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DOI: 10.1542/pir.12-4-1071990;12;107Pediatrics in Review

Marvin E. AmentPatient

Diagnosis and Management of Upper Gastrointestinal Tract Bleeding in the Pediatric

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The questions below should helpfocus the reading of this article.

1. How do the physiologic changesthat accompany gastrointestinalblood loss vary with the amount andrapidity of loss?2. What clinical or laboratory featuresguide management of patients withgastrointestinal hemorrhage?3. What constitutes an orderly diag-nostic approach to the patient withupper gastrointestinal bleeding?4. What constitutes an orderly diag-nostic approach to the patient withlower gastrointestinal bleeding?5. What constitutes appropriate man-agement of peptic ulcer disease inchildren and adolescents?

EDUCATIONAL OBJECTIVE

9. The pediatrician should haveknowledge to make an appropriateevaluation of an 18-year-old boywho has had abdominal pain forthree weeks and is now having he-matemesis, differentiating amongupper gastrointestinal bleeding,gastritis, duodenitis, gastric ulcer,duodenal ulcer, esophagitis, Mal-lory-Weiss syndrome, a bleedingdisorder, and esophageal varices,and develop an appropriate planfor management. (Topics, 90/91)

TABLE 1. Modes ofManifestation of UpperGastrointestinal Tract Bleeding inthe Pediatric Patient

HematemesisMelenaHematocheziaHemodynamic changes

“Department of Pediatrics, UCLA Medical Cen-ter, Los Angeles, California 90024-1752.

pediatrics in review vol. 12 no. 4 october 1990 PIR 107

Diagnosis and Management of UpperGastrointestinal Tract Bleeding in thePediatric PatientMarvin E. Ament, MD*

Gastrointestinal bleeding in pa-tients at any age is frightening. Thefear stems from the knowledge thatbleeding, if severe enough and sus-tamed for long intervals, may lead toshock and death. Fortunately, in bothpediatric and adult patients, in-stances in which bleeding is so mas-sive and uncontrollable that it leadsto rapid demise are extremely rare.The approach to diagnosis and treat-ment of gastrointestinal hemorrhageby the physician should be calm, log-ical, and expeditious to help allay thefears of the patient and family, and toreduce the morbidity associated withthe hemorrhage in the event its causeis found to be serious. Fortunately,the causes of gastrointestinal bleed-ing in the pediatric population arefewer than in adults; accordingly, thedifferential diagnosis is usuallyshorter, although not necessarily eas-ier. In contrast to adults, the age ofthe pediatric patient may play a keyrole in determining the differential di-agnosis.

MANIFESTATION OF BLEEDING(Table 1)

Before discussing the pathophysi-ology of bleeding, we will establish

definitions of the words frequently as-sociated with gastrointestinal bleed-ing.

Hematemesis is the vomiting ofblood. The blood may be either brightred or “coffee ground” in appearanceif it has been altered by gastric acid.Hematemesis implies that the site ofbleeding is proximal to the ligamentof Treitz. Blood from the upper gas-trointestinal tract may appear per rec-turn as black or tarry in color, causingthe so-called melanotic stool. Melenais typically coal black, shiny, sticky,and has a sickeningly sweet aroma.Very dark green stools are at timesconfused with melena. Therefore,when someone says their stool ismelanotic, it is always important toquestion whether or not they are talk-ing about a black, blackish maroon,or purple stool, versus one that ismerely dark green. The odor of me-lena is quite distinct and sets it apartfrom other causes of gastrointestinaldisease, such as malabsorption. Thecolor of blood in the stool, in part,depends on the volume of blood lostand the period over which it ispassed. The longer the transit time,the darker is the color of the stool.Hematochezia is the passage ofbright red or maroon blood from therectum. This may be pure blood,bloody diarrhea, or blood mixed withthe stool. The site of bleeding is al-most always in the left colon, andprimarily in the anorectal region. Pa-tients can have massive bleedingfrom the upper gastrointestinal tractand pass bright or near bright redblood rectally, but this is uncommon.

