Letters to the Editor

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LETTERS

TO

THE

EDITOR

607

compounds. Phenobarbital is a potent inducer of

micro-somal enzymes and increases conjugation of bilirubin. In

addition, phenobarbital increases canalicular bile flow

and enhances biliary excretion of bilirubin. The resultant

decrease in serum bilirubin may be one of the factors

involved in enhancement of “Tc-IDA excretion after

phenobarbital stimulation. The exact mechanism of the

effect of phenobarbital, however, is not well understood. We remain confident that hepatobiliary scintigraphy with “Tc-IDA derivatives is a reliable test for

differen-tiating biliary atresia from other causes of neonatal jaun-dice provided that the patient is treated with phenobar-bital in a dose of 5 mg/kg/day for five days prior to the

examination and both hepatic uptake and excretion of

tracer are taken into consideration in the interpretation of the scans.

REFERENCES

MASSOUD MAJD, MD

RICHARD C. REBA, MD

R. PETER ALTMAN, MD

Departments of Radiology and Surgery

Children’s Hospital National Medical Center

Washington, DC 20010

1. Majd M, Reba RC, Altman RP: Effect of phenobarbital on 99mTc-IDA scintigraphy in the evaluation of neonatal jaun-dice. Semin NucI Med 11:194, 1981

2. Harvey E, Loberg M, Ryan J, et al: Hepatic clearance mechanism of Tc-99m-HIDA and its effect on quantitation

of hepatobiliary function: Concise communication. J Nuci Med 20:310, 1979

3. Popescu HI: Hepatic clearance mechanism of Tc-99m-N-(Acetamlido)-iminodiacetic acid derivatives, letter. J Nucl

Med2l:1110, 1980

4. Loberg MD, Ryan JW, Porter DW: Hepatic clearance mech-anism of Tc-99m-N-(Acetamlido)-iminodiacetic acid

deriva-tives, reply to letter. (Ref. #3). J NucI Med 21:1111, 1980

initial intravenous treatment, failures were 67% higher on sucrose than on glucose, and vomiting leading to failure

was 10 times as common. In the study of Nalin et al3

babies on sucrose needed more than 24 hours treatment

compared with 15% of those on glucose. Of older

Bang-ladesh patients4 with cholera randomly allocated to

su-crose or glucose, 11 with severe diarrhea were on sucrose and five on glucose, and 15 of the glucose group cleared

rapidly compared with nine on sucrose. Chatterjee et al5

found 15% of Bengali infants in their study to be sucrase deficient.

At the start of acute diarrhea, mothers can give infants

plain water only (chronic diarrhea is a different matter). The condition of most infants will settle before they need

added sugar or salt, and before their circulation and

osmolarity are upset enough to give a risk of

disequilib-rium edema on straight water.6’7 After 16 to 24 hours

feeding can be rapidly restored after a cautious trial of

dilute milk. The few who do not immediately respond can

be treated with a glucose and salt mixture by mouth or

vein. This procedure avoids the risks of delay and of

contaminated or concentrated mixtures, and much of the

cost of glucose. In Guadalcanal, I recently found that this

had long been the custom, and I saw no children there as

dehydrated as those I saw in England before giving similar advice in the early 1960s.

Sucrose may not differ significantly from glucose in

trials, but the failures suggest a type II error.8 “The data

do not compel change” to quote Hirschhorn and Nalin,9

and further thought is needed before the World Health

Organization pontificates in some future “Year of the

Diarrhea.”

T. H. HUGHES-DAVIES, FRCP

Breamore Marsh

Fordingbridge, Hampshire, England

REFERENCES

Sucrose or Glucose for Diarrhea

To the

Editor.-Water moves along osmotic gradients. Acute diarrhea

is due to impaired solute absorption or to increased solute

excretion. It seems reasonable, as well as traditional, to lower the osmolarity of the gut’s contents in diarrhea by starvation and water.

Breast milk, when fully digested, has nearly twice the osmolarity of plasma, and giving it (or bread and butter’)

as advocated in Dacca2 might prolong diarrhea. The

24-hour purging rate of the patients of Black et al on an

unknown quantity of milk equalled that of the first eight

hours, and diarrhea persisted for 60 hours. Nalin et al3

gave Costa Rican babies half-strength milk only when

hydration was complete, at 16 ± 3 hours on glucose/salt

and 19 ± 2 hours on sucrose/salt, with added water.

Liquid stools stopped within 24 hours.

