testing should now be performed on the same day.

In
cases of fever without apparent source, reappraisal is
recommended within 24 to 48 hours.
typical febrile convulsion is a benign condition.
A
x
x
x
x
x
x
x
x
x
J. Blijham, M09 Acute Otitis Media (AOM) M29 Feverish Illnes in Childeren
Houten, DOI 10.1007/978-90-313-8872-1_2,
2011 Bohn Stafleu van Loghum, part of Springer Media, the Netherlands
26
Introduction
The NHG Clinical Practice Guideline on Feverish illness in Children provides

guidelines for the diagnosis and treatment of children with fever of brief
duration (1 week at most). What to do in the event of a febrile convulsion is
covered in a separate paragraph. Fever is an elevation of body temperature
above 38.0 C[1]. Body temperature is preferentially determined via a rectal
reading. Other forms of temperature measurement, such as infra-red tympanic thermometers, are less reliable[2]. Fever is almost always caused by infectious diseases. The vast majority of infections is caused by viruses. The clinical
guideline provides recommendations for recognising children at high risk
of serious illness and for advice and instruction of parents/carers of children
with feverish illness. The clinical guideline indicates under which conditions
additional examinations are warranted to identify infectious diseases, and
which conditions require specic treatment, such as meningitis. This clinical
guideline does not contain specic information on what additional testing is
required and which treatment for specic infectious diseases is indicated. For
more information, please refer to the relevant clinical guideline.
Background
Epidemiology
Fever is one of the most common disease symptoms. Given the variety of different denitions of fever and the different methods used to determine its
height, it is difcult to obtain incidence data. Fever is most common in the
age group of 0 to 4 years[3].
Pathophysiology
Fever usually occurs in response to the intrusion of micro-organisms into the

body. It is a normal physiological response, in which the release of cytokines
initiates a cascade of reactions. The thermoregulatory mechanism in the
hypothalamus responds by essentially turning up the body-thermostat[4].
Body temperature can only rise to above 42 C in cases of intracerebral infection (rare) or in cases of hyperthermia.
Hyperthermia in children may occur if body heat cannot be released sufciently[5].
M29 NHG Clinical Practice Guideline Feverish illness in Children
Diagnostic guidelines
Remote assessment by telephone
The GP, practice secretary or practice nurse actively asks about the following
characteristics and alarm symptoms to determine if and when the child needs
to be assessed.
The child with fever must be seen on a very short notice if one or more of the
alarm symptoms listed in the box below are present.
Alarm symptoms
Serious illness, quickly worsening condition, uid intake less than half of normal, drowsiness, inconsolable crying, rash appearing during fever, a change
in skin colour, changed breathing, moaning, apnoea; children younger than 1
month.
The recommendation is that children with feverish illness should be seen the
same day in case of:
Age between 1 and 3 months;
Compromised immune status or relevant comorbidity, for example children with congenital heart and lung conditions;
Fever for more than three days[6 ]or fever recurring after a number of feverfree days.
If the above characteristics or alarm symptoms are absent, the recommendation is to assess the child with fever the same day if:
The severity of the childs condition cannot be ascertained sufciently over
the phone;
The telephone conversation is complicated by irritation or even aggression,
difcult communication or a difference of opinion with the parents/caregivers;
Persistent parent worry[7].
In all other cases, a longer term appointment or self-care advice will sufce. A
home visit to a child with feverish illness is generally not indicated.
History
The GP asks about general signs and symptoms

Duration of the fever ;[6,8]
An impression of the childs condition ;[9] in the very young, parents/carers
can be asked about symptoms of drowsiness (is the child walking around,
does the child make eye contact) and crying (more than normal, can the
child be consoled);
27
28
Ask about urine production and uid intake. In infants, less than half of
normal (daily) intake is a alarm symptom.
The GP then checks for the presence of signs and symptoms that are associated with
specific diseases:
Skin: skin lesions/rash;
Central nervous system: decreased level of consciousness (less to no contact
with the child), vomiting and/or headache;[10]
Ear-nose-throat: throat ache, earache or rhinitis
Respiratory tract: breathing difculties, coughing or shortness of breath
and (in nursing infants) poor feeding;[11]
Digestive tract: vomiting and/or diarrhoea, possible relation to food intake;
Urogenital tract: stomach complaints, painful or burning sensation while
urinating, increased frequency of urination;
Hydration: urine production (in young children: enough wet diapers, at
least 4 per 24 hours). Drooling and ample tear production make dehydration unlikely.
The GP also asks about or checks the patient file for the following:
Relevant comorbidity, such as children with congenital heart, lung or urinary tract conditions, or immunocompromised children;
Vaccination status and most recent vaccination;[12]
Medication use (including immunosuppressants);[13]
Illness in the childs environment, for example cold sores;
Recent stay in a foreign country.
Physical examination
The objective of physical examination is to determine the severity of the illness and nd a potential source for the fever. The GP calmly approaches the
child, preferably at his or her own level. Children do nd examination of the
ear, nose and throat most unpleasant. It is therefore recommended that this
part of the examination is reserved for the end. Every child is examined fully,
unless there is an obvious source for the fever. Good observation is a key part
of the physical examination. Areas for attention during the examination are:
Temperature (always check rectally in children under the age of 3 months);
Is the child in a poor condition: irritability, decreased level of consciousness
(less to no contact), response to parents, crying and consolability;[9]
Skin: colour pale, cyanotic, patchy or grey; pale extremities; (maculopapular) exanthema or purpura (spots that cannot be pressed away); capillary
rell (increased > 1.5 to 2 seconds) should be determined on the sternum;
Signs and symptoms of meningitis: bulging fontanel, Brudzinskis sign,
Kernigs sign or Vincents sign;[10]
Inspection of the thorax to assess respiratory rate; count for one minute
(tachypnoea is dened as a rate of > 60/min in children younger than 2
months, > 50/minute in children between 2 months and 1 year and > 40
in children over the age 1. In individuals over the age of 18, tachypnoea is
dened as a respiratory rate of > 25/minute). Note chest in-drawings and

nasal aring. Listen for crackles in the chest and look for abnormalities
during auscultation and percussion;[11]
Inspection, auscultation, percussion and palpitation of the abdomen;
Kidney pain in the anks;
ENT: inspection of ears, nose, throat and mouth, palpation of regional
lymph nodes and assessment of mucous membrane hydration.
Additional examinations
Additional blood testing is of no added value.[14]

Urine testing for urinary tract infection (UTI) is indicated on the same day
in:
Children under the age of 2: if history or physical examination do not
reveal an source for the fever;[15]
Children over the age of 2: if there are signs of a UTI, or in the event of
fever lasting more than 3 days without a clear source.
In the event of abnormal urine test ndings, always perform a urine culture
(for criteria, see the NHG Clinical Practice Guideline UTI).
If there is any doubt about the presence of pneumonia, consider a chest xray. The diagnosis pneumonia is most likely in the event of fever combined
with coughing, tachypnoea, chest in-drawing or abnormalities on auscultation.[11] (see also the NHG Clinical Practice Guideline Acute Coughing).
A chest x-ray has no added value for children with fever without a source
after completion of the physical examination and history-taking.
Assessment
The GP determines whether there are any warning symptoms present (see
box).
Warning symptoms
The child seems seriously ill upon physical examination, with a decreased level
of consciousness, persisting vomiting, purpura, signs of severe tachypnoea
and/or dyspnoea, decreased peripheral circulation, pale, mottled, and/or
ashen countenance, meningeal signs.
If one or more warning symptoms are present, the child should be referred to
a paediatric specialist.
After history-taking and physical examination, the following diagnoses
may be considered.
Upper respiratory tract infection: throat ache, ear-ache, swallowing complaints or rhinitis, or abnormalities upon examination of the ENT area (see
29
30
NHG Clinical Practice Guideline Sore throat, NHG Clinical Practice Guideline OMA and NHG Clinical Practice Guideline Rhinosinusitis);
Lower respiratory tract infection: coughing, tachypnoea, dyspnoea and/or
abnormalities upon auscultation (see also NHG Clinical Practice Guideline
Acute Coughing);
Gastro-enteritis: vomiting and/or diarrhoea. In the event of persisting
abdominal pain, the possibility of appendicitis, UTI or pneumonia should
be considered (see NHG Clinical Practice Guideline Acute Diarrhoea);
Urinary tract infection: suspected in case of abnormal urine testing (for criteria, see NHG Clinical Practice Guideline UTI);[16]
Vaccinations: fever is a possible side-effect following recent inoculation;[12]
Fever without a source: if physical examination does not yield any indications for a specic diagnosis, this is called fever without a source;[17]
Sepsis: a septic child generally appears seriously ill; clinical signs consistent
with sepsis include a prolonged capillary rell (pale, cyanotic or ashen skin
colour), decreased level of consciousness (less contact), inconsolable crying
and/or moaning;[18]
Meningitis: clinical signs that may indicate this condition include (persistent) vomiting, meningeal signs, decreased level of consciousness (less
contact), purpura, pale, cyanotic, ashen or mottled skin colour, inconsolable crying and/or moaning.[10]
Guidelines on management and treatment

