Lower Gastrointestinal Bleeding Gary Silber Pediatrics in ......to test positive for blood (Table 2). In the majority of hospitals, guaiac, ben-zidine, or benzidine derivative test

DOI: 10.1542/pir.12-3-851990;12;85Pediatrics in Review

Gary SilberLower Gastrointestinal Bleeding

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The questions below should helpfocus the reading of this article.

1. What are causes of false positiveor false negative test results for bloodin stools?

2. Which conditions are most com-monly associated with lower intes-tinal bleeding in different agegroups?

3. What are the clinically significantfeatures of juvenile intestinal polyps?

4. Which conditions are most likely tocause major lower gastrointestinalbleeding?

EDUCATIONAL OBJECTiVES

4. The pediatrician should haveknowledge to make an appropriateevaluation of a 12-year-old boywith lower abdominal crampingpain and bloody stools, differen-tiating among infectious colitis,lower gastrointestinal bleeding, in-flammatory bowel disease (ulcer-

ative colitis, Crohn disease),Meckel diverticulum, hemolytic-uremic syndrome, bleeding disor-ders (von Willebrand disease, ce’Ion telanglectasla, Idiopathicthrombocytopenic purpura), is-chemic colitis, Henoch-Schoenleinnephritis, antibiotic-induced colitis,and colonic polyposis, and developa plan for management. (Topics,90/91)6. The pediatrician should haveknowledge to make an appropriateevaluation of a 20-day-old infantwith bright red blood In his stools,differentiating among anal fissure,infectious colitis, cow milk or soyprotein allergy, necrotizing enter-ocolftis, intussusception, Meckeldiverticulum, child abuse, volvulus,duplication cyst, and Hlrschsprungdisease with enterocolftis, and de-velop a plan for management.(Topics, 90/91)

“Pediatric Gastroenterologist, Phoenix Chil-

dren ‘s Hospital, Phoenix, Arizona.

pediatrics in review #{149}vol. 12 no. 3 september 1990 PIR 85

Lower Gastrointestinal BleedingGary Silber, MD*

IS IT REALLY BLOOD?

Finding blood in the stool of aninfant or child can be very alarming toparents. Fortunately, it is not neces-sarily a sign of serious illness. Thespectrum of disease to be consideredin the case of infants and children ismarkedly different from that of adults.Rarely does lower gastrointestinalbleeding portend malignancy.

During the past 25 years, our abilityto identify the source of a patient’sbleeding has improved markedly.Previously, 20% to 50% of infantsand children with blood in their stoolsremained undiagnosed. Today, weare able to diagnose or at least local-ize the bleeding site in over 90% ofcases.

The differential diagnosis of lowergastrointestinal bleeding is extensive,but can be greatly facilitated by takinginto account the patient’s age (Table1). Furthermore, the character of thebleeding, the volume of blood lost,and the absence or presence of as-sociated symptoms can also aid inidentifying both the cause and thediagnostic work-up needed. This pa-per focuses only on lower gastroin-testinal sources of bleeding. Discus-sion of other causes, such as gastn-tis, esophagitis, peptic ulcer disease,and esophageal varices, should besought elsewhere.

Before beginning an expensive andpossibly invasive work-up, confirma-tion that blood is being passed andan attempt to categorize the source,if possible, as the upper or lowerintestinal tract should be made.

Blood in the stool can vary in ap-pearance from bright red to tarryblack. Hematochezia is the passageof bright red blood, and melena refersto the passage of dark tarry stools.Certain foods and medicines maycause the stool to appear bloody orto test positive for blood (Table 2). Inthe majority of hospitals, guaiac, ben-zidine, or benzidine derivative testpads (Hemocult or Hemotest) areused to detect blood. These tests usea hydrogen peroxide developer andare based on the peroxidase activityof hemoglobin and its derivatives, in-cluding oxyhemoglobin, reduced he-moglobin, methemoglobin, and car-boxyhemoglobin. In the presence ofhydrogen peroxide, these sub-stances catalytically oxidize sub-strates such as guaiac or benzidine.This oxidation produces a colorchange in the substrate, thereby in-dicating a positive reaction.

