Vulnerable Sibling: Hyponatremia From Caries Prevention

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EXPERIENCE

AND

REASON

637

bellar cysts and the association of polycythemia. Arch

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18. Riddoch G: Discussion on vascular tumours of the brain and spinal cord. Proc R Soc Med 1931;24:382-383

19. Rowe PH: von Hippel-Lindau disease: Hereditary tendency in two families. Bull Northwestern Ciin 1955;6:117-125

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23. Hardwig P, Robertson DM: A familial, often lethal,

multi-system phakomatosis. Ophthalmology 1984;91:263-270

24. Cushing F!, Bailey P: Hemangiornas ofcerebellum and retina (Lindau’s disease). Arch Ophthalmoi 1928;57:447-462

25. Wing GL, Weiter JJ, Kelly PR, et al: von Hippel-Lindau disease: Angiomatosis of the retina and the central nervous

system. Ophthalmology 1981;88:1311-1314

26. M#{246}llerHU: Ophthalmic symptoms and heredity in cerebel-lar angioreticuloma. Acta Psychiatry Neurol

1944;19:275-292

27. Bird AV, Krynauw RA: Lindau’s disease in a South African family. Br J Surg 1953;40:433-437

28. Otenasek FJ, Silver ML Spinal hemangioma (hemangio-blastoma) in Lindau’s disease. J Neurosurg 1961;18:295-300

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Hudson Valley. J Neurosurg 1964;21:97-103

30. Rho Y: Von Hippel-Lindau’s disease: A report of five cases. Can Med Assoc J 1969;101:135-142

31. Schecterman L: Lindau’s disease: Report of an unusual case

and two additional cases in a Negro family. Med Ann Dis Coi 1961;30:64-76

32. Nyggaard KK, Walters W: Polycystic disease ofthe pancreas (dysontogenetic cysts): Report of a case with partial pan-createctomy. Ann Surg 1937;106:49-53

33. Fishman RS, Bartholomew LG: Severe pancreatic involve-ment in three generations in von Hippel-Lindau disease. Mayo Ciin Proc 1979;54:329-331

34. Jackaman FR: Polycystic pancreas: Lindau’s disease. J Coil Surg Edinb 1984;29:121-122

35. Steiner M, Klein E, Klein G: Antinuclear reactivity of sera in patients with leukemia and other neoplastic diseases. Ciin Immunoi Immunopathol 1975;4:374-381

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37. Pearson JC, Weiss ,J, Tanagho EA: A plea for conservation in renal adenocarcinorna associated with von Hippel-Lindau

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38. Adams JE: Familial hemangioblastoma of the cerebellum: Pedigree of two families. J Neurosurg 1953;10:421-423 39. Welch RB: Fluorescein angiography in side-cell retinopathy

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tomo-graphic and angiographic evaluation of hemangioblastomas. Radiology 1981;138:633-634

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kidney in association with Lindau’s disease. N EngI J Med 1951;244:633-634

43. Isaac F, Schoen I, Walker P: An unusual case of Lindau’s disease: Cystic disease of the kidneys and pancreas with renal and cerebellar tumors. AJR 1956;75:912-920

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45. Richards RD, Mebust WK, Schirnke RN: A prospective study on Von Hippel-Lindau disease. J Urol 1973;110:27-30 46. Goodbody RA, Gamlen TR: Cerebellar hearnangioblastoma

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Vulnerable

Sibling:

Hyponatremia

From

Caries

Prevention

Parental actions and beliefs shape every aspect

of a child’s health and development. Green and

Solnit’ described a vulnerable child syndrome in

which the child’s development was impaired when

the parents treated him or her in an inappropriate

fashion because they had an unreasonable

expec-tation that he or she would die. We recently cared

for a child who suffered a life-threatening event

(status epilepticus due to hyponatremia) because

the parents were trying to avoid reproducing a

serious, but not life-threatening, problem (nursing

bottle caries) that had occurred in the older sibling.

This distortion of professional advice created

vu!-nerability to significant neurologic problems.

Reprint requests to (D.L.C.) Department of Pediatrics, Medical College of Pennsylvania, 3300 Henry Ave., Philadelphia, PA

19129.

CASE REPORT

A 4#{189}-month-old male infant was brought to the

emer-gency room after the parents found him lying in bed without apparent respiratory effect. The mother had

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638 PEDIATRICS Vol. 79 No. 4 April 1987 checked on him because he was unusually quiet. She found him with his eyes rolled back. He did not move or breathe until she gave him two mouth-to-mouth breaths.

He had been well until one day before admission when

he was noted to have nasal congestion and a cough and to sleep more than usual.