Information and advice
Clear explanation of fever makes it easier for parents or caregivers to deal

with children with fever. The following is important:
Fever is a body temperature over 38.0 C.[1] Usually fever is a sign of infection. Fever causes dehydration and children with a feverish illness should
therefore be given extra uids.[19] Most children lose their appetite when
they are feverish, and they should not be forced to eat.
Fever generally does not require specic treatment. It is not necessary to
actively reduce the body temperature. Antipyretics do not help to speed up
recovery, although the fever-reducing and analgesic properties can help
children to feel better.[20] It is not necessary for a child with a feverish illness to stay indoors or in bed. Dress the child in light clothing and ensure
that the environment is not too warm, as body heat is released via the skin.
Applying cold compresses or sponging is not recommended.[21]
The most important reason for measuring the body temperature is to
determine whether or not a child has a fever. One measurement per day
will sufce. The temperature should be taken rectally as other ways of
measuring are less accurate.[28] Observing the child and noting any changes in behaviour are more important than continually taking the childs
temperature. Generally speaking, the higher the temperature, the more
31
worried the parents are, but in reality the extent to which the child seems
unwell is more important than the temperature itself. Pay much personal
attention to the child; this also provides a good opportunity to observe the
child.
Should any alarm symptoms appear (see also remote assessment by
telephone), a follow-up contact is mandatory.
To support verbal information, the following NHG patient information
letters: Aandachtpunten bij het zieke kind [What to watch out for in unwell
children], Kinderen met koorts algemeen [Children with feverish illness, general
information] and Koortsstuip [Febrile convulsions] can be given. These letters
are based on the NHG Clinical Practice Guideline and contain information
about fever in children and the treatment required. (See http://www.nhg.org,
patient information section for an overview of all NHG patient information
letters.)
Table 1
Recommended dosage for paracetamol (based on weight and short-term use; less
than 3 days)
weight and age
oral, maximum dose 90/mg/kg/day (syrup 24
rectal, maximum dose 90/mg/kg/day
mg/ml)
3 kg (birth)
2 ml four times daily
1 suppository (120 mg) twice daily
6 kg (3 months)
1 suppository (120 mg) three times daily
10 kg (12 months)
15 kg (3 years)
9 ml four times daily or 240 mg tablet four times
1 suppository (240 mg) four times daily
daily
20 kg (5 years)
1.5 tablet (240 mg) four times daily
25 kg (7 years)
1 tablet (500 mg) four times daily
30 kg (9 years)
1 tablet (500 mg) ve times daily
42.5 kg (12 years)
1 tablet (500 mg) six times daily
1 suppository (1,000 mg) three times

daily
Source: Pharmacotherapy Guideline on Pain Relief (http://www.nhg.org)
Medical therapy
Reducing fever is not an end in itself. In case of pain or discomfort, paracetamol may be given in concordance with the parents (see table 1).[22,23,24]
32
Response to paracetamol has no relation to the severity of the underlying

condition.[25]
How to handle fever without a source
If history and physical examination do not reveal an obvious cause for the
fever, this is called fever without a source. In most cases, the infection is
harmless, however in exceptional cases a serious condition may develop.[17] It
is important to carefully instruct parents/carers and discuss when to contact
their GP practice (see follow-up). In children younger than 3 months, signs
and symptoms indicating serious infection may be lacking or non-specic.
Because vaccinations in children younger than 3 months do not provide sufcient protection, the chances of infection by bacterial pathogens such as
Haemophilus influenzae and pneumococci are increased. All children younger
than 3 months with feverish illness without a source are referred to a paediatrician. Children older than 3 months suffering from feverish illness without
a source without warning symptoms should be reassessed (by telephone or in
person) after 24 to 48 hours.
Follow-up
Parents are instructed to contact the GP practice (again) for follow-up in the
following cases:
Alarm symptoms (Seriously ill, quickly worsening condition, poor uid
intake (less than half of normal), drowsiness, inconsolable crying, rash
appearing during fever, a change in skin colour, changed breathing, moaning, apnoea);
If they feel a need for reassessment;
After 24 to 48 hours for children older than 3 months and fever without a
source.
Referral
A child with feverish illness only rarely needs to be referred. Indications for
referral are:
All children younger than 1 month;[18]
All children between the ages of 1 and 3 months, unless there is a clear
source for the fever;
Presence of warning symptoms (see assessment and follow-up)
Suspected meningitis or sepsis;[10,18]
Signs of dehydration, particularly in children under the age of 1 year;
A need for diagnostic certainty.
Febrile convulsions
Two to ve percent of all children suffer at least one febrile convulsion

during childhood.[26] In a GP practice with a list of 2350 patients, a GP will
see less than one febrile convulsion each year. Most febrile convulsions occur
between the ages of 16 and 18 months. Most ts occur in children without any
neurological past medical history, in the age group of 6 months to 5 years,
during a period of fever.[27] Typical febrile convulsions do not lead to brain
damage. Many parents are afraid that their child will have a febrile t during
high fever, but the vast majority of febrile convulsions occur at the beginning
of a febrile period. In about half of all cases, the febrile convulsion is the rst
sign of feverish illness. About one third of children with febrile convulsions
have another t in the next febrile period. Most recurrences occur within six
months. The risk of recurrence is higher in cases of non-typical febrile convulsion. There seems to be a genetic predisposition for febrile convulsions.
The probability of suffering from a febrile convulsion is higher if one or more
rst-degree relatives did suffer from a febrile convulsion in the past.[28]
Diagnosis of febrile convulsions
A typical febrile convulsion begins with a tonic-clonic seizure with a decreased level of consciousness. The seizure does not last longer than 15 minutes,
and is followed by a post-ictal phase that can last up to one hour. During this
post-ictal phase, a source for the feverish illness should be sought, particularly signs of meningitis.[29] These symptoms are difcult to identify in the
post-ictal phase, and are often lacking in children under the age of 1 year. The
child also cannot be assessed properly if diazepam is given. In these cases,
reassess the child again later the same day. No additional examinations are
required in case of a typical febrile convulsion.
Management of febrile convulsions
While the parents or carers are on the telephone, instruct how the airway can
be kept free. Have the child placed on his front or side, with the head down.
An immediate home visit is indicated. If the child is still convulsing upon
arrival, diazepam is administered rectally.[30] The dosage is age-dependent:
under the age of 1 year 0.5 mg/kg of body weight, 1-3 years 5 mg, older than
3 years 10 mg of diazepam rectally. If the convulsion persists, the same dose
should be repeated after ten minutes. If the child still displays seizures after
fteen minutes, an emergency admission is indicated. If the child is already
in the post-ictal phase when rst assessed by the GP, or has responded well
to the treatment, a structured follow-up (by telephone or otherwise) must be
ensured. If there is any doubt, the child should be reassessed again after a few
hours.
In a typical febrile convulsion, consciousness is restored within 60 minutes,
unless diazepam has been administered. For reassurance, a rectiole with the
correct dose of diazepam (or a prescription for a rectiole) may be left with the
33
34
parents or caregivers, together with clear instructions on what to do in the

event of another convulsion. Antipyretic treatment is not helpful in preventing recurrence. Prescription of anti-convulsive medication to prevent recurrence of febrile convulsions is contra-indicated.[31]
Sharing information with the parents/carers is very important in handling
febrile convulsions, with an emphasis on the benign nature of a febrile convulsion, the chances of recurrence and what to do in such an event.[32,33]
Consultation and referral in case of febrile convulsions
In the following cases, serious illness is suspected and referral to a paediatric

specialist is indicated:
A febrile convulsion in a child with feverish illness younger than 6 months;
A recurrent febrile convulsion during the same febrile episode;
A febrile convulsion lasting longer than fteen minutes;
A febrile convulsion with focal signs: meningeal signs, signs of meningitis,
purpura and/or a decreased level of consciousness.
Establishment
In September 2006, a working group of six General Practitioners started writing the NHG Clinical Practice Guideline Children with Feverish Illness. The
working group consisted of M.Y. Berger, L.J. Boomsma, F.W. Albeda, R.H.
Dijkstra, T.A. Graafmans, J.R. van der Laan and W.H. Lemmen, all MDs and
General Practitioners. No conicts of interest were reported.
Comments were also received from a number of referees, namely: J.M.E.
Quak, paediatric nephrologist and Prof H.A. Moll, paediatrician, both on behalf
of the NVK; Dr M.A.H. Fleuren on behalf of TNO Quality of Life; Dr M. van
Stuijvenberg, paediatrician; P.J.M. Uitewaal, GP; A. Brand and C.A. de Kock,
GPs, on behalf of the NHG Standards Advisory Council; Dr H. van Weert, editor-in-chief of Huisarts & Wetenschap; A.C. van Loenen, hospital pharmacist,
clinical pharmacologist and editor in chief of the pharmacotherapeutic formulary Farmaceutisch Kompas, on behalf of the Health Care Insurance Board.
Referees do not necessarily all support every detail.
In March 2008, the standard was authorised by the NHG Authorisation
Committee.
N. Oteman, GP in Schoonhoven and scientic employee in the Guideline
Development and Science department of the NHG, provided the working
group and the editors of this standard with support and guidance.
Notes
Note 1 Fever Practically all of the literature refers to fever as a body temperature 38.0 C [Bonadio 1994, Baraff 1993]. This limit was also used in this set
of guidelines.
Note 2 Temperature measurement Palpation: Parents often diagnose fever by
feeling the forehead. A study in Zambia showed that in 94% of children (aged
1 month to 16 years), parents were able to recognise fever with a positive predictive value of 39%. If parents thought they did not feel fever, this proved
accurate in 95% of children. If parents indicate their child has a fever during
triage because of palpation, they are correct a good half of the time. Therefore, a temperature increase must always be veried using a rectal measurement [Whybrew, 1998].
Axilla: The conclusion of a meta-analysis of 20 articles (n=3,201 children
ages 0 to 18) showed that axillary temperature measurements often differ
from rectal temperature. In general, axillary temperature was lower, but the
difference varied from 0.17 C in infants (95% CI 0.15 to 0.5) to 0.93 C (0.15
to 1.98) in older children. In infants, axillary temperature correlated better
with rectal measurements, but this was only a small group. The general conclusion is that axillary temperature measurement is insufciently reliable
compared with rectal temperature measurement. No data is available on
sensitivity and specicity of axillary measured temperature compared with
rectally measured temperature. [Craig 2000].
Ear thermometer: In a meta-analysis of 44 studies (n=4,441 children aged 0 to
16 years), large differences were found between the rectal thermometer and
the ear thermometer. The differences were not correlated with temperature
or child age. It cannot be ruled out that the presence of acute otitis media
inuenced the correlation, as the involved studies did not supply sufcient
data on this subject. Measured temperatures deviated in both directions. The
average difference between rectal and ear measurements was 0.29 C [Craig
2002]. The pooled estimate for ear thermometer sensitivity was 63.7% (95%
CI 55.6 to 71.8) and specicity was 95.2% (93.5 to 96.9) compared to a rectally
measured temperature of > 38 C. There were few false-positives. This means
that if an ear thermometer registers fever, the likelihood of fever is high.
Conclusion: During telephone triage, all reports of fever regardless of how
it is measured must be taken seriously, as all measurement methods are
reasonably good at predicting the presence of fever. The ear thermometer is
the most practical, but is less reliable than rectal measurement. In children
under the age of 3 months, it is important to be certain of whether they are
febrile. It is recommended that rectal temperature always be taken in this
group.
Note 3 Epidemiology The Second Dutch National Study of general practice
returned an incidence for the diagnosis of fever of 6.7 per 1,000 patients per
year for all age groups pooled, with an incidence of 122 during the rst year
of life and of 41.5 in the age group 1 to 5 years. In the age group 5 to 14 years,
35
36
the incidence is 7.2 per 1,000 patients per year. There is no difference between
Dutch and immigrant children [Van der Linden 2004]. According to the Transition Project, incidence of a consultation for fever in general practice is about
430 per 1,000 children per year in the age group 0 to 4 years. In about 23% of
cases where fever is the reason for consultation, the diagnosis is a viral infection. This is followed by upper respiratory tract infections (16%) and acute
otitis media (14%) [Lamberts 1994, Van der Linden 2004].
For the period 2001 to 2004, there were 20 hospital admissions per 100
0-year-olds with the discharge diagnosis perinatal conditions in the Netherlands [Roedig 2007].
Note 4 Pathophysiology Under the inuence of exogenous pyrogens such as
viruses, bacteria and toxins, but also due to immune complement reactions,
macrophages and endothelial cells are triggered to produce endogenous
pyrogens, mostly interleukin-1, interleukin-6 and TNF-alpha. Interleukin-1
acts upon the endothelial cells in the anterior hypothalamus (and does not
pass the blood-brain barrier), releasing prostaglandins, mostly of the PGE2
type, which act on the thermostat in the anterior hypothalamus via cyclic
AMP, leading to an increase in the set point. The thermoregulatory centre in
the anterior hypothalamus receives information from skin and muscles via
afferent neurons, and also contains cells that measure temperature changes
in the blood. These cells respond to temperature changes of 0.02 C. Cells
with a thermostat function are located adjacent to them. These cells regulate the temperature set point. In case of fever, the set point is set to a higher
value. Interneurons transmit the information from the anterior hypothalamus to the posterior hypothalamus, which regulates the production and
release of heat via the autonomous nervous system (sympathetic and parasympathetic nervous activity, respectively). At the start of a febrile period, the
set point is set to a higher value and heat is retained through vasoconstriction
in the skin and increased muscle activity (sympathetic activity). The patient
experiences cold. At the end of a febrile period, the skin starts radiating heat
due to vasodilation, after which the patient starts sweating and feels clammy
due to evaporation (cold and wet; parasympathetic activity). This is a negative
feedback mechanism. Multiple inhibiting factors have been identied in the
hypothalamus-pituitary axis that limit body temperature to a maximum of
42 C, and rarely allows body temperature to rise above 41 C [Roberts 1979,
Bernheim 1979, Dinarello 1984, Dinarello 1988, Endres 1987, Robbins 1999].
Note 5 Hyperthermia Young children exposed to high temperatures, for
example because they are placed too close to a heat source, or left in a car in
hot weather, may suffer hyperthermia. The body temperature can rise to 44
C. The young infants lower capacity for perspiration contributes to hyperthermia. The skin often becomes warm and dry; the child is apathetic and
has red cheeks. Tachypnoea may occur, followed by stupor, coma and convulsions. Mortality and morbidity (brain damage) of hyperthermia are high.
When lowering temperature, attention must be given to potential uid and
electrolyte imbalance [Behrman 2004]. Unlike during infections, the body

