by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village,it has been published continuously since 1948. PEDIATRICS is owned, published, and trademarked PEDIATRICS is the official journal of the American Academy of Pediatrics. A monthly publication,
at Indonesia:AAP Sponsored on April 1, 2012pediatrics.aappublications.orgDownloaded from
Nutritional Management of Acute Diarrhea:An Appraisal of the Alternatives
Kenneth H. Brown, MD, and William C. MacLean, Jr, MD
From the Gastroenterology and Nutrftion Unit, Department of Pediatrics; Division ofGeographic Medicine, Department of Medicine, School of Medicine; and Division ofHuman Nutrition, Department of International Health, School of Hygiene and PublicHealth, Johns Hopkins University, Baltimore; lnstituto de lnvestigacion Nutricional,Apartado 55, Miraflores (Lima), Peru; and Ross Laboratories Columbus, Ohio
ABSTRACT. Whether fasting during an episode of acutediarrhea is necessary or desirable has recently been ques-
tioned. The principal argument advanced for limitedfasting is the avoidance of the consequences of malab-
sorption, namely acidosis, excessive fluid losses, depletionof the bile acid pool, and possible mucosal injury fromunabsorbed foods. Advocates of continued feeding duringacute diarrhea suggest that the practice will preventdeficits of intakes of protein and calories, maintain orstimulate repair of the intestinal mucosa, and sustain
breast-feeding in the breast-fed infant. There are only alimited number of clinical studies that address the issue.Available evidence suggests that, in most cases, currentpractice should be modified to minimize food withdrawal.Pediatrics 1984;73:119-125; diarrhea, malnutrition, nu-
trition, malabsorption.
Recent evidence has convincingly demonstrated
an inverse relationship between the prevalence of
diarrhea! disease and the growth of children in less
developed countries.13 Although less obvious for
developed populations as a whole, a similar rela-
tionship is clear in individual children in the more
developed countries.4 Growth failure secondary to
diarrhea has been attributed to the negative impact
of diarrhea on dietary intake57 and to impaired
Received for publication Aug 18, 1982; accepted May 25, 1983.Reprint requests to (W.C.M.) ROSS Laboratories, 625 Cleveland
intestinal absorption during and after enteric infec-
tions.8 Catabolic responses to infection also exact a
nutritional toll, especially in febrile illnesses.9 The
relative importance of these mechanisms has not
been conclusively determined, but a renewed appre-ciation of the complexities of the relationships
among enteric infection, dietary therapy, and ‘nu-tritiona! status following diarrhea has led to seriousrethinking of the most appropriate way to minimize
or replace both macronutrient and micronutrientlosses induced by diarrhea.
The approach to diarrhea by most pediatricians
in the United States and elsewhere consists of avariable period of food reduction or, more likely,
fasting-in order to avoid the clinical complicationof food-induced malabsorption-and compensatory
“overfeeding” during the recovery period. The ap-propriateness of this therapy has recently been
questioned by pediatricians in both developed’#{176}’1and Third World12 settings, who suggest as did
Park13 in 1924, that the child’s net balance ofnutrients, rather than the number of stools, should
be the primary clinical concern. These pediatriciansadvocate continued feeding during diarrhea. Al-
though the correct therapeutic approach is cur-rently debated, well-controlled studies of the alter-natives are, for the most part, lacking. Current
recommendations must, therefore, be based on the-oretical considerations while additional studies arebeing carried out. The purpose of this paper is toexamine the possible advantages and disadvantages
at Indonesia:AAP Sponsored on April 1, 2012pediatrics.aappublications.orgDownloaded from
of each of these approaches to the nutritional man-agement of childhood diarrhea and to review the
limited data available in the literature. Implicit in
our appraisal of the alternatives is the concept that
the outcome of nutritional therapy must be evalu-ated not only in terms of its short-term effect on
diarrhea, but also in terms of its longer range effecton intestinal function and nutritional status follow-ing recovery from the acute illness.