Unrestricted breast milk or bread will not only affect stool sugar assays, but blunt differences between sucrose

and glucose. Even so, among the patients not needing

1. Sack DA, Islam 5, Brown KH, et al: Oral therapy in children with cholera: A double blind comparison of sucrose with glucose electrolyte oral solution. J Pediatr 96:20, 1980

2. Black RE, Merson MH, Taylor PR, et al: Glucose vs sucrose in oral rehydration solutions for infants and young children

with rotavirus-associated diarrhea. Pediatrics 67:79, 1981

3. Nalin DR, Levine MM, Mata L, et al: Comparison of sucrose

with glucose in oral therapy of infantile diarrhoea. Lancet 2: 277, 1978

4. Palmer DL, Koster FVF, Islam AFM, et al: Comparison of sucrose and glucose in the oral electrolyte therapy of cholera

and other severe diarrheas. N Engl JMed 297:1107, 1977 5. Chatterjee A, Mahalanabis D, Jalan KN, et al: Evaluation of a sucrose/electrolyte solution for oral rehydration in acute

infantile diarrhoea. Lancet 1:1333, 1977

6. Hughes-Davies TH: Hyperosmolar coma in diabetes. Lancet

1:822, 1966

7. Hughes-Davies TH: Diseases of children, in Harvard CWH (ed): Current Medical Treatment. Bristol, 1975

8. Freiman JA, Chalmers TC, Smith H, et al: The importance of beta, the type II error and sample size in the design and interpretation ofthe randomized control trial. NEngI JMed

299:690, 1977

9. Hirschhorn N, Nalin DR: Sucrose or glucose for diarrhoea.

Lancet 2:1230, 1977

In

Reply.-Dr Hughes-Davies may feel justified to treat diarrhea

at Viet Nam:AAP Sponsored on September 7, 2020

www.aappublications.org/news

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608 PEDIATRICS Vol. 68 No. 4 October 1981 with “starvation and water” on the basis of reason and

tradition, but we do not feel that such treatment can be

supported by a review of the available evidence.

Rotaviruses, which were present in the stools of all

children in our study, appear to cause diarrhea by infect-ing epithelial cells in the small intestine. In animals, infection is segmental and progresses from proximal to

distal. Thus, only a portion of the mucosa is involved at one time.’ Temporary deficits in sodium transport result

in loss of excess water and electrolytes in the stool.’ Decreased levels of mucosal clisaccharidases have been

demonstrated in rotavirus diarrhea, as in many other

types of diarrhea, and children may have stools with increased reducing substances and an acid pH, indicating

incomplete absorption of carbohydrates.’2

It has long been recognized that feeding during

cliar-rhea may increase the water content and the volume of

stool. However, in the few controlled studies that have

been done, starvation during acute diarrhea failed to

shorten the duration of diarrhea.3’4 On the other hand,

Chung5 demonstrated that despite decreased absorption

of foods during diarrhea, children could still absorb

sub-stantial proportions offat and nitrogen ingested in a

milk-based formula. He stressed that we should be concerned

with “the infant rather than the stools” and that we

should focus on nutrients retained rather than nutrients lost, as long as feeding could not be shown to delay recovery. The demonstration that rare patients have char-rhea due to disaccharide intolerance does not negate this

general principal.6

Unfortunately, Hughes-Davies has incorrectly

inter-preted both our study and that of Nalin et al.7 In our

study, children were allowed to take breast milk from the

time ofadmission and the average total diarrheal duration

was 62 hours (38 hours before and 24 hours after

hospi-talization). In the study by Nalin et a!, milk was withheld

for 16 to 19 hours after admission and the total diarrheal

duration was more than 72 hours (most diarrhea ceased

or became minimal within 24 hours after hospitalization). Thus, a comparison of these studies does not reveal a

difference in the duration of diarrhea that might be due

to the time of introduction of milk feeding. A better

comparison can be made among three groups of children

treated in Dacca, Bangladesh.2 The duration of rotavirus

diarrhea in the hospital in groups of children given either

sucrose or glucose oral solutions with breast milk and other food did not differ from the duration in a group of children receiving intravenous therapy.

