Febrile seizures: An end to confusion

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services, etc.). Can we educate these professions for at least part of their time together? I believe

What Is There to Criticize in the Report?

REFERENCE

1. Fit for the Future: Report of the Committee on Child Health Services. London, Her Majesty’s Stationery Office, December 1976, vols 1 and 2.

806 PEDIATRICS Vol. 61 No. 5 May 1978

so.

From my enthusiastic review-not much. The

only fundamental area not addressed adequately

is the growing recognition that services are not

enough. While there is very adequate presenta-tion of the role of social factors in producing ill health, there is little attention to the need for basic changes in the cause of these social factors. Perhaps it is unfair to criticize a report on child health services for not tackling in their policy

recommendations the even more important

prob-lems of family jobs, income, environment, and

culture that so profoundly affect child health. But, every report has to have some boundaries. Fit for the Future has so much of importance that it

should not be too harshly criticized for this gap. Finally, there is the problem of

implementa-tion. Schemes for improving services abound.

Rereading the reports of past White House

Conferences on Children (especially the 1930

report) makes me realize that lack of

implemen-tation rather than lack of ideas is the major

problem in improving child health services.

Competing forces will always

find

alternative use of the limited resources-time and money-unless the steps to achieve change are detailed. Fit for the Future goes part way toward addressing this

issue with a chapter on “Transition to the New

Service”

and

on implications for training of the

new breed of physicians and nurses. But to

this

observer, too much faith is put on the power of

the logic of the blueprint (which is great) and on the goodwill of joint planning teams to achieve

the goals and too little on the incentives and

resources needed to accomplish them.

A

final chapter lists the priorities as seen by the

committee and recognizes the resource

con-straints.

Although this report is less concerned with

costs and benefits than I believe it should be, it

does what we in the United States have so far

failed to do. It sets clear goals for child health services in the United Kingdom, and it provides a

map of how to get there. A similar far-reaching report for the United States would advance child health.

Why not make this the goal of the next White House Conference?

Febrile

seizures:

An end to confusion

After years of conflicting advice from

numer-ous

experts about treatment or nontreatment of

febrile seizures, there is now a sound basis on

which the pediatrician can make decisions.

Recent studies14 have approached the problems of febrile seizures from different viewpoints and are beginning to present a coherent, understand-able picture of their outcome and the results and problems of therapy.

Nelson and Ellenberg in this issue (p. 720)

present the last in a series of articles on the 1,706

children with febrile seizures from the 54,000

pregnant women enrolled in the Collaborative Perinatal Project and followed up to the age of 7.

All

data were collected prospectively. They found

that 3.5% of white children and 4.2% of black

children between the ages of 1 month and 7 years had a seizure associated

with

fever unaccompan-ied by a recognized neurological illness. Of those

children who had one seizure, one third had a

second and one half of the latter had a third

seizure. Only 9% of the total population had three or more febrile seizures. Recurrences were more likely when the first seizure occurred during the first year of life. Three quarters of recurrences came within one year of the first febrile seizure,

and almost 90% of recurrences occurred within

two

years

of the onset. Nelson and Ellenberg found that febrile seizures caused no deaths, were not associated with permanent neurological defi-cit, and had no effect on IQ or academic perform-ance. Febrile seizures were associated with an increased risk of epilepsy, but only 2% of children

with

febrile seizures had become epileptic by age 7. Ninety-eight percent had not.

Nelson and Ellenberg found “risk factors”

which were associated with increased risk of

future epilepsy or “afebrile seizures.” When the first seizure was “complex,” i.e., longer than 15

minutes, focal, or part of a cluster, there was an

increased risk of epilepsy. A family history of

afebrile seizures

also

increased the risk of

subse-quent epilepsy. An important predictive factor of

subsequent epilepsy was whether the child was

neurologically normal or abnormal (or suspect)

prior to the first seizure. However, even when

two or more of these “high-risk” factors were

present, only 10% of the children developed

epilepsy; 90% did not.

These data thus document what most

pediatri-R.J.H. cians have long suspected: that febrile seizures are

both

common and benign.

Several questions might be posed. Can febrile seizures be prevented? Should they be prevented? What problems are associated with prevention?

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COMMENTARIES 807

The study of Wolf et al.,3 among others, would suggest that febrile seizures can be prevented, but only if phenobarbital is given daily and in suffi-cient dosage to achieve a blood level of 15 sg/ml.

Compliance must be assured and blood levels

monitored. Intermittent phenobarbital therapy at the time of fever is no better than no treatment at

all.’