Finally, upon initial examination,

patients may lack any objective signof bleeding and have only symptomsof blood loss: dizziness, dyspnea, orshock.

Color of bleeding does notdenote its severity, nor its

source.

PATHOPHYSIOLOGY OFBLEEDING

Our bodies can adapt to substan-tial blood loss without a noticable al-teration of function. This is especiallytrue in pediatric patients, who do nothave as severely altered cardiac, pul-monary, or renal function as manyadults who bleed. When an individualbleeds, a number of homeostaticmechanisms respond. These includean increase in sympathetic activity,with catecholamine and release ofadrenocorticotropic hormone, antidi-uretic hormone, aldosterone, gluco-corticoids, and prostaglandins.1 Ini-tially, the rapidity of blood loss maybe a more important factor than thevolume that is lost. As much as i 5%of our blood volume can be lostslowly without any hemodynamic re-sponse. With the use of several com-pensatory mechanisms, a patient canlose up to 30% of blood volumeslowly and still survive. A loss of over



Upper Gastrointestinal Tract Bleeding

PIR 108 pediatrics in review #{149} vol. 12 no. 4 october 1990

30% of blood volume rapidly resultsin shock and, without therapy, death.

Mild Blood Loss

If only i 0% to i 5% of blood volumeis lost, the intravascular volume ismaintained by several homeostaticmechanisms.2 First, the venous sys-tem contracts. The venous bed nor-mally contains a substantial volumeof blood, which can easily compen-sate for minor losses. Second, thereis a fluid shift that moves extravas-cular fluid into the vascular space.These changes prevent any changein cardiac output and oxygen con-sumption. The maintenance of circu-lating volume is more important thanthe actual red cell mass, as evidencedby patients with severe anemia whohave normal blood volumes and arehemodynamically stable.1

During the hemorrhage, blood flowto the brain and heart is maintainedpreferentially. This is critical becausethese organs are so susceptible todamage if oxygenation to them is notmaintained. If bleeding occurs morerapidly, changes in cardiac outputand arterial pressure become pro-nounced. A very narrow pulse pres-sure may be a valuable warning ofimpending vascular collapse as corn-pensatory vasoconstriction is ex-hausted. Patients may experienceshock with as little as i 0% volumeloss if the bleeding is extremely rapid.Cardiac output is near normal withslow bleeding in the early phases, butit is decreased markedly in patientswith rapid bleeding. Arterial pressureis decreased in the presence of bothslow and rapid bleeding, but to agreater degree with rapid bleeding.The first sign of bleeding is an in-crease in the pulmonary arterial pres-sure. Central venous pressure, pul-monary capillary wedge pressure,and arterial pressure are less accu-rate measures of volume depletionbefore, during, or after hemorrhage.

Restoration of the circulating bloodvolume following a loss of 10% to20% of the blood begins immediately.The total volume is restored in 30 to40 hours. The rate of vascular refill is0.10% to 1% per hour. With greaterblood loss, the replenishment ratemay approach 2% per hour.

Moderate Blood Loss

When blood loss exceeds 1 5% ofthe blood volume, compensatorymechanisms are no longer adequate.Cardiac output is maintained by sym-pathetic stimulation, resulting in in-creased heart rate and increasedforce of contraction. Peripheral vaso-constriction also assists in maintain-ing blood volume. Increased secre-tion of aldosterone and antidiuretichormone also assists in maintainingblood volume when the loss is at least1 5%. Blood sugar and fatty acid 1ev-els become elevated in response tothe release of the catecholamines.Oxygen consumption increases andblood lactate levels also become el-evated in response to tissue hypoxia.Hyperventilation may result in respi-ratory alkalosis before significantmetabolic acidosis is present. Lessrapid bleeding is associated more fre-quently with alkalosis, whereas rapidbleeding is associated with acidosis.Acidosis is due almost entirely to hy-perlactacidemia. Acidosis is not re-lated to arterial hypoxemia but is ameasure of tissue hypoxia. Althoughblood transfusion may increase bloodlactate levels, it is not a major con-tributor to acidosis. The degree ofacidosis correlates with the severityof shock.