On arrival in the emergency room, the baby was pale

but acyanotic. Vital signs were: temperature 35.2#{176}C (95.4#{176}F),heart rate 128 beats per minute, and respirations 32 breaths per minute. His weight was 6.9 kg with a body surface area of 0.32 m’. The child’s eyes were glazed, respiratory efforts were shallow and strained, and muscle

tone was poor. There were copious nasal secretions. Ox-ygen was given by mask, his nose was suctioned, and his respiratory effort improved. Multiple focal seizures oc-curred, which became generalized but then stopped spon-taneously. He received two doses of phenobarbital, 4 mg/ kg, im, and was then given iv diazepam when a

general-ized seizure developed. No further seizures occurred

dur-ing his hospital stay.

The initial blood chemistries were reported as Na 114

mEciJL, K 4.7 mEqJL, Cl 87 mEciJL, CO, 15.8 mmol/L,

BUN 7 mg/dL. An infusion of 9.5 mEq of Na as 3% NaCl was then given over one hour. Further history from the parents revealed that the child’s daily intake consisted of

960 to 1,200 mL (32 to 40 fi oz) of formula which was

diluted 1:2 with water rather than the appropriate

dilu-tion of 1:1. He also received water between feedings for a total of 960 to 1,200 ml (32 to 40 fl oz) of water per day.

The parents stated they gave dilute formula and water to

this child because their 2-year-old child had required

extensive dental work for nursing bottle caries. They had

been told that formula and juice in the bottle had

pro-duced this problem and were trying to avoid it in this

infant by limiting his exposure to sweetened solutions.

The baby was evaluated for sepsis with blood, urine,

and CSF cultures, but the only evidence of infection

found was an upper respiratory tract infection. The serum

sodium concentration became normal on the day of

ad-mission following fluid restriction and remained normal.

He was discharged on phenobarbital with instructions to

the parents to dilute the formula properly and to limit

water intake to 120 mL/d (4 fi oz/d). Nine days after the

seizures, the baby had normal findings on EEG. At his

last follow-up visit at 7 months of age, he was developing

normally and had had no more convulsions.

DISCUSSION

Parent counseling is an important part of the

pediatrician’s job. Numerous articles have dealt

with recognition of the overanxious parent who

brings the child for care because of fear that a

perceived problem is more serious than it

ap-pears.’4 The child whose parent perceives him or

her to be more ill than he or she is is at risk for

developmental problems related to an abnormal

parent-child relationship. We found another type

of vulnerable child, one whose sibling had a

pre-ventable medical problem and whose parents used

inappropriate means to avoid this problem in their

next child.

Water intoxication is not rare in children. It has

been caused by water swallowing during swimming,’

child abuse,6 voluntary water consumption,7

im-proper dilution of formula,8 and parental

misinter-pretation of physician’s advice to “give a lot to

drink.”9 However water intoxication due to a

par-ent’s attempt to prevent dental caries has not

pre-viously been reported.

Nursing bottle caries are severe decay of the

maxillary incisors due to prolonged contact of the

teeth with a sugar-containing substance, either via

sucking at a bottle nipple or at the breast.’#{176} Parents

are advised to prevent the condition either by not

leaving a bottle in the crib (or not giving the

breast-fed baby continuous access to the nipple) or by

providing plain water as a substitute for

sugar-containing liquids.” For most parents, this is

ade-quate advice. In a family in which baby bottle caries

has already occurred, there may be an attempt to

overcompensate. This infant had no teeth, but the

parents had already substituted water for half of

his feeding. Rather than find other means to help

the child to sleep, they used the water bottle

alter-native that had been proposed for the sibling.

In families with multiple children, it may be

believed that less time need be spent on parent

counseling because parents are experienced in child

care. This case highlights the fact that the

pedia-trician should especially evaluate what problems

previous children had (or were perceived to have)

and how the parents are attempting to avoid the

recurrence of the problem.

Dietary histories for infants should always

in-dude the amount of formula given per 24-hour

period and the method of preparation of the

for-mula. The amount of water given should be

ascer-tamed. Except during periods of hot weather, most

young infants do not require water. Water intake

in excess of 12 L/m2/d when the infant has about

30 m#{248}smof excretable solute per day may produce

water intoxication, which can, in turn, lead to

sig-nificant neurologic events.’2 In the absence of

in-take providing excretable solute, this volume may

be as little as 2.4 L/m2/d.12

The infant with strong sucking urges who has

insecure parents may always be “plugged into” a

bottle in an effort to calm him or her. Exploring

the baby’s temperament with the parents can be

used as an opportunity to suggest other means of

comforting the baby such as rocking, cuddling,

vo-calizing to him or her, or using a pacifier.