Even though this test is the basisfor our determination of blood in thestool, there are other problems withit. The amount of blood required toyield a positive reaction varies as aresult of differences in fecal hydra-tion, hemoglobin degradation, andthe presence of certain substancesthat inhibit the oxidation of the mdi-cator dye. False negative results canbe obtained if the patient is ingestinglarge doses of ascorbic acid or if in-testinal bacteria have degraded thehemoglobin to porphyrin. False posi-tive results can be obtained if thepatient has eaten rare red meat orperoxidase-containing fruits and veg-etables, such as broccoli, radishes,cauliflower, cantaloupe, or turnips.

Hemoquant is a test being mar-keted that appears to be more sen-sitive than other available testingmethods. This test is an assay basedon heme-derived porphyrin, and itquantifies both total fecal hemoglobinand that fraction of hemoglobin that

has been converted to porphyrin byintestinal flora. Its use is dictated bycost and the need for exactitude.

UPPER VS LOWERGASTROINTESTINAL TRACTBLEEDING

Once it has been established thata child has experienced intestinalbleeding, localization of the bleedingsite as in the upper or lower gastroin-testinal tract is important. Bright redblood that coats but is not mixed withthe stool is most likely to indicatebleeding from the anorectal area.Blood that is darker in color or moreintimately mixed with the feces indi-cates a bleeding site higher in theintestinal tract. Black tarry stools aregenerally indicative of bleeding sites







TABLE 3. Criteria for Diagnosisof Protein Sensitivity*

1. Symptoms subside after elimi-

nation of milk from diet.

2. Reoccurrence after a trial feed-

ing of milk within 48 h.

3. Results of three challenges areconsistently positive and simi-lar.

4. Symptoms subside after eachchallenge.

* Developed by Goldman.

Lower Gastrointestinal Bleeding

PIR 88 pediatrics in review #{149}vol. 12 no. 3 september 1990

first 24 to 48 hours of life. Commonsymptoms in those patients with en-terocolitis include abdominal disten-tion, diarrhea, and fever. Only onequarter of the patients have blood intheir stools.

Historically, the barium enema (Fig2) has been used to screen forHirschprung disease. However, thisstudy can be misleading, especially innewborns, because marked dilatationproximal to the aganglionic segmentmay not have had time to develop.Today, many institutions are usingrectal motility studies to determinewhich patients need further study.The definitive diagnosis is made byrectal biopsy showing the completeabsence of ganglion cells in the Meis-sner and the Auerbach plexus. His-tochemical staining for acetylcholin-esterase activity has been reportedto be beneficial in diagnosis.

The treatment of Hirschprung dis-ease usually involves surgical correc-tion. In most cases, a diverting cobs-tomy is created followed by a secondstage intestinal pull-through tech-nique of fully innervated intestine.

Finally, another cause of rectalbleeding in this age group is a coag-ubopathy. This can be the result ofinfection, platelet dysfunction or vita-mm K deficiency. With this problemone may also see petechiae, or ec-chymotic areas on the newborn.

One Month To Two Years of Age

In this age group, both very benignand very serious lesions may be as-sociated with lower gastrointestinalbleeding. These range from anal fis-sures and lymphonodular hyperplasiato intussusception and Meckel diver-ticulum. Furthermore, one should notforget that, except for necrotizing en-terocolitis, congenital diseases (es-pecially Hirschprung disease) need tobe considered.