Severe Blood Loss

When more than 30% of the cir-culating blood volume is lost, hypo-tension is invariably present. This isa major contributing factor to de-creased cardiac output. Metabolicacidosis also contributes to the se-verity of the patient’s symptoms.When loss of blood exceeds 30%,tissue damage occurs because of de-creased cardiac output.2 This can bereflected in every organ system.

Acute renal failure may develop.The most important determining fac-tor in development of renal failure isthe degree of vasoconstriction. Thisis initiated by the autonomic responseto blood loss, which can be exacer-bated by fear or anxiety. The devel-opment of renal failure is not neces-sarily determined by the duration ofthe hypotensive period. The liver, ifischemic, can effect tremendous ele-vations in transaminases, as well as

an elevation of bilirubin and a markedfall in the synthetic rate of clottingfactors. The ability of the liver to re-spond to intramuscular or intrave-nous vitamin K following restorationof blood volume is a good indicatorof the damage to the liver. In otherwords, if there is normalization of theprothrombin time within 24 hours ofadministering vitamin K, this wouldindicate, at most, mild injury to theliver. Very elevated bilirubin levels areassociated with acute liver damage.However, transaminase levels mayreturn to normal long before the bili-rubin levels.

Decreased cardiac perfusion canresult in infarction of the heart. Thiscan occur at any age. The gastroin-testinal tract, in addition to being thesource of the hemorrhage, can alsomanifest the side effects of the hy-poxia with ischernic bowel, coloniculcerations, and hemorrhagic gastri-tis. Other less common effects areacalculous cholecystitis and severeconjugated hyperbilirubinemia. Res-piratory insufficiency, secondary tocirculating microaggregates, may in-crease. Sepsis also can develop as aresult of impaired organ function ordepressed immune status. Both aci-dosis and sympathetic activity mayincrease the degree of myocardialdamage during shock. Arterial hy-poxia increases the sensitivity of theheart to shock. Myocardial damagemay be permanent if hypotension isprolonged and evidence of left yen-tricular failure appears. On rare oc-casions, long-term damage to theliver may occur as a result of severeshock.

ASSESSMENT OF THE PATIENT

It is the first obligation of the phy-sician to determine the quantity ofblood lost and the site of the bleeding.Information about the color and quan-tity of stool and/or emesis is helpful.Melena suggests, at minimum, ablood loss of 2% of blood volume. Itis important to remember that melenais defined as black, tar-like stool, notsimply black stool, which could besecondary to Pepto Bismol or ironintake. The physician also should re-member that parents often misjudgemelena. Melena typically indicates



Major gastrointestinalbleeding may manifest first

with symptoms of dizziness,tachypnea, and paleness.

TABLE 2. Role of NasogastricTube

Localization of gastrointestinalhemorrhage

Gastric lavageAids in endoscopic evaluation by

clearing stomach before ex-amination

Prevents hyperammonemia inthose with liver disease

Stops bleeding

GASTROENTEROLOGY

pediatrics in review #{149}vol. 12 no. 4 october 1990 PIR 109

bleeding from the upper gastrointes-tinal tract. Black stools can be causedby lesions in the right colon, althoughthe consistency is usually differentfrom that of true melena. The pres-ence of larger quantities of bright redblood per rectum represents either asource distal to the ligament of Treitzor the loss of 20% of blood volumefrom above the ligament.

Vomiting of coffee ground-like ma-terial does not necessarily signify aspecific quantity of blood, nor doesvomiting of bright red blood meanthat major bleeding is taking place.The volume of the emesis is helpfulin assessing the quantity of loss.Emesis without evidence of bloodloss does not rule out an upper gas-trointestinal source of bleeding, be-cause bleeding could have stoppedor could be in the duodenal bulb inthe case of a competent pylorus.

As much as 20% to 40% of uppergastrointestinal tract bleeding occurswithout hematemesis. Testing stooland vomitus for blood during an acuteepisode is not very helpful if it isobvious that the patient is passingbright red blood. If there is a questionabout whether the material passed isblood, it obviously should be testedwith guaiac or Hemoccult. Testingemesis or nasogastric return contain-ing nothing resembling blood is ofvery little value in the face of acutebleeding, because vomiting alone andthe passage of a nasogastric tubecould produce a positive test withoutthe presence of any real hemorrhage.