temperature regulation mechanisms function normally in hyperthermia.
Note 6 Duration and course of fever Some studies have found a weak association between the duration of fever and its course. The longer the fever lasts,
the higher the risk of a severe course [Berger 1996, Hsiao 2007, Richardson
2007, Trautner 2006, Bleeker 2007]. Another study found that fever lasting
longer than 3 days was associated with a signicantly greater probability of
severe infection [Goh 2006]. Two other studies however found that the probability of severe infection increased as the febrile period decreased [Teach 1997,
Haddon 1999].
Conclusion: There is insufcient evidence to support a relationship between
the duration of fever and the severity of the condition. In case of persistent
fever, a secondary bacterial infection with a potentially more severe course
must be considered.
Note 7 Worried parents General practitioners who had actually come in contact with a child with sepsis or meningitis and who indicated they could provide learning moments in addition to the listed warning symptoms, almost
unanimously mentioned uneasy parents. These are general practitioners
who, in hindsight, felt they could have referred sooner. Almost all of these
general practitioners noted the parents were capable of verbalising their
unease if asked about it specically [Fleuren 2002].
Note 8 Height of the fever The question of whether the height of the fever can
help differentiate between a severe and a mild infection is difcult to answer. There seems to be an association between the height of the temperature
and the presence of a urinary tract infection [Zorc 2005, Gorelick 2000]. The
association between a severe infection and the height of the temperature
is the strongest in young children [Pantell 2004]. There also seems to be an
association between the pathogen and the height of the temperature for
pneumococcal bacteraemia [Kupperman 1998]. Others did not nd any relationship between the height of the fever and the probability of severe infection
[Nademi 2001, Hsiao 2006]. Research into this association has only been performed in hospital settings. The low incidence of bacteraemia in primary care
limits the value of this clinical data [Lee 1998, Pantell 2004].
Conclusion: There is insufcient evidence to support the assertion that the
height of the temperature is an independent predictor of a severe course of
the infectious disease. The added diagnostic value is therefore minimal.
Note 9 Evaluation of severity of illness Over the years, various observational
scales have been developed to differentiate children at high risk of bacterial
infection from children with a viral or other infection and a benign course.
McCarthy was one of the rst to attempt this [McCarthy 1980]. This observational scale proved of no added value compared to traditional history-taking
and physical examination [McCarthy 1987]. In addition to the McCarthy
scale, the Yale Observation Scale (YOS) and the Young Infant Observation
37
38
Scale (YIOS) were developed for children with fever without a focus. The
goal was twofold; rst, to identify children with the highest risk of bacterial
infection in order to allow selective antibiotic therapy, and second, to prevent
unnecessary hospital admissions for children with non-severe infections.
Because YOS and YIOS missed too many children with severe infections, the
Philadelphia and Rochester protocols were drafted, which included additional tests (e.g. blood tests) and a chest x-ray [Baker 1993, Baker 1999, Anbar
1986, Dagan 1985]. Validation of these protocols showed high sensitivity
around 98% - and relatively low specicity, varying between 23.2 and 39.4%
[Garra 2005]. Both protocols can therefore only be used to rule out a severe
bacterial infection. Due to the low prevalence of severe bacterial infections in
children with fever in general practice, a test with a high specicity would be
very useful. No data is available on the usefulness of both YOS and YIOS in
Dutch general practice.
Conclusion: The use of above-mentioned observational scales and protocols
is advised against. A few items from history included in the YOS/YIOS are
copied in this guideline.
Note 10 Bacterial meningitis Background: Bacterial meningitis occurs 700 to
800 times per year in children in the Netherlands. The highest meningitis
incidence is found in the second half of the rst year of life, around the age of
7 months. The most common cause of bacterial meningitis is still the pneumococcus, which will likely change due to the introduction of the pneumococcal vaccine in 2006 [Netherlands Meningitis Foundation 2008, Fleuren
2002, Fleuren 2004].
Clinical features: classic symptoms headache, neck stiffness and skin rash
occur in 33%, 39% and 66% of cases, respectively. The combination of all
three symptoms only occurs in 13% of cases [Granier 1998]/
Meningeal irritation: Meningeal irritation may be determined using Brudzinskis sign (reexive bending of legs upon exion of the head), Kernigs
sign (severe pain upon extending the bent knee) and Vincents sign (keeping
the back straight when sitting with extended knees) or diaper pain (crying
when raising the buttocks when the child is supine). In only one-third of
cases of meningeal irritation a bacterial meningitis is present. Nevertheless,
lumbar puncture is indicated for all children with meningeal irritation [Van
Eeuwijk 2003].
Skin rash: maculopapular exanthema that is not yet haemorrhagic may
occur at the beginning of a meningococcal sepsis. Meningococcal sepsis
may also manifest with urticaria [Winterberg 1996]. The majority (82-97%)
of children aged 1 to 4 with meningococcal sepsis does have a haemorrhagic
rash, however. In the age group 4 to 15 years, this is true for 69-75%.
Age: In young children, symptoms are often non-specic. They may exhibit
elevated or decreased body temperature, changes in consciousness, irritability, hypotonia and eating disorders. In one third of cases, a bulging fontanel
is present [Roord 2001, Granier 1998]. Children aged 5 to 6 years often present
with headache. Fever is almost always present upon hospital admission, but
is less common in infants younger than 5 months [Roord 2001].
Course: A retrospective study among general practitioners and parents of