Anal fissures are the most commoncause of lower gastrointestinal bleed-ing, although statistics concerningthe actual incidence of the conditionare difficult to obtain, because mostcases go unreported. One group ofresearchers reported that 17% of allchildren with gastrointestinal bleed-ing studies had a fissure, the vastmajority of whom were less than 1

year of age. In most cases, fissuresare secondary to constipation. Con-stipation may result following thepassage of a large firm stool thatcauses a superficial tear of the squa-mous cell-lined anal canal. Becausethis area is extremely sensitive, thepatient experiences more pain witheach bowel movement. The childreacts by withholding stool, therebyincreasing constipation and pain andinitiating a vicious cycle. Diagnosis ismade on the basis of the patient’shistory and inspection of the analcanal, especially its posterior aspect.Treatment usually consists of stoolsofteners and warm sitz baths. Inmore severe cases, topical analgesicointments may be used; however, ahigh incidence of sensitization shouldpreclude general or chronic use.

The pediatrician should alwaysalso keep in mind that anal fissures,regardless of the age group and es-pecially in boys, may be the result ofsexual abuse. Careful questioningshould be done to rule out this pos-sibility. Internal examination may berequired.

Milk- or soy-induced enterocolitisusually occurs during the first monthof life or shortly thereafter. The prey-alence of this condition has been re-ported to be between 0.2% and7.5%, with one group in England re-porting it as the most common causeof infantile colitis. Enterocolitis canalso develop in the breast-fed baby.

Manifestations may be acute or in-sidious. Acute manifestations includevomiting and diarrhea, possiblystained with blood. These symptomscommonly develop 12 to 48 hoursafter the introduction of formula.More insidious symptoms include ab-dominal pain, persistent diarrhea ofmoderate severity, blood in thestools, and failure to thrive.

The diagnosis of this condition isclinical, based on a dietary oral-elimi-nation challenge test. Laboratorytests are usually not helpful. Proctos-copy or small bowel biopsy may bebeneficial. Hematochezia is usuallyassociated with frank colitis. Grossly,the cobonic mucosae can appear ery-thematous and friable; microscopi-cally, infiltrates of polymorphonuclearcells, plasma cells, and eosinophilscan be seen in the lamina propria.Goldman set up criteria to make this

diagnosis, consisting of three con-secutive challenge tests (Table 3).However, because it is very difficultto get parents to agree to repeattesting, many clinicians use only onechallenge.

Treatment for protein sensitivityusually consists of placing the infanton a casein-hydrolysate formula. Inunusual cases, the introduction ofsolids may result in other sensitivityreactions and so should be under-taken with caution. Cow milk and soyprotein sensitivity usually resolves by2 years of age, at which time the childcan be placed on a totally nonrestric-tive diet.

During late infancy, intussuscep-tion, Meckel diverticulum, and (lesscommonly) duplications of the smallintestine need to be considered ascauses of low gastrointestinal bleed-ing.

Idiopathic intussusception may oc-cur in children 3 months to 3 years ofage and usually occurs in patients 4to 10 months of age, with 65% ofcases occurring before 1 year of ageand 80% by 2 years of age. Thecause of idiopathic intussusception isunknown. The vast majority of casesoccurs in the region of the ileocecalvalve, and no lead point can be iden-tified. In an older child, a lead point-such as a polyp, Meckel diverticulum,or a hypertrophied lymphoid patch-is more likely to be found. Lympho-sarcoma must also be considered inpatients who experience symptomsafter the age of 6 years.

Typically, intussusception is indi-cated when healthy, well-nourishedinfants are awakened from sleep by



Fig 3. lntussusception. Barium enema show-ing coiled spring appearance of intestine onevacuation.

Fig 4. Lymphonodular hyperplasia of colon.Multiple 1-mm to 4-mm raised nodules.