On physical examination, measure-ment of vital signs provides the onlyaccurate assessment of volume loss.Presence of an orthostatic decreasein blood pressure of 10 mm Hg rep-resents a 10% to 20% volume lossof the intravascular volume. The pa-tient may complain of weakness ordizziness. Syncope or fainting usuallyaccompanies greater blood loss, al-though these also may be seen withrapid loss of as little as 10% of the

circulating volume. The presence ofhypotension and resting tachycardiausually signifies a loss of more than30% of the blood volume. Orthostaticblood pressure monitoring is usuallyadequate to monitor fluid and bloodreplacement unless a patient isknown to have cardiopulmonary dis-ease.

NASOGASTRIC TUBE (Table 2)

A nasogastric tube serves severalpurposes in the assessment andtreatment of gastrointestinal bleed-ing. First, it may help to determinewhether the bleeding is from the up-per gastrointestinal tract. A positivenasogastric return is conclusive;however, a negative return does notrule out an upper gastrointestinalsource. A study conducted by theNorth American Society of Gastroin-testinal Endoscopy found that 16%of patients with clear nasogastric re-turn had a lesion that was either ooz-ing or pumping at the time of uppergastrointestinal endoscopy (N =

21 4).3 Also, active bleeding was pres-ent at the time of endoscopy in ap-proximately 30% of patients with cof-fee ground-like return from the na-sogastric tube. Accordingly, thenasogastric tube has significant limi-tations in determining the presenceof active bleeding with any certainty.The nasogastric tube can be used toremove blood from the gastrointes-tinal tract, however. This is particu-larly important in those individualswith cirrhosis, in whom blood in thegastrointestinal tract could precipi-tate encephalopathy.

The size of the nasogastric tubeused depends, in part, on the size ofthe infant, child, or adolescent. The

limitations on passing the tubes arein part dependent on the size of thenasal passage or the decision ofwhether or not to pass the tube or-ally. The smaller bore tubes may beadequate for assessing bleeding butnot for removing large clots. Thelarger bore nasogastric tubes maycause trauma to the gastric mucosaand are not usually recommended be-cause of this factor. The trauma theymay induce during aspiration canmake assessment at the time of en-doscopy difficult. There is no ques-tion, however, that gastric lavagewith the nasogastric tube may aid theendoscopist in obtaining a clear viewof the bleeding site. There are fewcontraindications to passing a naso-gastric tube. The presence, or poten-tial presence, of esophageal varicesshould in no way preclude the use ofa tube. The presence of bright redblood assures one of active bleeding.However, red or pink fluid from gas-tnc lavage may just represent a gas-tric clot being slowly dissolved. Thisdistinction can at times be difficult tomake.

The choice of fluid to use to lavagethe stomach can be complicated.Water appears to be as efficaciousas saline solution and is certainly lessexpensive. Worries about water in-toxication, particularly in patientswho have had gastric surgery, havenot been substantiated. Iced orcooled solutions have been used todecrease mucosal blood flow, andthus to decrease bleeding. Cold so-lutions offer no recognized advan-tage over room temperature solu-tions in animal studies. Some observ-ers believe that solutions at 32#{176}For0#{176}Cmay interfere with local coagu-lation mechanisms. Thus, tap waterwould appear to be the solution ofchoice for gastric lavage because ofits cheapness and its temperature.4We do not know whether medicationinstilled into the stomach affectsbleeding. Studies in adults using 1ev-arterenol lavaged at concentrationsof 8 mg/i 00 mL have been reportedin uncontrolled studies to decreasebleeding.5 However, there are nodata to confirm that this is really ben-eficial. Antacids have not been shownto stop acute bleeding, and they willinterfere with any endoscopic evalu-ation.



