1

FEBRILE SEIZURES AS SEEN IN THE

CHILDREN’S EMERGENCY ROOM OF THE

UNIVERSITY COLLEGE HOSPITAL, IBADAN, NIGERIA

BY

OLUMIDE OLATOKUNBO JARRETT

MBBS (IBADAN) 1994

A DISSERTATION SUBMITTED TO THE NATIONAL

POSTGRADUATE MEDICAL COLLEGE OF NIGERIA IN PART

FULFILMENT OF THE REQUIREMENTS FOR THE FELLOWSHIP OF

THE FACULTY OF PAEDIATRICS

NOVEMBER, 2006

2

DECLARATION

I hereby declare that this work is original unless otherwise

acknowledged and that it has not been presented to any other

college for a fellowship or submitted elsewhere for publication.

Dr Olumide Olatokunbo Jarrett, MBBS (1994)

3

CERTIFICATION

The study reported in this dissertation was carried out by Dr. Olumide

Olatokunbo Jarrett under our supervision .We also supervised the writing of

the dissertation.

____________________________

DR O. J. FATUNDE MBBS, FMCPaed Consultant Paediatrician

University College Hospital

Ibadan. ________________________ PROF K. OSINUSI Professor of Paediatrics University College Hospital Ibadan.

4

DEDICATION

I dedicate this work to my Heavenly Father who makes all things

beautiful in His time.

Eccle 3:11

5

ACKNOWLEDGEMENTS

I give all glory to the Almighty God, the Lord Jesus Christ and the Holy Spirit

for granting me help on all sides throughout the period of my residency

programme and especially in the course of this study.

My sincere appreciation goes to my supervisors, Dr OJ Fatunde and Prof K

Osinusi for guiding this project from its inception and for impacting valuable

knowledge to me.

I also specially thank Drs Lagunju and Owoaje for the invaluable support

and encouragement that I received from them in the execution of this

project. I appreciate all the resident doctors in the Department of Paediatrics

for their support and love.

I am grateful to Mr Adewole and Mr James who were very helpful in the

analysis of my results. Special thanks go to Mr Fashina and Adeola Oloko for

their immerse assistance in making sure I had laboratory analysis done

accurately.

I appreciate the unflinching support of my beloved husband Mr Elvonuel BS

Jarrett who encouraged me to stay in the programme even when things were

tough. My lovely children; Bankoleoluwa, Emmanuel, and the twins, Esther

and Ruth, were very patient, enduring several moments when mummy just

could not be at home for them.

Many thanks to all my parents both Spiritual and Physical, who were always

in support of my progress.

May the Good Lord reward you all Amen.

6

TABLE OF CONTENTS

Page no.

Declaration---------------------------------------------------------- ii

Certification--------------------------------------------------------- iii Dedication----------------------------------------------------------- iv

Acknowledgements------------------------------------------------- v

Table of contents--------------------------------------------------- vi

Glossary of Abbreviations----------------------------------------- vii List of Tables-------------------------------------------------------- viii

Summary------------------------------------------------------------ x

Introduction -------------------------------------------------------- 1

Literature Review -------------------------------------------------- 4 Aims and Objectives ----------------------------------------------- 57

Subjects and Methods -------------------------------------------- 58

Results -------------------------------------------------------------- 70

Discussion --------------------------------------------------------- 98

Conclusions ------------------------------------------------------- 109 Recommendations ----------------------------------------------- 110

Limitations of study ---------------------------------------------- 111

References --------------------------------------------------------- 112

Appendix 1 ------------------------------------------------------- 130

Appendix 2--------------------------------------------------- 131

7

GLOSSARY OF ABBREVIATIONS

AVP Arginine vasopressin

AAP American Academy of Pediatrics

BPA British Paediatric Association

CSF Cerebrospinal fluid

CHES Child Health Education Study

EEG Electroencephalogram

FBC Full Blood Count

GABA Gamma aminobutyric acid

IQ Intelligence Quotient

Kg Kilogram

MRI Magnetic resonance imaging

NMDA N- methyl D-aspartate

NCPP National Collaborative Perinatal Project

OFC Occipito Frontal Circumference

OTCHEW Otunba Tunwase Children’s Emergency Ward

PGE2 Prostagladin E2

PHC Primary Health Care

RBM Roll Back Malaria

SPSS Statistical Package for Social Sciences

TNF Tumor necrosis factor

UCH University College Hospital

UTI Urinary tract infection

URTI Upper respiratory tract infection

UNICEF United Nations Children’s Fund

WHO World Health Organization

8

LIST OF TABLES

Table

Title Page no No

Table 1

Table 2

Table 3

Table 4

Table 5

Table 6

Table 7

Table 8

Table 9

Table 10

Table 11

Table 12

Table 13

Age and Sex distribution of 147 children in the study.

Classification of children into seizure categories.

Type of seizures in relation to the age of children with febrile seizures.

The socioeconomic class of parents in relation to the type of febrile seizures in the children of the study.

The socioeconomic class of parents in relation to past history of seizures in the children of the study.

Pre-hospital management given to 59 children with febrile seizures.

Pre-hospital intervention in relation to the socioeconomic class of the parents.

Pre-hospital intervention by mothers in relation to

recurrence of febrile seizures in children of the study.

The type of pre-hospital intervention given by mothers in relation to the type of seizures in the children with febrile

seizures.

Relationship between the etiology of fever and age of the children in the study.

Relationship between aetiology of fever and the pattern of

febrile seizures.

The degree of parasitaemia in relation to the type of seizure in the children in the study.

Packed cell volume values in 147 children with febrile seizures.

71

72

73

74

76

79

80

81

81

83

86

87

89

9

Table 14

Table 15

Table 16

Table 17

Packed cell volume in relation to the etiology of fever.

The white blood cell counts in relation to the etiology of

fever in 147 children with febrile seizures. Cerebrospinal fluid sugar in relation to the aetiology of

fever in the children studied.

Cerebrospinal fluid -protein in relation to the aetiology of fever in the children studied.

89

91

94

95

10

SUMMARY

A prospective study was carried out at the University College

Hospital (UCH), Ibadan, between November 2002 and December 2003

to determine the prevalence, aetiology and short-term prognosis of

febrile seizures in childhood.

One hundred and forty-seven children with febrile seizures

admitted into the Children Emergency Room of the UCH Ibadan were

studied. Their ages ranged from four months to sixty months (five

years) with a mean age (SD) of 26.35 (13.76) months.

A detailed history was taken and a thorough physical

examination was carried out on each patient, while investigations

performed were recorded in a proforma. The duration of hospital stay

and the presence of neurological deficits were also recorded.

The proportion of children who presented with febrile seizures

amongst the paediatric admission into the hospital during the study

period was 9.9 %. There was a slight male preponderance among those

with febrile seizures, with a male to female ratio of 1.3:1.Complex

febrile seizures occurred more frequently with a simple to complex

ratio of 1:2.1.

The leading causes of febrile seizures were malaria (40.1%),

septicaemia (15%), urinary tract infection (12.3%) and pneumonia

(8.2%). Other less common causes were otitis media, measles and

gastroenteritis.

11

Pre-hospital intervention was given to 59 patients (40.1%). Of

these, native concoction was given to 15(25.4%) children. There was

statistically significant relationship between pre-hospital management

and socioeconomic class of parents (P value = 0.008). The mean (SD)

duration of hospital stay of the children studied was 6.37 + 8.067

days. Children with bacterial infections spent a longer period in the

hospital as compared with children with malaria.

Two (1.3%) of the 147 children died. Neurological deficits, mainly

cranial nerve palsies and hypertonia, were found in six survivors.

It is concluded that febrile seizures remain a major cause of

morbidity in children presenting to the Children’s Emergency Room of

UCH, Ibadan and that the major aetiological factor is malaria.

Therefore, measures to control malaria amongst our children should

be improved to reduce its prevalence. Effective health education of the

general public should be undertaken emphasizing the relative benign

nature of this condition, thus allaying the fear and apprehension and

panic associated with the disease, the dangers of offering harmful

methods of intervention should also be highlighted.

12

INTRODUCTION

A febrile seizure is a seizure occurring in infancy or childhood

usually between three months and five years of age associated with

fever but without evidence of intracranial infection or a defined cause.1

Seizures with fever in children who have had afebrile seizures are

excluded.1

Febrile seizures are a common problem encountered in

emergency paediatric practice occurring in about 2-4% of children

under 5years of age.2,3 It has been found to contribute significantly to

childhood morbidity in our environment,2 complicating common

childhood febrile illnesses such as malaria, which was responsible for

45% of the febrile illnesses associated with febrile seizures in the

study by Familusi et al.2 Conditions likely to precipitate febrile

seizures vary depending on the most prevalent fever-inducing illness

or disease in a given location.4

A febrile seizure causes intense parental anxiety.5 This coupled

with some degree of ignorance, is usually responsible for the various

forms of intervention offered by parents and caretakers when a child

has an episode. These interventions include the use of cow urine

concoction,2, 3 burning of parts of the body, application of substances

to the eyes and mouth and so on.2 Such practices may account for

13

the high mortality of 6.4% obtained in the previous study at our

centre.2

There is a genetic predisposition to febrile seizures with an

autosomal dominant inheritance pattern having been demonstrated.6

The risk of recurrence and epilepsy are important issues in

febrile seizures. The temperature at time of seizure, the age of onset

and the record of family history of febrile seizures determines the

probability that there would be a recurrence.7,8 Recurrence refers to a

situation whereby a child who has had a previous febrile seizure goes

on to have a repeat episode during another febrile illness.1, 9 The type

of febrile seizure, family history of non-febrile seizures and abnormal

neurologic or developmental status prior to febrile seizures are some of

the factors that determine the risk of developing epilepsy.7,8

The issue of relevant investigations and their indications has

also been the subject of study.10 For example; lumbar puncture is

perhaps the most relevant investigation to be carried out in order to

rule out the presence of meningitis.10

While there have been previous reports on febrile seizures in

Nigerian children, 2,4,11-18 only one of such studies has been conducted

at our centre more than 30 years ago.2 It is important to review the

subject from time to time in order to document changes, if any, in the

presentation, causes and management of the condition.

14

The purpose of this study was therefore to determine the current

pattern and aetiology of febrile seizures in children seen at the

Children Emergency Ward of the University College Hospital, Ibadan,

as well as the practice of caregivers with regard to febrile seizures. The

results will help to focus on possible interventions needed to change

perceptions about this disorder in bid to reduce morbidity and

mortality.

LITERATURE REVIEW

Definition

15

A seizure is an abnormal involuntary paroxysmal neuronal

discharge from the brain, which could manifest as motor

abnormalities and/or sensory and autonomic disturbances with or

without loss of consciousness. 1, 19

The definition of febrile seizures has been the subject of

controversy in recent times. 1,20,21 The Joint Working Group of the

Research Unit of the Royal College of Physicians and the British

Paediatrics Association20 defined febrile seizures as “an epileptic

seizure occurring in a child aged six months to five years precipitated

by fever arising from infection outside the nervous system”.1, 20 They

considered that it was proper to use the term ‘epileptic’ in so far as the

neurophysiological substrate of a febrile convulsion is a paroxysmal

neurological discharge as it is in an epileptic seizure.

Wallace,21 however, felt that the definition should not be

restricted because she felt once restrictions such as intracranial

infection, presence of chronic neurological disorder or duration or

lateralization of convulsion are placed on the definition it becomes

extremely difficult to decide whether a convulsion should be

characterized as ‘febrile’ or not. She accordingly defined it as ‘any

seizure occurring in association with any febrile illness’.

Arguments have ensued because of these varying views in terms of

exclusive and inclusive criteria and therefore, this amongst other issues

necessitated a consensus meeting.19 The Panel18 defined febrile seizure

16

as “an event in infancy or childhood usually occurring between three

months and five years of age associated with fever but without evidence

of intracranial infection or defined cause.” Members concluded that

febrile seizures are to be distinguished from epilepsy, which is

characterized by recurrent non-febrile seizures. Febrile seizures cannot

be referred to as “epileptic” because this is the term used in describing

non-febrile recurrent seizures. The definition by the panel appears to

properly define the condition with emphasis on the absence of an

intracranial involvement.

Epidemiology

Febrile seizures are a common problem encountered in

emergency paediatrics practice.2, 6, 11, 21 It is the commonest cause of

seizures in children younger than five years.2 Its prevalence varies

from one geographical location to the other.2, 11,12, 22-24

In the United States of America, studies have shown that 2-4%

of children will experience a febrile seizure prior to the age of five

years1,3 Costeff25 reported an incidence of 3% amongst Israeli children,

while Webb26 found an incidence of 5.1% in India. Nakayama et al27 in

a population- based study, reported an incidence of 7% amongst

Japanese children. Incidence is as high as 9.7% in a country like

Ghana.11

17

In Nigeria, the few studies2, 11-18 that have been carried out

reveal a somewhat higher incidence of febrile seizures when compared

to other parts of the world.2 Familusi et al2 in 1971 reported a 15.1%

prevalence of febrile seizure in children admitted to an emergency

room in Ibadan. Izuora and Azubuike13 in 1977 reported an prevalence

of 15.6% among admissions to the University of Nigeria Teaching

Hospital Emergency Paediatric Unit in Enugu, while Angyo et al18

reported a prevalence of 8.08% in Jos.

In contrast to the very high prevalence reported from Ibadan and

Enugu, Scott-Emuakpor and Longe12 reported a lower prevalence of

5.8% at the children’s emergency unit of the University of Benin

Teaching Hospital. Out of the 1,207 children admitted to the

emergency unit during the study, 104 (8.6%) had a provisional

diagnosis of febrile seizures, but 34 were later excluded because of the

presence of metabolic derangement and features of meningitis.

All the Nigerian studies were hospital-based and can thus be a

gross misrepresentation of the actual population affected. Also, the

hospitals involved are all referral centres and so some bias could have

been introduced. Since the occurrence of a seizure will in many cases

prompt the parents to take the child to a health facility, it is to be

expected that these hospital-based figures will be higher than those

obtained in population –based studies. These factors can account for

the higher prevalence reported from Nigeria.

18

Febrile seizures are primarily a disease of infants and young

children, 2, 3, 11, 12, 20, 21-23 which occur more in the first year of life.2, 24

In the past, the age range for febrile seizures was set at 6

months to 6 years2, 29 but in recent times this age limit has been

reviewed.19 The National Institute of Health Consensus Development

Conference in its definition stated that febrile seizures are ‘… seizures

occurring in children between 3 months and 5 years associated with

fever…’.19 The majority of cases of febrile seizures occurred between

six months and 4 years of age in the study by Familusi et al2 and

occurred rarely below the age of 6 months or above the age of 5 years.