448 children with a meningococcal sepsis or meningitis attempted to chart
the disease course. This revealed that classic symptoms such as haemorrhagic rash, decreased consciousness and meningeal irritation often occurred
late, on average only after 13 to 22 hours. In 72% of children, there were early
symptoms of sepsis. The most common symptoms muscle aches in the
legs, cold extremities and abnormal skin colour occurred between four and
six hours after the beginning of the disease [Thompson 2006]. Two types of
disease course may be identied. In the rst, the child is ill for one to a few
days, with fever and signs of an upper respiratory tract infection (caused by
Staphylococcus pneumoniae and Haemophilus inuenzae). In the other, less
common form, the course is acute and fulminant, and sometimes fatal. In
this case, signs of sepsis and meningitis (primary cause Neisseria meningitidis)
appear within a few hours [Roord 2001, Granier 1998]. In the case of Meningitis, the greatest morbidity and mortality is caused by the pneumococcus
[Roord 2001].
Conclusion: Children with fever must undergo extensive physical examination, among other things to detect meningitis. The absence of classic
symptoms, particularly in infants, does not entirely rule out meningitis. In
these cases, watch for general alarm symptoms and symptoms, and ensure
good follow-up or refer to a paediatrician if meningitis is suspected.
Note 11 Pneumonia A systematic literature review shows there is no gold
standard for differentiating between a viral and bacterial pneumonia. The
meta-analysis ultimately included ve studies that attempted to compare
chest x-rays to a reference test. No studies used bronchoalveolar lavage or pulmonary aspiration as a reference test to determine whether the patient had a
bacterial pneumonia. Performing a chest x-ray does not seem useful in order
to differentiate between a viral and a bacterial pneumonia [Swingler 2000].
Little research has been conducted examining the relationship between
clinical symptoms and the presence of pneumonia in primary care. Data is
however available from hospital studies.
Palafox et al examined whether tachypnoea (using the WHO denition) is
a sufciently valid characteristic to diagnose pneumonia in children with a
respiratory infection. A total of 110 children, aged 3 months to 5 years with an
acute respiratory infection, 51 of whom with tachypnoea, were included. The
clinical diagnosis of pneumonia was made in 35 children (32%), conrmed
via chest x-ray, the gold standard for diagnosing pneumonia. The sensitivity
of tachypnoea as a sole clinical sign was 74%, specicity was 67%. In children
with less than three days of fever, sensitivity and specicity were both lower.
Age and undernourishment had no effect. The presence of retractions was
also a discriminating factor, with a sensitivity of 71% and a specicity of 59%.
Abnormal auscultation was far less reliable, with a sensitivity of 46% and a specicity of 79%. The absence of audible abnormalities does not rule out pneumonia. The diagnosis was made most reliably in children under the age of 6
months with tachypnoea [Palafox 2000].
39
40
Another hospital study was a prospective trial in 147 children suspected

of pneumonia. The clinical signs that best predicted pneumonia were determined retrospectively (with a chest x-ray as a golden standard). The most sensitive parameters were: tachypnoea (sensitivity 99%, specicity 88%), coughing
(sensitivity 98%, specicity 70%), retractions (sensitivity 88%, specicity
77%),and fever (sensitivity 78%, specicity 42%).
The most relevant nding was tachypnoea; its absence almost entirely
ruled out pneumonia [Shamoon 2004].
A third prospective study also found an association between tachypnoea
and pneumonia. The prevalence of pneumonia in this study was 7%. Per
degree of temperature increase, respirator rate increased by 2.5 per minute.
This study showed tachypnoea had a sensitivity of 73.8% and a specicity
of 76.8%. The positive predictive value of tachypnoea is only 20%, while the
negative predictive value and the lack of tachypnoea is 97.4% [Taylor 1995].
Conclusion: Pneumonia is likely in the event of fever combined with
coughing, tachypnoea, retractions or abnormalities upon auscultation.
Tachypnoea is the most sensitive symptom. The absence of these symptoms
makes the probability of pneumonia very low. The working group therefore
recommends against routine chest x-rays for children with fever without
pulmonary complaints.
Note 12 Vaccinations Most vaccines can cause a fever within 24 to 48 hours of
administration. Clinical studies indicate that the number of fever reactions is
higher when the pneumococcal vaccine and hexavalent (Dtak/Hib/Hepatitis
B) vaccine are given together than if a hexavalent vaccine is given alone. Fever
is frequently (> 10%) reported in association with the meningococcus C vaccine. For the BMR vaccine, fever only occurs ve to twelve days after vaccination (Pharmaceutical Aids Committee 2007].
Note 13 Immunocompromised patients A patient may be immunocompromised
due to any number of conditions and treatments. Conditions that affect the
immune system include HIV infection, Downs syndrome, combined immunodeciency syndrome, hypogammaglobulinemia, agammaglobulinemia,
leukaemia, lymphomas and generalised malignancies. Immunosuppressive
therapies are treatments with corticosteroids, cytostatic agents, radiotherapy,
status post splenectomy or bone marrow transplantation.
Note 14 Additional blood tests Little to no primary care research has been
done examining the added value of blood testing in children with a fever.
Most children with fever have a viral infection with a benign course. A small
proportion of them will develop a bacterial infection with a serious course,
such as meningitis or sepsis. The question is whether blood testing in a primary care setting can identify those children with the highest risk of a severe
disease course. Severely ill children will be referred to a hospital, and the
question is whether blood testing in children with a good clinical condition
has any consequences.
41
Initially, blood testing was primarily focused on the number of white blood
cells. Various studies among children with fever in hospital care showed that
a high white blood cell count had a sensitivity of 69-80% and a specicity of
58-80% for predicting severe bacterial infection. These values are based on a
cut-off value of 15-18 x 109/l [Isaacman 2000, Isaacman 2002, Pulliam 2001].
Two studies looked at the value of the neutrophil count, with a cut-off value
of 10.2 and 10.6 x 109/l. The sensitivity for bacterial infection was 69-71%, and
the specicity was 76-79% [Pulliam 2001, Isaacman 2002].
More studies have been conducted assessing CRP, particularly in children
younger than 36 months. Table 2 provides an overview of various cut-off
values and sensitivity and specicity for predicting bacterial infection with a
potentially severe course. All studies were performed in a hospital setting.
A systematic review of 46 articles assessed the role of procalcitonin (PCT) as
an early marker of severe infection in children. PCT has a sensitivity varying
from 83-100% and a specicity of 70-100% for diagnosing sepsis and meningitis. The cut-off value varies in the studies, but in general, 2 ng/ml is used to
differentiate between viral and bacterial infections. The role of PCT in diagnosing a bacterial pneumonia remains unclear. This is largely because a bacterial pneumonia is often diagnosed using a chest x-ray, which cannot be considered a gold standard. The specicity of PCT for diagnosing pyelonephritis
is 82-86%, and the sensitivity is 70-73% when compared to renal scintigraphy
(DMSA scan) as the gold standard. In a hospital population of children with
fever without a focus, a sensitivity of 93% and a specicity of 74% have been
found for tracing a severe bacterial infection. Unfortunately, this study also
made the diagnosis of bacterial pneumonia based on a chest x-ray [Van Rossum 2004].
Conclusion: There is no single laboratory test that is sufciently specic to
identify the early stages of an infection with a potentially serious course in
children. PCT seems to be the most promising marker for the future. However, there is insufcient evidence available from primary care research to
assess the value of PCT in general practice. Given the low a priori probability
of severe infection in primary care (which will probably be lowered even
further thanks to the introduction of the Hib and pneumococcal vaccines),
markers would have to become even more specic [Black 2004, Lee 1998,
Kourtis 2004]. Additional blood testing in general practice is therefore not
recommended.
Table 2
study
Galetto-Lacour
Predictive value of CRP in children with fever

cut-off value
sensitivity
specicity
relative risk in the event of a positive
(mg/l)
(%)
(%)
result
40
79
79
6.1
30
81
89
3.79
2003
Carrol 2002
42
study
cut-off value
sensitivity
specicity
relative risk in the event of a positive
(mg/l)
(%)
(%)
result
Pulliam 2001
70
79
91
13
Isaacman 2002
44
63
79
3.3
Gendrel 1999
20
73
88
5.43
Thayyil 2005
50
75
68.7
5.23
Note 15 Risk factors for developing a urinary tract infection (UTI) A study among
children with fever in a hospital setting showed that 3-10% of children
younger than 3 months had a urinary tract infection [Newman 2002]. It is
estimated that 5% of all children with fever without a focus suffer from a
urinary tract infection [Hoberman 1993]. In newborns and infants, the classic
symptoms of a urinary tract infection are often lacking [Van Wijk 1998]. Additional urine testing is therefore recommended in high-risk groups. Three different studies identied comparable risk factors, and none were performed
in a primary care setting. In a cross-sectional study in the emergency department among girls younger than 2 years and boys younger than 1 year with
a temperature of over 38.5 C, young age (< 12 months old), uncircumcised
males, fever without a focus, supra-pubic discomfort during medical examination and fever higher than 39 C were found to be independent risk factors
[Shaw 1998]. In a prospective tertiary care study among 1,469 girls with fever
without a focus (> 38.3 C), the following risk factors were identied: age less
than 12 months, Caucasian race, temperature higher than 39 C, more than
two days of fever and the absence of an origin for the fever [Gorelick 2000].
A prospective study among paediatricians working outside the hospital showed that the duration of fever, high temperatures, young age and not being
circumcised could be identied as risk factors.
Conclusion: Young age, uncircumcised males and high fever are associated
with the occurrence of a urinary tract infection. In children under the age of
2 years, symptoms consistent with a urinary tract infection may be difcult
to identify. The working group chose to perform urine tests on the same day
on children under the age of 2 with fever without a focus. The reason is that
children under the age of 2 are at greater risk of developing kidney damage
after a urinary tract infection (see note 16).
Note 16 Treatment of urinary tract infections Urinary tract infections in young
children can quickly lead to renal damage, and always require immediate
antibiotic treatment [Hansson 1997, Pylkknen 1981]. Retrospective British
research found kidney damage in 5% of all children referred with a urinary
tract infection [Coulthard 1997, Pylkknen 1981]. Another British study in
children with a history of urinary tract infection showed that the probability
of developing new renal damage decreases in children past the age of three
[Vernon 1997]. Other studies did not duplicate this decrease [Benador 1997].
It is assumed that pyelonephritis may eventually lead to hypertension and
renal insufciency [Jacobson 1989].
Note 17 Fever without a focus By far the most research into children with
fever without a focus is conducted in a hospital setting, mostly in the emergency and paediatric departments. This means data is not easily translated
to primary care. In children younger than 3 months, clinical presentation is
often atypical, making the presence of bacterial infection difcult to predict
[Ishimine 2006, Baker 1999, Klassen 1992, Bleeker 2002]. Children over the
age of 3 months have a lower risk of bacterial infection than young infants, as
good protection is only achieved after three vaccinations [Oostenbrink 1999].
Furthermore, only a small percentage of bacterial infections in this age group
is caused by the pneumococcus [Baker 1993]. The introduction of the Hib vaccine has signicantly decreased the number of Haemophilus influenzae infections [Lee 1998, Sur 2007, Bleeker 2002]. The pneumococcal vaccine was also
introduced in the Netherlands in 2006. It is expected this will further reduce
the number of bacterial infections caused by the pneumococcus [Black 2004].
A small percentage an estimated 0.02% - of children has a meningococcal
infection [Lee 1998]. Ninety percent of children over the age of 3 months with
a meningococcal infection have a clinical picture consistent with meningitis
or meningococcal sepsis, and 10% have an unexpected meningococcal bacteraemia. A retrospective study showed that additional blood testing did not
affect treatment policy in children who later proved to have positive blood
cultures with meningococci [Kuppermann 1999]. Observational scales such
as the YOS also proved not to be useful for identifying occult bacteraemia in a
clinical setting [Teach 1995]. About 5% of children with fever without a focus
are found to have a urinary tract infection [Hoberman 1993].
Conclusion: In children younger than 3 months with fever without a clear
focus, the clinical presentation of severe disease is often atypical. It is important to consider bacterial infections in this group in particular. The working
group therefore recommends that all children under the age of 3 months
without a clear focus for the fever be referred to a paediatrician. Early urine
testing is advised for children younger than 2 years without a clear focus for
the fever.
Note 18 Children younger than 1 month The probability of a severe course of
an infectious disease is greater in newborns. Infants younger than 1 month
do not have a fully mature immune system and are unprotected by vaccines.
Additionally, presentation may be very non-specic [Bleeker 2002]. Infections
occurring during or shortly after birth are often caused by long-term ruptured membranes (> 24H) or are acquired during passage through the birth
canal. An infection occurring within the rst 28 days after birth is a perinatal
infection [Merkus 2008]. Common pathogens are the Group-B Streptococcus
(GBS), Listeria monocytogenes, the herpes simplex virus, Staphylococcus aureus,
Staphylococcus epidermidis, Escherichia coli, Klebsiella spp, Haemophilus influenzae,
the hepatitis B virus and Chlamydia spp. In premature infants, necrotising
43
44
enterocolitis (NEC) must also be considered as a differential diagnosis in the