TABLE 3. Resuscitation ofPatients With GastrointestinalBleeding

Physical examination and contin-ued monitoring of vital signs

Expansion of intravascular volumeTyping and cross-matching of

bloodOxygenationFoley catheterization of bladderPlacement of central venous lineTransfusion of whole blood or

packed erythrocytesPharmacologic assistanceIntubation and ventilator support


PIR 110 pediatrics in review #{149}vol. 12 no. 4 october 1990

RESUSCITATION (Table 3)

Intravascular Replacement

The volume of blood lost and theactivity of the bleeding determine thechoice of fluid used to stabilize thepatient. Typing and cross-matchingof the blood of all such patientsshould be done immediately if bleed-ing is present, so that no delays areencountered should blood beneeded. The patient who has lost1 0% to 20% of blood volume doesnot necessarily require blood replace-ment, providing the bleeding hasstopped. To correct fluid depletion,initial replacement can be accom-plished with isotonic saline solution.The rate of saline infusion should beas fast as necessary to reverse or-thostatic hypotension. Children vir-tually never go into failure followingrapid repletion of intravascular vol-ume. If orthostatic hypotension re-sponds to isotonic saline solution,that alone may be sufficient. If after20% of the blood volume is replaced,the patient is still has orthostatic hy-potension without any improvement,blood should be given.

The age and underlying physicalcondition of the patient also deter-mine whether or not blood is needed.A healthy young individual can toler-ate a lower hemoglobin than an olderindividual who may have some un-derlying heart disease. Obviously,children who have heart disease mayneed to be transfused with bloodsooner. Similarly, children with hem-orrhage who have chronic lung dis-ease may require transfusion earlier

because of their problems with oxy-gen diffusion. Saline solution shouldbe avoided in the cirrhotic patient,except in true emergencies, becausethe sodium will be difficult to eliminateduring the recovery period. If the pa-tient is stabilized with saline solution,he or she can be monitored for furtherbleeding and transfusion may be un-necessary. During this time, urineoutput should be measured carefully.Catheterization of the bladder is usu-ally required only in case of massivebleeding. In massive bleeding, re-placement ideally should consist ofwhole blood. If whole blood is notreadily available, packed erythro-cytes will suffice. The volume re-placed should equal the measuredvolume lost, because replacementwill always be behind to some de-gree. Massive bleeding may requireunmatched blood to keep the patientalive long enough to stop the bleed-ing. For bleeding of lesser degrees,packed red cell transfusion is pre-ferred. Fresh-frozen plasma can begiven to approximate the volume ofblood lost, if necessary, and to re-store the blood pressure to normal. Itcan also be used if there is a recog-nized deficiency in clotting factors inpatients with acute or chronic liverdisease. Platelet transfusions mustbe given if the volume of blood lostapproximates more than 50% of thepatient’s total blood volume, unlessthe platelet count is depressed be-cause of another illness.

The patient’s vital signs are an in-dication of blood volume to be re-placed. The hemoglobin and hema-tocrit are not accurate reflections ofblood volume during an acute hem-orrhage. Equilibration of hematocrittakes a minimum of 24 to 72 hours.The value of the initial hematocrit isto determine the patient’s startingpoint and not to determine the quan-tity necessary to replace. Monitoringof hematocrit after transfusion is notnecessary more frequently thanevery 6 hours, because values atmore frequent intervals will not trulyreflect the patient’s status. The usualgoal of transfusion in the patient whohas stopped bleeding is to restore anadequate circulating volume to allowfor tissue perfusion. A hemoglobinlevel of i 0 g/mL with a hematocrit of30% is adequate in most patients and

allows for some downward equilib-rium. In the patient who continues tobleed, monitoring of vital signs is farmore important than monitoring hem-atocrit.

Significant decline inhematocnt may take 24

hours.

Oxygen

The need for oxygen in bleedingpatients depends on several factors.Tissue hypoxia can be aggravatedbecause of the effects of suddenblood and volume loss. The monitor-ing of blood gases is important inthose patients who have severebleeding and underlying heart andlung disease. Poor tissue perfusionwill be manifested by metabolic aci-dosis, the systemic effects of whichare exacerbated by hypoxia. All pa-tients with massive hemorrhage, inshock, should receive oxygen.