However 29(4.9%) out of the 590 patients with febrile seizures studied

were less than 6 months of age, while 42(7.1%) were over 5 years of

age.

The peak age for febrile seizures is between the age of 6 months

and 12 months, 23 but12-14 months has been noted in some review.6

Febrile seizures have been shown to have a slight male

preponderance.2, 4 They, Fagbule et al4 reported M: F ratio of 1.3:1,

Familusi et al2 a ratio of 1.36:1 and Angyo et al18 a ratio of 2:1.

Seasonal variation has also been observed.4 In the tropics, about

two thirds of episodes of febrile seizures occur during the rainy

season,4 which corresponds to the season of highest incidence of

malaria. Racial differences in prevalence rates have also been reported

being 3.5% in whites and 4.2% in blacks.9

19

The socioeconomic status of the parents of children with febrile

seizures could affect the prevalence and outcome of febrile seizures.5

Parmer et al5 reported in their study that prior awareness of febrile

seizures was significantly higher in the upper and middle social class,

so also was awareness of correct measures to take in prevention and

treatment of febrile seizures.

Pathogenesis of Fever

Fever is an elevation of body temperature mediated by an

increase of the hypothalamic heat regulatory set point.29 The

hypothalamic thermoregulatory centre controls body temperature by

balancing signals from peripheral cold and warm receptors. Another

regulatory factor is the temperature of blood circulating in the

hypothalamus. The integration of these signals maintains normal core

temperature at the set point of 370C ± 0.50C.30

In the pathogenesis of fever, there is usually a stimulus.29,, 30 Most

often these are bacteria and their endotoxins, viruses, yeasts,

spirochetes, protozoa, immune reactions, several hormones,

medications and synthetic polynucleotides. These substances are

commonly called exogenic pyrogens. Cells stimulated by exogenic

pyrogens form and produce cytokines called endogenic pyrogens. The

most important endogenic pyrogens are interleukin1, interleukin 6 and

cachetin also called Tumours Necrosis Factor (TNF). Endogenic

pyrogens are glycoproteins that also have other important effects.30

20

Interleukin 1 and TNF increase the immune response by activation of T

cells and stimulation of interleukin 2 production. Interleukin 1 enhance

B cell proliferation. Fever and specific effects of interleukin 1 and TNF

form highly integrated processes that are involved in the response to

infection and acute inflammation processes. Interleukin 1 and TNF are

produced not only by monocytes and macrophages but also by

endothelial cells and astrocytes.30 Other endogenic pyrogens include

interleukin beta and gamma.

In the presence of sepsis, there is usually increasing levels of

interleukin 1 and TNF which are transported by blood. In the

hypothalamus, they trigger the synthesis of prostaglandin of group E

(PGE2) from the arachidonic acid of cytoplasmic membrane of target

cells.29 The precise mechanism by which PGE2 resets the central

thermostat is not known. PGE2 alters the hypothalamus heat-

regulating set point resulting in heat generation and heat

conservation.29 Heat generation is brought about by increased cell

metabolism, muscle activity and involuntary shivering, while heat

conservation is by vasoconstriction and heat preference behaviour.

Glucocorticoids inhibit the production of interleukin 1 and TNF

while Aspirin and other non- steroidal- anti- inflammatory drugs

inhibit cyclooxyygenase responsible for PGE2 production.29In the

majority of diseases, fever is caused by pyrogens. There are situations

however when fever may be caused directly by changes in the centre of

21

thermoregulation without the participation of exogens and endogenic

pyrogens. This occurs in brain tumors, intracranial bleeding and

thrombosis. 30

Pathogenesis of Febrile Seizures

Febrile seizures result from an age- dependent hyper excitability

of the brain that is induced by fever.31 Although there are important

genetic influences that render a febrile child more likely to develop

seizures, it is the fever per se that causes the seizures.31

Various authors have reviewed the mechanism by which fever

leads to seizures in these children.32-36 These studies were mostly

carried out on animals. Some reported that the height and rapidity of

body temperature were pathogenetic while another author reported

that a lack of arginine vasopressin increased the threshold for febrile

seizures or prevented it altogether.32 GABA (gamma aminobutyric

acid) has also been impilicated.33,34 A study reported low levels of

GABA in the animals they studied33 while another study by Knight et

al34 did not report any significant difference in the levels of GABA in

children with febrile seizures and those without.

Loscher and Siemens35 reported that the concentration of PGE2

in the central nervous system was significantly elevated in children

22

before febrile seizures and there was a significant positive correlation

between temperature and PGE2 levels.

Another report suggested that N-methyl L-D aspartate (NMDA)

receptor- mediated mechanisms may be involved in the production of

febrile seizures in response to hyperthermia.36 This is because its

antagonist produced dose- dependent increases in latency to the onset

of seizures. NMDA receptors are the major group of glutamate

receptors in the central nervous system upon which excitatory amino

acid neurotransmitters (glutamate and asparate) act to generate the

neuronal impulse that may be manifested as a seizure. It was deduced

that fever may lead to the generation of the NMDA receptor agonist.36

Genetics

The fact that there is a genetic predisposition to febrile seizures

cannot be doubted.27,35,37-39 The most useful information comes from

studies of children preferably in a large area.1 The American National

Collaborative Perinatal Project found family history to be the major

identified contributor to vulnerability to febrile seizures1.

The mode of inheritance of febrile seizures has been the subject

of considerable debate. Some workers have postulated an autosomal

mode of inheritance.6 There have also been suggestions of a polygenic

mode of inheritance but no report of sex linked inheritance has been

postulated.12 Tsuboi and Okada40 in a population and family- based

study, in Fuchu City, Japan, assessed 6,706 children aged 3 years.

23

Four hundred and fifty children had febrile seizures while 620

randomly children selected served as controls. The incidence of febrile

seizures amongst siblings of the 450 children with febrile seizures was

21.9% compared to 6.2% amongst the controls. Surprisingly, the

incidence amongst sisters was more than amongst brothers. This is at

variance with previous studies which showed a male predilection in

febrile seizures.6 The incidence among siblings was higher if one

parent had had febrile seizures and lower if neither parent had had

seizures.40 The incidence was highest if there were two family members

with febrile seizures, lowest if no family member had had a seizure

and intermediate if one relative had a history of febrile seizure.40 The

differences among these 3 categories were significant. Tsuboi and

Okada40 concluded that a multifactoral inheritance was most likely

involved.

Scott Emuakpor et al12 in a hospital-based study carried out at

the University of Benin Teaching Hospital reported the risk of full

siblings having febrile seizures to be 50%, indicating an autosomal

dominant mode of inheritance, with complete penetrance. This study

cannot, however, conclusively claim this, since several generations of

the families would have to be analyzed and the behavior of the gene

studied to come to this conclusion. Secondly, since the study was

hospital-based, samples were highly selective and may not necessarily

portray accurately what occurs in the general population.

24

Eric et al38 reported another autosomal dominant febrile

convulsion locus on chromosome 19p. This study brought to light the

fact that febrile seizures occur with higher frequency in families where

there was already a documented history of febrile seizures with

children from such families showing a three-fold or greater risk than

the general population of children with febrile seizures.

Recently, Nakayama et al27 reported the existence of a gene on

chromosome 5q 14-q15 which confers susceptibility to febrile seizures.

This study was however hospital based. Pieffer et al39 reported a large

family with 21 members affected by febrile seizures inherited as

autosomal dominant trait. Linkage analysis, genome wide scan and

subsequent fine mapping revealed significant evidence for a febrile

seizure locus on chromosome 2q 23-24.39 The findings from these

studies38,39 suggest that there may be at least four possible loci for

febrile seizures.

Other predisposing factors

There is evidence that maternal habit/ill health can predispose a

child to febrile seizures.1 These include prenatal maternal cigarette

smoking, and maternal alcohol intake, maternal seizures and

maternal renal problems. In a case- control study, Cassario et al41

found that prenatal cigarette smoking doubled the risk of simple

febrile seizures while alcohol intake doubled the risk of complex febrile

seizures.

25

Maternal medication during pregnancy has also been

implicated.21 Examination of the types of drugs given in pregnancy

shows that those known to have an effect on the central nervous

system for example, barbiturates, antidepressants and antiemetics

were frequently implicated in a report by Wallace.42 It seems

possible that these agents have adverse effects on the developing

cerebrum. Diuretics were given significantly more often to mothers of

patients. Diuretics, in altering electrolyte balance and in the case of

thiazides, carbohydrate metabolism, they could adversely affect the

fetal environment during brain maturation. Prolonged use of these

drugs during pregnancy could be deleterious to the growing fetus.

Perinatal predisposing factors that have been implicated include

breech presentation, antepartum hemorrhage, delivery by caesarian

section and intrauterine growth retardation.21

There are two bodies of opinion on the relationship between

pregnancy and perinatal factors and the risk of febrile seizures.

Wallace43 compared the birth history of 132 patients with febrile

seizures with the birth history of 180 of their siblings without febrile

seizures, 80(61%) of the children with febrile seizures had perinatal

and neonatal problems while only 39(22%) of their normal siblings had

abnormal perinatal history. Wallace43 concluded that abnormal

pregnancy with brain damage might be important in the pathogenesis

of febrile seizures.

26

Lennox44 in a hospital-based study reviewed the records of 240

children with a history of febrile seizures. He reported that 74% had a

normal birth history, while 26% had an abnormal perinatal history.

This included breech delivery, placenta praevia with severe bleeding,

use of high or middle forceps, caesarian delivery, twin birth and

prematurity. The author, however, did not proceed to determine the

importance of individual factors to the subsequent development of

febrile seizures.

In contrast to the foregoing report, the CHES45 in a population

study did not find any appreciable contribution of pregnancy and birth

factors to the risk of febrile seizures. Zhao et al46 in china, in a case

control study also found that none except maternal acute respiratory

infection was associated with increased risk.

Aetiology of the fever associated with Febrile seizures

The leading aetiology for the fever depends on which infection is

commonest in the environment.14 Virtually any cause of fever other

than central nervous system diseases is a potential etiology in febrile

seizures.14

Documented causes include: 2,14 malaria, pneumonia, upper

respiratory infections, (tonsillitis, pharyngitis), otitis

27

mediasteomyelitis, cellulitis, urinary tract infection, septicaemia or

bacteraemia, gastrointestinal infections and viral infections e. g.

measles.

In both the Northern and Southern parts of Nigeria, the etiology

of fever causing febrile seizures is similar.2,4,12,18 In a study by

Familusi et al2 at the University College Hospital Ibadan, it was found

that the commonest cause of fever that triggered off seizures was

malaria. This is similar to what Fagbule et al4 reported from Ilorin

where 71.1% of the children with febrile seizures had Plasmodium

falciparum infection. Malaria was also the commonest cause of fever in

studies by Angyo et al18 in Jos, Iloeje15 in Enugu and Akpede47 in

Benin. Malaria being the commonest aetiological agent is not

surprising in this country considering the fact that Nigeria is stable for

the malaria infection which necessitated our being a member of the

Roll back malaria programme (RBM) as a nation.48 RBM is a

partnership working worldwide to halve the burden of malaria by

2010.48,49 Malaria is responsible for over one million deaths each year

all over the world, about 3,000 a day; the majority of victims being

children. The policy of malaria control should be maintained. If

malaria could be properly controlled the incidence of febrile seizures

will be reduced.

In contrast, Lewis et al50 in their study of children with

febrile seizures in a temperate country traced a viral etiology in 86% of

28

the children. The viral infections manifested as various infections like

pharyngitis, tonsillitis, gastrointestinal infection, otitis media and

measles.

Familusi et al2 isolated viruses from 14(13.3%) of the 105

children that had viral studies. Fagbule et al4 did not carry out viral

studies. This could have affected the results obtained.

McIntyre et al51 in their retrospective study on occult

pneumococcal bacteraemia and febrile seizures, reported that 10 out

of the 29 patients managed in their hospital at Liverpool with

bacteraemia, had been admitted and managed as cases of febrile

seizures. They inferred that bacteraemia could be an important cause

of febrile seizures and those complications of focal infections; e.g.

meningitis and pneumonia were issue for concern. In another study by

the same author, positive blood cultures were obtained in 12 (4.3%) of

the 282 patients they reviewed, six of whom actually had a clinical

picture suggestive of septecaemia while the other 6 did not.51 They

concluded that bacteraemia are detected more frequently in children

who are admitted to hospital with febrile seizures when cultures are

performed as a routine. Teah et al52 also in a retrospective study

reported a 2.9% incidence of septicaemia in the patients they

reviewed.

There is a significant difference between the pattern of

bacteraemia seen in children in the temperate and tropical countries.53, 54

29

This has been attributed to the difference in climatic conditions. While

the predominant organism isolated from cultures in the temperate

regions are streptococcus pneumonia and Haemophilus influenza, 55

Staphylococcus aureus is more predominant in the tropics.54

Prevalence of bacteraemia also defer in the tropics and

temperate countries, being as low as 3% in the latter and as high as 11%

- 12.4% in the former.53,54 The report by Lepage et al53 gave the

prevalence of 12.4% among Rwanda children while Teele et al56 reported

a prevalence of 3 – 4% among young febrile children who were sent home

at first visit with bacteraemia in a walk in clinic in boston. Akpede et al47

found an incidence of 11% in one of their reports.

There is no specific symptom and sign associated with malaria.

In the tropics acute fever without localizing signs is often equated with

malaria and the risk of bacteraemia in such children has remained

unknown.47 Although malaria is a predominant infection in healthy

under-fives with fever without localizing signs in the tropics, bacteraemia

with or without malaria occur with an important high frequency and

some have recommended that while presumptive treatment of malaria is

justified in such children, evaluation for bacteraemia should be given

consideration.47 In the study by Akpede54 12 of the 14 children with

bacteraemia had concurrent malaria infection.

The higher prevalence of bacteramia in the tropics could be due to

the influence of malaria. Hemolysis induced by malaria cause

30

hypotransferinaemia, which can enhance susceptibility to staphylococcus

aureus infection.47 Sequestration of erythrocytes containing maturing

schizonts of plasmodium falciparum in deep tissues; capillaries,

including that of the gut, causes microinfarct formation which can

enhance blood stream invasion by enterobacteriae. Acute malaria

infection is also known to cause immunosupression.

Although asymptomatic parasitaemia is a frequent problem in

febrile patients in endemic areas, those with double infection of malaria

and other bacterial infections experience greater morbidity and

mortality.54 Hendrickse57 reported in 500 severely ill children in the

emergence room showed that 25% of the 20 children with malaria and

bacterial infection died as compared to 3.7% of 164 children with malaria

alone. In contrast, Lepage et al53 found no significant difference in the

mortality rate between children with bacteria infection and the control

group with malaria alone. It would be, however, unwise to disregard the

presence of bacteria infection in children with malaria.