rst month.
The course of infections in newborns depends on the virus or bacteria
causing it. Contamination can lead to sepsis. A viral or bacterial infection in
a newborn can quickly worsen, and lead to death within a few hours. The
prognosis of an infected newborn is heavily dependent on the timing of the
diagnosis and start of treatment. Mortality among newborns with sepsis lies
around 20-50%. Sepsis caused by a Group-B Streptococcus has a mortality
even under optimal treatment of 40%. Mortality for a generalised herpes
infection is 70%. Surviving children run the risk of brain damage following
certain infections. This is particularly common after meningitis, with the
herpes simplex virus an E. coli being two notorious pathogens (see also http:
//www.rivm.nl/vtv/object_class/kom_problgeboren.html) [Van den Brande
1998]. Based on this information, the working group decided to refer all
children under the age of 1 month with fever to the paediatrician.
Note 19 Fluid balance Children under the age of 2 years are most sensitive to
dehydration. Infants are more likely to suffer dehydration than older children and adults, as increased uid loss in infants leads to swift changes to
extracellular volume [Kist-Van Holthe 1999]. Infants also lose a relatively larger amount of uid via the skin than an adult due to their large surface area
to volume ratio. Finally, the infants renal concentration ability in the event
of hypovolaemia is limited, contributing further to dehydration. Sufcient
uid intake is required to compensate for the uid loss caused by fever. Based
on the literature, no recommendations can be made regarding whether hot,
cold or lukewarm uids should be administered.
Note 20 Some ideas people have about fevers Parents are often needlessly afraid
of complications caused by fever [Crocetti 2001]. Fever need only be treated
when the child is experiencing discomfort [Taylor 2006]. Evidence shows that
parents are mostly frightened of the harmful effects of fever, such as convulsions (40% of parents), brain damage (12%), death (2%) and coma (1%). Many
parents also believe that a fever will continue to increase if left untreated
[Stephenson 1988]. Research among a representative sample of the Norwegian population shows that a third of people think that a body temperature
over 40.5 C is life-threatening [Eskerud 1991].
Fever in children is a symptom for which help is often sought outside ofce
hours. Fear of the consequences of fever and earlier experiences of medical
intervention play a signicant role in this [Kai 1996]. Parents often experience
inconsistencies in the approach of care providers and they are not sensitive to
reassurance (for example: Its only a virus) [Blumenthal 1998]. No literature
could be found about beliefs ethnic minority parents may hold concerning
fever in children.
Conclusion. There are many misconceptions about fever. It is therefore
important to provide parents and carers with a comprehensive explanation.
45
Note 21 Non-medical lowering of temperature A Cochrane review showed that

sponge-bathing has some effect on body temperature. The seven included
(quasi) randomised trials were heterogeneous and all had methodological
limitations. The authors of the review concluded that the physical methods
alone are not useful in lowering temperature, but that combination with
an antipyretic may lead to swifter temperature drops [Meremikwu 2002].
Sponge-bathing can be unpleasant for the child. As temperature decrease is
not an end in itself, sponge-bathing is not recommended.
Note 22 Choice of antipyretic Various studies have compared the efcacy of
paracetamol and ibuprofen (see table 3).
Table 3
author and
Effects of paracetamol versus ibuprofen on temperature

type of study
year
Goldman 2004
number of
medication
patients
Systematic
1,982
outcome
effect
measures
Paracetamol
review (14
(8-15 mg/kg)
trials, 11 RCTs)
versus ibupro-
Temperature
No signicant
difference
fen (2.5-10
mg/kg)
Perrot 2004
Meta-analysis
1,820
(17 studies)
Paracetamol
Pain
Pain: no
(10-15 mg/kg)
Temperature
signicant dif-
versus ibupro-
Safety
ference
fen (10 mg/kg)
Temperature:
ibuprofen
signicantly
better at lowering after 4-6
hours
Erlewyn-Lajeunesse 2006
RCT
123
Paracetamol
Temperature
Combination
(15 mg/kg) ver-
Absence from
of paracetamol
sus ibuprofen 5
school
and ibuprofen
mg/kg) versus
Stress score
signicantly
a combination
better for all
of both
end points
Studies have also been done examining the effect and height of the dosage.
An RCT with 121 children showed that paracetamol administered with a rectal loading dose of 30 mg/kg was more effective and faster when it came to
lowering temperature than a dose of 15 mg/kg [Treluyer 2001]. For ibuprofen,
a dose of 10 mg/kg proved more effective than 5 mg/kg [Goldman 2004].
Conclusion: Paracetamol and ibuprofen are comparable in terms of effectiveness for lowering body temperature. Ibuprofen may initially work slightly
46
faster and more powerfully, but the effect is comparable to paracetamol after
a few hours. The combination of both medicines may be more effective for
lowering body departure, but, given the high risk of dosage errors, monotherapy with paracetamol is the recommended treatment for lowering temperature. This standard recommends only combating fever in the event of
pain or discomfort. Combating fever is not an end in itself.
Note 23 Side-effects of paracetamol and ibuprofen In terms of side-effects, a
paracetamol overdose may cause acute liver damage. A review article shows
that this very rarely occurs in children. It is nonetheless important to realise
that glutathione is important for paracetamol detoxication. Malnutrition
and interactions with other medication and alcohol can reduce this detoxifying effect, leading to an increased risk of toxic effects. In children younger than 7 years, even a dose of 200 mg/kg did not lead to severe problems
[Bromer 2003]. Other authors set the cut-off for overdose lower (140 mg/kg)
[Lall 1998]. While paracetamol is safe to use, parents often dose it incorrectly
due to incorrect weight estimation, calculation errors and the like. Studies
conducted among 100 parents showed that 30% dosed correctly, 13% dosed
correctly despite incorrect calculations, 48% under-dosed and 9% overdosed
[Simon 1997].
Short-term use of ibuprofen in an RCT with 27,065 children showed the
risk of gastrointestinal bleeding was 7.2 (95% CI 2 to 18) per 100,000 children.
This was not signicantly different from the risk for paracetamol. The number of cases of renal insufciency (5.4 per 100,000 children) was not signicantly different compared with paracetamol use. The limitation of this study
is that not all children were screened as standard; renal failure or gastrointestinal bleeding was determined based on complaints [Lesko 1995, Lesko 1997].
Ibuprofen may cause kidney damage in children with decreased kidney
function or signs of dehydration [Moghal 1998].
Conclusion: Severe side effects rarely occur with paracetamol. Use of ibuprofen does not seem to cause a signicant increase in side-effects. However, as
additional tests were only performed in the event of complaints in the large
groups studied, no denitive statements can be made.
Note 24 Ibuprofen dosage Because ibuprofen is available over the counter,
ibuprofen dosage is included in this note for the sake of completeness (see
table 4). Paracetamol remains the recommended treatment in cases of pain or
discomfort.
Note 25 Response to antipyretics and course A literature search only revealed
ve prospective cohort studies examining the predictive value of lowered
body temperature following paracetamol administration for disease course.
In these ve studies, temperature was measured in a variety of ways, and
differing doses of paracetamol were given. However, all studies came to the
same conclusion: lowering of body temperature after paracetamol administration was not a predictor for disease course [Weisse 1987, Torrey 1985,
Yamamoto 1987, Baker 1987, Richardson 1999].
Table 4
47
Child dosage of ibuprofen: 20-30 mg/kg of body weight in 3-4 doses, for a maximum of 3 days
weight and
oral dose
rectal dose
10-15 kg (1-3
3-5 ml of syrup (20 mg/ml) three to four times daily
1 suppository (125 mg) twice/three
years)
or 1 orodispersible tablet (100 mg) three to four times
times daily
age
daily
15-20 kg (3-5
5-7 ml of syrup (20 mg/ml) three to four times daily or
1 suppository (125 mg) three/four
years)
1 orodispersible tablet (100 mg) four times daily
times daily
20-25 kg (5-7
7-9 ml of syrup (20 mg/ml) three to four times daily or
1 suppository (125 mg) four times
years)
2 orodispersible tablets (100 mg) three times daily
daily
25-30 kg (7-9
200 mg (tablet, coated tablet, capsule) three to four
1 suppository (125 mg) four times
years)
times daily
daily or 0.5 suppository (500 mg)

