Tuberculosis Screening Pediatrics in Review 1982;3;271 DOI: 10.1542/pir.

3-9-271

The online version of this article, along with updated information and services, is located on the World Wide Web at: http://pedsinreview.aappublications.org/content/3/9/271

Pediatrics in Review is the official journal of the American Academy of Pediatrics. A monthly publication, it has been published continuously since 1979. Pediatrics in Review is owned, published, and trademarked by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village, Illinois, 60007. Copyright 1982 by the American Academy of Pediatrics. All rights reserved. Print ISSN: 0191-9601.

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DEVELOPMENTAL

ANOMALIES

alies. They are mostly of mnemonic value to aid diagnostic investigation. Thus, an infant with feeding problems and pulmonary aspiration who is found to have thoracic vertebral anomalies should be checked for tracheo-esophageal fistula, and is also more likely to have congenital heart disease, renal anomalies, etc. In case of a causally defined syndrome such as the Ellis-van Creveld syndrome, the multiple manifestations of the patient are referred to as pleiotropy.

normal from the abnormal and to be able to evaluate the severity and ramifications of the abnormality; to document objectively by measure-

7.

Heinonen

OP.

Slone

D, Shapiro

S: Birth

Defects
8.

ment

and

photograph;

to examine
minor anomdevelopmental
9.

relatives to distinguish alies from normal

Littleton, MA, PSG PubI Co. 1977 Miller ME, Graham JM Jr, Higginbottom MC, et al: Compression related defects from early amnion rupture: Evidence for mechanical teratogenesis. J Pediatr 98: 292, 1981 Matsunaga nancy and E. Shiota K: Ectopic myoma uteri: Teratogenic pregef-

and Drugs

in Pregnancy.

variants;
technical

and
terms

to use
pertaining

correctly

the de-

to cause
1 0.

and
fect.

pathogenesis

of congenital

ACKNOWLEDGMENT I am most grateful to LaVelle expert secretarial collaboration. Spano for

11.

CONCLUSION The vis medicatrix naturae can be relied on to heal the child in most illnesses in which cause and pathogenesis are unknown. This is not true in most cases of congenital anomaly; it is the rare deformity (breech head, mild bowing of legs, etc) that will improve spontaneously. The other anomalies, malformations, dysplasias will stay to challenge pediatricians to a deeper pathogenetic and causal understanding so that they can give better genetic and prognostic counseling and guide parents and professionals with an effective habilitative plan. Such an understanding is also needed to identify neonatally the hopeless cases before attempts to save life and to treat have gone too far. To attain such an understanding there must be a willingness to learn to do a complete and accurate physical examination; to learn to tell the

1 2.

REFERENCES (Asterisk reference recommended office.) 1.

()

indicates general for the pediatricians

3.

2.

Smith DW: Recognizable Patterns of Human Malformations: Genetic, Embryologic and Clinical Aspects, ed 2. Philadelphia, WB Saunders Co. 1976 Spranger JW, Opitz JM, Smith DW, et al: Errors of morphogenesis: concepts and terms. Recommendations of an international working group. J Pediatr, in press 1981 Opitz JM, Herrmann J, Pettersen JC, et al: Terminological. diagnostic, nosological and anatomical-developmental aspects of developmental defects in man. Adv Hum Genet 9:71, 1979 Opitz JM, Gilbert EF: Pathogenetic analysis of congenital anomalies in humans. Pathobiol Annu, in press 1981 Warkany J: Congenital Malformations: Notes and Comments. Chicago, Year Book Medical Publishers Inc. 1971 Shepard TH: Catalog of Teratogenic Agents, ed 3. Baltimore, Johns Hopkins University Press, 1 980

14.

15.

16.

3.

17.