Diagnosis

In the case of a pediatric patientwho has a presumed gastrointestinalhemorrhage, the physician must firstdetermine if bleeding is truly present.Sometimes the source of the bleed-ing is naso- or oropharyngeal. Carefulexamination of the anterior nares andthe oral pharynx should be under-taken quickly, looking for blood drain-ing from the posterior nasopharynxinto the esophagus and stomach. Ifthere is a significant amount of gas-trointestinal bleeding, it is critical thata nasogastric tube be inserted andfluid aspirated, unless a distal sourceis obvious. If the aspirate is positivefor blood, the site of the bleeding isalmost certainly proximal to the liga-ment of Treitz, but the physician mustremember that a negative aspiratedoes not exclude an upper gastroin-testinal bleeding site beyond the py-lorus. Other characteristics of uppergastrointestinal tract bleeding are el-evated levels of blood urea nitrogenand hyperactive bowel sounds.Lower gastrointestinal tract bleedingis characterized by normal blood ureanitrogen levels and normal bowelsounds.



Endoscopy is most useful ifdone within 24 hours of

bleeding.

TABLE 4. DiagnosticIntervention With PositiveNasogastnc Aspirate

Physical examinationPlain radiographs of abdomenUpper gastrointestinal endoscopyUpper gastrointestinal seriesArtenographyTagged erythrocyte study

TABLE 5. DiagnosticIntervention With NegativeNasogastric Aspirate

Inspection of the anus and rectalexamination

Plain radiographs of abdomenProctosigmoidoscopy or colonos-

copyUpper gastrointestinal series with

small bowel follow-throughBarium enemaScan for Meckel diverticulumArteriographyTagged erythrocyte studyWork-up for positive aspirateLaparotomy

TABLE 6. Causes of UpperGastrointestinal Tract Bleeding

Barrett ulcerDuodenal ulcerDuodenitisEsophageal or gastric varicesEsophagitisGastric ulcerGastritisMallory-Weiss tearMenetner diseaseNeoplasmsPolypsStress ulcersVascular anomalies

GASTROENTEROLOGY

pediatrics in review #{149}vol.l2no.4octoberl99O PIR 111

POSITIVE NASOGASTRICASPIRATE (Table 4)

The source of the upper gastroin-testinal tract bleeding can be deter-mined in 90% of cases if endoscopyis done within the first 24 hours.6 Anyfurther delay may defeat attempts toidentify the exact source. Flexible fi-beroptic upper intestinal endoscopyin pediatric patients has shown thatthe most common causes of bleedingare gastritis, esophagitis, duodenalulcers, and esophageal varices.7 En-doscopy should be performed on pa-tients with active bleeding who areknown to have esophageal vances,because the source of bleeding maybe from lesions other than the var-ices. For patients who have majorgastrointestinal hemorrhage, bariumupper gastrointestinal studies are farless accurate than endoscopy andmay interfere with subsequent endo-scopic examination. Additionally, bar-ium studies do not usually reveal thesuperficial lesions of esophagitis,gastritis, or Mallory-Weiss tears.

In a small percentage of cases ofupper gastrointestinal tract bleeding,when endoscopic and barium studieshave failed to determine a source ofbleeding or when bleeding is massive(more than 0.5 mL per minute, mak-ing endoscopic visualization impos-sible), artenography should be per-formed. This examination of the su-perior and inferior mesenteric arteriesand the celiac axis may reveal somecommon causes of bleeding, as wellas unusual causes, such as hepaticartery aneurysms, hematobilia after

trauma, gastropancreatic duplicationcyst, or arteriovenous malformationsand hemangiomas. If angiographyhas not proved diagnostic or cannotbe performed, erythrocytes labeledwith technetium-99 pertechnetateand observed using an abdomenscan can detect the site of activebleeding.8 Some physicians preferthis to angiography, because it hasfewer complications. If a bariumstudy has been done recently, bothangiography and pertechnetate stud-ies may be uninterpretable.