THEORETICAL ADVANTAGES OF DELAYEDFEEDING DURING DIARRHEA
The advantages of delayed feeding are primarily
related to the variety of proven and theoretical
consequences of malabsorption of ingested foods(Table). Malabsorption of carbohydrate, particu-
larly, of lactose, is common during and after diar-rhea. Decreased mucosal surface area, alterationsof the villus-crypt ratio, and decreased concentra-
tions of the disaccharidases have all been observed
during and following diarrhea associated wth a va-riety of pathogens.14’15 These injuries of the intes-
tinal mucosal, along with alterations in intestinaltransit time, undoubtedly account for the diarrhea-
related malabsorption of carbohydrates.The dura-tion of carbohydrate malabsorption is typically self-
limited, but may continue well beyond the periodof symptomatic illness in individual cases.16
Malabsorption of fat may also persist longer than
the episode of symptomatic diarrhea.’7 Although
excessive fecal losses of bile acids have been blamedfor steatorrhea,18 pancreatic injury’9 and intestinal
mucosal abnormalities may also be important. Mildfat malabsorption also has been described inasymptomatic enteric infections.20 Although the ab-sorption of protein appears to be maintained closer
to normal, increased fecal loss of endogenous aminoacids has been reported in infants with acute diar-rhea fed only glucose water.21 The loss of endoge-nous protein can be substantial in dysenteric syn-
dromes. Compromised absorption of nitrogen isprobably better tolerated nutritionally than corre-
sponding impairments of carbohydrate and fat ab-sorption, inasmuch as the percentage of nitrogen
TABLE. Theoretical Advantages of Delayed Feedingand Continued Feeding During Acute Diarrhea
Delayed feedingAvoid consequences of malabsorption
AcidosisFluid lossDepletion of bile acid poolMucosal injury
Continued feedingPrevent protein/energy deficitsMaintain or induce repair of intestinal mucosaSustain breast-feeding
retained and utilized, under normal conditions, is
rarely more than 50% of that absorbed. Conse-quently, a moderate degree of nitrogen malabsorp-
tion is still compatible with adequate retention.Urinary nitrogen excretion decreases in this situa-tion. In contrast, any malabsorption of fat or car-bohydrate represents a loss of energy that can be
compensated for only by a decrease in energy ex-
penditure or growth rate.Although the loss of potentially available nutri-
ents is one obviously undesirable nutritional effectof malabsorption, perhaps the clinically more im-
portant consequences are the short-term and long-
term complications induced by the unabsorbed
foods. Unabsorbed substances, particularly carbo-
hydrates, create an intraluminal osmotic force thatdraws water and, to a lesser extent, electrolytes intothe gut lumen. Bacterial fermentation of carbohy-
drates in the colon produces an increased number
of small molecules, further increasing the number
of osmotically active particles in the lumen. Accu-mulated fluid and solutes can distend the gut andstimulate its motility. The role of nonabsorbed
carbohydrates in the production of diarrhea-related
systemic acidosis has been described.22’23 Not onlydoes this combination of factors produce more diar-rhea and its associated symptoms, but carbohydrate
malabsorption in its more severe forms may ac-
tually induce a greater net fecal loss of endoge-nously secreted nutrients than would have been
engendered by the infection alone.