4.

fects and maternal characteristics. Teratology 21 :61 , 1980 Hoyme HE, Higginbottom MC, Jones KL: The vascular pathogenesis of gastroschtsis: Intrauterine interruption of the omphalomesenteric artery. J Pediatr 98: 228, 1981 Schinzel AAGL, Smith DW, Miller JR: Monozygotic twinning and structural defects. JPediatr95:921, 1979 Livingston JE, Poland BJ: A study of spontaneously aborted twins. Teratology 21:139, 1980 Shiota K: Neural tube defects and maternal hyperthermia in early pregnancyepidemiology in a human embryo population. Am J Med Genet, in press 1981 Smith DW, Clarren 5K, Harvey MAS: Hyperthermia as a possible teratogenic agent. JPediatr92:873, 1978 Lademacher DS, Vermeulen RCW, vd Harten JJ, et al: Circumvallate placenta and congenital malformation. Lancet 1: 732, 1981 Carmi R, Sofer 5, Karplus M, et al: ApIasia cutis congenita-An autosomal recessive form with variable manifestations in two sibs. Am J Med Genet, in press 1981 Penrose LS: Memorandum on Dermatoglyphic Nomenclature BDOAS. IV(3): 11 3, 1968 (available for free from the March of Dimes) Schaumann B, Alter in Medical Disorders. ger Verlag. 1976 Reed T: Review: medicine-problems pected chromosome J Med Genet 8:411, M: Dermatoglyphics New York, SprinDermatoglyphics and use abnormalities. 1981 in susAm

18.

5.

19.

6.

in

Tuberculosis EDUCATIONAL OBJECTIVE

Screening Tuberculosis be a major

that ideally

13. Appropriate awareness of the current epidemiologic status of tuberculosis among children in the United States and of the methods for screening and early detection (81/82).

American Thoracic Society: Toward Irradication-A Contemporary Control Strategy. Am Rev Respir Dis 1 1 8:641 1978,
,

The epidemiology
in determining

of tuberculosis
screening

in a given
programs,

community
It can be

should
argued

factor
every

tuberculosis

child should have a tuberculin skin test performed yearly, but the risk is so low in many suburban populations that the yield from such testing will be very low and the cost for each case found high. There is no question, however, about the need to
have a systematic and complete screening in populations at high risk. These include

inner city children, the socioeconomically disadvantaged, ers who come in contact with such populations, and

immigrants,

health work-

all family and other close contacts of known cases. The tine test and other multiple skin puncture tests yield unacceptably high rates of false-positives and false-negatives. Intradermal tests are best, preferably with PPD, but of course these must be read by someone trained to evaluate reactions. (R.J.H.)

pediatrics

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Congenital EDUCATIONAL OBJECTIVE An Update

Horm Res,

Adrenal

Hyperplasia

146. Appropriate understanding of the value of serum I 7-hydroxyprogesterone (1 7-OHP) in the diagnosis and management of congenital adrenal hyperplasla in infancy (81/82).

of Congenital Adrenal Hyperplasia (CAH). New Ml, et al, Rec Prog in press, 1981, Adrenal Hyperplasia in Intersex States. New MI, et al. Pediatr Ado! Endocrino! 8: 147, 1981. Microfilter Paper Method for 1 7 Alpha-Hydroxyprogesterone Radioimmunoassay (RIA): Its Application for Rapid Screening for CAH. Pang S, et al, J C!in Endocrino! Metab 45:1003, 1977. Serum Androgens as a Continuing Index of Adequacy of Treatment of CAH. Korth-Schutz S, et al. J C/in Endocrino! Metab 46:452, 1978. The Application of a Serum I 7 OH Progesterone RIA to the Diagnosis and Management of CAH. Hughes IA, et al, J Pediatr 88:766, 1976. Serum 17 Alpha-Hydroxyprogesterone in CAH. Lippe BM, et al, J Pediatr 85:

...

782,

1974.