GASTROENTEROLOGY


severe abdominal pain. They willdraw up their legs and subsequentlyvomit. They may then pass a normalstool and show marked improve-ment. Shortly thereafter, however,pain reappears that lasts a couple ofminutes and recurs at regular inter-vals. Eventually, the infants will be-come pale, apathetic, and diaphor-etic, and may pass stools mixed withblood and mucus. These stools maybe currant jelly in color because ofthis mixture; however, this is not aconsistent finding. Hematocheziamay not occur if symptoms havebeen present less than 12 hours. Inmany cases, physical examinationmay help to determine that a sau-sage-shaped abdominal mass can bepalpated on the right side. Plain radio-graphs may show evidence of ob-struction, but they are relatively in-sensitive early in the course of thiscondition. Diagnosis is confirmed bybarium enema, which may also betherapeutic (Fig 3).

In fact, barium enema examinationdelivering hydrostatic pressure mayresolve the episode entirely. Studiesindicate that this is successful in 75%of cases. If this approach fails, lapa-rotomy is warranted. Recently, stud-ies from Japan have shown good re-sults with air reduction of intussus-ception, and this technique is now

being used in the United States on alimited basis. Additionally, a recentreport details the use of normal salinehydrostatic enema.

Meckel diverticulum may be foundin this age group as well as in thepreschool child with either intermit-tent bleeding or massive gastrointes-tinal bleeding. Meckel diverticulum isthe result of incomplete obliterationof the omphabomesenteric duct, andit is usually located within 100 cm ofthe ileocecal valve. This conditionmay be totally asymptomatic orcause complications, such as hem-orrhage or intestinal obstruction. Inthose patients having complications,60% are less than 2 years of age andmore than 30% are less than 1 yearof age.

In most cases, the cause of bleed-ing is ectopic gastric mucosae withinthe diverticulum. Acid productionhere causes ulceration opposite oradjacent to the orifice of the divertic-ulum. The bleeding is usually painlessand can vary from being minimal re-current episodes of hematochezia toa massive shock-producing hemor-rhage. The diverticulum can be con-firmed by performing a 99m techne-tium pertechnetate or Meckel scan, astudy based on the affinity of theradioisotope for gastric mucosae.The accuracy of this study can beimproved if the infant is given H-2histamine antagonists for 24 to 48hours before the test. False positiveresults have been reported in patientswith intussusception, hydrone-phrosis, arteriovenous malforma-tions, and inflammatory bowel dis-ease. At times, an exploratory lapa-rotomy may be the only way toconfirm a suspected Meckel divertic-ulum.

All symptomatic Meckel diverticulishould be excised surgically. Be-cause bleeding usually stops spon-taneously, patients with massivehemorrhage can be stabilized beforesurgery.

Duplications of the small intestineare uncommon, but they can causelower gastrointestinal bleeding. Suchduplications are usually found in theileum as long tubular crypts that givean appearance of doubling over ofthe intestine. They usually connectwith the bowel at their distal end andmay contain gastric mucosae, caus-

ing peptic ulceration of the intestineand subsequent bleeding. Treatmentis surgical resection of the affectedsegment.

Lymphonodular hyperplasia of thecolon is a benign lesion seen in thisage group and in preschool children.Controversy exists as to whether ornot rectal bleeding should be attrib-uted to this condition. Infants andchildren with this condition areasymptomatic except that blood,bright red in color, is present in mul-tiple stools. Blood loss is usually mm-imal and only rarely will be associatedwith anemia. Diagnosis of lymphon-odular hyperplasia is made by sig-moidoscopy (Fig 4) or by air contrastradiography, although radiographicappearance can be misinterpreted asminute mucosal ulcerations. There isno treatment for this problem, butit usually resolves spontaneouslywithin 3 months.

Preschool (2 to 5 Years of Age)Period

Although the preschool child posesa specific set of diagnostic consider-ations, there is a fair amount of over-lap between this age group and thatof the infant.

The two conditions most likely tocause bleeding in this age group arejuvenile polyps and infectious enter-ocolitis.