In the study by Musa-Aisien et al 58 UTI prevalence was 9%.

Prevalence was higher in girls than in boys. Angyo et al18 reported a

prevalence of only 3(1.8%) of the 163 patients studied, while Fagbule et

al4 did not report any case of UTI in their study. This is not surprising

since urine culture was not done routinely in the patients they studied

but was restricted to patients in whom UTI was suspected. Familusi et

al2 reported a diagnosis of UTI in 2.8% of their patients. They stated

31

that this was probably an under-representation since the number of

children who had urine culture was small. A study in South Africa by

Jeena et al 59 had a very high yield of 17%, gram negative organism being

responsible for 87.5% of the cases. Teah et al52 in Washington DC,

reported a 0.7% yield of bacteria pathogens in a retrospective study

where the incidence of UTI in children with febrile seizures was reviewed.

Trainer et al60 found an incidence of 5.9% amongst 171 patients in a

retrospective study in Chicago while Lee et al61 in Wales reported an

incidence of 8%.

In the report by Lewis et al50 it was implied that though majority of

the causes of febrile seizures they saw were elucidated by a systemic viral

illness, some had generalized bacterial infection. There were cases where

bacteria pathogens were isolated in the blood, along with a virus being

isolated from body fluids. In temperate regions the occurrence of a virus

isolated in a febrile child does not exclude a possibility of a super-

imposed bacterial infection hence the need for proper clinical assessment

and evaluation of a febrile child and cultures taken in these children in

spite of the obvious viral infection.

Immunization seems to precipitate febrile seizures only rarely.62

Only 1.4% of the children in the NCPP (National Collaboration

Perinatal Project) who had had seizures in the first seven years of life

had been immunized within two weeks of the episode and in about one

third of them, other potential causes of fever were present. DPT

32

(diphtheria, pertussis, tetanus) vaccine has been implicated

particularly the pertussis component. 63 In a study following

administration of DTP vaccines 9 out of 15,752 children developed

convulsions meanwhile none of the 784 children with DT (diphtheria,

tetanus) vaccine convulsed.

Types of Febrile Seizures

There are two types of febrile seizures

1. Simple: defined as a primarily generalized seizure lasting less

than 15 minutes and not recurring within 24 hours or during

that particular febrile illness;7 and

2. Complex: defined as a seizure which is focal, or prolonged

(>15minutes) and or recurring within 24 hours of the initial

seizure.7 Focal seizures may involve an arm, leg or face on one

side only or eye deviation towards one side.

Out of the 590 children studied by Familusi et al, 2 only

27(4.6%) had focal seizures, it was however not stated explicitly the

number of children with complex febrile seizures. In a study of Saudi

Arabian children64 8.4% had complex febrile seizures. However, In this

study, children were recruited after their first febrile seizure. This

would, therefore, not have included patients with multiple seizures in

a febrile episode. Excluding this latter group of patients would have

reduced the proportion of patients with complex febrile seizures.

33

Fagbule et al4 found that 58.5% of cases had one episode of

seizures in 24 hours, 20.8% had 2 episodes, while another 20.8% had

3 or more episodes in 24 hours. Thus 41.6% of the children had

complex febrile seizures based on occurrence of multiple seizures in a

24-hour period. Iloeje15 in Enugu stated that 67(38.9%) of the 172

children studied had seizures lasting longer than 30minutes while

Angyo et al18 in Jos did not mention the pattern of seizures in the

children they studied.

Investigations

Several authors10,23, 65- 72 have reviewed the indications, cost and

benefits of various laboratory tests in the child with febrile seizures.

This issue has generated the most controversial aspects in the

evaluation of febrile seizures.10

The investigations that have been considered as ‘work up’ after a

febrile seizure have included: 10

Full blood count;

Blood culture;

Lumbar puncture;

Skull X-ray;

Electroencephalogram;

Electrolytes;

Urinalysis and culture; and

Random blood sugar

34

In the tropics, blood film for malaria parasites has been included

in this list especially as malaria is the commonest cause of fever in

febrile seizures.2,4 .The above laboratory investigations are expensive,

being worth much as 286 dollars in one study.10 In University College

Hospital Ibadan, with the current pricing of laboratory tests, this

would cost well over five thousand naira (40 dollars). The value of

these procedures to the clinicians in assessing the child with febrile

seizures is reviewed below.10, 23, 65 - 72

Lumbar Puncture Meningitis is the most important differential

diagnosis in the child with a febrile seizure.10 Most febrile seizure

episodes are benign and self-limited and do not require treatment.28

Several studies, 23,28,65-72 however, have shown that meningitis can

occasionally occur with a clinical picture indistinguishable from febrile

seizures.28

Thirteen percent of children with meningitis have convulsions

with fever and these seizures are almost always brief and

generalised.23,65 In 30% to 35% of these children (primarily those

children younger than 18 months) meningeal signs and symptoms

may be lacking.23 A recognized source of fever e.g. otitis media,

pneumonia, does not exclude the presence of meningitis. 23,66

The wide spectrum of presenting clinical manifestations and the

high degree of morbidity associated with the delayed treatment of

bacterial meningitis makes it essential to separate the child with

35

meningitis from among those with febrile seizures as soon as

possible.66

Although there is universal concern about the possibility that

meningitis may not be diagnosed quickly enough; there is

disagreement about the indicators for lumbar puncture.69 Some

reports are in support of routine lumbar puncture in all children

presenting with fever and seizure aged less than 18months while some

are not.16,64,67 A 6.3% yield for meningitis in a study by Laditan66 on

routine lumbar puncture after first febrile seizure, made him to

recommend continued performance of lumbar puncture in such

children especially under the age of 18months. So also did Rutter et

al67 report that it is not sufficient to limit lumbar puncture to the

children who did not have localizing signs of infection, for example a

child with a pneumonia could have a co-existing bacterial meningitis.

Another author65 argued that lumbar puncture is a reasonable

screening procedure and avoids unnecessary admission to the hospital

of children less than 18 months with simple febrile siezures.65 Only

those children who actually have meningitis are at risk of herniation

from the procedure but need a diagnostic tap anyway especially in a

hospital where supervision from experienced clinician is not always

available.

Lorber and Sunderland68 and Akpede16 had a different view

about routine lumbar puncture. Akpede et al16 reported a 4.2% yeild

36

of meningitis amongst the 522 children with fever and seizure.

Although six (27.3%) of the children with meningitis lacked the

classical signs, they had other indications for lumbar puncture

including; age less than six months, focal or multiple seizures,

absence of a past or family history of seizures, unrousable coma, and

an extracranial focus of infection. Akpede et al16 concluded that the

decision on the need for a lumbar puncture in children with febrile

seizures should not only be guarded by clinical evidence of meningitis,

but should take account also of features such as complex febrile

seizures, state of consciousness and previous or family history of

seizures. This also agrees with the recommendation of the RCP and

BPA.20

Lorber and Sunderland68 in the same vein argued that the risk of

coning/herniation after a lumbar puncture should be an indication for

not performing it routinely in febrile seizures. Review by an

experienced member of staff (senior resident, consultant) successfully

identified all cases of meningitis with the exception of one case of viral

meningitis in a group of 452 children with fever and seizure in their

study. It was however, not stated what parameters were considered in

the evaluation.

Some children with initial negative lumbar puncture later can go

to develop meningitis.67,68 This was observed by Rutter et al67 who

reported the case of 2 children who developed menigits withn 1- 2

37

days of a negative LP. This could be very dangerous considering the

prognosis of meningitis is related to the promptness of diagnosis and

early commencement of proper treatment in other to reduce morbidity

and mortality.

A major argument for the continuation of routine lumbar

puncture in children with fever and seizure in developing countries is

that other diagnosis such as Tuberculosis meningitis may be missed

or that it is not possible to exclude cerebral malaria.71 It is pertinent to

note that the simple addition of a broad spectrum antibiotic such as

chloramphenicol in a situation where pyogenic meningitis is a

possibility but LP is considered unsafe might no longer be adequate

because of the increasing problem of antibiotic drug resistance. The

differentiation of cerebral malaria from pyogenic meningitis is of

therapeutic importance bearing in mind that the use of

dexamethasone could be deleterious in cerebral malaria but

considered beneficial and desirable in pyogenic meningitis.71

Treatment of both infections concomitantly may be an unbearable

extra financial burden for some families.

Performing an LP in a person who has bacteraemia may cause

meningitis.71 Teele et al56 found an important association between LP

during bacterial infection and meningitis. This was most prominent in

children under the age of one year.

38

The American Academy of Pediatrics (AAP) and the Provisional

Committee on Qualitative Improvement in collaboration with expert

neurologists have developed a practice algorithms on the

neurodiagnostic evaluation of the child with the first febrile seizure.23

They reviewed over 200 medical journals and articles addressing the

diagnosis and evaluation of febrile seizures and concluded that an

increased risk of failure to diagnose meningitis occurs in:

1. Children less than eighteen months of age, who may show no

signs of meningitis.

2. Children who are evaluated by a less experienced health care

provider; and

3. Children who may be unavailable for follow-up.

It was concluded that the cerebrospinal fluid was more likely to

be abnormal in children initially seen with fever and seizures who

have had:

1. Suspicious findings on physical and neurological

examination;

2. Complex febrile seizures;

3. Physician visit within 48 hours before the seizures;

4. Seizures on arrival at emergency department;

5. Prolonged post ictal state; and

6. Initial seizures after 3 years of age.

They therefore made these recommendations:

39

1. After the first episode of seizures with fever in an infant less

than 12 months, performance of a lumbar puncture be

strongly considered, because the clinical signs and symptoms

associated with meningitis may be minimal or absent in this

age group;

2. In a child between 12 and 18 months a lumbar puncture

should be considered because signs of meningitis may be

subtle;

3. In a child older than eighteen months, although lumbar

puncture is not routinely warranted, it is recommended in the

presence of meningeal signs and symptoms (i.e. neck

stiffness, Kernig’s and Brudzuki’s signs) or for any child

whose history or examination results suggest the presence of

intracranial infection; and

4. In infants and children who have had febrile seizures and

have received prior antibiotics treatment, clinicians should be

aware that treatment could mask the signs and symptoms of

meningitis. As such a lumbar puncture should be strongly

considered.

In summary the AAP and the BPA recommended lumbar

puncture in every child less than 18months with their first febrile

seizure; a child older than 18 months if on antibiotics already before

the seizure; the presence of signs of meningeal irritation and after a

40

complex febrile seizure or if the child is unduly drowsy or irritable or

systemically ill.20,23

Full Blood Count (FBC) Full blood count is a routine investigation. In

a febrile child the presence of a leucocytosis of > 15,000/mm3 could be

an indication of a bacteraemia especially in children with acute fever

without localizing signs.71,72 AAP stated that FBC is useful in the

evaluation of fever in young children as the incidence of bacteraemia

in children younger than 2years with or without febrile seizures is the

same.23 By combining age, temperature and white blood count it is

possible to delineate a group of children with a very high incidence of

bacteraemia.71 Mc Gowan et al74 found a 28% incidence of

bacteraemia in children aged 7- 14 months with temperature > 39.5oC

and white blood count of > 20,000/mm3. Ayoola et al72 reported that

age less than 6months, restlessness and a WBC of > 15,000/mm3 are

associated with significantly increased risk of bacteraemia. Thirty-

eight percent of the infants with fever had bacteraemia in their report.

When fever is present, the decision regarding the need for

laboratory testing should be directed towards identifying the source of

fever rather than as part of the routine evaluation of the seizure

itself.23 Leucocytosis in the presence of a neutrophilia is an indication

of an underlying bacterial infection.71 The result of a segmented

Neutrophil count > 10,000/mm3 or a band neutrophil count >

5,000/mm3 increased the risk of severe bacterial infection to 80%. All

41

of their patients with occult bacteraemia had high white cell and

neutrophil counts.71

Blood Culture There is adequate data existing to show that

bacteraemia is a relatively common disease in young apparently mildly

ill febrile children.56 Although bacteraemia resolves spontaneously in

some children, many remain ill. Some have persistent bacteraemia, in

others a focal infection develops and in a few, severe disease like

meningitis occurs.

The problem of accurate diagnosis in children presenting with

fever especially without a localizing sign cannot be underrated. In the

tropics children presenting with fever could have positive malaria

parasitaemia but studies have shown this does not rule out the

presence of a bacteraemia or even a urinary tract infection.54,56 Blood

cultures have been considered an important part of the evaluation of

febrile children with underlying illnesses and those with selected soft

tissue infections.55 The issue arises of whether to do routine blood

culture in these children as they present in the clinic and also whether

treatment with an antimicrobial empirically is beneficial. The presence

of bacteraemia without a soft tissue focus is a therapeutic challenge

and the use of empirical antimicrobial has been suggested.55 There

are reports on this issue.56,75 In some reports, the outcome of children

sent home at first visit with unsuspected bacteraemia indicated that

children treated at first visit had a superior outcome when compared

42

to those left untreated.56,75,76 There is still no non invasive readily

available technique for distinguishing the febrile child with a non

bacterial infection who is likely to have spontaneous resolution from

the child with invasive bacterial infection requiring aggressive

management hence adequate clinical assessment should be done with

consideration of age of the child, temperature at presentation and

white blood cell count because they have been found to be indices of

the presence of bacterial infection.54,56,75

In a report, the outcome of children sent home at first visit with

unsuspected bacteraemia indicated that children treated at first visit

had a superior outcome when compared to those left untreated.76 It is

believed that presumptive therapy is warranted for the children from 6

– 24 months of age who have both a fever of > 38.90C and a WBC of >

15,000/mm.3

The use of blood culture in the out-patient department could be life

saving would help in accurate and prompt management of children with

fever.

Patients with simple febrile seizures are at approximately the

same risk for bacteraemia as children with fever alone.70 Out of the 93

patients with simple febrile seizures that James et al 70 studied, 5.4%

had positive blood culture. It was discovered that neither age nor

history of febrile seizures affected the risk of bacteremia. They argued

that patients with simple febrile seizures should be treated in the

43

same manner as other patients of the same age with regards to the

performance of blood culture.

Occult pneumococal bacteraemia may be an important cause of

febrile seizures. A study carried out on children in the outpatients

department showed that occult pneumococal bacteraemia occurred

frequently in young febrile children whose illness seemed trivial, and

thus did not warrant blood samples being taken.72 Persistent

bacteraemia and the development of focal infection including

pneumonia and pneumococal meningitis have been reported.72 Ayoola

et al72 suggested that age less than six months; restlessness and a

white blood count of 15,000/mm3 are associated with significantly

increased risk of bacteraemia. Thirty-eight percent of the infants with

fever in their study had bacteraemia.