Increased intraluminal osmolality can, by itself,initiate derangements of intestinal function. Intra-
gastric instillation of hypertonic mannitol (nonab-
sorbable) in the rat, for example, has been shown
to produce deficiencies in the intestinal disacchar-idases.24 Similarly, the infusion of hypertonic man-nitol solutions into the duodenum of rats produces
transient malabsorption of glucose and fat.25 In theformer study the addition of disaccharides in the
solution tended to mitigate the reduction of thecorresponding disaccharidase.24 These studies aredifficult to interpret, however, because the infused
or force-fed solutions were made hypertonic (800 to
1,300 mosm/kg of H2O) by nonabsorbable solute. It
is questionable whether the human small intestine
is ever subjected to osmolalities this high when
potentially absorbable solute is fed. Studies in thepig have demonstrated that the osmolality of duo-
denal contents approximates 450 mosm/kg of H20
60 minutes after gastric instillation of diets rangingfrom 250 to 700 mosm/kg.26 Moreover, net absorp-
tion of water, carbohydrate, and electrolyte wassignificantly better when the more hypertonic dietswere consumed.27
Coello-Ramirez and Lifshitz28 observed a rela-
tionship between the severity of carbohydrate in-
at Indonesia:AAP Sponsored on April 1, 2012pediatrics.aappublications.orgDownloaded from
tolerance and the proliferation of bacteria in thesmall intestine during the acute phase of diarrhea.They speculated that the presence of high loads of
aerobic enteric bacteria in the small intestinecaused carbohydrate intolerance. Equally plausible
is the interpretation that carbohydrates malab-
sorbed because of infection-induced intestinal dys-
function encouraged bacterial proliferation by pro-viding a metabolic substrate and by interfering with
normal intestinal motility. Thus, unabsorbed car-
bohydrate could conceivably lead to bacterial cob-nization of the small bowel and its attendant nu-
tritional problems.29’3#{176}
Two final theoretical problems raised by the issueof feeding during diarrhea are the possible effect of
the absorption of whole protein by the damagedintestine31’32 on the later development of foodsensitivity33 and the possible effect of unabsorbed
protein and/or fat on the conservation of bile acids.Although proteins in foods can clearly cause dam-age to the intestinal mucosa, as in gluten enterop-
athy, there are no convincing data that this is more
likely to occur after acute infection or that absorp-
tion of these proteins during the period of infectionresults in an increased prevalence of food sensitiv-
ity.
There are precedents linking malabsorption with
poor intestinal conservation of bile acids. Whenpancreatic replacement is withheld from childrenwith cystic fibrosis, for example, the resulting de-
terioration of the absorption of macronutrients isaccompanied by increased fecal losses of bile
acids.34 It is possible that unabsorbed dietary com-
ponents bind bile acids and inhibit their reabsorp-tion in the ileum. Excessive losses of bile acids
could deplete the bile acid pool, which is relatively
smaller in the infant and young child than in the
adult, and result in an intraluminal bile acid con-
centration insufficient to achieve micellar solubili-
zation of fats. Malabsorption of foods offered early
in the course of diarrhea might thereby contribute
to more chronic steatorrhea.
THEORETICAL ADVANTAGES OF CONTINUEDFEEDING DURING DIARRHEA
To understand the potential magnitude of thenutritional deficit imposed by fasting during diar-
rhea, one has only to consider the epidemiologicdata concerning childhood diarrhea in less devel-oped countries. A World Health Organization-sponsored review of epidemiologic studies from de-
veloping countries has estimated that children less
than 5 years of age suffer an average of two episodes
of diarrhea per year.35 A recent intensive village-level study of diarrheal diseases in one such coun-
try, Bangladesh, documented an annual incidence
rate of 6.8 episodes and an annual prevalence rate
of 15% (55 d/yr) for children less than 3 years ofage.36’37 If these children were to fast during all days
of symptomatic diarrhea, they would forfeit a siza-ble proportion of their potential annual nutrientintake during those years. Assuming that intestinal
absorption normalizes at the same time that symp-
tomatic diarrhea subsides (which, in fact, is not thecase), children in Bangladesh would have to con-
sume an average of 17% more than their recom-
mended intake on symptom-free days to compen-
sate for their days of fasting. It is not certainwhether infants and young children can consis-
tently consume and absorb the additional food re-
quired, particularly if the diet is at all bulky or of
inferior digestibility, ie, not primarily milk- or for-mula-based. Thus, a policy of withholding food
from children with diarrhea could result in irre-placeable nutritional losses in some settings.
Because of the potentially sizable deficit of nu-trients induced by fasting during diarrhea, manypublic health planners now encourage continuedfeeding throughout the diarrhea! episode. An em-
phasis on malabsorption during diarrhea neglects
the degree of absorption that does occur when nu-
trients are offered. It can be argued that, from the
point of view of total body nutrient balance, sub-
optimal absorption of some food is preferable to nomalabsorption of no food.