Congenital adrenal hyperplasia (CAH) is the inborn error of metabolism resulting from deficiency of enzymes involved in normal adrenal steroidogenesis. CAH should be suspected in cases of intersex (sexual ambiguity), salt wasting syndromes, forms of complete or incomplete premature pubertal development, and unexpected or

excessive virilization. In the newborn period, 21 -hydroxylase deficiency

ditism) or 1 lfl-hydroxylase males 1 7a-hydroxylase extremely rare) will lead ysteroid dehydrogenase

intersex problems (the most frequent

may be seen in genetic females with cause of female pseudohermaphro-

deficiency (hypertensive form of CAH). In genetic deficiency and cholesterol desmolase deficiency (both to intersex, In both genetic males and females, 3/3-hydroxdeficiency may cause sexual ambiguity,

As none

of the deficient

enzymes

involved

in these

conditions

can

be routinely

measured directly, the diagnosis of CAH is made by measuring the compounds accumulating in excess just prior to the defective enzymatic step, The most common form of CAH is that due to 21-hydroxylase deficiency, an HLA-linked, autosomal recessive disease. One third to one half of patients with this disorder exhibit overt, clinical salt wasting. The diagnosis is made by measuring serum levels of 1 7hydroxyprogesterone (1 7OHP), the compound just before the enzymatic block, or its urinary metabolite pregnanetriol, Serum 1 7OHP can now be reliably measured on filter paper specimens. Levels of serum androgens, and their urinary metabolites, will also be elevated. Some patients with overt salt wasting may have measurable serum and urinary aldosterone levels but these levels do not rise appropriately following a low sodium challenge. Plasma renin activity (PRA), an indicator of intravascular volume repletion, is markedly elevated in overt salt wasters but may

also be elevated
the

in some

patients

without

clinical

evidence

of salt wasting

(indicating

presence of subtle salt loss). Treatment of CAH involves, when necessary, correct and timely surgical correction, as well as replacement

and prompt therapy with

sex assignment glucocorticoids

(hydrocortisone,

20 to 25 mg/sq

rn/day)

and where

indicated

(ie, elevated

PRA)

mineralocorticoid replacement (9e-fluorohydrocortisone, Florinef), Adequacy of control should be judged on clinical grounds (normal growth rate, bone age advancement, and normal pubertal development) and confirmed by laboratory means. Measurements of serum 1 7OHP and androgens, especially 34-androstenedione, taking into consideration their diurnal variation, and urinary pregnanetriol excretion are the most valuable indicators of adequate glucocorticoid replacement. Normalization of PRA is an index of adequate mineralocorticoid replacement. Oversuppression of 1 7OHP, serum androgens, and PRA should be avoided. (R. Rapaport)

Routine Prospective
AmJDis

Urinalysis

Questioned of Routine 1981. Admission Urinalysis. Hermansen MC, et al.

Child

Evaluation 135:126,

A total of 954 patients had admission urine analysis. Four new diagnoses resulted: diabetes (one patient), sickle cell trait (one patient), asymptomatic bacteruria (one patient) and pelvic kidney (one patient), None of these patients benefitted. It is
difficult (R.H.R.) to justify routine dip stick urinalysis on every pediatric admission

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ENDOCRINOLOGY

sue of a patient perplasis. Acta 1972 31

.

with lipoid Endocrinol

adrenal hy1 71 :51 2, 39.

consistent with 1 7-20 desmolase deficiency. Gyneco/ Invest 7: 1 38, 1976 Goebelsmann U. Horton JR, Mestman

tal hypospadias. 1974 47.

N EngI

J Med

291 :944,

Bongiovanni

AM: The adrenogenital

of 3fl-hydroxysteJ Clin Invest JA, Anast CS,

syn41: et at: 40.

32.

drome with deficiency roid dehydrogenase. 2086, 1962 Parks GA, Bermudez

JH, et at: Male pseudohermaphroditism due to testicular 1 7$-hydroxysteroid dehydrogenase deficiency. J C/in Endocrinol Metab 36:867, 1973
Saez JM, de Peretti E, Morera AM, et al: Familial male pseudohermaphroditism with gynecomastia due to a testicular 1 7ketosteroid reductase defect. I. Studies in vivo. J Clin Endocrinol Metab 32:604, 1971
.

lmperato-McGinley J. Peterson A, Leshin M, et at: Steroid 5n-reductase deficiency in a 65-year old male pseudohermaphrodite: The natural history, ultra struc-

ture

of the testes,

and evidence
J C/in

for ge-

33.