A history of febrile seizures should not dissuade the

emergency room physician from performing blood culture.

Electroencephalogram (EEG) The EEG is abnormal in 90% of

children on the day after the febrile seizure. During the first week,

tracings are abnormal in about one third of cases, but afterwards only

5% or less are abnormal.10

Paroxysmal abnormalities in the EEG are not predictive of

recurrent febrile seizures.16 Some have found that the EEG predicts

44

later epilepsy,77,78 but others23 have not. The AAP’s review23 also

stated that there was no evidence that an abnormal EEG after the 1st

febrile seizure is predictive of either the risk of recurrence or the

development of epilepsy. Since EEG is expensive and unhelpful in

management, it should not be routinely carried out in children with

febrile seizures.

Skull X-rays The expense, radiation exposure, and lack of clinical

value suggests that skull x-rays, should be done only if there is a

suspicion of underlying brain disease or afebrile seizure.10 However in

current practice, Computerized Topographic Scan or Magnetic

Resonance Imaging may be more useful in these conditions.

Electrolytes These tests are rarely indicated and should be reserved

for children in whom significant fluid loss and dehydration occurs.10

Hospitalization

Several authors 10,69 have reviewed the issue of routine

hospitalization of children with febrile seizures and it was concluded

that admission should be considered only in those in whom serious

underlying disease is suspected.69

Some authors 10,69 state that clinicians often give parental

anxiety as an indication for admission10 but recommend that the

physician should emphasize the benign nature of febrile seizures and

not reinforce parental fears by admitting the child.69

45

There are principles guiding the issue of whether a child with

febrile seizures should be admitted or not. In UCH, children with

febrile seizures are not routinely admitted rather each child is

stabilized, a good history and examination done and the child is

assessed for cause of the fever and the severity of the illness. If it is a

first episode of febrile seizure, lumbar puncture is done to rule out

meningitis while other investigations are done as indicated. If the child

is alert, active after a period of observation the child is sent home on

medications to be seen on follow up. If the child’s condition, depending

on the cause of the fever, indicates further monitoring, then admission

is imperative.

The RCP/BPA joint working group decided that the following

factors would favor admission after a first febrile seizures:

Complex febrile seizures

Child less than 18 months

Unusual parental anxiety or inability of the parents to cope

Doctor not easily available to review at home20

The child should be kept for observation for few hours while

awaiting retrieval of CSF results and other basic investigations.

Hospitalization of patients with febrile seizure should not be

routine, rather each child’s case should be judged appropriately by the

attending physician who has been trained and is skilled to do so.

46

Parental Role and Socioeconomic factors in the outcome of

febrile seizures

It has been observed that the majority of parents have gross

misconceptions about febrile convulsions and hence take inappropriate

or even harmful actions in an attempt to control the convulsions.11 It is

believed that their social attitudes and behavior contribute immensely

to the high morbidity and unfavorable prognosis of febrile seizures in

this part of the world.2, 11

Iloeje11 carried out a population study of 845 Enugu parents

regarding their views of the causes, prognosis, best treatment options

and prophylaxis in febrile seizures. The parents were also asked to

state what steps they took whenever their children had fever with or

without seizures. Most (64.9%) of them gave a native concoction.

Others (16.9%) took harmful actions such as burning of the so le of

the feet, scarification, etc. Fifteen parents (9.4%) took measures to

bring down the child’s temperature such as tepid sponging and

fanning the child; only 14 parents (8.8%) took the child immediately to

the hospital. Many (56%) of parents either did not know the cause of

the convulsion or attributed them to evil spirits, God or as secondary

to constipation. Familusi et al 2 also recorded a high number (52%) of

parents administering native concoction (cow urine concoction) to

their children with febrile seizures. This was found to be contributory

to the high mortality rate of 6.4%.

47

With respect to the reaction of people who witnessed the attack,

Rutter et al79 reported that the reaction of the first person to witness

the convulsion was often one of fear and panic. They usually shouted

for help from the household or from neighbours. Some called their

doctor or an ambulance at once. Reactions towards the child are also

extremely variable. Some would lie the child down, others would place

the child in the sitting position while some would hit the child on the

back or even try to prise the child’s clenched teeth apart. Some

parents are known to actually attempt mouth-to-mouth resuscitation.

In the study by Rutter et al 79 30% of the parents interviewed

spontaneously volunteered that they thought their child was dying or

dead. These observations were further buttressed by Parmer et al5 who

reported that up to 90% of parents thought their child was dying

during the convulsion. After the acute episode, recurrence and

epilepsy were the major parental concerns. Most parents thus show a

severe psychological reaction to their child’s convulsion. This,

however, contrasts with the doctor’s consideration of febrile seizures

as a benign phenomenon. It is possible that these contrasting

perceptions are a result of the communication between the doctor and

parents being ineffective in imparting the right information and

knowledge. It is therefore essential that the physician know about

parental concern and anxieties in order to establish a meaningful

dialogue and allay their fears effectively.5

48

It has also been shown that parental anxiety and apprehension is

related to inadequate knowledge of fever and febrile seizures.80

Maternal education plays an important role in the quality of health

care a child receives.81 Children of mothers with no formal education

are at least twice as likely to die before age five than children of

mothers with post primary education.81

Correct and adequate knowledge of the relationship between fever and

febrile seizures, and its usual good prognosis, are important for

lessening the parental anxiety and apprehension associated with

febrile seizures. Many parents even develop fever phobia and each

febrile episode in the child can be a nightmare for the parents.5,79

Mothers constitute a good target group for specific health

education. Basley as cited by Oseni14 reported those parents with

previous knowledge of febrile seizures took more appropriate measures

during a convulsion than parents without such knowledge. It is

therefore very important that caregivers are educated on the

acceptable ways of managing febrile seizures when a child is brought

to the hospital. This is particularly relevant, given the propensity for

recurrence of seizures in the same child. Mothers irrespective of their

educational of social background should be taught on specific things

they should do when a child has a seizure.

Specific things to do when a child has a seizure include;

don’t panic

49

remove the child from harmful substances

lay him/her on the side and hold the child

If seizure does not stop after 10 minutes take to the hospital.

In places where there are home services the doctor could be

called in.

Basic health education can be incorporated into the curriculum

in both the primary and secondary schools. If topics such as

management of febrile seizures are taught, especially emphasizing

what not to do during a seizure, the impact on the children of such

students when they become parents will be appreciable. Such basic

health education can also be offered in programmes in the print and

the electronic media. In this way, even people who have not had the

opportunity of formal education can benefit.

Treatment

A rational approach to the management of febrile seizures

should take into account that the long-term prognosis is excellent,

and that there is no evidence that prophylaxis reduces the risk of

subsequent non-febrile seizures.19

An initial work up of febrile seizures should include a complete

history and complete physical examination with emphasis on

neurological examination, including characterization of the febrile

50

illness, degree of temperature elevation and complete description of

the febrile seizures.19

The management of a child with febrile seizures involves

1. Acute Stage

a. Control of seizures

- Some children are be brought into the hospital

convulsing and hence need to be resuscitated by

maintenance of airway, oxygen administration and

aborting the seizures .21

b. Control of fever

This is achieved by administration of antipyretics.1, 21

Acetaminophen produces relatively prompt lowering of the

temperature. However, some studies have shown that

antipyretics therapy is not effective in preventing febrile

seizures.20,21 This may partly be because the seizures can

occur during the rapid rise of temperature even before the

elevated temperature is noticed by the care-giver. The child

could also benefit from tepid sponging and fanning. It is

advisable to offer these latter therapies about 30 minutes

after the administration of acetaminophen, otherwise tepid

sponging will induce shivering which can increase the

temperature again.80

c. Treatment of the aetiology of the febrile illness.

51

Since febrile seizure is always a symptom of a generalized

illness, adequate physical examination and appropriate

laboratory investigations should be carried out and specific

treatment given for specific illness e.g. antimalarials for

malaria and antibiotics for pneumonia.

2. Prophylaxis

This is usually with the use of anticonvulsants.1, 82

There are two types:

(1) Intermittent: medications are given whenever the

temperature is greater than 380C and is continued

throughout the febrile illness.

(2) Prolonged or continuous: medication is given on a daily

basis.19

The use of prophylactics for treating febrile seizures is

controversial.83 Some doctors think that long term treatment with

phenorbarbitone is indicated after one episode,84,85 others do not.86

Some believe long term treatment with phenorbarbitone prevents

recurrence84,87 others consider it of limited or no prophylactic value.88

However, nearly all agree that side effects and non compliance are

common.84-88

Fransten et al89 reported a one year recurrence rate of 25% in

172 children who were not given any anticonvulsant treatment as

52

compared to 16% obtained in Knudsen et al”s study90 in which

diazepam or phenobarbitone was administered.

In a report by Wallace91 of 116 children who did not receive

anticonvulsants after their first febrile seizures, 55(47%) had a

reccurence with a subsequent febrile illness. A significantly increased

risk was present in:

Those with perinatal neurological abnormality

With a complicated initial fit

Males with history of convulsion disorder in parents and

wards

Females with age of onset less than 19 months.

The findings could be used for selecting children with a

higher possibility of a recurrence.

Regular administration of phenobarbitone significantly reduced

the recurrence rate of febrile seizures when compared to no

treatment or intermittent treatment in a study by Wolf.87

Fifty percent of febrile seizures occur in the first 24hours of an

illness.85 Knowledge of pharmacology indicates the futility of

administering phenobarbitone for the prevention of febrile seizures

when fever is detected.92 It must be administered for at least 5 half

lives to achieve a steady level of the drug in the serum. While the half-

life may be variable and age dependent, at least several days of

administration is required to achieve an effective therapeutic level of

53

15micro gram per milliliter when the usual therapeutic doses of 3 – 5

mg/kg are prescribed.92

The condition for an effective intermittent prophylalaxis of febrile

seizures with diazepam must be to give the drug in sufficient dosage

and to give it on time as soon as the symptoms and signs of ill health

occur in the child.93 In a report by Dianese, et al93 the parents of 101

children were interviewed about the children who had had febrile

seizures for recurrence and also all the records of readmissions as a

result of a new febrile seizure or other illnesses were reviewed. Of

these, 90 had febrile episodes after the first febrile seizure and met the

criteria for intermittent prophylaxis. Forty-eight received diazepam

adequately and in the doses suggested, 42 did not.

Continuous phenobabitone (3-5mg/kg/d) and short-term

diazepam (0.3-0.5mg/kg/dose 8 hourly, rectally) at the first sign of

febrile illness till the second day of complete recovery have been

compared.14 They were all found to be effective in the prevention of

febrile seizures but there is controversy on the choice of drugs because

of the problem of side effects.

The side effects of phenobarbitone which include; irritability,

hyperactivity, negativistic behaviour and rashes are sometimes severe

enough to warrant withdrawal of the drug or produce poor compliance

in other cases.94.

54

Evidence suggests that the frequency of febrile seizures may be

reduced by the prompt administration of diazepam per rectum at the

onset of acute febrile illness.19, 82,83 Side effects include lethargy,

ataxia, irritability and sedation, though these are rarely seen.

Knudsen and Vestermark90 carried out a cohort study

comparing, the rate of recurrence of febrile seizures after the first

episode in two groups of children. The first group was given

intermittent diazepam (suppositories) any time temperature was

greater than 38.50C whilst the other group was given daily

phenorbabitone. It was discovered that the recurrence rate was

similar and so also the duration of seizures. They concluded that

long-term treatment with phenobarbitone offered no advantage over

intermittent diazepam.

Sodium valproate at a dose of 20 – 40mg/kg/day has been

reported to be effective, but hepatic toxicity following the prolonged

use has been reported.10,95 However in a study by Ogunmekan et al95

no patient receiving Sodium valproate as the first anticonvulsant

prophylactic drug experienced a second during the first 6months. In

patients who had previously received phenobarbitone, there was a

90% reduction in seizure recurrence. Recurrence was also decreased

in 3 of the 4 children who had had side effects to phenobarbitone

before withdrawing it. There was no significant side effect with sodium

valproate.

55

Recurrence

It has been suggested that each seizure makes it easier for

another to occur.1 Of the children with febrile seizure, 30-40% who do

not receive prophylactic therapy will experience a second.19

There have been various reports on the recurrence rates of

febrile seizures.9, 14,43 Most of the recurrences occur within six to

twelve months of the initial febrile seizure.7

The risk of recurrence is influenced by the neurological status of

the child prior to the seizures, the age of the patient at the time of the

first seizure and the character of the seizure.92

Risk factors for recurrence include; 7,21

- Family history of febrile seizures and or epilepsy.

- Age less than fourteen months at the first seizure

- A short duration of illness (<24hrs) prior to febrile seizures

- Low temperature at time of febrile seizure

- Attendance in day care centre

- Developmental delay.

The single most important factor in predicting recurrence is the

age at the time of the seizures.95 Nelson and Ellenberg96 found 50%

recurrence rate in children with onset of febrile seizures in the first

year of life as opposed to a 28% recurrence rate with onset after the

first year of life. In a population- based study by Nelson et al9 it was

56

found that a third of the children (30%) who experienced a febrile

seizure had at least one recurrence and half of those who had at least

one recurrence had a further episode. Nine percent of the 1706

children they studied had over 3 or more recurrences. Males and

females and blacks and whites did not differ significantly in their

vulnerability to recurrence in the study. It was postulated that the

likelihood of recurrence was related to age at onset of febrile seizures.

In children who experienced their first episode of febrile seizures

before their first birthday, 30% later experienced multiple recurrences,

while only 11.1% of those whose first episode occurring after their first

birthday experienced multiple recurrences.

Airede97 found that patients with moderate degrees of pyrexia

(39-39.90C) at first febrile seizure were 10 times more likely to have

subsequent recurrence than those with low or high degree of pyrexia.

This is at variance with what is popularly stated that recurrence is

more likely when first seizure occurs at a lower temperature.7

Imuekheme17 from Benin, measuring serum CSF Copper and

Zinc levels on admission in febrile seizure patients found low serum

zinc levels on admission to be significantly associated with recurrence

of the seizure and therefore helpful in deciding the risk of recurrence.

Complications

Epilepsy Only 2-4% of children with febrile seizures develop

57

epilepsy.7 Risk factors for developing epilepsy include a family history

of non-febrile seizures, abnormal neurological or developmental status

prior to febrile seizures and atypical febrile seizures.

Nelson and Ellenberg96 carried out a prospective population

study of 1706 children with febrile seizures over a period of years till

age 7 years. They discovered that only 3% of these children developed

afebrile seizures by the seventh year of life. Lennox,78 reported a

higher incidence of 5- 12% amongst the 240 children febrile seizures

studied over a 3 year period. However, the number of febrile seizures

these children had had in the past was not stated.