Numerous infectious agents causeblood in the stool, usually in associ-ation with diarrhea (Table 4). Viralagents generally do not cause overtblood losses in the stool. Althoughdifferent organisms vary in clinical



TABLE 4. Infectious Agents

Associated With Hematochezia

SalmonellaShigellaCampy!obacterjejuniYersinea enterocoilticaEnterohemorrhagic Escherichia

coilEnteroinvasive Escherichia coilClostridium difficileAeromonas hydrophilaEntamoeba histolytica



manifestation (Table 5), a stool cul-ture typically is needed to identify theoffending organism. Several orga-nisms merit discussion.

Clostridium diffidile is a bacteriathat causes pseudomembranous co-litis in association with the use of anumber of antibiotics (Table 6). Thepathogenesis of pseudomembranouscolitis is thought to be secondary tothe proliferation of the clostridia or-ganism during the course of antibiotictreatment. Antibiotics decrease nor-mal bowel flora, allowing the cbostri-dia to predominate. Consequently,the quantity of toxin produced bycbostridia increases, inciting a cobonicmucosal reaction termed pseudo-membranous colitis. Clinical symp-toms from pseudomembranous coli-tis can occur either during antibiotictreatment or 1 to 3 weeks after treat-ment has ceased. Patients commonlyhave watery diarrhea with blood andmucus, and may experience feverand abdominal pain. Diagnosis re-quires demonstration of the cbostridiatoxin in stool; simply verifying thepresence of C diffidile does not con-firm the diagnosis of pseudomem-branous colitis. Special caution is re-quired regarding diagnosis in infancy.One study has demonstrated that30% of infants up to 3 months of ageand 10% of infants up to 2 years ofage may carry the organism, as wellas its toxin, but be totally asympto-matic. Proctoscopy or sigmoidos-copy also can be helpful in diagnosis(Fig 5). Grossly, whitish-yellow ele-vated plaques appear on the wall ofthe cobonic mucosae. Microscopi-cally, an intense inflammatory reac-tion with polymorphonuclear cells, fi-brim, and cellular debris replacing thelamina propria occurs.

The first approach to treatment isthe cessation of the offending antibi-otic. Oral vancomycin and metroni-dazole both have also been used ef-fectively in the treatment of pseudo-membranous colitis. There is,however, a relatively high recurrencerate of up to 20%.

Entamoeba histolytica is a water-borne protozoan parasite that alsocan cause bloody diarrhea. The mci-dence rate for infection by this orga-nism is highest on Indian reservationsand in lower socioeconomic areas ofthe south central and southwesternUnited States. In up to 1 0% of thepopulation, infection is asympto-matic, which is especially importantgiven that humans are the only res-ervoirs for this parasite and thattransmission is by the fecal to oralroute through hands, food, or water.

Clinical symptoms of an amoebicinfection include abdominal pain andacute diarrhea with blood and mucusin the stools. Complications second-ary to amoebic infection include intes-tinal perforation and liver abscesses.Examination of the stool for ova andparasites will not always yield an or-ganism because microscopic exami-nation may miss the cysts or tropho-zoites. Amoebic serology can be ben-eficial, however; up to 90% of thosepatients with amoebic colitis havepositive serology. Treatment for thisorganism involves using two antibi-otics, metronidazole and iodoquinol.

Aeromonas hydrophila has alsobeen implicated recently in gastroin-testinal bleeding. This organism ismore commonly found during thewarm weather months and survivesin both fresh and salt water. Threemain patterns of illness are seen withinfection by this organism. In the ma-jority of cases, individuals developwatery diarrhea without blood thatresolves after 1 week. About 25% ofthose infected with A hydrophila de-velop diarrhea with blood and mucusthat can last up to 1 month. Finally, athird group of patients experiencesymptoms for as long as 3 months,requiring physicians to consider in-flammatory bowel disease in the dif-ferential diagnosis.

The mechanism of action of theenterotoxin produced by A hydro-phila is unknown. Diagnosis is madeby stool culture on special media not

commonly used in most microbiologylaboratories. Because this is a self-limited disease, antibiotics usually arenot used. However, in those childrenwith a malignancy or liver disease,therapy should be considered withTMP-SMX.