Pubertal boy with the 3f./-hydroxysteroid dehydrogenase defect. J Clin Endocrinol Metab33:269. 1971 Jahhe 0, Perheentupa J, Viinikka L, et
at: Testicular endocrine function in a pubertal boy with 3/l-hydroxysteroid dehydrogenase deficiency. J C/in Endocrinol Metab 39:206, 1974

netic heterogeneity. Metab50:15, 1980

Endocrinol

48. 49.

41

Peterson
tier

RE, lmperato-McGinley
Male pseudohermaphrodit-

J, Gaudefi50.

T, et at:

Jagiello G, Atwell JD: Prevalence of testicular feminization. Lancet 1 :329, 1962 Ross GT, Vande Wiele AL: The ovaries, in Williams RH (ed): Textbook of Endocrinology. ed 5. Philadelphia. WB Saunders, 1974, pp 368-422
Manuel M, Katayama The age of occurrence in intersex patients some. 1976 Sweet KP, Jones of gonadal with a Y HW Jr: tumors chromo124:293, A, et at:

34.

Neumann F. Elger W: The effect anti-androgen 1 ,2n-methylene-6-chloro-

of the
42.

ism due to steroid 5a-reductase ciency. Am J Med 62:1 70, 1977

Pang S. Levine LS, Chow

D, et al: Dihy-

.4, 6-pregnadiene-1 7-o-ol-3-20-dione1 7o acetate (cyproterone acetate) on the development of the mammary glands of the male foetal rats. J Endocrino/ 36:

drotestosterone

and

its

relationship

to
51.

Am
A.

J Obstet
Schrott H,

Gynecol
Kurland

43.

347,
35. Kenny

1966
FM, Reynolds JW, Greeny

OC:
44.

36.

Partial 3/l-hydroxysteroid dehydrogenase (3fi-HSD) deficiency in a family with congenital adrenal hyperplasia: Evidence for increasing 3fl-HSD activity with age. Pediatrics 48:756, 1971 Biglieri E. Herron MA, Brust N: 1 7-Hydroxylation deficiency. J C/in Invest 45: 1946, 1966 New Ml: Male pseudohermaphroditism due to 1 7-hydroxylase deficiency. J C/in Invest 49:1930, 1970 Goebelsmann u. Zachmann M, Davajan V. et al: Male pseudohermaphroditism

testosterone in infancy. J C/in Endocrinol Metab48:821, 1979 lmperato-McGinley J, Guerrero L, Gautier T. et al: Steroid 5o-reductase deficiency in man: An inherited form of male pseudohermaphroditism. Science 186: 1213, 1974

Study of the incidence of hypospadias in Rochester, Minnesota, 1940-70, and a case-control comparison of possible etiologic factors. Mayo C/in Proc 49:52,
52. 1974 Aarskog D: Maternal progestins as a possible cause of hypospadias. N EngI J Med 300:75, 1979 Jones HW, Scott WW: Hermaphroditism, Genital Anomalies and Related Endocrine Disorders. Baltimore, Williams & Wilkins, 1971, p97 Jeune M, David L: Le pseudo-hermaphrodisme masculin: Essai de classification apropos de 33 observations. Pediatre 27:891, 1972

45.

Saenger P. Goldman AS, Levine L5, et at: Pre-pubertal diagnosis of steroid 5oreductase deficiency. J C/in Endocrinol Metab46:627, 1978 Wilson JD: Dihydrotestosterone formation in cultured Chem 250:3408, human 1975 fibroblasts. J Biol

53.

37.

46.

Walsh

PC, Madden

JD, Harrod

MJ, et al:

54.

38.