Thirty percent of the mothers in Wolf and

co-workers’ study were unaware that their child had a fever until the convulsion occurred. Even

had they known, 15 mg/kg of phenobarbital

given orally or intramuscularly would have taken

several hours to reach therapeutic blood levels5,6

and would have caused marked sedation as well.

Administration of the usual dose (4 to 6 mg/kg) or even twice the usual dose will take days to reach therapeutic levels. Thus, febrile seizures usually

can be prevented, but only if phenobarbital is

given daily, compliance is assured, and blood

levels are maintained at greater than 15 tg/ml. Should febrile seizures be prevented? Various

authors recommend prevention of recurrent febrile seizures (1) to prevent infantile hemipare-sis, (2) to prevent temporal lobe epilepsy, (3) to prevent status epilepticus, (4) to prevent brain damage, (5) to prevent subsequent epilepsy, (6) to allay anxiety in the parents. Nelson and Ellenberg

found no evidence that febrile seizures were associated

with

the first four of these, regardless of the number of seizures. Regarding subsequent

epilepsy, there are no studies to date which

indicate that phenobarbital prevents subsequent epilepsy or that febrile seizures cause subsequent

epilepsy. While phenobarbital therapy seems to

be commonly utilized “to allay parental anxiety,” the low compliance rate in Wolf and co-workers’ patients3 might suggest that physicians’ anxiety about parental anxiety is higher

than

parental

anxiety

about febrile seizures. Furthermore, adequate discussion of the meaning, management, and significance of febrile seizures might more effectively alleviate parental anxiety than admin-istration of phenobarbital to the child. Ninety-four percent of children with a febrile seizure will

have “pure” febrile seizures or only one risk

factor and a 2% risk of subsequent epilepsy. Even in the children whose febrile seizures start before the age of 1, who are neurologically abnormal, or

who

have two or more risk factors, the risk of

epilepsy does not reach 10%. Thus, 90% of even

these “high-risk” children will not develop

epilepsy.

It would appear that there is little reason to treat the “low-risk” group, and treatment of the

“high-risk” group should be decided by the

parents and the physician with knowledge of the

problems associated with prevention.

What are the problems of prevention? In

another article in this issue (p. 728), Wolf and

Forsythe further document the problems, such as

hyperactivity, with phenobarbital prophylaxis

and elucidate some of the determinants of the

hyperactivity. They have previously shown that

despite major efforts to monitor blood levels and

assure compliance, daily phenobarbital therapy was discontinued in one third of the children.

Behavioral abnormality occurred in 42% of the

children and hyperactivity was sufficiently severe to cause discontinuation in 20% of those treated.

In

a total one third of patients, phenobarbital therapy was discontinued because of hyperactivi-ty, behavior, problems, rash, or lethargy. Further-more, assurance of compliance required constant reinforcement of mothers as well as monitoring of the child’s blood levels.

As a result of the recent studies, I have begun to treat fewer cases of febrile seizures. The problems

of continuous therapy appear to outweigh the

benefits for the 94% of children with pure febrile seizures or only one risk factor. If the child’s seizures start before the age of 1, or if the child is neurologically abnormal, and has an additional

risk factor, then I discuss the problems and

possible benefits of therapy with the parents.

Since only half of the high-risk group have a

second seizure, and since the risk of epilepsy in

this

group only increases substantially after

two

seizures,

I

prefer to wait until after the second seizure before beginning therapy.

Even then, the reason for initiating therapy is not entirely clear. If therapy is initiated, pheno-barbital should be utilized once a day in sufficient

dosage to produce blood levels of 15 tg/ml. It

should be continued for

two

years from onset

(

since 90% of recurrences will have occurred by that time). if the child becomes hyperactive,

medication is tapered and the drug’s use is

discontinued. if afebrile seizures occur, the child is treated as if he had epilepsy.

In every case, the meaning of the seizures is

discussed

with

the parents at the first visit. They are instructed that if the child has a fever they

should

use

antipyretics and sponging, and if the child

has

another seizure they should stay calm. They

are

told that if a seizure lasts more than 15 minutes, the child should be taken to an

emergen-cy room (so that intravenous medication can be

used if necessary). Most of all, the parents are

given reassurance that, as Nelson and Ellenberg

have shown, these children do well-even without therapy.

Baltimore, MD 21205

J

OHN

M.

FREEMAN, M.D.