twice/three times daily
30-42 kg (9-12
200 mg (tablet, coated tablet, capsule) three to ve
0.5 suppository (500 mg) twice/three
years)
times daily
times daily
Source: Pharmacotherapy Guideline on Pain Relief (http://www.nhg.org)
Note 26 Incidence of febrile convulsions A large retrospective study in Rotterdam (3,570 children) found that 3.9% of the children have had at least
one febrile convulsion [Vink 1990]. A stratied sample among 103 general
practices in the Netherlands showed the incidence of febrile convulsions to
be 4.8 per 1,000 patient years. The probability of febrile convulsion between
the ages of 3 months and 6 years was estimated at 2.7% [Speelman-Verburgh
1996].
Note 27 Typical and atypical febrile convulsions A typical febrile convulsion
consists of a persistent extension cramp (tonic) followed by a series of generalised seizures (clonic), followed by a post-ictal phase of lowered consciousness
with complete recovery within 60 minutes. A febrile convulsion is the occurrence of the above event in children between the ages of 6 months and 5 years
with fever (38 C), without signs of intracranial pathology. An atypical fever
convulsion entails a duration of longer than 15 minutes and focal aspects
or recurrence within the same febrile period, particularly within 24 hours.
This may indicate a higher risk of severe pathology, including meningitis. A
typical febrile convulsion is not associated with an increased risk of epilepsy
[Sadleir 2007].
Note 28 Risk factors for febrile convulsion Predisposition to febrile convulsions
is largely determined by a positive family history of convulsions [Verity 1985].
A large-scale study in Rotterdam showed that children with a positive family
48
history had a 4.5 times higher risk of febrile convulsions [Offringa 1991].
Children with long admissions to neonatology units, frequent stays in day
care centres or slowed development were more likely to suffer febrile convulsions [Brouwer 1996].
Note 29 Additional examinations in the event of a febrile convulsion A review estimated the probability of meningitis in the event of a febrile convulsion to be
0-4%. It is worth noting that bacterial meningitis is very unlikely if no warning symptoms are found during physical examination, specically petechial
bleeding, neck stiffness or lowered consciousness [Offringa 2001]. A second
review put the probability at 0.23% [Sadleir 2007].
Note 30 Medication for terminating febrile convulsions A prospective randomised trial in secondary care compared intranasal midazolam (0.2 mg/kg) to
intravenous diazepam (0.3 mg/kg). A total of 47 children, aged 6 months to
5 years,were included,. No signicant side-effects were reported in either
group, and both medications were effective in terminating the seizure [Lahat
2000]. A second RCT performed in the emergency department compared
buccal midazolam to rectal diazepam. Dosage was age-related, varying from
2.5 to 10 mg. A total of 177 patients from the age of 6 months were included,
however children with a diagnosis of epilepsy were not excluded. The population was therefore heterogeneous, with convulsions caused both by fever
and epilepsy. Only 56 children had a febrile convulsion. The conclusion in
this heterogeneous group was that buccal midazolam was more effective
than rectal diazepam in combating the convulsion and preventing recurrence
[McIntyre 2005]. A third prospective study conducted in secondary care included a total of 43 children aged 2 to 12 months, and compared buccal midazolam with rectal diazepam. In this study, only 12 children were found to have a
febrile convulsion. Buccal midazolam proved just as effective as rectal diazepam [Baysun 2005].
Conclusion: Rectal diazepam remains the medication of choice for febrile
convulsion. Advantages of midazolam have not been demonstrated convincingly. A prospective trial conducted in a primary care setting with large
groups of patients could clarify the value of midazolam for this indication.
Note 31 Prophylaxis for febrile convulsions A meta-analysis of nine RCTs examined the question of whether prophylaxis can be given to prevent recurrent
febrile convulsions. The risk of recurrent convulsions was signicantly lower
under continuous administration of phenobarbital or valproate compared
with placebo. Administration of pyroxidine or phenytoin compared with
placebo did not show a signicant difference. Intermittent administration of
diazepam also did not show any signicant difference compared to placebo.
The number needed to treat (NNT) to prevent a convulsion was four for valproate and eight for phenobarbital [Rantala 1997]. There is no evidence that
anti-convulsive medication decreases the risk of developing epilepsy. However, it is known that anti-convulsive medication has signicant side-effects,
such as irritability, lethargy and ataxia [Sadleir 2007]. There is insufcient
evidence to support the assertion that paracetamol or ibuprofen use may prevent a convulsion [Van Stuijvenberg 1998b, Baumann 2000].
Conclusion: Only valproic acid and phenobarbital are effective in preventing
recurrent febrile convulsions. As febrile convulsions are a benign condition,
and these medications have signicant side-effects, prophylaxis is recommended against.
Note 32 Prognosis Children with epilepsy have been found to have a higher
prevalence of past febrile convulsions [Baumann 2000]. If risk factors are
present, such as an atypical febrile convulsions, problems in the childs past
medical history (developmental disorders or motor disorders) and convulsions without fever in rst-degree family members, the risk of developing
epilepsy is signicantly higher [Brouwer 1996]. There is no evidence that
children function less well cognitively following a febrile convulsion [Sadleir
2007, Verity 1998, Brouwer 1996].
Note 33 Educating parents A retrospective questionnaire study among parents
with children who had suffered a febrile conversion showed high anxiety
levels among parents. Forty-seven percent of parents were afraid that their
child would die during the convulsion. Twenty-one percent indicated they
were no longer worried about the outcome thanks to good information provision. The study showed that non-Western parents were more fearful. It is
worth noting that this study took place in secondary care [Van Stuijvenberg
1998a].
Literature
1
2
In case of references to NHG products: see www.nhg.org

Anbar RD, Richardson-de Corral, V, OMalley PJ. Difculties in universal application of criteria identifying infants at low risk for serious bacterial infection. J Pediatr
1986;109:483-5.
Baker MD, Fosarelli PD, Carpenter RO. Childhood fever: correlation of diagnosis with
Baker MD, Bell LM, Avner JR. Outpatient management without antibiotics of fever in
temperature response to acetaminophen. Pediatrics 1987;80:315-8.

selected infants. N Engl J Med 1993;329:1437-41.
5
Baker MD, Bell LM, Avner JR. The efcacy of routine outpatient management without
antibiotics of fever in selected infants. Pediatrics 1999;103:627-31.
Baraff LJ, Bass JW, Fleisher GR, Klein JO, McCracken GH, Jr., Powell KR et al. Practice
guideline for the management of infants and children 0 to 36 months of age with
fever without source. Agency for Health Care Policy and Research. Ann Emerg Med
1993;22:1198-210.
Baumann RJ, Duffner PK. Treatment of children with simple febrile seizures: the AAP
Baysun S, Aydin OF, Atmaca E, Gurer YK. A comparison of buccal midazolam and rectal
practice parameter. American Academy of Pediatrics. Pediatr Neurol 2000;23:11-7.

diazepam for the acute treatment of seizures. Clin Pediatr (Phila) 2005;44:771-6.
49
50

9
Behrman RE, Kliegman RM, Jenson HB. Nelson textbook of pediatrics. 17th ed. Philadelphia (PA): Saunders, 2004.
10 Benador D, Benador N, Slosman D, Mermillod B,Girardin E. Are younger children at

highest risk of renal sequelae after pyelonephritis? Lancet 1997;349:17-9.
11 Berger RM, Berger MY, Van Steensel-Moll HA, Dzoljic-Danilovic G, Derksen-Lubsen
G.A predictive model to estimate the risk of serious bacterial infections in febrile
infants. Eur J Pediatr 1996;155:468-73.
12 Bernheim HA, Block LH, Atkins E. Fever: pathogenesis, pathophysiology, and purpose.
Ann Intern Med 1979;91:261-70.
13 Black S, Shineeld H, Baxter R, Austrian R, Bracken L, Hansen J, et al. Postlicensure
surveillance for pneumococcal invasive disease after use of heptavalent pneumococcal conjugate vaccine in Northern California Kaiser Permanente. Pediatr Infect Dis J
2004;23:485-9.
14 Bleeker SE, Moll HA. Het jonge kind met koorts zonder focus in het post-Haemophilus inuenzae-tijdperk. Ned Tijdschr Geneeskd 2002;146:3-5.
15 Bleeker SE, Derksen-Lubsen G, Grobbee DE, Donders AR, Moons KG, Moll HA. Validating and updating a prediction rule for serious bacterial infection in patients with fever
without source. Acta Paediatr 2007;96:100-4.
16 Blumenthal I. What parents think of fever. Fam Pract 1998;15:513-8.
17 Bonadio WA, Smith DS, Sabnis S. The clinical characteristics and infectious outcomes
of febrile infants aged 8 to 12 weeks. Clin Pediatr (Phila) 1994;33:95-9.
18 Bromer MQ , Black M. Acetaminophen hepatotoxicity. Clin Liver Dis 2003;7:351-67.
19 Brouwer OF, Kamphuis DJ, Begeer JH. Koortsconvulsies: prognose en behandeling.
Ned Tijdschr Geneeskd 1996;140:1801-4.
20 Carrol ED, Newland P, Riordan FA, Thomson AP, Curtis N, Hart CA. Procalcitonin as
a diagnostic marker of meningococcal disease in children presenting with fever and a
rash. Arch Dis Child 2002;86:282-5.
21 Commissie Farmaceutische Hulp. Farmacotherapeutisch Kompas 2007. Amstelveen:
College voor zorgverzekeringen, 2007.
22 Coulthard MG, Lambert HJ, Keir MJ. Occurrence of renal scars in children after their
rst referral for urinary tract infection. BMJ 1997;315:918-9.
23 Craig JV, Lancaster GA, Williamson PR, Smyth RL. Temperature measured at the
axilla compared with rectum in children and young people: systematic review. BMJ
2000;320:1174-8.
24 Crocetti M, Moghbeli N, Serwint J. Fever phobia revisited: have parental misconceptions about fever changed in 20 years? Pediatrics 2001;107:1241-6.
25 Dagan R, Powell KR, Hall CB, Menegus MA. Identication of infants unlikely to
have serious bacterial infection although hospitalized for suspected sepsis. J Pediatr
1985;107:855-60.
26 Dinarello CA. Interleukin-1 and the pathogenesis of the acutephase response. N Engl J
Med 1984;311:1413-8.
27 Dinarello CA, Cannon JG, Wolff SM. New concepts on the pathogenesis of fever. Rev
Infect Dis 1988;10:168-89. Endres S, Van der Meer JW, Dinarello CA. Interleukin-1 in the
pathogenesis of fever. Eur J Clin Invest 1987;17:469-74.
28 Erlewyn-Lajeunesse MD, Coppens K, Hunt LP, Chinnick PJ, Davies P, Higginson IM, et
al. Randomised controlled trial of combined paracetamol and ibuprofen for fever. Arch
Dis Child 2006;91:414-6.