Familial incomplete male pseudohermaphroditism type 2: Decreased DHT formation in pseudovaginal perineoscro-

Bladder EDUCATIONAL 79. Appropriate the management bladder paralysis OBJECTIVE understanding of a child (81/82). of with

Paralysis

with

Myelomeningocele

Current Approaches to Evaluation and Management of Children with Myelomeningocele. Action Committee on Myelodysplasia, Section on Urology. Pediatrics 63:663, 1979. Clean Intermittent Catheterization in Children. Plunkett JM, et al. J Urol 1 21: 469, 1979.
The
(1

urologic

) the preservation The

development

management of renal of appropriate

of children born with myelodysplasia function; (2) the control of urinary urinary continence for age.

has infection;
in 1 972

three and
by

goals: (3) the

Lapides

introduction

of clean

intermittent

catheterization

(CIC)

has proven to be a superior method of bladder drainage. neonatal period. Children with normal intelligence are able from the age of 6 to 7 years. Continence can be achieved
by the use of pharmacologic drugs. Adjunctive surgery can

CIC can be started in the to catheterize themselves in most children on CIC

also be used to increase

bladder Plunkett
showed
complications patient),

outflow resistance and bladder capacity which will improve continence. and Braren reported their results of CIC in 34 children. Only one child
radiotogic
and bladder

evidence
included acute neck

of upper
spasm (one

tract

deterioration
(two

while
patients),

using
urethral

CIC.

Their

major
(one

pyelonephritis patient).

stenosis

Another when the

in the

modality of bladder bladder can be easily

of vesicoureteral

emptying, emptied,
reflux.

suprapubic expression, when post-cred#{233} residual

In order to assure that

is indicated is negligible,
this procedure

only and
is

absence

safe, cystography should be performed should be measured. The procedure

vesicoureteral reflux when high

and post-expression residual urine volumes is definitely dangerous in the presence of

pressures are transmitted directly to the

kidney

during

bladder

expression.

intravesical (C. Uy)

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Dysmenorrhea EDUCATIONAL OBJECTIVE New

833,

134. ApproprIate acquaintance with the possible use of Inhibitors of prostaglandin synthesis In the treatment of primary dysmenorrhea (81/82).

Concepts
1978.

in Dysmenorrhea.
Med Lett

Vlikorkala Drugs Ther

0,

et al. Am 21 :81
,

J Obstet

Gynecol

1 30:

Drugs

for Dysmenorrhea. dysmenorrhea

all postpubertal it is thought which augment

1979.

Primary
50#{176}/oof

is a form
females. to be the myometrial

of painful

menstruation

which

affects

more

than

understood, glandins pain. Clinical trials with agents that inhibit prostaglandin production (aspirin, ibuprofen, mefenamic acid, indomethacin, naproxen) have demonstrated an amelioration of the symptoms. Other forms of therapy-inhibition of ovulation, surgery, and tocolytic agents-achieve effectiveness through the limitation of prostaglandin activity.

Although its pathophysiology is still not fully result of excessive levels of endometrial prostacontractility producing uterine ischemia and

Comment. It seems that we are finally putting aside the wholly psychiatric nations for this disorder. We should not forget, however, that a longstanding

expla-

and

predictably periodic discomforting symptom will frequently cause anxiety which may linger on after the institution of medical therapy. This is particularly true of the adolescent who may have devised a number of intrapsychic mechanisms to cope with the pain. If any of these mechanisms are responsible for a secondary pain, they may tend to perpetuate the primary symptom-menstrual pain. If the health provider is aware of such a complex, an attempt should be made to institute some form of psychotherapy. (R. L. Johnson)

Zinc EDUCATIONAL OBJECTIVE

Deficiency Infants
Pediatrics

159. ApproprIate knowledge of the conditions with which zinc deficiency may be associated (81 / 82).

Plasma Zinc Levels in Premature DD, et al. J Pediatr 92:798, 1978. Zinc. AAP Committee on Nutrition. Zinc has been recognized

Receiving 62:408, trace

Parenteral 1978.

Nutrition.