Johns Hopkins Hospital

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808 PEDIATRICS Vol. 61 No. 5May 1978

REFERENCES

1. Nelson KB, Ellenberg JH: Predictors of epilepsy in

children who have experienced febrile seizures. N

Engi I Med 295: 1029, 1976.

2. Ellenberg JH, Nelson KB: Febrile seizures and later

intellectual performance. Arch Neurol 35:17,

1978.

3. Wolf SM, Carr A, Davis DC, et al: The value of

phenobarbital in the child who has had a single

febrile seizure: A controlled prospective study. Pediatrics 59:378, 1977.

4. Homer WA, Annegers JF, Kurland LT: Febrile seizures, prognosis for subsequent seizures, abstracted.

Neurology 23:341, 1977.

5. Jalling B: Plasma and cerebrospinal fluid concentration of phenobarbital in infants given single doses. Dev Med Child Neurol 16:781, 1974.

6. Pearce JL, Sharman JR. Forster RM: Phenobarbital in

the acute management of febrile convulsions. Pedi-atrics 60(suppl):569, 1977.

Perspectives

on chronic

nonspecific

diarrhea:

Dietary

management

Chronic nonspecific diarrhea (CNSD) of child-hood, originally thought to be part of the celiac

syndrome, was described as a separate clinical entity by Cohian’ in 1956. In the ensuing years,

CNSD has been appreciated to represent one of

the most common causes of prolonged diarrhea in

the infant and toddler. Yet confusion remains

regarding its cause and treatment.

Drs. Davidson and Wasserman’ have described consistent diagnostic criteria further

characteriz-ing CNSD as a recognizable syndrome. The onset

of symptoms occurs classically between 6 and 30

months of age with the development of three to

six loose and often mucousy stools per day. With

no associated malabsorption, growth and

devel-opment remain normal. While spontaneous

reso-lution of CNSD is anticipated by 39 months of

age, longitudinal observations indicate that these

patients have a high incidence of functional

bowel complaints during adolescence and

beyond. From the standpoint of the child, this “complaint” all too frequently becomes a

“prob-lem” when the frequency and/or consistency of

the bowel movements impair bowel training or

become intolerable to the parents.

With cause and pathophysiology remaining

ill-defined, the cornerstone of therapy to the

physi-cian has been reassurance.’ Bowel movements

have been occasionally reduced in frequency by

decreasing intestinal stimulation through

elimina-lion of snacks and avoidance of cold or

hyperos-molar beverages. Though bacterial overgrowth

has not been documented, the problem has

improved in some children following a course of antimicrobial therapy.’

The role of dietary intake in the cause and

management of CNSD has received relatively

little attention. In their original report, Drs.

Davidson and Wasserman2 noted that many of their patients were on high-protein, low-carbohy-drate, and low-fat diets at the time of referral; however, they did not feel that dietary manipula-tions were of benefit.

Our own experience with CNSD has suggested

a significant role for nutritional management.4 On reflection, the parents often note that the diar-rhea began in association with a transient upper

respiratory tract illness. In a large number of

patients, with persistence of the symptoms and

the failure of lactose elimination to modify the course, diets became increasingly restricted and

the daily fat intake was markedly reduced. In

addition, fluid and caloric requirements are

increasingly met with foods containing large

amounts of carbohydrates. The role of reduced fat intake in CNSD is also seen in a second, smaller

group of our patients who were receiving less than 20 gm of fat per day as a result of unsuper-vised, parentally prescribed elimination to reduce the risk of later atheromatous vascular disease.’

Our initial observation and approach to

thera-py came while excluding malabsorption states

with 72-hour stool fat excretions. With the daily

minimum intake of 50 gm of fat required for interpretation of the study, the parents of many

patients with CNSD reported resolution of the

diarrhea. Thereafter, careful nutritional counsel-ing led to the use of a therapeutic diet containing 30% to 50% of its calories from fat. This regimen

alone has resulted in resolution of symptoms in

more than 90% of both groups of patients with

CNSD.

In addition to suggesting another diagnostic

criterion for many patients with CNSD, this

finding may also allow us to better define the pathophysiology. The shortened mouth-to-diaper transit time noted in infants with CNSD6 has been attributed to an increase in colonic mass move-ment, propelling fecal material into the rectosig-moid. Our observation suggests a role for

made-quate dietary fat, fat that normally would delay gastric emptying and slow intestinal transit. Any

associated compensation for reduced calories by

the use of hyperosmotic carbohydrate beverages

would further enhance intestinal motility. We

feel that this latter explanation is secondary,

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1978;61;806

Pediatrics

John M. Freeman