Abnormal neurological or developmental status, occurrence of

complex first febrile seizures and history of non- febrile seizures in a

parent or older sibling were found to be significant predictors of

epilepsy in a report by the NCPP.9 The number of episodes of febrile

seizures has also been found to have a positive relationship with

epilepsy as reported by Lennox44 and Wallace.77

In a retrospective study by Annegers et al 8 the medical histories

of residents of Rochester, Minnesota who had a diagnosis of febrile

seizures within a period of 40 years were reviewed. The relative risk of

epilepsy following febrile seizures declined with increasing age. They

reported further that the occurrence of subsequent partial unprovoked

seizures was strongly associated with all the three complex features

whereas the occurrence of subsequent generalized seizures was

58

associated with the number of febrile seizures and a family history of

unprovoked seizures.

Pathogenesis of epilepsy following febrile seizures may be

different amongst various seizure types.98-100 Konishi et al98 studied

the clinical, EEG and developmental factors of 46 epileptic children

following febrile seizures. Eleven hade generalized seizures while 34

had partial seizures. Intractable seizures were recognized in 9% of the

partial seizure group. Motor and mental defects were more frequently

associated with the partial seizure group than with the group with

generalized epilepsy following febrile seizures. Complex febrile seizures

are associated with increased risk of epilepsy.3 A study by kanemoto

et al99 confirmed the close association between complex febrile

seizures and temporal lobe epilepsy.

Hippocampal sclerosis is the most common pathology in

intractable temporal lobe epilepsy.101 Bower et al 101 in reviewing the

relationship between the degree of hippocampal atrophy and the

incidence of febrile seizure in patients with temporal lobe epilepsy,

reported that the degree of MRI-determined hippocampal atrophy was

not related to a history of febrile seizures. They were more in support

of the hypothesis that hippocampal sclerosis is a pre-existing

abnormality in patients with febrile seizures who later develops of

temporal lobe epilepsy.

59

It is therefore apparent that the issue of later onset of recurrent

non-febrile seizures should be addressed when managing cases of

febrile seizures, with emphasis on taking a good history, especially

the premorbid neurological status, family history of seizures and the

nature of the seizures.

Neurological Deficits

The child with febrile seizures may have neurological deficits

such as motor deficits, sensory and perception abnormalities.19

There is some controversy regarding the effects of cow’s urine

mixture. Some authors2,102 believe cow urine mixture is responsible for

the neurological complications seen in patients with seizures while

some do not.103 Some authors believe hypoglycemia which is induced

by some unknown component of cow urine mixture is responsible for

the permanent neurological sequelae and prolonged coma seen in

some patients given this mixture,2,57,102,104 while some do not see any

correlation between the administration of cow urine mixture to

children with seizures and the incidence of hypoglycemia, neurological

sequelae and death.103

Familusi et al2 reported persistent neurological deficits in 49

(8.3%) of the 590 children with febrile seizures. The neurological

deficits included generalized spasticity, behavior disturbances,

hemiplegia, decerebrate rigidity, blindness, deafness and

choreathetosis. However, the deaths and neurological deficit were

60

more common among patients to whom traditional concoctions (cow

urine) were administered for control of seizures. Thirteen percent of

the 309 patients who received cow’s urine mixture developed

permanent neurological sequelae as compared with only 2% of the 197

patients who did not receive the mixture.

The popular native concoction used in the part of the country

where this study was done is the cow’s urine concoction. This contains

tobacco leaves, garlic leaves, basil leaves, lemon juice, rock salt, bulb

of onions all soaked in cow’s urine or human urine in varying

strengths and for varying lengths of time.105 Oyebola106 in his review of

the chemical components and pharmacological actions of cow’s urine

concoction reported the deleterious effects of native concoction on the

brain and other body systems. These include; cardiovascular effects

like tachycardia, blood pressure and electrocardiographic changes.

Respiratory complications include: respiratory depression and

respiratory failure while other effects are profound hypoglycaemia,

reduced neutrophil and monocyte counts (thus increasing the risk of

infection), restlessness, spasms, intracranial haemorrhage, paraplegia,

coma and death.

The clinical findings in patients given cow’s urine mixture are,

on the whole compatible with nicotine poisoning and the occurrence of

toxic symptoms in those who have only had the mixture rubbed into

61

the skin supports the concept of nicotine poisoning because of the

known ease with which nicotine is absorbed from the skin.57 Some

findings in cow’s urine mixture poisoning, such as prolonged coma

and permanent neurological sequelae do not however accord with

nicotine toxicity and suspicion has long centered on hypoglycemia

induced by unidentified constituents of the concoction, as the cause of

these complications. This suspicion has been reinforced by the

frequent detection of hypoglycemia in patients given cow’s urine.107

Familusi et al2 found hypoglycemia and low CSF glucose in 19% of

patients given cow’s urine mixture, but in only 1.5% of those not

given. Severe hypoglycemia was also found in 24 out of 70 epileptics

known to have had the mixture.104, These are indications but not proof

of a causal relationship between cow’s urine poisoning and

hypoglycemia. In a study by Ojewole et al102 on rats, they reported a

firm evidence of a time and dose related hypoglycemic effect of the

cow’s urine mixture. The mechanism by which it is induced is however

not known. Some authors do not agree with this correlation, Ransome

kuti et al103 reported that there was no correlation between the

administration of cow urine to children with convulsion and the

incidence of hypoglycemia, neurological sequelae and death

Verity et al45 reported speech problems in patients with febrile

seizures. Curiously, it was children who had had simple rather than

complex febrile seizures that were affected. Eleven out of the 42

62

children they studied had recovered fully within 5years and only one

case was said to have been severe. Aicardi et al 107 in a series of 402

patients with febrile seizures hospitalized or seen as outpatients

reported that 37(9.2%) had neurological sequelae out of which 24%

had hemiplegia. Wallace111 reported that 27 out of 100 children

followed up for 2-4years after hospitalization for febrile seizures had

evidence of seriously disturbed behavior.

Some authors are however, of the opinion that these neurological

deficits usually antedate febrile seizures.1, 19 Their argument is that

there is no epidemiological evidence that these deficits reflect

neurological injury at the time of the febrile seizure. It is therefore

possible that neurological deficits following febrile seizures are not

purely as a result of the seizures. Rather, they may represent the

premorbid status of the patient or are secondary to the form of

treatment offered.

Intellectual Outcome

In children admitted to hospital with febrile seizures Lennox109

found mental retardation at follow up in 22%. However the author did

not do a premorbid IQ assessment of the children. About half the

reports reviewed by Wallace21 reported that 5-10% of their patients

were retarded. Nelson and Ellenberg96 selected 431 children from the

1,706 with febrile seizures in the National Collaborative Perinatal

63

Project. Siblings in the study who had not had febrile seizures acted

as control for intellectual testing at seven years of age. Children who

were normal before any febrile seizure did not differ in intelligence

quotient (1Q) from their normal seizure- free siblings, while children

who were suspect or mentally challenged before the first febrile

seizures scored significantly lower IQs than their siblings. Neither

recurrent seizures nor seizures lasting longer than 30 minutes were

associated with IQ deficit. A population based study in the United

Kingdom101 also found little difference in intelligence outcome between

children with febrile seizures and their peers if the children with

febrile seizures had no other known neurological abnormality. It is

therefore doubtful if recurrent febrile seizures have any significant

effect on IQ.

64

AIM AND OBJECTIVES

The general objective of this study was to evaluate the pre- hospital

management, pattern, aetiology and outcome of febrile seizures in

children seen at the Children’s Emergency Ward of the University

College Hospital, Ibadan.

The specific objectives are;

1. To determine the prevalence of febrile seizures amongst children aged

3months - 5years admitted into the Children’s Emergency Ward of the

University College Hospital Ibadan.

2. To determine the pattern of febrile seizures in affected children.

3. To determine the underlying cause of fever in children with febrile

seizures.

4. To determine the influence of socioeconomic class and maternal

education on the type of pre-hospital management given to children

with febrile seizures.

5. To determine the short-term morbidity and case fatality rate

among affected children with febrile seizures.

65

SUBJECTS AND METHODS

STUDY SITE

This study was carried out between November 2002 and

December 2003 at the University College Hospital (UCH), a tertiary

health institution with 805 beds in Ibadan, Oyo State, Nigeria. UCH

caters for patients from Ibadan and its environs and sometimes for

patients from other parts of Nigeria.

The Paediatric unit is made up of an emergency ward named

Otunba Tunwase Children’s Emergency Ward (OTCHEW) and 5 other

wards for the admission of patients. Most of the patients admitted to

the wards are initially seen in the emergency ward, while a few

patients, usually with chronic illnesses are admitted to the wards from

the outpatient clinics. A patient with an emergency such as febrile

seizures would be seen initially in the emergency ward. For this reason,

the study was conducted at the OTCHEW.

The emergency ward has a resuscitation area where critically ill

children are nursed till stable before being transferred to the ward

area. There is also a general ward, measles bay, a diarrhea therapy

unit, a neonatal ward, a laboratory, a pharmacy and a records and

accounts unit.

Children brought to OTCHEW are seen by the registrar on duty

66

who does a brief clinical assessment and resuscitates the child

depending on how critical the case is. There are house physicians

and nurses on the ward to assist in managing the children. The senior

registrars conduct wardrounds regularly and see to the smooth

operation on the ward.

Children stay for a maximum of 48hrs and afterwards they are

either discharged to follow up or transferred to the other wards hence

creating room for more admissions.

The cases seen in OTCHEW include: - severe malaria, severe

anaemia, acute respiratory infections, neonatal problems, burns,

measles, tetanus, diarrhea cases, septicaemic illnesses, severe

malnutrition, seizures, coma cases and so on.

67

SAMPLE SIZE ESTIMATION

The sample size was calculated using the formula110 n =Z2pq d2

nf =n

1 + n N Where,

n = the desired sample size when the population is greater than

10,000.

nf = the desired sample size when the population is less than 10,000.

z = the standard normal deviate, usually set at 1.96, which

corresponds to the 95% confidence level.

p = the proportion of the target population estimated to have a

particular characteristic (0.04) q = 1.0 –p

d = degree of accuracy desired usually set at 0.03. N = the estimate of the population size. The admission records of the last year preceding this study were

reviewed and these showed that, 1640 patients were admitted into the

children’s emergency ward. Of these, (3.7%) had febrile seizures.

The estimated prevalence (p) is 60 1640

68

= 0.037

= 3.7% n = (1.96)2 (0.037) (0.963)

(0.03)2 = 152 nf = 152 1 + 152 1640

= 139

The calculated minimum sample size was 139. However, the

sample size was increased to 147 to accommodate for attrition.

Procedure

This was a 14-month prospective study carried out at the University

College Hospital Ibadan, from November 2002 to December 2003.

Children were recruited from the OTCHEW. Inclusion Criteria

The following inclusion criteria were used to select children for the

study.

(i) age 3 months to 5 years

(ii) History of seizures in the presence of a fever ( axillary

temperature >37.50C) at presentation in hospital or fever and

seizure occurring while in the hospital.

(iii) normal cerebrospinal fluid.

69

Exclusion Criteria

(i) children below 3 months and above 5 years of age.

(ii) children with previous or on-going nonfebrile seizures

(iii) children with acute head trauma associated with seizures

(iv) children with congenital or acquired central nervous system

abnormality

(v) children with abnormal cerebrospinal fluid.

70

RECRUITMENT OF PATIENTS AND CONDUCT

OF THE STUDY

Ethical Clearance

Ethical clearance for the study was obtained from the Joint

University of Ibadan/University College Hospital Ethical Committee.

(Appendix I)

The investigator evaluated all new patients admitted into the

paediatric emergency room of the University College Hospital Ibadan

on the first day of admission into the hospital to identify those with

febrile seizures and this was done on a daily basis over the period of

the study.

Methodology

The investigator obtained verbal consent from the parents or

caregivers of the children before they were recruited into the study. A

history of the illness was obtained from the caregivers and the patients

when this was possible. The name, age, sex, presenting complaints,

duration of symptoms before presentation, birth weight if available,

and pre-hospital management were recorded in a proforma designed

for the study (Appendix II). A thorough physical examination was

performed on each patient at admission with particular emphasis on

the central nervous system. Anthropometric measurements were taken.

71

These included weight (kg) on admission, occipitofrontal circumference

(OFC) in cm, and the length or height (cm).

Temperatures were taken using clinical mercury-in-glass

thermometers. The bulb of the thermometer was placed at the apex of

the axilla, halfway between the anterior and the posterior margins of the

axilla and read after four minutes.111 Children less than two years of

age were weighed using the Way Master Model 1615K Infant Scale (Way

Master Co Reading, England) while those aged two years and above

were weighed using a flat scale (Hanson, Model: 89p, Ireland), and the

weight measured to the nearest 0.5kg. The scale was checked for zero

error before weighing. The OFC was measured by passing a tape

measure around the forehead and the occiput without the measuring

finger getting in between the tape and the head. Length was measured

using a tape measure from the vertex to the heel of the child in patients

who could not stand. Older children were made to stand with the heels

of the bare feet against a wall on which was a tape accurately calibrated

in centimeters. The findings on examination were recorded on the

proforma (Appendix II). The clinical diagnosis, the results of

investigations and the final diagnosis were also recorded on the

proforma (Appendix II). All the patients were seen and examined by the

investigator.

Laboratory Investigations

72

The extent of laboratory investigations was determined by the

clinical diagnosis. However, the following investigations were

performed on each recruited patient irrespective of the clinical

diagnosis: packed cell volume, full blood count, blood film for malaria

parasites, blood culture, urine microscopy, culture and sensitivity,

random blood sugar and CSF analysis. The Technologists in the

Microbiology, Haematology and Chemical Pathology departments who

routinely analyzed such specimens performed the laboratory analyses.

Lumbar puncture was performed on each child at presentation. The

patient was placed in the lateral recumbent position while an assistant

flexed the neck and legs of the patient. The skin of the lower back was

thoroughly cleaned with methylated spirit. A 23 or 21 gauge needle

was introduced into the midsaggittal plane at L4/5 or L3/4 spinal

space directed slightly in the cephalic direction. About 2 mls of

cerebro-spinal fluid was obtained for microscopy, culture and

sensitivity and also for sugar and protein content.