Painless rectal bleeding in an oth-erwise healthy preschool child shouldimmediately arouse suspicion of a ju-venile polyp. Polyps are seen mainlyin children 2 to 8 years of age, with apeak incidence occurring at 3 to 4years of age; polyps rarely occur be-fore 1 year of age or during adoles-cence. Juvenile polyps account for90% of all polyps found in childrenand carry no malignant potential. Theaverage polyp (Fig 6) is about 1 cmin diameter, has a thin stalk (or apedicle) covered by normal cobonicmucosae, and may be ulcerated. Pre-viously, it was thought that 85% ofthese lesions were found in the rec-tosigmoid colon and the remainder inthe proximal colon; as many as 75%of the polyps were believed to besolitary. However, more recent databased on cobonoscopy indicate thatthe frequency of multiple polyps maybe as high as 60%, and as many as25% of polyps may be located prox-imal to the transverse colon.

Children with juvenile polyps willusually have minimal rectal bleeding,with streaks of fresh blood on theoutside of the stool. Less frequently,a child will experience profuse bloodloss or a chronic iron deficiency fromoccult blood loss. There may besome associated abdominal pain sec-ondary to traction on the polyp. Thepolyp may protrude or prolapse atthe anus if it is rectal in location andcan be felt by digital exam. Manyautoamputate before treatment. Di-agnostically, an air contrast bariumenema, performed after a completecleaning of the colon using a bal-anced electrolyte solution, may aidin establishing the definitive diagno-sis. However, if a pediatric gastroen-terobogist is available, cobonoscopy isbecoming the procedure of choice.Currently, treatment of juvenilepolyps consists of full colonoscopywith endoscopic polypectomy. In thehands of a trained pediatric gastroen-terobogist or surgeon, this procedurecan be performed safely using seda-tion in the outpatient setting.



TABLE 5. Organisms Associated With Gastrointestinal Bleeding

Shigella

Campylobacterje-

juni

Yersinia enterocoli-tis

EnteroinvasiveEscherichia coil

EnterohemorrhagicEscherichia coil

Fever None unless bacter-Diarrhea emic, immune-Abdominal pain Large inoculum required compromised or

<6 months ofage

Fever Secondary to mucosal Person-to-person YesVomiting invasion Small inoculum (1 0 orga-Diarrhea nisms)

Fever Can be seen in infants Contained in water, milk, YesDiarrhea <7 wk of age meat, and poultryAbdominal pain Person-to-person trans-

missionSmall inoculum (100 or-

ganisms)

Fever Up to 25% of cases Milk Not establishedDiarrheaAbdominal painMay mimic acute

appendicitis

Fever Yes Food or water SymptomaticVomiting Large inoculum neededDiarrhea

Diarrhea May be cause of 30% of Diarrhea SymptomaticAbdominal pain undiagnosed casesFever (rare) Self-limited

Bloody

TABLE 6. Antibiotics AssociatedWith the Occurrence ofPseudomembranous Colitis

ClindamycinLincomycinAmpicillinPenicillinTetracyclineChboramphenicolCarbenicillinOxacillin

DicloxacillinCephabothinCephabondineCefazolinCephalexinCephradineStreptomycmnNovobiocin

Fig 5. Pseudomembranous colitis. Whitish-yellow raised plaques on colonic mucosae.

GASTROENTEROLOGY


Symptoms Blood in Stool Transmission Antibiotic Treatment

Salmonella Up to 10% gross blood Food or drink

Several polyposis syndromes havebeen observed during infancy andchildhood of which pediatricians needbe aware, because treatment strate-gies differ for each.

Hematochezia may be found oninitial examination in the case of sev-eral multisystem diseases, includinghemolytic uremic syndrome, which isthe most prevalent of these condi-tions reported in infants and childrenup to 3 years of age. Thus, a gas-trointestinal manifestation may delay

the diagnosis until renal or hemato-logic abnormalities are recognized.The intestinal manifestations are usu-ally self-limiting and rarely result inmajor morbidity.