Michie

in nutrition. More than 40 zinc-containing enzymes have been identified including alkaline phosphatase, carbonic anhydrase, alcohol and glutamic dehydrogenase, and the carboxypeptidases. Zinc appears to play a role in nucleic acid metabolism and protein synthesis. Approximate nutritional requirements for zinc have been formulated. The recommendations for infants and children are 3 mg/day from birth to 6 months, 5 mg/day from 6 to 1 2 months, 1 0 mg/day from 1 to 1 0 years, and 1 5 mg/day for older children and adolescents. It should be pointed out that the bioavailability of this metal varies considerably according to the dietary source so that the quantity

as an important

metal

absorbed may range from 20% to 60% Zinc deficiency in infants and children

of that ingested. may result from

inadequate

dietary

intake,

impaired absorption, excessive excretion, and an inherited defect in zinc metabotism. Most cases of severe intake deficiencies have occurred in infants and children receiving total parenteral nutrition without zinc supplements. This is especially a problem in premature infants who have lower body stores of zinc than full-term infants. Intestinal malabsorption syndromes probably give rise to zinc deficiency but more studies need to be done in this area. Hyperzincuria may potentially contribute to deficiency and may be seen in sickle cell disease, catabolic states, liver disease, burns, diabetes mellitus, and the nephrotic syndrome. Acrodermatitis enteropathica represents a rare inherited disorder of zinc absorption which is potentially fatal. Symptoms incude growth failure, anal and orificial skin lesions, glossitis, conjunctivitis, alopecia, diarrhea, depression, loss of appetite,

and

loss

of taste.

There

is also

an increased

susceptibility

to infection.

Lesser

expressions of the above occur in zinc deficiency related to deficient intake or increased excretion. The diagnosis of zinc deficiency can be made by determination of the plasma zinc level. In healthy children and adults, the mean value is 90 jig/100 ml with a

lower limit established

and nails

of normal in infants
may also

of 65 to 70 j.tg/100 and premature infants.

information

ml. The normal range Determination of zinc

zinc nutrition.

is not as well content of hair

provide

regarding

Comment. Therapy of zinc deficiency Zinc sulfate may cause gastrointestinal

may be accomplished irritation. For simple

with oral zinc acetate. nutritional deficiency in

is probably with 10 to (K. Nord)

infants and children, 0.5 to 1 mg of zinc per kilogram adequate. Patients with acrodermititis enteropathica 45 mg of zinc per day. Plasma levels should be used

of body weight should be treated

to guide

therapy.

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NEONATOLOGY

drawal, it should be relieved by panegonic, however relief could merely reflect a nonspecific effect of the opiate. We prefer the continuation of phenobarbital and the addition of chlorpromazine. If the diarrhea is
due to withdrawal, response to

chlonpromazine will occur within 24 hours. If that occurs, the chlorpromazine is continued and the phenobarbital is stopped. MORTALITY During the late 1 9th century and early years of this one almost all infants of addicted women died. Cyanosis was such a prominent feature of abstinence that theories were propounded concerning the ability of the narcotic to cause poor fetal circulatory maturation. Therefore, it was said, the foramen ovale did not close after birth and cyanosis resulted. During the first half of this century cyanosis lost its prominence, yet approximately half of the infants who suffered withdrawal died. Death was usually the result of severe vomiting and diarrhea. In the main, death resulted from failure to appreciate the problem or from inadequate use of drugs. Today, although much about narcotic withdrawal remains unknown, our awareness of the problem and the variety of therapeutic agents available have eliminated neonatal abstinence as a life-threatening illnessno infant should die of narcotic withdrawal. FOLLOW-UP Several reports indicate that the