One to three mls of venous blood was obtained from a peripheral

vein after the skin surface had been cleaned with methylated spirit. A

new hypodermic needle was then attached to the syringe containing

the blood and the blood was injected into a culture bottle containing

glucose broth for the detection of organisms after cleaning the rubber

cap of the culture bottle with methylated spirit. This culture bottle was

immediately taken to the laboratory to be incubated. This was done

73

aerobically at 370C for 7 to 10 days. Facility for anaerobic culture was

not available in our centre during this study. Venous blood was also

taken for packed cell volume, full blood count and random blood

sugar. The sample for random blood sugar was taken before the

lumbar puncture was performed. Peripheral blood films (thick and

thin) were prepared in a standard manner, Giemsa stained and

examined under oil immersion; 200 thick film fields were examined

before findings were declared negative. Parasitaemia was graded from

+1 to +4 where one plus = 1 to 10 parasites per 100 thick fields, two

pluses = 11 to 100 parasites per 100 thick film fields, three pluses = 1

to 10 parasites per one thick film field and four pluses = more than 10

per one thick film field. One to three millilitres of “clean catch” urine

was collected in to a sterile universal bottle and sent to the

microbiology laboratory for microscopy, culture and sensitivity. The

samples were processed within one hour of collection. Chest X-rays

were done in children who had clinical evidence of lower respiratory

tract infection.

The patients were followed up till discharge with regular

examinations to detect neurological deficits and the total duration of

hospital stay was noted.

In UCH, lumbar puncture is done on every child presenting with

the first febrile seizure but for the purpose of this study, every child

presenting with fever and seizure had a lumbar puncture done.

74

Treatment and Monitoring of Patients

Convulsions were aborted with deep intramuscular injection of

paraldehyde (1ml/year of life to a maximum of 5mls) or intravenous

diazepam at 0.1-0.3mg /kg given slowly until the seizure stopped with a

maximum dose of 10mg. Repeated convulsions were controlled with a

loading dose of intramuscular phenobarbitone at 15-20mg/kg stat then 3-

5mg/kg/day in two divided doses.

Patients who had packed cell volume less than 15% had packed red

cell transfusion. In children with malaria parasitemia, antimalarial

therapy was instituted. Uncomplicated malaria where only one episode of

febrile seizure had occurred was treated with oral chloroquine. If

chloroquine had been used previously, alternatives in the form of

amodiaquine or primethaime/sulfadoxine were used. In the presence of

repeated seizures or other indications of complicated malaria, quinine or

artemisinine was the drug of choice. In children with clinical diagnosis of

septicaemia, urinary tract infection or other bacterial infection,

appropriate antibiotic therapy was instituted based on the usual drugs

normally administered to treat various infections pending results of

investigations.

Statistical Analysis

Data analysis was done using Statistical Package for Social

Sciences (SPSS) version 10 and exported into Epi info version 5

75

software package for formal analysis on anthropometry. The initial

frequencies of the variables were done to generate the mean, standard

deviation, minimum and maximum values. Categorical data were

compared using Chi-squared test and Fisher’s exact test where

applicable. Differences were deemed to be statistically significant

where p<0.05.

Anthropometric analysis

The formal analysis on anthropometry was done by taking the

weight and height measurements and comparing them with the

National Centre for Health Statistics (NCHS) growth charts (these now

constitute the World Health Organization international growth

reference curves). using the Epinut analysis module of Epi Info

version5.112,113 To determine the proportion of stunting, wasting,

underweight and over-weight the following cut off points were used:

Stunting: z score of height for age <-2SD; wasting: z score of weight for

height <-2SD; under-weight: z score of weight for age <- 2SD; over-

weight: z score of weight for height >+ 2SD.114 `

Socioeconomic classification

The socioeconomic classification was done using Oyedeji’s

method.115 This classification considers the level of education and the

occupation of both parents:

No formal education 5 unemployed/housewife/farmer 5

76

Primary education 4 unskilled worker 4

Secondary education 3 skilled worker 3

Post secondary nonprofessional (secondary

education 2 school teacher/senior civil

servant/well to do business-

University/HND 1 man or woman) 2

Professionals 1

The scores are added together for both parents and the average score

obtained. A score of 1-2 = upper class, 3 = middle class, and 4-5 =

lower class.

77

RESULTS

During the 14-month period of this study, from November 2002

to December 2003, 147 children admitted to the OTCHEW at the UCH,

Ibadan, Nigeria, satisfied the criteria for inclusion into the study.

Prevalence of febrile seizures

There were a total of 1,487 paediatric admissions into OTCHEW

during the study period. Of these 147 were cases of febrile seizures

giving a prevalence of 9.9%.

Age and Sex Distribution

Table I shows the age and sex distribution of the children studied.

There were 83(56.5%) males and 64(43.5%) females giving a male:

female ratio of 1.3:1. The ages of the children ranged between

4months and 60 months (5 years) with a mean + standard deviation of

26.35 + 13.76 months. The mean age of the males was 25.71 + 13.24

months while that of the females was 27.19 + 14.4 months. The

highest numbers of children were in the13 - 24 age groups.

78

Table I .Age and Sex distribution of 147 children in the study.

Age Male Female Total

(in months) n(percent) n(percent) N(percent)

3 - 12 13(62) 8(38) 21(14.3)

13 - 24 35(56.5) 27(43.6) 62(42.2) 25 – 36 24(68.6) 9(25.7) 35(23.8)

37 – 48 12(66.7) 6(33.3) 18(12.3)

49 – 60 3(27.3) 8(72.7) 11(7.5)

Total 83(56.5) 64 (43.5) 147(100)

P = 0.305, df = 4, x2 = 4.835. mean age of females = 27.19 + 14.4 months.

mean age of males = 25.71 + 13.24 months

Type of seizures

As shown in table II, the type of seizure was classified into

simple and complex seizures taking into consideration the duration of

the seizures, pattern of seizures and the number of occurrences within

that febrile episode.

Forty- seven cases (32%) qualified to be referred to as simple

while 100 cases (68%) fell under complex febrile seizures. The seizures

were described as generalized in 129 cases (87.8%) and focal in 18

cases (12.2%). There was no statistically significant relationship

between the type of seizures and the age of the children (p= 0.936, df =

79

4, x 2 =0.822) (table III). In all the age groups complex febrile seizures

occurred more frequently than simple febrile seizures.

Table II. Classification of children into seizure categories

___________________________________________________________________

Characteristic seizure type Number

of seizure (%)

___________________________________________________________________

1. single, generalized simple 47(32%)

<15minutes

2. single generalized complex 20 (13.6%)

>15minutes

3. Multiple seizures complex 62 (42.2%)

in 24hrs

4. Focal complex 18 (12.2%)

___________________________________________________________________

Total 147 (100)

___________________________________________________________________

80

Table III: Type of seizures in relation to the age of children with febrile

seizures

___________________________________________________________________

Age in months Simple Complex Total

N(percent) N(percent) N(percent)

___________________________________________________________________

3- 12 8(38) 13(62) 21(14.3)

13- 24 18(29) 44(71) 62(42.2)

25- 36 12(34.3) 23(65.7) 35 (23.8)

37- 48 6(33.3) 12(66.7) 18(12.2)

49- 60 3(27.3) 8(72.7) 11(7.5)

__________________________________________________________________

Total 147(32) 100(68) 147(100.0)

P = 0.936, df = 4, x2 = 0.822.

Demographic Characteristics of the Parents

The socioeconomic status of the parents of the children in the

study is highlighted in Tables IV and V. The socioeconomic status of

the parents of these patients was determined using Oyedeji’s

method.119 Forty (27.2%) parents belonged to the upper class, 75(51%)

to the middle class and 32(21.8%) the lower socioeconomic class.

As shown in table IV, there was no statistically significant

difference in the type of seizure in relation to the socioeconomic class

of the parents.(p = o.658, df = 2, x2 = 0.838).

Table IV. The socioeconomic class of parents in relation to the type of

81

febrile seizures in the children of the study.

___________________________________________________________________

socioeconomic class simple complex Total

n (percent) n(percent) N(percent)

___________________________________________________________________

Upper 15(37.5) 25(62.5) 40(27.2)

Middle 23(30.7) 52(69.3) 75(51)

Lower 9(28.2) 23(71.9) 32(21.8)

___________________________________________________________________

Total 47(32) 100(68) 147(100)

___________________________________________________________________

p = 0.658, df = 2, x2 = 0.838.

Past Medical History and Family History

A family history of febrile seizure in a first degree relative was

obtained in 42(29%) cases of the 147 children studied. A history of

febrile seizures in one or more of their siblings was present in

23(15.7%) patients. Nine (6.1%) mothers knew that they had

convulsions in childhood, while 10(6.8%) fathers were similarly

affected.

A past history of febrile seizures was volunteered in 23(15.6%) of

the patients, most first recurrences occurred within a year of the first

episode in 17(74%); 16 had one previous episode, 3 had 2 episodes,

and 4 patients had 3 or more episodes. Age at first episode in the

82

children with recurrence varied from 3 months to 48 months. Twenty

(87%) of the 23 patients with recurrence in this study had their first

episode at age one year and above, with only 3(13%) being less than a

year at first episode. The mean age at first episode was 20.29 + 12.75

months compared with 27.4 + 15.4months obtained in the general

group. Only in one instance was a history of epilepsy in the family

obtained. Eight (34.8%) of the 23 patients with recurrent febrile

seizures had a family history of febrile seizures compared with

36(28.1%) of the 127 cases presenting with their first episode of febrile

seizure. The difference was not statistically significant (P value = 0.53,

X2 = 0.39). Nine of the 23 children (39%) had or were attending day

care centers.

Table V. The socioeconomic class of parents in relation to past

history of seizures in the children of the study

83

_______________________________________________________________

socioeconomic class recurrent non-recurrent Total(percent)

_______________________________________________________________

upper 7 33 40(27.2)

middle 10 65 75(51)

lower 6 26 32(21.8)

_______________________________________________________________

Total 23 124 147(100)

_______________________________________________________________

P= 0.726,df = 2, x2= 0.642

Predisposing Factors

Sixty-four (43.5%) of the children studied had attended or were

attending day care while nine (6.1%) were born preterm.

History of medication in pregnancy was obtained in 130(88%).

The medications included mostly haematinics (85%) like folic acid and

iron tablets and multivitamins. Four mothers had taken one form of

antibiotic or the other while none use of native concoction. History of

perinatal abnormalities was obtained in 19(12.9%) cases: 7 mothers

had antepartum haemorrhage, 1 had severe anaemia, 2 had breech

delivery and 6 caesarian section delivery.

Temperature

The temperature on admission or at the time of seizure varied in

84

the children studied. In 3(2%) children temperature at admission was

less than 37.5OC, 142(96.6%) had temperatures between 37.50C and

400C. Only two patients (2%) had temperatures above 40.00C. There

was no difference in the mean temperatures (38.30C) of the children

with recurrence and those without.

Pre-hospital intervention given

Out of the 147 patients studied only 59(40.1%) were given a pre-

hospital treatment of some sort after or during the seizure. (Tables VI

to IX). Fifteen (25.4%) out of the 59 gave native concoction. Nine

(15.3%) children had substances applied to the eyes. The substances

included salt, wine, onions, coconut oil, palm oil and metholatum.

One child had subsequent visual impairment. Three children (5%)

were subjected to burning of parts of the body e.g. both feet and

buttocks and one had to have plastic surgery done as a result of this.

One child had deep knife incisions inflicted on her face, feet and

trunk. Other forms of treatment given included application of things

like eucalyptus oil, palm oil, pepper, kerosene, lime and adiagbon

(coconut oil) to the body. The children to whom substances were given

by mouth also had the same substance rubbed on the body. None of

the children was tepid sponged or given any drug to stop the seizure

associated with fever.

Table VII shows that of the 59 parents who treated their children

85

at home, 9(15%) were in the upper class, 36(61%) were in the middle

class while 14(23.7%) were in the lower class. Seventeen percent of the

children in the upper class had pre-hospital intervention, 47% of the

76 in the middle class and 44% of the children in the lower class.

There was a statistically significant difference between the types of

pre-hospital intervention given in the different socioeconomic classes.

(p= 0.008,df = 8, X2 = 20.8). None of the children in the upper class

had native concoction.

Forty- seven of the 124 children with first febrile seizure versus

12 of the 23 with recurrent febrile seizures had pre-hospital

intervention. (P = 0.25,df = 1, X2 = 1.32) (Table VIII). There was no

statistically significant relationship in the type of seizure and the pre-

hospital intervention administered in the children (p= 0.981, df = 1, x2

= 0.002)(table IX).

86

Table VI. Pre-hospital management of 59 children with febrile seizures

___________________________________________________________________

Type of intervention Frequency Percent

___________________________________________________________________

1. Agents given by mouth

Native concoction 15 25.4

Salt and water 8 13.6

Milk 4 6.8

Anointing oil 2 3.4

Palm oil 1 1.7

Pepper 1 1.7

2. Agents rubbed into eyes

onions 3 5.1

metholatum 1 1.7

canel oil 1 1.7

palm oil 1 1.7

wine 1 1.7

salt 1 1.7

3. Burning of body 2 3.4

4. Cut to the body 3 5.1

5.water to the body 8 13.6

5. Others 7 11.9

___________________________________________________________________

Total 59 100

___________________________________________________________________

87

Table VII. Pre-hospital intervention in relation to the socioeconomic

class of the parents.

_________________________________________________________

Type of intervention upper middle lower total

___________________________________________________________________

Native concoction 0 7 8 15(10.2)

Other agents to drink 2 12 2 16(10.9)

B&C/S 2 10 1 13(22)

Others 5 7 3 15(10.2)

No intervention 30 40 18 88(60)

___________________________________________________________________

Total 39 76 32 147(100)

___________________________________________________________________

X2 = 20.8, P value =0.008,df = 8.

B&C/S = Burning and cutting of parts of the body or application of

substances to the eyes

others = kerosene, lime, adiagbon, eucalyptus oil and pepper

88

Table VIII. Pre-hospital intervention by mothers in relation to

recurrence of febrile seizures in children of the study

___________________________________________________________________

Intervention recurrence non-recurrent Total (percent)

__________________________________________________________________

Yes 12(20.3) 47(79.7) 59(40.1)

No 11(12.5) 77(52.4) 88(59.9)

___________________________________________________________________

Total 23(15.7) 124(84.4) 147(100)

___________________________________________________________________

p = 0.251, X2 = 1.32, df = 1)

Table IX. The type of pre-hospital intervention given by mothers in

relation to the type of seizures in the children with febrile seizures

__________________________________________________________________

Intervention simple complex total

N(percent) n(percent) n(percent)

__________________________________________________________________

Yes 19(32.2) 40(67.8) 59(40.1)

No 28(31.8) 60(68.2) 88(59.9)

_________________________________________________________________

Total 47(32) 100(68) 147(100)

_________________________________________________________________

( p = 0.981, X2 = 0.002, df = 1)

89

Aetiology of fever in children with febrile seizures

Tables X and XI show the causes of the fever that provoked

seizures in these children.. Malaria was responsible for 59(40.1%) of

the cases. Septicaemia was diagnosed in 22(15%) of the cases while

18(12.3%) had urinary tract infection. Twelve patients (8.2%) had

positive cultures of both blood and urine.