In a series of trials comparing sucrose- and glucose-based oral therapy solutions, glucose has demonstrated a consistent but slight advantage.27#{176} Although many of these studies have involved small numbers of patients, we

anticipated that the difference between the solutions may

be small and included nearly 400 children per group. If

we consider a 10% difference in failure rates between the groups to be clinically important we could expect a power of 0.99. Even with a 5% difference in failure rates, the

power would still be more than 0.75. Taken together,

these studies indicate that glucose is preferred to sucrose

and that the differences are most marked in persons with high rates of stool output, such as may be seen in

chol-era.’#{176}However, these studies also indicate that sucrose can be substituted with minimal loss of efficacy in

situa-tions in which lower cost and greater availability of

su-crose make it a more practical alternative for widespread

use.

We are concerned about Hughes-Davies’

recommen-dation that diarrhea in children of developing countries

be treated with starvation, including the withdrawal of

breast milk, and with water for several reasons. First,

breast milk is a critical source of nutrients for young

children in most developing countries and interruption of

feeding during the four to eight episodes of diarrhea these

children have each year could threaten the successful

continuation of breast feeding.” Second, diarrhea has

been found to be an important cause of malnutrition in

developing countries’2 and withdrawal of food during

illness is one reason for this adverse consequence.’3 When one considers that children less than 5 years old in rural

Bangladesh have diarrhea for an average of 13% of their

lives and have some type of illness on more than half of

all days, it is easy to see how food withdrawal during

illness may contribute to growth faltering and malnutri-tion. Children receiving a bulky, cereal-based diet with a low energy density may not be able to “catch-up” rapidly enough to regain weight losses before the next illness.’4 The continuation of breast-feeding wifi ensure a substan-tial dietary intake during and after diarrhea.’5 Third, the

failure to provide oral replacement of the electrolytes being lost in diarrheal stool and the continued ingestion of water or low solute fluids is likely to lead to hypona-tremia and hypokalemia.’6’7 Last, the failure to provide

adequate amounts of sodium and a source of glucose to

facilitate its absorption by the use of an oral therapy

solution can be expected to result in a higher risk of

dehydration and death.’8 Thus, we feel that treatment of

diarrhea with starvation and water is not in the best

interests of children in developing countries.

ROBERT E. BLACK, MD, MPH

Center for Vaccine Development

University of Maryland School of Medicine

29 South Greene St

Baltimore, MD 21201

MICHAEL MERSON, MD

Diarrhoeal Diseases Control Programme

World Health Organization

DAVID SACK, MD

Division of Infectious Diseases The Baltimore City Hospitals

REFERENCES

1. Davidson GP, Gall DG, Petric M, et al: Human rotavirus enteritis induced in conventional piglets: Intestinal structure and transport. J Clin Invest 60:1402, 1977

2. Sack DA, Chowdhury AMAK, Eusof A, et al: Oral hydration in rotavirus diarrhea: A double-blind comparison of sucrose

with glucose-electrolyte solution. Lancet 2:280, 1978

3. Chung AW, Viscorova B: The effect of early oral feeding versus early oral starvation of the course of infantile char-rhea. J Pediatr 33:14, 1948

4. Rees L, Brook CGD: Gradual reintroduction of full-strength milk after acute gastroenteritis in children. Lancet 1:770,

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LETTERS

TO

THE

EDITOR

609

5. Chung AW: The effect of oral feeding at different levels on the absorption of foodstuffs in infantile diarrhea. J Pediatr

33:1, 1948

6. Sunshine P, Kretchmer N: Studies of small intestine during development. III. Infantile diarrhea associated with

intoler-ance to disaccharides. Pediatrics 34:38, 1964

7. Nails DR, Levine MM, Mata L, et al: Comparison of sucrose with glucose in oral therapy of infant diarrhoea. Lancet 2:

277, 1978

8. Palmer DL, Koster PT, Islam AFM, et al: Comparison of sucrose and glucose in the oral electrolyte therapy of cholera and other severe diarrheas. N Engl J Med 297:1107, 1977 9. Chatterjee A, Mahalanabis D, Jalan KN, et al: Evaluation

of a sucrose/electrolyte solution for oral rehydration in acute infantile diarrhea. Lancet 1:333, 1977

10. Sack DA, Islam 5, Brown KH, et a!: Oral therapy in children with cholera: A comparison ofsucrose and glucose electrolyte

solutions. J Pediatr 96:20, 1980

1 1. Mata L: Breast-feeding: Main promoter of infant health. Am J Clin Nutr 31:2058, 1978

12. Rowland MGM, Cole TJ, Whitehead RG: A quantitative

study into the role of infection in determining nutritional status in Gambian village children. Br J Nutr 37:441, 1977