frequency of sudden infant death syndrome (SIDS) among infants of addicted women is four to nine times that expected for the general infant population. Even should the socioeconomic pool from which addicts are drawn have twice the 3/i ,000 frequency for SIDS seen among the general infant population, the nearly 20/1 ,000 reported for infants of addicted mothers is startling. Appanently, opiates and methadone are not different in this regard, but the evidence is meager. Growth patterns following discharge from the nursery are difficult to assess because of lack of good socioeconomic controls. It appears that infants of mothers addicted to opiates or methadone grow slower than expected during the first three months, then slowly achieve the growth rate expected for the normal population. Preschool children of addicted mothers tend to be small for their age. Following discharge from the nursery, narcotic-exposed infants are commonly apparently hungry, demanding, difficult to satisfy, irritable, and irritating. They are restless, have exaggerated rooting, sleep for only short periods, and demonstrate poor socialization. This lasts for three on four months, but not beyond six. These drag on symptoms occur whether the infant required treatment or not and whether the infant was discharged to the parent(s) or not. It seems to be more pronounced among infants of methadone-treated mothers. Motor development is above average during the initial six to nine

months and then levels off at one yean. Fine motor coordination during the first year is equally poor among opiate-addicted and methadone-addicted infants. Similarly, both are poorly attentive, whereas language development appears to be normal. Follow-up studies are limited, troubled by lack of controls and, especially among infants of mothers not in methadone maintenance programs, compounded by family disruption and foster home care. Because of the association of all of these adverse factors vigorous attempts to achieve follow-up care are imperative.

REFERENCES
1
.

Gluck

L, Kulovich

MV:

Lecithin,.

sphyn-

2.

3.

gomyelin ratios in amniotic fluid in normal and abnormal pregnancy. Am J Obstet Gynecol 1 1 5:539, 1973 Zelson C. Rubio E, Wasserman E: Neonatal narcotic addiction: 10 year observation. Pediatrics 48:178, 1971 Nathenson G, Cohen Ml, Litt IF, et at:

The effect

of maternal

heroin

addiction

4.

on neonatal jaundice. J Pediatr 81:899, 1972 Cornblath M, Schwartz A: Disorders of Carbohydrate Metabolism in Infancy, ed 2. Philadelphia, WB Saunders. 1976, p 1 57

5. Finnegan LP: Pathophysiological and behavioral effects of the transplacental transfer of narcotic drugs to the foetuses and neonates of narcotic-dependent mothers. Bu//Narc 31:1, 1979 6. Lipsitz PJ: A proposed narcotic withdrawal score for use with newborn infants: cacy. A pragmatic C/in Pediatr evaluation 14:592, of its
1975

effi-

Groups

in Well

Child
in Well

Care Child Care.

The Osborn population LM, was et at. Pediatrics 67:701 class, and
,

Use of Groups Small

five

1 981.

group

visits
formed

were
a group.

compared

to individual

visits
white,

for well child

middle

care.

Three
Mormon.

to

patients

After were

a 45-minute performed.

group counseling session, individual brief physical examinations The group method was efficient; no more time was spent; no
mothers used the of 38 to how
thing.

reduced fees were changed. The group changed the process of well visits; took more initiative, reassured one another, asked more questions, and clinician as a resource. There was an increase in explanations. Thirty-seven

mothers Comment:
find the

were
time

very satisfied
and
to counsel

and stated
simple
advise, and

they
rather

preferred
Perhaps
than just

group
this

care.
is an answer
the whole

A wonderful

innovation.

to

ignoring

(R.H.R.)

pediatrics

in review

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Small EDUCATIONAL
154.

Bowel

Resection After Intestinal Resection. Philadelphia, WB Saunders

Gryboski J, in: Gastrointestinal Co, 1 975, pp 298-300.
Prob-

OBJECTIVE The Small

lems Although syndrome Necrotizing

Appropriate familiarity with the complications which may follow resection of significant portions of small bowel in infants and children, and their prevention or management (81/82).

Bowel

in the Infant.

the small bowel may be congenitally short, most in the newborn are the result of problems requiring enterocolitis, malrotation with volvulus, omphalocele,

cases of short bowel massive resection. and gastroschisis

with

volvulus,

and

jejunoilial

atnesia

are

the

most

common

conditions

for

which

surgery proximal resections

may result in short bowel syndrome. Resections small bowel do not significantly affect growth involving 75#{176}/o are followed by negative nitrogen

of up to 25% of the or nitrogen excretion; balance and impairment

of folate,

iron, vitamin,

calcium,

and magnesium

absorption.