Family history taking must include all

child-related problems, not just genetic or fatal ones, so

that areas in which the parents are using unusual

means of dealing with their children may be

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No reprints available.

American Academy of Pediatrics.

EXPERIENCE

AND

REASON

639

ered. Even a more broad-based question such as,

“Are there any problems that occur in children that

you believe are a special risk for your child?” may

alert the pediatrician to potentially dangerous

sit-uations.

Counseling about developmental and behavioral issues is an important part of the pediatrician’s

role. Care must be taken that the remedies we

provide for one problem are not taken to such an

extreme that they create another.

REFERENCES

DEBORAH L. CALLANAN, MD

LINDA B. HINER, MD

Department of Pediatrics

Medical College of Pennsylvania

Philadelphia

1. Green M, Solnit AJ: Reaction to the threatened loss of a child: A vulnerable child syndrome. Pediatrics

1964;34:58-66

2. Bass LW, Cohen RL: Ostensible versus actual reasons for seeking pediatric attention: Another look at the parental ticket of admission. Pediatrics 1982;70:870-874

3. Poole SR: The over-anxious parent. Gun Pediatr 1980;

19:557-562

4. Yudkin 5: Six children with coughs: The second diagnosis. Lancet 1961;2:7202

5. Kroop RM, Schwartz JF: Water intoxication from swim-ming. J Pediatr 1982;101:947-948

6. Mortimer JG: Acute water intoxication as another unusual manifestation of child abuse. Arch Dis Child

1980;55:401-403

7. Gold I, Koenigsberg M: Infantile seizures caused by volun-tary water intoxication. Am J Emer Med 1986;4:21-23

8. Partridge JC, Payne ML, Leisgang JJ, et al: Water intoxi-cation secondary to feeding mismanagement. Am JDis Child

1981;135:38-41

9. Etzioni A, Benderley A, Levi Y: Water intoxication by the oral route in an infant. Arch Dis Child 1979;54:551-553 10. Brams M, Maloney J: “Nursing bottle caries” in breast fed

children. J Pediatr 1983;103:415-416

11. Shelton PG, Berkowitz RJ, Forrester DJ: Nursing bottle caries. Pediatrics 1977;59:777-778

12. Sweeney MJ: Fluid therapy, in Hoekelman RA, Blatman SA, Brunell PA, et al (eds): Principles of Pediatrics. New

York, McGraw-Hill Book Co, 1978, p 257

Are You Overlooking

Fractures

of the Mandibular

Condyle?

Little has been published in the pediatric

litera-ture about fractures of the mandibular condyle, and

pediatricians may not be familiar with the types of

trauma leading to such fractures, current

tech-niques of physical and radiographic examination,

and other commonly associated injuries. While

working at a children’s hospital for more than 10

years, we have found that condylar fractures can go

undiagnosed, leading to serious long-term

conse-quences. This view is supported by Proffitt et al’

who reviewed the records of patients attending a

large dentofacial clinic and found 25% had

abnor-mal jaw shape and malocclusion attributable to an

overlooked or inappropriately treated condylar

fracture. For these reasons, we embarked on a

ret-rospective study of a group of children with

frac-tures of the mandibular condyle who sought

treat-ment at Children’s Orthopedic Hospital in Seattle.

The mandible is the second most frequently

frac-tured facial bone after the nasal bones.2 It is the

largest bone of the face and is horseshoe shaped,

with the main portion being referred to as the body

and the part extending superiorly as the ramus (Fig

1). The ramus is surmounted by the mandibular

condyle, which fits into the glenoid fossa of the

temporal bone, forming the temporomandibular

joint. The condylar area is the most fragile portion

of the mandible and is involved in most mandibular

fractures. Hall et a!3 analyzed 263 fractures of the

mandible in children and found 40.0% involved the

condyle.

MATERIALS

AND

METHODS

The records of 49 children, 33 boys and 16 girls,

who sustained fractures of the mandibular condyle

in the 14-year period from 1969 to 1982 and received

initial treatment at the Children’s Orthopedic

Hos-pital and Medical Center in Seattle were available

for scrutiny. Information regarding the injury was

obtained retrospectively from the medical and

den-tal charts.

The patients were grouped by age: group 1, 15

preschool children 1 to 5 years of age; group 2, 25

grade school children 6 to 12 years of age; and group

3,

eight teenage patients 13 to 18 years of age. The

type of trauma, associated injuries, and treatment

were recorded.

RESULTS

The causes of the condylar fractures are shown

in Table 1 and indicate that the type of trauma

causing fracture varied with the age group. In the

preschool children, motor vehicle collisions were

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1987;79;637

Pediatrics

DEBORAH L. CALLANAN and LINDA B. HINER