Studies of enzyme concentrations of villus enter-
ocytes in transmissible gastroenteritis in pigs, an
infection that resembles rotavirus infection in thehuman, have shown near normal sucrase concen-
trations 40 hours after the episode began. At itsnadir, sucrase concentration was still more than
40% of normal.’5 Given the relatively high concen-
tration of this enzyme under normal conditions,considerable sucrose absorption should be possibleeven at these reduced concentrations.
Continued feeding during diarrhea has also beetspromoted because of the observation that intestinal
mucosal disaccharidase levels are dramatically re-duced during fasting.� Some investigators havespeculated that the diminished intestinal enzymelevels might interfere with the subsequent reintro-
duction of feeding. It can be argued, however, thatthe duration of fasting in such studies is frequently
considerably greater than the one or two days usu-ably recommended for the treatment of diarrhea
and that the decrease in intestinal enzyme levels ismerely a temporary adaptive response to reduced
oral intake that rapidly reverses in response tofeeding. Indeed, studies in animals suggest that therenewed production of protein in the intestinal
epithelial cell following refeeding is rapid, occurringwithin a matter of hours.39 Pancreatic secretionsare a potent stimulus for intestinal mucosal hyper-
at Indonesia:AAP Sponsored on April 1, 2012pediatrics.aappublications.orgDownloaded from
enzyme secretion sufficient to maintain a near nor-ma! mucosa. The consequences of limited fastingmay not, therefore, have major importance on sub-
sequent intestinal function.A final argument for continued feeding during
diarrhea pertains to the breast-fed infant. Nipplestimulation and periodic emptying of the breast are
critical to ongoing milk secretion. Interruption ofnursing for several or, frequently, more days, espe-cially in the first several months of lactation, mayhave a long-term negative impact on the ability of
the mother to meet her infant’s nutrient needsthrough exclusive breast-feeding. Although expres-
sion of breast milk during the period that nursingis interrupted should help to maintain the milksupply, this practice may not always be successful.
STUDIES OF CONTINUED FEEDING DURINGACUTE DIARRHEA
Surprisingly, there are few studies that look spe-cifically at the common approach to nutritional
therapy of diarrhea, ie, fasting plus oral glucose-electrolyte solutions for 24 to 48 hours followed by
a gradual reintroduction of formula and other foodsover the subsequent two to five days. This approach
has evolved over many years and apparently works,at least in the United States, but has not been wellstudied in rigorous comparative trials. (Many work-ing outside the United States would contend that
the appallingly high rates of malnutrition second-ary to diarrhea are proof that this approach, whichis also commonly adopted in the less developedcountries, is less than optimal.) It cannot be as-
sumed that because current practice works another
approach might not be preferable even in cleanenvironments.
The early investigations of Chung (1948)42 arefrequently cited to support the fact that, despite
extensive malabsorption in diarrhea, a considerable
amount of nutrients can, nevertheless, be absorbed.Chung studied six infants admitted to Bellevue
Hospital with diarrhea, dehydration, and acidosisof varying degrees. Balance studies were carried out
during feeding of milk-based formulas providing 35to 45, 60 to 69, or 100 to 137 kcal/kg/d, assigned inrandom order. Balances of protein and fat were
generally positive throughout. Because of increasedstool output, however, five of six children required
from 38 to 258 mL/kg/d of intravenous fluids tomaintain hydration, a fact frequently overlooked.
In the same year, Chung and Viscorova43 com-pared the effects of full feeding (n = 60) and star-vation with gradual reintroduction of food (n = 55)
on the course of acute infantile diarrhea. The fedgroup received 40% more calories during the first
week than did the starved group. These investiga-
tors found no difference between the two regimenswith regard to duration of diarrhea. They did com-ment that stools were more frequent and volumi-
nous in the fed group. Unspecified, but assumedfrom Chung’s first paper and the practices of the
time, is the use of intravenous fluids to maintainhydration.