29 Eskerud JR, Hoftvedt BO, Laerum E. Fever: knowledge, perception and attitudes.
Results from a Norwegian population study. Fam Pract 1991;8:32-6.
30 Fleuren MAH, Paulussen TGWM. Meningitis en sepsis bij kinderen. Ervaringen van
huisartsen. Leiden: TNO Preventie en Gezondheid, 2002.
31 Fleuren MAH, Paulussen TGWM. Vroegsignalering van meningitis en sepsis door huisartsen. TSG 2004;82:97-103.
32 Galetto-Lacour A, Zamora SA, Gervaix A. Bedside procalcitonin and C-reactive protein
tests in children with fever without localizing signs of infection seen in a referral center. Pediatrics 2003;112:1054-60.
33 Garra G, Cunningham SJ, Crain EF. Reappraisal of criteria used to predict serious bacterial illness in febrile infants less than 8 weeks of age. Acad Emerg Med 2005;12:921-5.
34 Gendrel D, Raymond J, Coste J, Moulin F, Lorrot M, Guerin S, et al. Comparison of
procalcitonin with C-reactive protein, interleukin 6 and interferon-alpha for differentiation of bacterial vs. viral infections. Pediatr Infect Dis J 1999;18:875-81.
35 Goh PL, Lee SW, Wong EH. Predictors of serious bacterial infection in children aged 3
to 36 months with fever without source. Singapore Med J 2006;47:276-80.
36 Goldman RD, Ko K, Linett LJ, Scolnik D. Antipyretic efcacy and safety of ibuprofen
and acetaminophen in children. Ann Pharmacother 2004;38:146-50.
37 Gorelick MH, Shaw KN. Clinical decision rule to identify febrile young girls at risk for
urinary tract infection. Arch Pediatr Adolesc Med 2000;154:386-90.
38 Granier S, Owen P, Pill R, Jacobson L. Recognising meningococcal disease in primary
care: qualitative study of how general practitioners process clinical and contextual
information. BMJ 1998;316:276-9.
39 Haddon RA, Barnett PL, Grimwood K, Hogg GG. Bacteraemia in febrile children presenting to a paediatric emergency department. Med J Aust 1999;170:475-8.
40 Hansson S, Martinell J, Stokland E, Jodal U. The natural history of bacteriuria in childhood. Infect Dis Clin North Am 1997;11:499-512.
41 Hoberman A, Chao HP, Keller DM, Hickey R, Davis HW, Ellis D. Prevalence of urinary
tract infection in febrile infants. J Pediatr 1993;123:17-23.
42 Hsiao AL, Chen L, Baker MD. Incidence and predictors of serious bacterial infections
among 57- to 180-day-old infants. Pediatrics 2006;117:1695-701.
43 Isaacman DJ, Shults J, Gross TK, Davis PH, Harper M. Predictors of bacteremia in
febrile children 3 to 36 months of age. Pediatrics 2000;106:977-82.
44 Isaacman DJ, Burke BL. Utility of the serum C-reactive protein for detection of occult
bacterial infection in children. Arch Pediatr Adolesc Med 2002;156:905-9.
45 Ishimine P. Fever without source in children 0 to 36 months of age. Pediatr Clin North
Am 2006;53:167-94.
46 Jacobson SH, Eklof O, Eriksson CG, Lins LE, Tidgren B, Winberg J. Development of
hypertension and uraemia after pyelonephritis in childhood: 27 year follow up. BMJ
1989;299:703-6.
47 Kai J. Parents difculties and information needs in coping with acute illness in preschool children: a qualitative study. BMJ 1996;313:987-90.
48 Kai J. What worries parents when their preschool children are acutely ill, and why: a
qualitative study. BMJ 1996;313:983-6.
49 Kist-van Holthe JE, Van der Heijden AJ. Dehydratie ten gevolge van gastro-enteritis bij
kinderen. Ned Tijdschr Geneeskd 1999;143:193-6.
51
52

50 Klassen TP, Rowe PC. Selecting diagnostic tests to identify febrile infants less than 3
months of age as being at low risk for serious bacterial infection: a scientic overview. J
Pediatr 1992;121:671-6.
51 Kourtis AP, Sullivan DT, Sathian U. Practice guidelines for the management of febrile
infants less than 90 days of age at the ambulatory network of a large pediatric health
care system in the United States: summary of new evidence. Clin Pediatr (Phila)
2004;43:11-6.
52 Kuppermann N, Fleisher GR, Jaffe DM. Predictors of occult pneumococcal bacteremia
in young febrile children. Ann Emerg Med 1998;31:679-87.
53 Kuppermann N, Malley R, Inkelis SH, Fleisher GR. Clinical and hematologic features
do not reliably identify children with unsuspected meningococcal disease. Pediatrics
1999;103:E20.
54 Lahat E, Goldman M, Barr J, Bistritzer T, Berkovitch M. Comparison of intranasal
midazolam with intravenous diazepam for treating febrile seizures in children: prospective randomised study. BMJ 2000;321:83-6.
55 Lall SB, Paul R. Paracetamol poisoning in children. Indian J Pediatr 1998;65:393-400.
56 Lamberts H. In het huis van de huisarts: verslag van het Transitieproject. 2e dr. Lelystad: Meditekst, 1994.
57 Lee GM, HarperMB. Risk of bacteremia for febrile young children in the post-Haemophilus inuenzae type b era. Arch Pediatr Adolesc Med 1998;152:624-8.
58 Lesko SM, Mitchell AA. An assessment of the safety of pediatric ibuprofen. A practitioner-based randomized clinical trial. JAMA 1995;273:929-33.
59 Lesko SM, Mitchell AA. Renal function after short-term ibuprofen use in infants and
children. Pediatrics 1997;100:954-7.
60 McCarthy PL, Jekel JF, Stashwick CA, Spiesel SZ, Dolan TF, Jr. History and observation
variables in assessing febrile children. Pediatrics 1980;65:1090-5.
61 McCarthy PL, Lembo RM, Fink HD, Baron MA, Cicchetti DV. Observation, history, and
physical examination in diagnosis of serious illnesses in febrile children less than or
equal to 24 months. J Pediatr 1987;110:26-30.
62 McIntyre J, Robertson S, Norris E, Appleton R, Whitehouse WP, Phillips B, et al. Safety
and efcacy of buccal midazolam versus rectal diazepam for emergency treatment of
seizures in children: a randomised controlled trial. Lancet 2005;366:205-10.
63 Meremikwu M, Oyo-Ita A. Paracetamol for treating fever in children. Cochrane Database Syst Rev 2002;CD003676.
64 Merkus JMWM. Perinatale sterfte in Nederland: audit dringend nodig. Ned Tijdschr
Geneeskd 2008;152:603-5.
65 Moghal NE, Brocklebank JT, Meadow SR. A review of acute renal failure in children:
incidence, etiology and outcome. Clin Nephrol 1998;49:91-5.
66 Nademi Z, Clark J, Richards CG, Walshaw D, Cant AJ. The causes of fever in children
attending hospital in the north of England. J Infect 2001;43:221-5.
67 Nederlandse Meningitis Stichting. Verwekkers bacterile meningitis. Amsterdam 2008.
http://www.meningitisstichting.nl/.
68 Newman TB, Bernzweig JA, Takayama JI, Finch SA, Wasserman RC, Pantell RH.
Urine testing and urinary tract infections in febrile infants seen in ofce settings: the
Pediatric Research in Ofce Settings Febrile Infant Study. Arch Pediatr Adolesc Med
2002;156:44-54.

69 Offringa M, Hazebroek-Kampschreur AA, Derksen-Lubsen G. Prevalence of febrile seizures in Dutch schoolchildren. Paediatr Perinat Epidemiol 1991;5:181-8.
70 Offringa M, Moyer VA. An evidence-based approach to managing seizures associated
with fever in children. West J Med 2001;175:254-9.
71 Oostenbrink R, De Groot R. Het jonge kind met koorts zonder focus; diagnostiek en
beleid. Ned Tijdschr Geneeskd 1999;143:185-90.
72 Palafox M, Guiscafre H, Reyes H, Munoz O, Martinez H. Diagnostic value of tachypnoea in pneumonia dened radiologically. Arch Dis Child 2000;82:41-5.
73 Pantell RH, Newman TB, Bernzweig J, Bergman DA, Takayama JI, Segal M, et al.
Management and outcomes of care of fever in early infancy. JAMA 2004;291:1203-12.
74 Perrott DA, Piira T, Goodenough B, Champion GD. Efcacy and safety of acetaminophen vs ibuprofen for treating childrens pain or fever: a meta-analysis. Arch Pediatr
Adolesc Med 2004;158:521-6.
75 Pulliam PN, Attia MW, Cronan KM. C-reactive protein in febrile children 1 to 36
months of age with clinically undetectable serious bacterial infection. Pediatrics
2001;108:1275-9.
76 Pylkkanen J, Vilska J, Koskimies O. The value of level diagnosis of childhood urinary
tract infection in predicting renal injury. Acta Paediatr Scand 1981;70:879-83.
77 Rantala H, Tarkka R, Uhari M. A meta-analytic review of the preventive treatment of
recurrences of febrile seizures. J Pediatr 1997;131:922-5.
78 Richardson AC, Roghmann KJ, White KC. Use of clinical observation scales following antipyretic therapy to predict serious illness in febrile children. Am J Dis Child
1999;144:435.
79 Richardson M, Lakhanpaul M. Assessment and initial management of feverish illness
in children younger than 5 years: summary of NICE guidance. BMJ 2007;334:1163-4.
80 Robbins, Cotran R. Pathologic basis of disease. 7th ed. Saunders, 2004.
81 Roberts NJ, Jr. Temperature and host defense. Microbiol Rev 1979;43:241-59.
82 Roedig A. Ziekenhuisopnamen perinatale aandoeningen, oorzaak bij de pasgeborene
2001-2004. Nationaal Kompas Volksgezondheid. RIVM, Bilthoven 2007. http://www.
rivm.nl/vtv/object_map/o1729n21477.html
83 Roord JJ, Kaandorp CJE. CBO-richtlijn Bacterile meningitis. Ned Tijdschr Geneeskd
2001;211-4.
84 Sadleir LG, Scheffer IE. Febrile seizures. BMJ 2007;334:307-11.
85 Sarrell EM, Wielunsky E, Cohen HA. Antipyretic treatment in young children with
fever: acetaminophen, ibuprofen, or both alternating in a randomized, double-blind
study. Arch Pediatr Adolesc Med 2006;160:197-202.
86 Shamoon H, Hawamdah A, Haddadin R, Jmeian S. Detection of pneumonia among
children under six years by clinical evaluation. EastMediterr Health J 2004;10:482-7.
87 Shaw KN, Gorelick M, McGowan KL, Yakscoe NM, Schwartz JS. Prevalence of urinary
tract infection in febrile young children in the emergency department. Pediatrics
1998;102:e16.
88 Simon HK, Weinkle DA. Over-the-counter medications. Do parents give what they
intend to give? Arch Pediatr Adolesc Med 1997;151:654-6.
89 Speelman-Verburgh ME, Bruynzeels MA, Van Suylekom-Smit LWA, Van der Velden J,
Hoes AW, Van der Wouden JC. De incidentie van koortsconvulsies bij kinderen van 3-72
maanden oud. Ned Tijdschr Geneeskd 1996;140:664-7.
53
54