In the case of Henoch-Schoenleinpurpura, gastrointestinal manifesta-tions occur in 50% of cases and in-dude colicky abdominal pain, melena,or bloody diarrhea. These symptomsmay precede the characteristic rashin 20% of cases, often delaying theestablishment of the diagnosis. Gas-trointestinal complications related toHenoch-Schoenlein purpura includeacute gastrointestinal hemorrhage(5%) and intussusception (3%). Phy-sicians differ concerning the use ofcorticosteroids to alleviate these gas-trointestinal problems. However, a re-cent study indicated that these prob-lems were self-limiting and did notjustify the use of steroids.

School-Aged Children

For the most part, the diagnosticconsiderations relevant to the pre-

school child also apply to the school-aged child, with the single addition ofinflammatory bowel disease. Thistopic was recently reviewed in thispublication (Pediatrics in Review1 987;8) and so will not be discussedin great detail here.

The most common symptom of in-flammatory bowel disease is diarrhea



Fig 6. Juvenile polyp of colon. 0.5 mm = 1.0mm.



with or without blood. This is an initialfinding in 80% of patients with Crohndisease and in all patients with ulcer-ative colitis. In some cases, extrain-testinal manifestations (such asweight loss, anorexia, or arthralgias)may predominate. It is necessary todistinguish between ulcerative colitisand acute self-limited colitis, whichcan usually be accomplished by per-forming cobonoscopy and evaluatingbiopsy specimens and cultures.

Evaluation and Management

Initially, for a patient with sus-pected gastrointestinal bleeding, anassessment of cardiovascular statusand the degree of blood loss must bemade to allow stabilization of the pa-tient before consideration of amy di-agnostic work-up. Vital signs, espe-cially heart rate and blood pressuremust be monitored continually, es-pecially if blood loss is ongoing. Theestablishment of venous access andfluid resuscitation is mandatory, par-ticularly if tachycardia or hypotensionis present. Initial laboratory studies ofthe blood should include a completeblood cell and platelet count, a retic-ulocyte count, a prothrombin and par-tial prothromboplastin time, typingand cross-typing of the blood, and adirect Coombs test.

Hospital admission is dependenton the clinical condition of the patient.If massive bleeding has occurred, thechild should be hospitalized. In caseswith intermittent or minor bleedingupon admission, it is not necessary.Many tests, including cultures, radio-

logic and nuclear medicine scans, aswell as sigmoidoscopy or colonos-copy, can be performed on an out-patient basis.

SUMMARY

The differential diagnosis of lowergastrointestinal bleeding in childrencan be reduced markedly simply bytaking into account the age of thechild. The clinical condition of the pa-tient can further help narrow the di-agnostic possibilities. Newborns andinfants who are clinically unstable aremore likely to have diseases such asnecrotizing enterocolitis, volvulus,Hirschprung disease, intussuscep-tion, or Meckel diverticulum. A babywho appears healthy should be ex-amined for swallowed blood, allergiccolitis, anal fissures, or lymphomodu-bar hyperplasia. An older child ofhealthy appearance with bleeding islikely to have a juvenile polyp or in-fectious colitis, but a child who ap-

pears sick may have hemolyticuremic syndrome, Henoch-Schoen-lein purpura, or inflammatory boweldisease. This information, along withthat gleaned from the physical ex-amination, can lead the pediatricianto determine the need for specifictests, such as abdominal radio-graphs, stool cultures, and am endo-scopic evaluation.

We have come a long way in ourability to diagnose the causes oflower gastrointestinal bleeding. Withthe availability of newer radiographicand nuclear medicine modalities andthe ability to visualize the colon en-doscopically, the need for exploratorylaparotomy for diagnosis is rarer.While surgery may still be the therapyof choice, new diagnostic modalitiesgive the surgeon much more preop-erative information.