Since these early observations, additional studies
of feeding during diarrhea have been completed.
Mahalanabis44 gave reconstituted powdered milk tosix infants aged 12 to 24 months with cholera. The
diet was introduced between 24 and 48 hours afteradmission to the hospital. The resumption of milk
feedings was uniformly associated with a promptimprovement in nitrogen balance, and no increase
in stool output or systemic acidosis was observed.All of the patients, however, received significantlyless than their daily energy requirements during
the study period, ie, less than 50 kcal/kg/d duringmost of the study period. Thus, the effect of contin-
ued complete feeding during diarrhea was not eva!-uated in these patients. Furthermore, as the author
recognized, the apparently good results observed
with cholera, a relatively noninvasive pathogen,may not necessarily be applicable to other more
invasive infectious agents. They may be applicable,however, to other secretory diarrheas, such as that
caused by enterotoxigenic Escherichia coli, an or-ganism that accounts for approximately 25% ofdiarrheal episodes in young children in developing
countries.37 Differences in macronutrient absorp-
tion during the acute episode and the recoveryperiod have recently been documented between
children with rotavirus-caused diarrhea and thosewith diarrhea due to cholera.45
Rees and Brook’#{176}compared three feeding regi-mens in 46 British children between 6 weeks and 4
years of age with “mild” acute diarrhea of less than5 days’ duration and dehydration less than 5%. The
patients received either immediate feeding withfull-strength milk, glucose-electrolyte solution untildiarrhea improved followed by full-strength milk,
or glucose-electrolyte solution followed by gradual
reintroduction of increasing concentrations of milk
by “quarter-strength” increments every eight
hours.There was no difference among groups in theduration of hospitalization (range 3.2 to 3.6 days),
but there tended to be more vomiting among chil-dren receiving the more concentrated feedings. The
authors concluded that full-strength milk feedingscould be introduced rapidly in cases of uncompli-cated diarrhea. Inasmuch as their patients wereadmitted for study as long as four days after theillness began, however, the effect of truly immediatemilk feeding cannot be determined from their data.
A similar study was completed by Soeprapto et
at Indonesia:AAP Sponsored on April 1, 2012pediatrics.aappublications.orgDownloaded from
al’2 among Indonesian infants aged 4 to 24 months.
Unfortunately, the duration of diarrhea before hos-pitalization was not reported. Milk feedings wereintroduced immediately after oral or intravenousrehydration, and full intake was achieved during
the subsequent three days or nine days in the twostudy groups. Patients with fecal-reducing sub-
stances were treated with a low-lactose formula inplace of ordinary milk. No difference in the dura-
tion of diarrhea was observed despite the different
pace of reintroduction of milk.
In contrast to the above studies, Torres-Pinedo
et �J22 studied the metabolic consequences of milk
feeding during diarrhea in nine infants in PuertoRico. They encountered not only a dramatic in-crease in stool volumes associated with milk con-sumption but a simultaneous elevation in fecal acid
excretion and systemic acidosis. They postulatedthat the ingestion of carbohydrate was at least
partially responsible for the generation of metabolicacidosis during diarrhea, a hypothesis recently con-
firmed in a study of 12 children with rotavirus
infection.23 These findings are consistent with sev-eral other studies of the consequences of carbohy-
drate malabsorption during diarrhea.46’47It is difficult to explain the discrepancies in the
results of these studies. Factors that may determinethe patient’s response to diet include the duration
of diarrhea before the reintroduction of feeding, thenutrient load and osmolality presented to the intes-
tine, and the severity and etiology of diarrhea.