Two children with UTI were correctly identified and commenced

on antibiotics before culture results were obtained while three children

with septicaemia were correctly diagnosed clinically and commenced

on antibiotics before culture results were obtained.

The predominant organism isolated from the blood of these

patients was staphylococcus aureus found in 22(68.8%) of the 32

patients with positive blood culture. Other organisms were Salmonella

species 3(9.4%), Pseudomonas species 2(6.3%), unidentified gram-

negative bacilli 4(12.5%) and Klebsiella species in one (3%) patient.

The predominant organism isolated from the urine of these

children studied was Escherichia coli in 16 (53.3%) of the 30 children

with UTI; the other organisms were Klebisella species 8 (25%)

Staphylococcus aureus 3 (1%) and non- Haemolytic streptococcus 2

(6.7%). A patient had Candida albican infection (3.3%).

Table X. Relationship between the etiology of fever and age of the

children in the study.

_____________________________________________________________________

90

Etiology 3-12 13-24 25-36 37-48 49-60 total

_____________________________________________________________________

Malaria 7 26 14 9 3 59

Septicaemia 1 9 7 1 4 22

UTI 2 10 3 2 1 18

Pneumonia 3 6 1 2 0 12

Sept & UTI 3 3 4 1 1 12

Unknown 2 6 4 3 1 16

Others 3 2 2 0 1 8

_____________________________________________________________________

total 21 62 35 18 11 147

_____________________________________________________________________

(P = 0.79, df = 4, X2 = 18.265)

UTI = urinary tract infection

Sept & UTI = septicaemia & urinary tract infection

Others = measles, otitis media, gastroenteritis, typhoid enteritis and

tonsilopharyngitis

3 patients with pneumonia, 13 patients with septicaemia, 11 patients with

UTI and 7 patients with other infections also had malaria

The antibiotics that were sensitive to the organisms cultured

were mostly the cephalosporins like Ceftazidine and Cefuroxine and

91

also quinolones like ofloxacin, Ciprofloxacin and Sparfloxain. Amoxil

and genticin were also included in the drugs sensitive to the

organisms. Resistant drugs included Septrin, chloramphenicol and

tetracycline.

Pneumonia was diagnosed and confirmed by chest x-rays in

12(8.2%) children. Two children had clinical features in keeping with

measles. Two children presented with otalgia, ear discharge and

examination of the ear revealed pus in the middle ear and perforation

of the tympanic membrane. They both had positive ear swab cultures.

One child each was diagnosed with gastroenteritis and typhoid

enteritis. Two children had inflamed tonsils while in 16 (10.9%)

children the cause(s) of the fever could not be ascertained. There was

no statistically significant relationship between etiology of fever and

the age of the children (table X) (P = 0.79, df = 4, X2 = 18.265).

Malaria apart from occurring in some of the children alone it also

was seen in the children with other infections. Malaria was found in

13 of the cases of Septicaemia, 11 in the UTI cases, 3 in the

pneumonia cases and in 7 children with other infections. Table XI

shows the relationship between the etiology of fever and the type of

febrile seizures. Complex febrile seizure was more frequently seen in

all the etiological groups. Only one of the 18 children with UTI had

simple febrile seizures (0.1>p > 0.05). There was no statistically

significant difference in the type of seizure in relation to the degree of

92

parasitaemia (p= 0.089,

df = 2, x2 = 4.835)(table XII).

Twenty-five children had one plus of malaria parasitaemia, 11

had 2 pluses, 13 had 3 pluses while 10 had 4 pluses amongst the 54

with malaria only. There was no statistically significant relationship

between the degree of malaria parasitaemia and the type of seizure

(table XII) (P = 0.115, df = 2, x2 = 4.319).

There was no statistically significant difference in the aetiology of

fever among the different socioeconomic class (p = 0.50, df = 12, x2 =

11.37), and the type of pre-hospital intervention offered these children

(p = 0.10, df = 18, x2 = 5.86).

Table XI. Relationship between aetiology of fever and the pattern

of febrile seizures

_______________________________________________________________

93

Aetiology of fever simple complex total

(percent) (percent) (percent)

_______________________________________________________________

Malaria 24(40.7) 35(59.3) 59(40.1)

Septicaemia 7(31.8) 15(68.2) 22(15)

UTI 1(5.6) 17(94.4) 18(12.3)

Pneumonia 6(50) 6(50) 12(8.1)

Septicaemia

And UTI 4(33.3) 8(66.7) 12(8.1)

Unknown 3(18.8) 13(81.2) 16(10.9)

Others 2(25) 6(75) 8(5.4)

_______________________________________________________________

Total 47(32) 100(68) 147(100)

_______________________________________________________________

p = 0.082, df = 6, x2 = 11.212

Others = measles, otitis media, gastroenteritis, typhoid enteritis and

tonsilopharyngitis

3 patients with pneumonia, 13 patients with septicaemia, 11 patients with

UTI and 7 patients with other infections also had malaria.

Table XII. The degree of parasistaemia in relation to the type of

seizure in the children in the study.

_______________________________________________________________

94

degree of parasitaemia complex simple total

(percent) (percent) (percent)

_______________________________________________________________

< ++ 23(63.9) 13(36.1) 36(61.1)

> +++ 12(52.2) 11(47.8) 23(38.9)

_______________________________________________________________

total 35(59.3) 24(40.7) 59(100)

_______________________________________________________________

p = 0.115, df = 2, x2 = 4.317.

Packed cell volume

Table XIII shows the PCV values in the patients studied. The

mean PCV was 25.3 + 9.4 %. Anaemia was present in 89 patients

(61%), with 30 of them having a PCV of < 15% and 52 (35.4%) of the

patients having severe anaemia.

The least PCV was 8% while the highest value was 49%. There

was no relationship between the packed cell volume and the pattern of

seizures, socioeconomic status and the degree of parasitaemia. There

was no statistically significant difference in the packed cell volume in

the children with malaria (p = 0.55, df = 16, X 2 = 14.63). There was

however a statistically significant relationship in the PCV and the

etiology of fever in these patients(p = 0.01, df = 6, x2 = 16.81)(tableXIV)

95

Table XIII. Packed cell volume values in 147 children with febrile

seizures

_______________________________________________________________

PCV No of cases Percent

(percent)

_______________________________________________________________

<15 30 20.7

15 – 20 22 15

21 – 25 14 9.5

26 – 30 30 20.4

> 30 51 34.7

_______________________________________________________________

total 147 100

_______________________________________________________________

PCV = Packed cell volume

96

Table XIV. Packed cell volume in relation to the etiology of fever.

Aetiology presence of anaemia

Yes (%) no(%)

Malaria 38(64) 21(36)

Sept 19(86) 3(14)

UTI 14(78) 4(22)

Pneumonia 4(33) 8(67)

S & U 8(67) 4(33)

Unknown 11(69) 5(31)

Others 2(25) 6(75)

Total 96(65) 51(35)

_______________________________________________________________

P = 0.01, df = 6, x2 = 16.81

sept = septicaemia,

UTI = urinary tract infection

S&U = septicaemia and urinary tract infection,

others = gastroenteritis, measles, typhoid enteritis, otitis media,

tonsilopharyngitis.

White cell count

97

Table XV shows the white blood cell count in relation to the aetiology

of fever. Normal levels were found in 83(56.5%) of the children. There

was no statistically significant difference in the white cell count

amongst the different aetiological groups.

(p = 4.81, df = 18, x2 = 17.62).

Table XV. The white blood cell counts in relation to the etiology

98

of fever in 147 children with febrile seizures

_______________________________________________________________

WBC mal sept uti pneu s&u others un total

_______________________________________________________________

a 18 5 6 3 1 4 3 40

b 28 15 10 8 8 3 11 83

c 12 1 1 0 3 1 1 19

d 1 1 1 1 0 0 1 5

_______________________________________________________________

Total 59 22 18 12 12 8 16 147

_______________________________________________________________

p = 4.81, df = 18, x2 = 17.62

a = <5,000/mm3

b = 5,000 – 10,000/mm3

c = > 10,000 - < 15,000/mm3

d = > 15,000/mm3

99

Cerebro-spinal fluid

Tables XVI to XVII give details of the CSF findings in the patients

studied. The CSF protein was <10mg/100mls in 24.5% of the children,

while the highest value was 45mg/100mls seen in 2 patients. The CSF

protein mean and SD value was 23.98 + 0.774 mg/100mls.

The CSF sugar mean and SD value was 65.84 +

29.28mg/100ml. In 11 patients CSF sugar was less than

40mg/100ml.

The mean (SD) RBS was 97.42 + 36.38 mg/100ml. The RBS was

< 40mg/100mls in 4 children while 28 patients had RBS >

120mg/100mls. In every case, including the cases of hypoglycemia,

the CSF sugar was 50% or more of the blood sugar. The cellular

contents of the CSF were within normal limits in all the children

studied. There was no statistically significant relationship between the

CSF sugar levels, aetiology of fever and the pre-hospital intervention

given in the children studied (p = 0.686, df = 12, x2 = 9.202) (table

XVI). (p = 0.23, df = 6, x2 = 8.07) There was no statistically significant

relationship between the CSF protein and the aetiology of fever in the

children studied (p = 0.7, df = 12, x2 = 19.503)(table XVII).

There was no statistically significant relationship between the

CSF protein, CSF sugar and the pattern of seizures. (p = 0.339, df = 2,

x2 = 2.162) (p = 0.606, df = 2, x2 = 1.003).

100

In the 10 children with hypoglycorhachia 2 had simple febrile

seizures while the others (10) had complex febrile seizures. Four of

them had malaria, 1 had Septicaemia,3 had UTI, 1 had both positive

blood and urine cultures while 1 had pneumonia. The 2 children with

hypoglycemia had complex febrile seizure and fever was caused by

malaria and UTI respectively.

Table XVI. Cerebrospinal fluid sugar in relation to the aetiology of

fever in the children studied.

101

_____________________________________________________________________

CSF sugar mal sept pneu uti s&u others un total

_____________________________________________________________________

< 40 3 4 1 1 1 0 1 11

40 – 80 38 14 7 13 9 4 12 97

> 80 18 4 4 4 2 4 3 39

_____________________________________________________________________

Total 59 22 12 18 12 8 16 147

_____________________________________________________________________

p = 0.686, df = 12, x2 = 9.202

sept = septicaemia,

UTI = urinary tract infection

S&U = septicaemia and urinary tract infection

Mal = malaria

Pneu = pneumonia

Un = unknown

Others = gastroenteritis, measles, typhoid enteritis, otitis media,

tonsillopharyngitis.

Table XVII. Cerebrospinal fluid protein in relation to the aetiology

of fever in the children studied.

102

_____________________________________________________________________

CSF protein mal sept pneu uti s&u un others total

_____________________________________________________________________

<10 13 5 1 2 4 8 3 36

10 – 40 46 17 11 16 8 7 5 110

41 – 80 0 0 0 0 0 1 0 1

_____________________________________________________________________

Total 59 22 12 18 12 16 8 147

_____________________________________________________________________

p = 0.077, df = 12, x2 = 19.503

sept = septicaemia,

UTI = urinary tract infection

S&U = septicaemia and urinary tract infection

Mal = malaria

Pneu = pneumonia

Un = unknown

Others = gastroenteritis, measles, typhoid enteritis, otitis media,

tonsillopharyngitis.

Outcome

Duration of hospital stay

The duration of hospital stay ranged from 24hrs to 90 days. The

mean duration (SD) of stay was 6.37 + 8.067 days. Forty-four (29.9%)

103

were discharged within 72 hours of admission, 71 (48.3%) after a

period of 4 – 7 days while 2 (1.3%) stayed for a period of more than 4

weeks.

Majority (75%) of the patients with malaria stayed for less than a

week. None stayed beyond 2 weeks. Patients with bacterial infection

spent a longer period in the hospital as compared to patients with

malaria.

Neurological deficit

At the time of discharge persisting neurological deficits were seen

in 6 of the 145 survivors. Four of them had generalized hypertonia

while 2 children each had 6th and 7th cranial nerve palsies. Five of the

children presented with complex febrile seizures while one had simple

febrile seizures.

There was no statistically significant relationship between the

occurrences neurological deficits pre-hospital intervention and the

etiology of fever. (P = 0,0602, df = 6, x2 = 523).

Mortality amongst the 147 patients with febrile seizures

Two patients died giving a case fatality of 1.4%. One was a 30-

month-old child with severe malaria who had greater than 10

parasites per high power field and also had severe anaemia. He had

104

blood transfusion and antimalarial therapy administered, but died

after 5 days of admission. The other child was a 5-year-old child with

typhoid perforation who died 4 days after surgery. None of the deaths

could be directly attributed to febrile seizures.

105

DISCUSSION

Febrile seizures remain one of the commonest emergencies in

Nigeria.116 – 119 The prevalence rate of 9.9% obtained in this present

study is lower than that obtained by famulusi et al2 in the same centre

over 30 years ago. It is also lower than figures obtained by Izuora and

Azubuike13 of 15.6% in Enugu. It is however higher than what was

obtained in Jos by Angyo18 and in Benin by Scott-Emuakpor et al12

where a prevalence of 5.8% was reported.

Though there seems to be an improvement by the reduced

prevalence, the figures are still higher than what is obtained in

developed countries.

Our poor environmental hygiene makes a young child infection

prone. Poor health care delivery system in the midst of economic

instability limits availability, accessibility and affordability of health

services as well as prompt diagnosis and management of fever and

this may contribute to higher prevalence. The sociocultural habits and

beliefs can contribute immersely to the high prevalence rate of febrile

seizures.11

While dealing with children with fever and seizures who are

under 6 months and above 5 years it is particularly necessary to rule

out meningitis in them because there is a greater risk of mistaking

serious illness such as pyogenic meningitis for febrile seizures in this

age group. Onset of febrile seizures before the age of 6 months is

106

uncommon as evident in this study as only 2 children were less than 6

months old. The age distribution in the present study is similar to that

reported by previous workers.2,4,14,18

This study showed only a slight male preponderance with a male

to female ratio of 1.3:1. This is similar to previous reports.2,4 In Jos

Angyo18 however obtained a male: female of 2:1.

In this study complex febrile seizures occurred more commonly

than simple febrile seizures with a ratio of 2.2: 1. This agrees with the

report of Akpede et al47 but at variance with what is reported in

literature including previous reports from Nigeria.4,14,64 Berg et al3

reported 35% of complex febrile seizures amongst first febrile seizure

children and 41.2% complex febrile seizures amongst children with

recurrent febrile seizures in a study in New York. Poor reckoning of

the duration can lead to wrong diagnosis of complex febrile seizures.