ACKNOWLEDGMENTS

The author wishes to thank Dr RoxanneHecht for her helpful advice and criticism inreviewing the manuscript and Stephanie Havellfor assisting in preparing the manuscript.

SUGGESTED READING

Andrassy RJ, Mahour H. Malrotation of themidgut in infants and children. Arch Surg.1981 116:158-1 60

Bishop W, Ulsher M. Bacterial gastroenteritis.Ped Clin North Am. 1988;34:69

Bruce J, Hieh YS, Gooney DR, et aI. Intussus-ception: evolution of current management. JPediatr Gastroenterol Nutr. 1987;6:663-674

Cynamon H, Milov D, Andres J. Diagnosis andmanagement of colonic polyps in children. JPediatr. 1989;1 14:593-596

Jenkins HA, Pincott JR. Soothill JF, MilIa PJ,Harries JT. Food allergy: the major cause ofinfantile colitis. Arch Dis Child. 1984;59:326-329

Kaplan B, Benson J, Rothstein F, Dahms B,Halpin T. Lymphonodular hyperplasia of thecolon as a pathologic finding in children withlower gastrointestinal bleeding. J PediatrGastroenterol Nutr. 1984:3:704-708

Kleinhaus S. Boley SJ, Sheran M, Sieber W.Hirschprung’s disease, a survey of the mem-bers of the Surgical Section of the AmericanAcademy of Pediatrics. J Pediatr Surg.1979;1 4:588-597

Kliegmien AM, Fanaroff A. Necrotizing entero-colitis. NEnglJMed. 1984;310:1093-1103

Lake A. Recognition and management of in-flammatory bowel disease in children andadolescents. Curr Probl Pediatr.1988;1 8:377-437

Lake A, Whittington P, Hamilton S. Dietaryprotein-induced colitis in breast-fed infants.J Pediatr. 1982;101 :906-910

Martin L, Torres M. Hirschprung’s disease.Surg Clin North Am. 1985;65:1 171-1180

Powell G. Milk and soy induced enterocolitis ofinfancy. J Pediatr. 1978;93:553-560

Santulh T, Schullinger J. Polypoid disease ofthe gastrointestinal tract. In: Welch K, Ran-dolph JG, Aavitch MM, et aI, eds. PediatricSurgery. 4th ed. Year Book Medical Publish-ers; 1986;2:932-944

Stevenson AJ. Non-neonatal intestinal ob-struction in children. Surg Clin North Am.1985:65:1217-1233

Stewart DA, Colodry AL, Daggett WC. Malro-tation of the bowel in infants and children, a15 year review. Surgery. 1976;79:71 6-720

Teitelbaum DH, Qualman S, Caniano D. Hirsch-prung’s disease, identification of risk factorsfor enterocolitis. Ann Surg. 1988;207:240-244

Walsh MC, Kliegman A, Farnaroff A. Necrotiz-ing enterocolitis: a practitioner’s perspective.Pediatr Rev. 1988:9:219-226

Self-Evaluation Quiz

6. Each of the following is a true statementpertaining to chemical tests for blood (eg,guaiac), except:

A. They can be used to confirm that bloodis actually being passed in stool.

B. Ingestion of large doses of ascorbic acidmay cause false negative results.

C. Eating rare red meat may cause falsenegative results.

D. Ingestion of peroxidase-containing fruitsand vegetables may cause false positiveresults.

E. Their use to test nasogastric tube aspi-rates may allow detection of upper gas-

trointestinal bleeding.



DOI: 10.1542/pir.12-3-851990;12;85Pediatrics in Review

Gary SilberLower Gastrointestinal Bleeding

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Lower Gastrointestinal Bleeding Gary Silber Pediatrics in ......to test positive for blood (Table 2). In the majority of hospitals, guaiac, ben-zidine, or benzidine derivative test