Information on severity and etiology, especially, israrely presented in the studies to date. Inasmuch
as the half-life of the intestinal mucosal cells isapproximately 36 hours, relatively rapid replace-
ment of injured mucosal cells is expected. Becauseof rapid migration from crypt to villus during repair,however, concentrations of peptidases and disac-
charidases will still be suboptimal at the villus tipfor a number of days. Relatively small differencesin the timing of reintroduction of feeding mighthave marked effects on the clinical outcome of
dietary therapy. The concentration and composi-tion of the diet are also important, because malab-
sorption is not absolute but depends on the ratiobetween the amount of nutrients presented to the
gut and the amount of available digestive enzymesand mucosal absorptive surface. Malabsorption canbe avoided, to some extent, by reducing the amountof nutrients presented to the small intestine perunit time, ie., by more frequent feeding of smaller
amounts.48 Known lactose malabsorbers, for ex-ample, benefit from milk supplementation whenthe milk is given in limited amounts and combinedwith other foods.49 Finally, the etiology of diarrhea
may be important because individual infectiousagents induce specific pathophysiologic changes.
Carbohydrate malabsorption is expectedly more
pronounced following rotavirus-caused diarrhea,for example, in which mucosal injury is marked,
than following diarrhea caused by enterotoxigenicE coli.50’5’ Conceivably, the results of previous stud-
ies have been unknowingly biased by a preponder-
ance of one or another specific etiologic agent.
CURRENT THERAPEUTIC RECOMMENDATIONS
Realizing the limited availability of pertinent,well-designed studies, it is difficult to make dietary
recommendations with complete confidence. Nev-ertheless, until a definite causal relation between
dietary therapy and chronic malabsorption can beestablished, the only aspects of early feeding duringdiarrhea that are proven to be potentially detrimen-tal are excess fluid loss and increased acidosis. Asthese complications are easily monitored clinically,it is possible to reintroduce foods immediately fol-lowing rehydration or to continue feeding when
there is no evidence of dehydration and to observe
the subsequent clinical course. With excessive fecal
losses leading to increasing dehydration, food canbe temporarily withdrawn. It is critical that themothers of ambulatory patients be taught to rec-ognize excessive stool losses and signs of dehydra-
tion. Once food has been withdrawn, there is nonecessity to resume feeding immediately; kwashi-orkor and marasmus do not develop in hours. How-
ever, there is also no justification for fasting morethan 24 to 48 hours in the majority of cases. The
failure to recognize starvation stools (small, fre-quently passed greenish mucous stools) for whatthey are, often results in unjustifiable continuation
of fasting while waiting for “diarrhea” to stop. Theappropriate response to starvation stools is in-creased food intake.
The WHO Programme for Control of Diarrhoea!Diseases has made fairly specific and generallyquite reasonable recommendations for feeding dur-
ing diarrhea.52 Once rehydration, if required, iscomplete, breast-feeding should be continued. It is
recommended that children who are fully weanedshould receive their usual diet, but that milk and
milk-based formulas should be diluted at least two-fold. (Others prefer to remove all milk for 24 to 36hours. Lactose-free formulas are often substituted.)Although it may appear illogical that consumptionof breast milk is recommended at normal levelswhile dilution of cow milk is encouraged, clinical
experience suggests that breast milk is generallywell tolerated.53 Quantitative studies of the absorp-tion of breast milk by babies with diarrhea would
provide a valuable addition to our knowledge.
Consumption of complementary foods shouldalso be encouraged for those children more than 3
at Indonesia:AAP Sponsored on April 1, 2012pediatrics.aappublications.orgDownloaded from
months of age who cannot satisfy their energyrequirement by exclusive breast-feeding. We have
shown that wheat noodles are well tolerated anddigested during recovery from acute diarrhea.54Similar experience has been found with rice in
Bangladesh.55 Whether the same holds true forother major staples, particularly the legumes, has
not been documented and calls for caution in their
use. Solid food should have the additional advan-
tage in the breast-fed or milk-based formula-fedinfant of slowing gastric emptying, thereby reduc-ing the amount of lactose in the small intestine perunit tiltie. More frequent, smaller feedings wouldhave the same beneficial effect on lactose digestion
and absorption. Generally, the child should deter-mine the amount of food to be consunied. Foodshould not be forced upon unwilling, anorectic in-
lants, but food should be offered to the hungryinfant despite ongoing diarrhea. Once diarrhea sub-sides, extra food should be made available to enablerecovery of any nutritional deficit imposed by the
acute illness.Clearly, there is a great need for additional stud-
ses of the quantitative relationships among feeding
during diarrhea of defined etiologies, recovery fromthe acute illness, and the nutritional outcome.Eventually, specific recommendations may dependon the age and nutritional status of the child, the
habitual feeding practices, the type and severity of
diarrhea, the site of initiation of therapy (ie, inpa-
tient V outpatient), and the financial resources ofthe himily or institution in question. Studies ad-
dressing some of these issues are currently in prog-ress and should add to our understanding of the
correct nutritional therapy for childhood diarihea.