13. Martorell R, Yarbrough C, Yarbrough 5, et al: The impact

of ordinary illnesses on the dietary intakes of malnourished children. Am J Clin Nutr 33:345, 1980

14. Rohde JE: Preparing for the next round: Convalescent care

after acute infection. Am J Clin Nutr 31:2258, 1978 15. Hoyle B, Yunus M, Chen LC: Breast feeding and food intake

among children with acute diarrheal disease. Am J Clin Nutr 33:2365, 1980

16. Finberg L: The management of the critically ill child with dehydration secondary to diarrhea. Pediatrics 45:1029, 1970 17. Kingston ME: Biochemical disturbances in breast-fed infants

with gastroenteritis and dehydration. Trop Pediatr 82:1073,

1973

18. Hirschhorn N: The treatment of acute diarrhea in children:

An historical and physiological perspective. Am J Clin Nutr

33:637, 1980

Pharyngeal Gonorrhea

To the

Editor.-Farrell and co-workers’ make a strong case for the

suspicion of sexual abuse in all children who have vaginal cultures that are positive for Neisseria gonorrhoeae. We

want to add our support to their conclusions with an

additional contribution: to extend their findings to include

throat cultures positive for N gonorrhoeae. We have

found this to be true in children of both sexes victimized

by sexual abuse.

From January through December 1979 at our

Chil-dren’s Hospital National Medical Center we reviewed all

cultures done on patients suspected of sex abuse. This

included throat cultures for isolation of N gonorrhoeae.

The technique utilized was the following: Specimens were

obtained from tonsils or the posterior pharynx using a

sterile swab. Immediately after being obtained, the swab

was rolled gently over approximately one third of the surface of a Thayer-Martin agar plate and of a 5% sheep blood agar plate. Care was taken to ensure that the entire

swab face touched the agar surface during inoculation.

The plates were then sent immediately to the clinical

laboratories. There, the plates were placed in an

atmo-TABLE. Five Patients with Positive Pharyngeal Cul-ture Sex Age (yr) Medical-Psychosocial History Associated Findings

F 3 Consulted for frequent

masturbation

Erythema

around vagina,

strong suspi-cion of sexual abuse

F 4 Past history of

fore-head hematoma,

tib-ial fracture

Laceration of va-gina, child abuse

M 7 Admitted to being

sub-jected to sodomy by

older boy

None

M 10 Immature, victim of

so-domy; violent against another boy; in psy-chotherapy.

None

F 13 Sexual assault by

step-father

None

* None of the patients had pharyngeal pathology.

sphere of 10% CO2 at 35 C. Negative plates were held a

minimum of three days. Colonies having organisms that

stained as Gram-negative diplococci and a positive

oxi-dase test were confirmed as N gonorrhoeae if they

fer-mented glucose, but not sucrose or maltose and lactose. A special effort was made to ensure that the specimens were labeled, “throat culture,” as opposed to “cervical” or “rectal” cultures, so that the bacteriologist could dif-ferentiate N gonorrhoeae from Neioseria meningitidis

or other species of Neisseria.2 We found five patients,

referred to the Sex Abuse Team, whose only positive

culture was pharyngeal (Table). Their age range was from 3 to 13 years; two were boys; none had clinical

manifes-tations of pharyngeal gonorrhea.3 We exclude from this

report all patients who, in addition, had positive cervical or rectal cultures for N gonorrhoeae.

We concluded that pharyngeal colonization may be at

times the only bacteriologic manifestation of a child’s

contact with a person affected by gonorrhea. We thus

recommended that the pharyngeal culture be obtained in

addition to the traditional vaginal and rectal culture in any child suspected to be the victim of sexual abuse.

TOMAS JOCE SILBER, MD

Adolescent Medicine Outpatient Department

REFERENCES

GUIDO CONTRONI, MS

Microbiology Laboratory

Children’s Hospital National Medical Center

111 Michigan Avenue, NW

Washington, DC 20010

1. Farrell MK, Bilimire E, Shamroy JA, et al: Prepubertal

gonorrhea: A Multidisciplinary Approach. Pediatrics 67:151,

1981

2. Silber TJ, Controni G, Korin E: Pharyngeal gonorrhea in children and adolescents. Clinical Proceedings, Children’s Hospital National Medical Center 33:79, 1977

3. Silber TJ: Pharyngeal gonorrhea in children. Pediatrics 61: 674, 1978

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1981;68;607

Pediatrics

Robert E. Black, Michael Merson and David Sack