A convulsing child presents an alarming picture and onlookers

very often exaggerate the duration of the seizure.

The author in interviewing the caregivers of the patients in the study

took particular care in trying to obtain reasonable estimates of the

duration of the seizure. In spite of this, it is possible that a number of

children were wrongly classified as having complex febrile seizures

based on the duration of seizures. It is notable though that only 14 of

the seizures were classified as complex based solely on the prolonged

duration of a single generalized seizure.

107

Another possible explanation for the predominance of complex

febrile seizures is the fact that this is a hospital-based study. It is

more likely that a child who has had a prolonged or multiple seizures

would be rushed the hospital than the child who has had a single brief

attack. This will tend to exaggerate the proportion of complex febrile

seizures among hospital patients when compared with its occurrence

in the general population.

A family history of febrile seizures in the first-degree relatives of

29% is higher than what was obtained at this centre in previous

reports.2, 119 Osuntokun et al119 reported 3.9%, while Familusi et al2

reported 18.1% prevalence of positive family history of febrile seizures

in Ibadan. Reports from Shagamu118 and Ilesha14 were 12.3% and

43.5% respectively. Livingstone120 reported a prevalence of 58% while

Lennox121 in America, reported a rate of 45%. Positive history is

defined primarily by parental recollection and willingness to disclose

information. Low figures obtained in previous studies in this center

could be attributed to denial as a result of social stigma attached to

convulsions in this part of the world. The result of the present study

suggests increased level of parental education and enlightenment as

compared to the past, as the rate of disclosure by the informant

reflects.

It has been reported that most recurrences occur within

6 – 12 month of the initial seizure.7 The finding in this study is in

108

keeping with this. Twenty-three (15.6%) of the patients studied had a

history of recurrence, 17(74%) had the 2nd episode within a year of the

first. It has been reported that the risk of recurrence is influenced by

the age of the patient at the time of the first seizure.92, 95 This is not

supported by the results of this study. The results also do not support

literature reports of family history as a risk factor for recurrence.

The aetiology of the fever causing febrile seizures in the children

studied bears several similarities to what has been previously

documented in our area.2, 4, 18 Malaria plays a significant role in febrile

seizures in this geographical area.4 The role of malaria in these

children is in keeping with past observations that malaria is the

commonest cause of fever in children in the tropics.47 The 40.1%

prevalence of malaria in the study is similar to the prevalence of

45.2% earlier reported in Ibadan,2 but lower than the prevalence of

71.2% and 74.8% reported in Ilorin4 and Jos 18 respectively. It’s

however surprising that a higher prevalence of malaria is reported in

the middle belt.

The policy of malaria control should be maintained. If malaria

could be properly controlled the incidence of febrile seizures will be

reduced.

The finding in this report supports previous reports about the

possible co-existence of malaria with other infections.47,54

Community acquired bacteria is an important problem in the

109

tropics.47 Septicaemia was the 2nd commonest cause of fever in this

study and it was responsible for 15% of the causes of fever. The

predominant organism isolated was staphylococcus aureus (68.8%).

The results are in keeping with some previous reports, 53,54 but at

variance with some other reports. 2,18,51,52

Akpede et al47, 54 reported incidence of bacterial infections in

children of 9% and 11% in 2 different studies done in Nigeria.

Lepage53 reported an incidence of 12.4% among Rwanda children.

Familusi et al2 and Angyo et al18 reported bactiraemia in 3.3% and

3.7% respectively in the children they studied while James et al70

reported 5.4% and Teah et al52 a 2.9% incidence. James and Teah’s

studies were retrospective and not all the children studied had blood

culture, Familusi et al2 and Angyo et al18 studies were prospective

however not all the children studied had blood culture.

Bacteraemia in young children is a reasonably frequent

occurrence with occasionally serious sequelae; most patients however,

do quite well. The problem is more perplexing in infants and young

children with high fever and no focus.122

A history of febrile seizures should not dissuade an emergency

room physician from performing a blood culture.70 In a study by

James et al70 2 of the 5 patients with bacteraemia had had febrile

seizures. Documentation of parasitaemia does not exclude other

110

infections but can be misleading in sick child, this is confirmed in this

present study. Other reports53, 54 have highlighted the problems of

concurrent infections, including bacteraemia in children with malaria.

In an endemic area for malaria like Nigeria, febrile children should be

investigated for the presence of bacteraemia and other infections even

with a positive malaria parasitaemia.

Septicaemia is a serious infection, which can lead to multiple

complications and even death. Therefore the possibility of this

diagnosis should be kept in mind when managing a child with febrile

seizures.

Urinary tract infection was the 3rd commonest aetiological factor

found in this study. It accounted for 12.3% of the cases. The finding in

this study is similar to that of James et al70 and Ibadin et al58 in which

incidences of 17% and 9% were reported respectively, but were at

variance with other reports.2, 18,52,60 The difference may be related to

differences in methodologies. This study was prospective whereas

others52, 60 were not. All the patients in this study had a urine culture

whereas not all the patients in these other studies did.2, 18,51,60

Pneumonia was responsible for fever in 8.2% of the children

studied rating as the fourth commonest cause of fever in the study.

Only 2 children had Upper respiratory tract infection (URTI). This is at

variance with what obtained in previous reports2, 4,18 which had higher

incidences.

111

Viral agents account for a large proportion of fever causing

febrile seizures in temperate regions. The role of viruses in this study

will remain undetermined since viral studies were not done. It would,

however, have been very informative to compare the results of viral

studies with Familusi et al’s2 finding of virus isolates in 14(13.3%) of

the 105 patients with febrile seizures. This is an area for further

research.

The problem of multiple infections in children is highlighted in

this study and this could make assessment and management of these

children very challenging for the Paediatrician.

The role of predisposing factors in febrile seizures could not be

fully assessed in this study because there were no controls to compare

with. However, the fact that 64(43.5%) of the children were attending

daycare might be a pointer to its contribution to the disease. Nineteen

(12.9%) children had perinatal abnormalities in the study. This

supports the finding of Wallace42 but not that of CHES19 and Zhao.46

Pre-hospital intervention was given to 59(40.1%) children. Eight-

eight (59.9%) of the parents did not administer anything harmful but

rather brought the children straight to the hospital. This is

comparable with the report by Familusi et al2 where 60% did not give

any form of harmful intervention. Native concoction was administered

to 10.2% of the children studied. This is considerably lower than the

52.4% reported by Familusi et al2 in the same hospital in 1971. Also

112

2.7% children had parts of their body burnt or knife incisions made on

them compared with 7.8% in Familusi’s study. The difference between

the 2 studies could be a reflection of the degree to which health

education has been able to impact on the use of harmful measures by

people when managing febrile seizures. Native concoction are popular

remedies used all over the country for the treatment of febrile seizures.

This is shown by reports from other parts of Nigeria.2,4,12,18 It is

important to educate caregivers when they present at the health

centre because some of them are rather fixed in their ways handling

situations. They need to be enlightened on the dangers of persisting in

such practices for example, risk of infections, gangrene, neurological

sequelae and even death.

This study showed that socioeconomic status influenced the type

of pre-hospital intervention administered. None of the parents in the

Upper class gave native concoction, majority (76.9%) of them took

their children to the Hospital. Mothers contribute a good target group

for specific health education.

There was a relationship between the duration of hospital stay

and the aetiology of fever causing febrile seizures. Majority of the

children with malaria stayed for less than a week. This is expected

since malaria is usually effectively treated in three to seven days.

However, children with Septicaemia, UTI, and other bacterial and

mixed infections are usually admitted for several days of intravenous

113

antibiotics. This was similar to what was reported in other studies.18

Various neurological complications of febrile seizures have been

reported from Nigeria. Familusi et al2 and Angyo et al18 reported

neurological complications in 8.3% and 1.8% respectively while

Imuekheme17 reported a rate of 12.5%. However, in this present study,

only six children (4%) had neurological deficits. This is within the

reported range of 1.8 – 12.5%. 2,17,18

The finding of 28(19%) patients with hyperglycemia is not

unusual and agrees with previous reports.124 Seizure is known to

produce an increase in circulating levels of both cortisol and

adrenaline and these raise the blood sugar by their anti- insulin

action.124 Only four (2.7%) of our patients had hypoglycemia, whereas

Familusi et al2 reported 13% prevalence. The occurrence of

hypoglycemia could have been as a result of anorexia or vomiting

preventing feeding which could usually follow some childhood illnesses

especially malaria.

Severe anaemia (< 20%) was present in 35.4%) of the patients.

This could be related to the high incidence of malaria plus the problem

of malnutrition. It also agrees with previous reports.2,4

The children with septicaemia were more likely to have anaemia

in this study so also were the children with urinary tract infections.

This could also have been as a result of the co – existence of malaria

with these infections.

114

The case fatality rate of 1.4% in this study is comparable to that

reported by Angyo et al18, Oseni14 and fagbule4, however, it is at

variance with the 6.4% reported by Familusi et al2 and the 9.2% by

Ejeheri.125 The report is in conformity with several reports from

developed countries like USA.126,127

Febrile seizures are generally considered benign with a

favourable outcome.128, 129 In our environment certain adverse factors

combine to bring about poor outcome. The administration of native

concoction to convulsing children is a common practice associated

with poor outcome. This is responsible for most of the deaths, which

occurred, in the previous study at our centre.2 All the 4 children that

died in Fagbule’s study4 also had native concoction administered. The

use of these concoction must be rigorously discouraged through

health education.

115

CONCLUSIONS

1) The prevalence of febrile seizures among children admitted to the

Children’s Emergency Ward of UCH, Ibadan has declined to

9.9% from 15.1% about 3 decades ago.

2) Complex febrile seizure is the predominant type of febrile seizure

in children presenting to the UCH.

3) Malaria is the commonest cause of febrile seizures in children

presenting to the UCH, but Septicaemia, Urinary Tract infection

and Pneumonia are also important causes.

4) Significantly fewer people are now administering native

concoctions to children with febrile seizures, when compared

with 30 years ago.

5) Socioeconomic status has an effect on the type of pre-hospital

management given to children with febrile seizures.

6) The mortality and neurologic sequelae rates in children with

febrile seizures at the UCH has declined considerably

since 30 years ago.

7) The low incidence of adverse neurological outcome and mortality

could be related to the less frequent use of native concoctions in

the home management of the disease.

8) The presence of bacterial or other infections does not rule out

malaria infection in children.

116

RECOMMENDATIONS

1) The general public especially mothers need to be educated on

the correct attitude to febrile seizures and appropriate

management of the convulsing child.

2) Malaria control in this environment should be intensified,

especially the recognition of symptoms and early treatment at

home.

3) Bacteraemia and UTI oftentimes present with non-specific

manifestations and a high index of suspicion is required in

diagnosis.

117

LIMITATIONS OF STUDY

1) Viral studies were not done as part of the search for aetiology of

the fever in these children because of financial constraints.

118

119

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136

137

APPENDIX II

PROFORMA

A STUDY OF FEBRILE SEIZURES IN CHILDREN

1. Chronological No:…………….. 4. Date of Admission:…………

2. Name:…………………………… 5. U.C.H No:…………………..

3. Age (months):…………………... 6. Sex: Male =1 Female = 2

7. Father’s Education 8. Father’s Occupation

1 No formal education 1 Unemployed

2 Koranic 2 Unskilled worker

3 Primary 3 Petty trader

4 Secondary 4 Artisan

5 Post Secondary 5 Middle level prof.

6 High level prof.

7

9. Mothers Education 10. Occupation

1 No formal education 1 Unemployed

2 Koranic 2 Unskilled worker

3 Primary 3 Petty trader

4 Secondary 4 Artisan

5 Post Secondary 5 Middle level prof.

6 High level prof.

7

11. Pregnancy and Delivery history

a. Maternal smoking Yes = 1 No = 2

b. Pregnancy Cx; APH = 1 Others = 2 (specify):………………….

c. Medication in Preg. Yes = 1 No = 2

d. Delivery; SVD = 1 Breach = 2 CS = 3 Instrumentation =4

Others = 5 (specify:………………………..

e. Birth weight(kg):..; AGA = I SGA = 2 LGA = 3 Term= 4 preterm = 5

12. Child care attendance; Day care/Nursery Yes = 1 No 2

13. P.M.H

a. Past History of f.s. Yes = 1 No = 2 If No of time …………………

If Yes: i. No of times:………………………………

ii. Age at 1st episode:………………………..

iii interval between 1st and 2nd episodes (month): ………………

b. Development delay Yes = 1 No = 2

c. Family history of febrile seizures Yes = 1 No = 2

d. If Yes who: mother = 1 father = 2 sibling = 3

e. Family history of epilepsy. Yes = 1 No = 2

f. If Yes, who; mother = 1 father = 2 sibling = 3

138

14. Presenting complaints

a. Fever ; duration (in days):…………………..

b. Seizures

i. No of times: Once = 1 twice = 2 > thrice = 3

ii. Focal = 1 or generalized = 2

iii. Duration:………………………………….

iv. Post ictal state:…………………………….

c. Other symptoms; cough = 1 vomiting = 2 diarrhea = 3

Ear pain/ discharge = 4 others = 5 (specify):………………….

15. Pre hospital treatment. Yes = 1 No = 2

a. Native concoction = 1 salt and water = 2 milk = 3 other = 4

b. Other treatment; substances applied to eyes = 1 burning of part of body = 2

(specify):………………… Others = 3 (specify):………………….

16. Physical Examination

a. Weight (kg):……… (b) Ht (cm):…… (c) OFC (cm):…………..

d. Temperature (oC) (at admission/time of seizure):…..

17. Clinical Diagnosis; Malaria = 1 ARI = 2 UTI = 3 G.E = 4 Others = 5

(specify):……………………………

18. CNS examination;

level of con : lethargy = 1, drowsy = 2, Alert = 3, coma = 4,

Neck stiffness :present =1,absent = 2

kerning sign : post = 1,neg = 2.

Brudzuki’s sign : post = 1, neg = 2

Tone : normal = 1, red = 2, increased = 3

Reflexes : normal = 1, red = 2, increased = 3.

19. Investigations

a) CSF: (i)wbc:………….. (ii)rbc:………………..(iii) protein:……………..

(iv)sugar:…………………. (v)rbs:……………………………

b) blood film for malaria parasite……………………..

c)PCV………………………………………………...

d) FBC………………………………………………...

e) Blood culture………………………………………

f) Urine culture……………………………………….

g) others(specify)…………………………………….

20. Final Diagnosis:……………………………………………………………

21. Outcome: Discharge = 1 Died = 2

22. If discharged duration of stay (in days):……………………………..

23. Neurological deficit (specify):…………………………………………

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