REFERENCES
I, Martorell R. Habicht JP, Yarbrough C, et a!: Acute morbid-ity and physical growth in Guatemalan children. Am J Dis
(‘htld19i5;129:1296 1299
2. Rowland MGM, Cole TJ, Whitehead RG: A quantitative
study into the role of infection in deterniining nutritional
status in Gambian village children. Br J Nutr 1977:37:441-
45()3. Brown KH, Black RD: The nutritional cost of’ infections, in
� of the XII International Nutrttion Con�res�,, San
Diego, 1952
4. Cushing AH, Anderson L: Diarrhea in breast-fed and non-breast -ted infants. Pediatrics 1982;70:92 1
5. Mata L�J, Krumal RA, Urrutia JJ, et a!: Effect of infectionon food intake and the nutritional state: Perspective as
viewed from the ‘� illage. Am J Clin Nut,- 1977;30:1215- 1227
6. Marturell R. Yarbrough C, Yarbrough S, et al. The impact
of ordiiiary illnesst.s ‘ it the dietary intakes of malnourished
children Am .J (,‘j� tVutr 19811,33:345-3#{244}0
7. Suzker SA. Moila AM, Karim AKMM. et al: Calorie intake
in childhood diarhea. Nutr Rept mt 1982;26.581 590
and its significance in infantile diairhea. Pediatr Res
1973� 7:161-168
22 Torres-Pinedo R, Lavastida M, Rivera CL: Studies on infant
diarrhea: I. A comparison of the effects of milk feeding and
intravenous therapy upon the composition and volume of
the stool and urine. J Clin invest 1966;45:469-480
23. Sack DA, Rhoads M, Molla A, et a!: Carbohydrate malab-sorption in infants with rotavirus diarrhea. Am J Clin Nutr1982;36:1112- 1118
24 Pergolizzi R, Lifshitz F, Teichberg 5, et al: Interaction
between dietary carbohydrates and intestinal disacchari-
dases in experimental diarrhea. Am J Clin Nutr1977;30:482 -489
25. Nasrallah SM, Margolis S Iber FL: Fat and glucose mal-
absorption after hypertonic mannitol. Johns Hopkins Med
J 1970:127:38-41
26. Case GL, Phillips RW, Lewis LD, et al: Effects of osniolality
of liquid nutrient diets on meal passage and nutrient ab-sorption in Yucatan miniature swine. Am J Clin Nutr1981;34:1s68- 1878
27. Case GL, Lewis LD, Phillips RW, et al: Effects of osmolalityof liquid nutrient diets on plasma equilibration of water andcarbohydrate in Yucatan miniature swine. Am J Clin Nutr1981;34:1861-1867
33. Walker-Smith JA: Cow’s milk intolerance as a cause of post-enteritis diarrhea. J Pediatr Gastroenterol Nutr 1982;1:163-173
34. Weber AM, Roy CC, Morin CL, et al: Malabsorption of bileacids in children with cystic fibrosis. N Engi J Med1973;289:1001-1005
35. Snyder JD: The magnitude of the global problem of acutediarrhoeal disease: A review of active surveillance data. Buil
WHO 1982;60:605-61336. Black RE, Brown KH, Becker 5, et al: Longitudinal studies
of infectious diseases and physical growth of children in
rural Bangladesh: I. Patterns of morbidity. Am J Epidemiol1982;115:305-314
37. Black RE, Brown KH, Becker S, et al: Longitudinal studiesof infectious diseases and physical growth of children in
rural Bangladesh: II. Incidence of diarrhea and association
with known pathogens. Am J Epidemiol 1982;115:315-32438. Knudsen KH, Bradley EM, Lecocq FR, et al: Effect of