90 Stephenson MJ. Childhood fever: Parental beliefs and management. Can Fam Physician 1988;34:63-5.
91
Sur DK, Bukont EL. Evaluating fever of unidentiable source in young children. Am
Fam Physician 2007;75:1805-11.
92 Swingler GH. Radiologic differentiation between bacterial and viral lower respiratory
infection in children: a systematic literature review. Clin Pediatr (Phila) 2000;39:627-33.
93 Taylor C. Managing infants with pyrexia. Nurs Times 2006;102:42-3.
94 Taylor JA, Del BM, Done S, Winters W. Establishing clinically relevant standards
for tachypnea in febrile children younger than 2 years. Arch Pediatr Adolesc Med
1995;149:283-7.
95 Teach SJ, Fleisher GR. Efcacy of an observation scale in detecting bacteremia in
febrile children three to thirty-six months of age, treated as outpatients. Occult Bacteremia Study Group. J Pediatr 1995;126:877-81.
96 Teach SJ, Fleisher GR. Duration of fever and its relationship to bacteremia in febrile
outpatients three to 36 months old. The Occult Bacteremia Study Group. Pediatr
Emerg Care 1997;13:317-9.
97 Thayyil S, Shenoy M, Hamaluba M, Gupta A, Frater J, Verber IG. Is procalcitonin
useful in early diagnosis of serious bacterial infections in children? Acta Paediatr
2005;94:155-8.
98 Thompson MJ, Ninis N, Perera R, Mayon-White R, Phillips C, Bailey L et al. Clinical recognition of meningococcal disease in children and adolescents. Lancet
2006;367:397-403.
99 Torrey SB, Henretig F, Fleisher G, Goldstein RM, Ardire A, Ludwig S, et al. Temperature response to antipyretic therapy in children: relationship to occult bacteremia. Am
J Emerg Med 1985;3:190-2.
100 Trautner BW, Caviness AC, Gerlacher GR, Demmler G, Macias CG. Prospective evaluation of the risk of serious bacterial infection in children who present to the emergency
department with hyperpyrexia (temperature of 106 degrees F or higher). Pediatrics
2006;118:34-40.
101 Treluyer JM, Tonnelier S, dAthis P, Leclerc B, Jolivet-Landreau I, Pons G. Antipyretic
efcacy of an initial 30-mg/kg loading dose of acetaminophen versus a 15-mg/kg maintenance dose. Pediatrics 2001;108:E73.
102 Van den Brande JL, Heymans HSA, Monnens LAH. Kindergeneeskunde. 3e dr. Maarssen: Elsevier/Bunge, 1998.
103 Van der Linden MW, Westert GP, De Bakker DH, Schellevis FG. Tweede Nationale Studie naar ziekten en verrichtingen in de huisartspraktijk: klachten en aandoeningen in
de bevolking en in de huisartspraktijk. Bilthoven: RIVM, 2004.
104 Van Eeuwijk JS, Brand PLP. Nekstijfheid bij kinderen: wel of geen meningitis? Ned
Tijdschr Geneeskd 2003;147:321-3.
105 Van Rossum AM, Wulkan RW, Oudesluys-Murphy AM. Procalcitonin as an early marker of infection in neonates and children. Lancet Infect Dis 2004;4:620-30.
106 Van Stuijvenberg M. Febrile seizures: clinical and genetic studies [dissertation]. Rotterdam: Erasmus Universiteit, 1998a.
107 Van Stuijvenberg M, Derksen-Lubsen G, Steyerberg EW, Habbema JD, MollHA. Randomized, controlled trial of ibuprofen syrup administered during febrile illnesses to
prevent febrile seizure recurrences. Pediatrics 1998b;102:E51.

108 Van Wijk JA, Van der Heijden AJ. Urineweginfecties bij zuigelingen, een verraderlijk
ziektebeeld. Ned Tijdschr Geneeskd 1998;142:2385-8.
109 Verity CM, Butler NR, Golding J. Febrile convulsions in a national cohort followed up
from birth. I-Prevalence and recurrence in the rst ve years of life. BMJ (Clin Res Ed)
1985;290:1307-10.
110 Verity CM, Greenwood R, Golding J. Long-term intellectual and behavioral outcomes
of children with febrile convulsions. N Engl J Med 1998;338:1723-8.
111 Vernon SJ, Coulthard MG, Lambert HJ, Keir MJ, Matthews JN. New renal scarring in
children who at age 3 and 4 years had had normal scans with dimercaptosuccinic acid:
follow up study. BMJ 1997;315:905-8.
112 Vink R, Offringa M, Van der Does E. Het beleid van huisartsen bij convulsies met
koorts. Huisarts Wet 1990;33:263-7.
113 Weisse ME, Miller G, Brien JH. Fever response to acetaminophen in viral vs. bacterial
infections. Pediatr Infect Dis J 1987;6:1091-4.
114 Whybrew K, Murray M, Morley C. Diagnosing fever by touch: observational study.
BMJ 1998;317:321.
115 Winterberg DH. Exanthemen bij kinderen. Ned Tijdschr Geneeskd 1996;140:1494-9.
116 Yama moto LT, Wigder HN, Fligner DJ, Rauen M, Dershewitz RA. Relationship of bacteremia to antipyretic therapy in febrile children. Pediatr Emerg Care 1987;3:223-7.
117 Zorc JJ, Kiddoo DA, Shaw KN. Diagnosis and management of pediatric urinary tract
infections. Clin Microbiol Rev 2005;18:417-22.
55

Textbook Oma 2

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Textbook Oma 2

Uploaded by

Copyright:

Available Formats

NHG Clinical Practice Guidelines

NHG Clinical Practice

M09 NHG Clinical Practice Guideline Acute Otitis Media

M29 NHG Clinical Practice Guideline Feverish illness in

Ruim 20 jaar geleden is de eerste standaard van het Nederlands Huisartsen

M09 NHG Clinical Practice Guideline

Huisarts Wet 2006;49(12):615-21

NHG Clinical Practice Guidelines

AOM is a common condition: an estimated one-half to three-quarters of the

M09 NHG Clinical Practice Guideline Acute Otitis Media (AOM)

Various signs and symptoms can be a reason to consider a diagnosis of acute

The GP should query the following:[9]

NHG Clinical Practice Guidelines

No additional examinations are required to conrm AOM.[10]

M09 NHG Clinical Practice Guideline Acute Otitis Media (AOM)

swimming with their head underwater; this recommendation also applies to

The GP starts symptomatic treatment in all cases. The treatment comprises

children aged 3-12

2.5 ml syrup (24 mg/ml) 4-6 times daily

1 suppository (120 mg) 2-3 times

1 suppository (240 mg) 2-3 times

children aged 2-4

6-7 ml syrup (24 mg/ml) or 1 tablet 120 mg 4-6

1 suppository (240 mg) 3 times

children aged 4-6

8 ml syrup (24 mg/ml) or 1.5 tablets 120 mg 4-6

1 suppository (240 mg) 4 times

children aged 6-9

10 ml syrup (24 mg/ml) or 0.5 tablet 500 mg 4-6

1 suppository (500 mg) 2-3 times

children aged 9-12

0.75 tablet (500 mg) 4-6 times daily

1 suppository (500 mg) 3 times

1 suppository (1000 mg) 2-3

NHG Clinical Practice Guidelines

(not < 6 months)

caps. or disp. tab. 250 mg

Paediatric dosages of the recommended antibiotic agents

M09 NHG Clinical Practice Guideline Acute Otitis Media (AOM)

NHG Clinical Practice Guidelines

Dutch College of General Practitioners

M09 NHG Clinical Practice Guideline Acute Otitis Media (AOM)

NHG Clinical Practice Guidelines

According to the literature overview mentioned above, 10 to 20% off all

M09 NHG Clinical Practice Guideline Acute Otitis Media (AOM)

children below the age of 16. Otorrhoea through a spontaneous perforation of

NHG Clinical Practice Guidelines

M09 NHG Clinical Practice Guideline Acute Otitis Media (AOM)

NHG Clinical Practice Guidelines

M09 NHG Clinical Practice Guideline Acute Otitis Media (AOM)

NHG Clinical Practice Guidelines

Note 23 Recurrent acute otitis media In studies and international guidelines,

M09 NHG Clinical Practice Guideline Acute Otitis Media (AOM)

In case of references to NHG products: see www.nhg.org

siteit Utrecht, 1992.

10 Commissie Farmaceutische Hulp. Farmacotherapeutisch Kompas 2006. Amstelveen:

NHG Clinical Practice Guidelines

M09 NHG Clinical Practice Guideline Acute Otitis Media (AOM)

M29 NHG Clinical Practice Guideline

Huisarts Wet 2008:51 (6):287-96

NHG Clinical Practice Guidelines

The NHG Clinical Practice Guideline on Feverish illness in Children provides

Fever usually occurs in response to the intrusion of micro-organisms into the

M29 NHG Clinical Practice Guideline Feverish illness in Children