Resections

of the distal

small bowel result in B12 and bile salt malabsorption. Resection of the iliocaecal valve results in rapid transit time and allows bacterial proliferation in the small bowel. The remaining intestine may adapt over time to allow improved absorptive function. Villous hypertrophy may occur and there may be mucosal cell hyperplasia of the epithelium. Disacchanidases, enterokinase, and peptide hydrolase increase in proportion to the mucosal cell population. These adaptive changes occur to a

greater extent in the distal small bowel after proximal resection than in the proximal bowel after distal resection. Because the newborn must contend with a physiologic malabsorption due to inefficient bile salt absorption and limitation of exocnine pancreatic function, extensive resection of bowel often results in severe malabsonption and malnutrition. By using parentenal hyperalimentation, adequate nutrition can be maintained and only in this setting can adaptive hyperplastic changes in the remaining bowel develop.

Comment.

Central panenteral hyperalimentation should be used in the early postoperative period and continued as the infants tolerance to a predigested formula, such as Pregestamil, increases. Such adaptation may take weeks to months. If resection is very extensive, and especially if the iliocaecal valve has been resected, hyperalimentation may be the only adequate way to maintain nutrition. In some cases of massive resection, adaptive changes will never be adequate to allow
independence from hypenalimentation. Unfortunately, we have no early absolute markers to indicate which infants will ever achieve independence from parenteral hyperalimentation, but resections sparing less than 1 5 cm of small bowel with an intact iliocaecal valve and those sparing less than 40 cm without an iliocaecal valve carry a grim prognosis. Supporting such patients raises difficult questions for family and medical staff alike, although some centers have chosen to use hyperalimentation in the hospital or at home for an indefinite period. (K. Nord)

Pseudoepilepsy EDUCATIONAL OBJECTIVE Neurogenic 44. Appropriate recognition management of the child pseudoseizures (81/82). and with
at. Am 210,

and Hysterical
1 35:82,

Seizures
1978. in Adolescent

in Children
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and Adolescents.
Gross

Williams

DT, et
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Pseudoepilepsy:

A Study

M. Am J Psychiatry

Psychic stress may trigger seizure activity in children and adolescents who may or may not have neurogenic epilepsy. Such seizure activity is known as pseudoepilepsy. The physician usually becomes aware of this syndrome after finding that the patients seizure cannot be controlled even with increasing dosages of varying medications. In addition, these patients fail to bite their tongues or have fecal or urinary incontinence during the episode. The episodes are slow in onset and are not associated with bodily injury. Postictal stupor is absent and the patient may have complete recall for events that occurred during the seizure. Psychotherapy is a necessary adjunct in the treatment of these patients and should be directed toward the definition and alleviation of the psychic stress.

Comment. Pseudoepilepsy is a mechanism that the child or adolescent is using to cope with some form of stress. If it successfully removes the stress-as it frequently does if the patient is hospitalized-it may quickly become a fixed psychodynamic mechanism. This outcome can best be prevented by early recognition and treatment in patients who meet the criteria described above. (R. L. Johnson)

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1982

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Rotavirus
Stool

Diarrhea Content and Purging E coil, and V Cholera were made The results Rates in Diarrhea in Children. Molla and electrolyte Caused by Rotavirus, AM, et al: J Pediatr 98: losses in diarrhea from

Electrolyte Enterotoxigenic 835, 1981. Comparisons three etiologies.

regarding fluid are as follows:

Water Loss
(ml/kg/8 hr) Na

Stool K

Cholera
Escherichia co/i

Rotavinus

60 40 33

90 54 37

30 38 37

The conclusions are that notavinus, the commonest cause of infantile a hypotonic stool, and the formula suggested by the World Health replacement therapy in cholera may be inappropriate. (R.H.R.)

diarrhea, yields Organization for

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pediatrics

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vol. 3 no. 9 march

1982

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Tuberculosis Screening Pediatrics in Review 1982;3;271 DOI: 10.1542/pir.3-9-271

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