fasting and refeeding on the histology and disaccharidaseactivity of the human intestine. Gastroenterology 1968;
55:46-5139. Hagemann RF, Strogand JJ: Fasting and refeeding: Cell
kinetic response of jejunum, ileum, and colon. Cell Tissue
Kinet 1977;10:3-1440. Williamson RCN: Intestinal adaptation: I. Structural, func-
tional and cytokinetic changes. N Engi J Med 1978;298:1393-1402
41. Williamson RCN: Intestinal adaptation: II. Mechanisms ofcontrol. N Engi J Med 1978;298:1444-1450
42. Chung AW: The effect of oral feeding at different levels onthe absorption of foodstuffs in infantile diarrhea. J Pediatr1948;33:1-13
43. Chung AW, Viscorova B: The effect of early oral feedingversus early oral starvation on the course of infantile diar-rhea. J Pediatr 1948;33:14-22
44. Mahalanabis D: Nitrogen balance during recovery from se-cretory diarrhea of cholera in children. Am J Clin Nutr
1981;34:1548-155145. Molla A, Molla AM, Rahim A, et a!: Intake and absorption
of nutrients in children with cholera and rotavirus infectionduring acute diarrhea and after recovery. Nutr Res1982;2:233-242
46. Lifshitz F, Coello-Ramirez P, Guiterrez Topete G, et al:Carbohydrate intolerance in infants with diarrhea. J Pediatr1971;79:760-767
47. Sutton RE, Hamilton JR: Tolerance of young children with
severe gastroenteritis to dietary lactose. Can Med Assoc J1968;99:980-982
48. Parker P, Stroop 5, Greene H: A controlled comparison of
continuous versus intermittent feeding in the treatment ofinfants with intestinal disease. J Pediatr 1981;99:360-364
49. Brown KH, Khatun M, Parry L, et al: Nutritional conse-quences of low dose milk supplements consumed by lactosemalabsorbing children. Am J Clin Nutr 1980;33:1054-1063
50. Sack DA, Chowdhury AMAK, Eusof A, et al: Oral rehydra-
tion in rotavirus diarrhea: A double blind comparison of
sucrose with glucose electrolyte solution. Lancet 1978;2:280-
283.
51. Sack DA, Islam S, Brown KH, et al: Oral therapy in children
with cholera: A comparison of sucrose and glucose electro-lyte solutions. J Pediatr 1980;96:20-25
52. A Manual for the Treatment ofAcute Diarrhea: Programme
for Control of Diarrhoeal Diseases, World Health Organiza-tion publication No. WHO/CDD/SER/80.2. Geneva
53. Finberg L, Harper PA, Harrison HE, et al: Oral rehydrationfor diarrhea. J Pediatr 1982;101:497-499
54. Brown KH, Lopez de Roma#{241}aG, Graham GG, et al: Expe-rience with a mixture of wheat-noodles and casein in theinitial dietary therapy of infants and young children with
protein-calorie malnutrition or acute diarrhea. J Hum Nutr1982;36A:354-366
55. Molla AM, Hossain M, Sarker SA, et al: Rice-powder elec-trolyte solution as oral therapy in diarrhoea due to Vibriocholerae and Escherichia coli. Lancet 1982;1:1317-1319
at Indonesia:AAP Sponsored on April 1, 2012pediatrics.aappublications.orgDownloaded from
This article has been cited by 3 HighWire-hosted articles:
Permissions & Licensing
http://pediatrics.aappublications.org/site/misc/Permissions.xhtmlor in its entirety can be found online at: Information about reproducing this article in parts (figures, tables)