NEGATIVE NASOGASTRICASPIRATE (Table 5)

The approach to patients with rec-tal bleeding and a negative nasogas-tric aspirate is predicated on the colorand amount of blood and the child’ssymptoms. A recent study of childrenwith rectal bleeding, with and withoutother symptoms, showed that in-spection of the anus and proctosig-moidoscopy identified the source ofbleeding in nearly 80% of the pa-tients. Only 20% needed additionalstudies to determine the etiology. Abarium enema, scan for Meckel di-verticulum, or colonoscopy was re-quired to make the diagnosis in theremaining cases. This study sug-gested that a systematic approach tothis problem, beginning with an analexamination and following it with aproctosigmoidoscopic examination,is the most effective way to proceed.9If the blood is darker in color, is mixedwith stool, and is usually unasso-ciated with abdominal pain or diar-rhea, a Meckel diverticulum, intestinal

duplication, or right-sided colonic pol-yps should be suspected. A bleedingMeckel diverticulum of the ileum is, in80% of cases, associated with me-lena and blood volume depletion. Apertechnetate scan should be per-formed first; if it is inconclusive, itshould be followed by a colonoscopyand then, ultimately, an air contrastbarium enema.

GASTROINTESTINAL BLEEDINGIN THE NEWBORN PERIOD (Table6)

Gastrointestinal bleeding in thenewborn period differs from that inthe older child. More often than not,the cause of major bleeding is notdetermined and the bleeding fre-quently ceases in less than 24 hours.Major bleeding in the neonatal periodmay be the result of hemorrhagic gas-tritis or stress ulcers caused by aperinatal insult of hypoxia, sepsis, orlesions of the central nervous sys-tern.9 Other more frequently recog-nized causes of neonatal bleeding arehemorrhagic disease of the newbornsecondary to vitamin K deficiency andanal fissures. The latter, however, isnot a major source of blood loss.Swallowed water and maternal bloodcan appear as hematemesis or evenmassive dark red rectal bleeding, butit is easily diagnosed by performingthe alum-precipitated toxoid test.This examination differentiates fetalfrom maternal blood by the additionof sodium hydroxide to the blood.Fetal blood remains pink, owing tothe alkaline resistance of fetal hemo-globin, whereas adult hemoglobingives a brown color.





Necrotizing enterocolitis in the pre-term or stressed term infant and en-terocolitis secondary to Hirschsprungdisease may frequently cause occultto moderate rectal bleeding. How-ever, it is rarely massive. A midgutvolvulus associated with malrotationof the bowel may lead to melena orhematochezia secondary to the ob-struction of the blood supply to theintestines. All of these entities arepotentially life-threatening and re-quire rapid diagnosis and aggressiveintervention with fluid replacement,antibiotic therapy, bowel decompres-sion, even surgery. Some neonateswho have no recognized stress in theneonatal period may develop massivebleeding secondary to ulcers in theduodenal bulb and stomach. Thecause of this is yet unknown but,fortunately, the bleeding usually re-sponds to supportive measures anddoes not require any surgical inter-vention. There is no evidence thatneonates who develop ulcers withbleeding are at increased risk of de-veloping chronic peptic ulcer disease.

Intolerance to cow milk and soyprotein (so-called “protein” allergies)can lead to vomiting or hematemesisand occult or gross rectal bleedingwith weight 1055.10 The bleeding,however, is seldom massive. Af-fected patients may exhibit dysen-tery-like symptoms, including feverand diarrhea, and are often confusedwith those who have a dysentery-likesyndrome. Typically, young infantswith cow milk or soy protein intoler-ance have elevated white bloodcounts, with neutrophilia. Most do nothave recurrent pulmonary infectionsor wheezing and do not have eosin-ophilia. In rare cases, infants will haveallergic dermatitis, pulmonary in-volvement, as well as gastrointestinalinvolvement. If the patient has allergicgastroenteropathy with colitis, thesymptoms usually begin to declinewithin a period of 24 to 48 hours ofwithdrawing the offending formula.However, if the damage is severe,the diarrhea may persist for days orweeks, even after the withdrawal ofthe offending protein. Patients whohave suspected intolerance to cowmilk and soy protein should be puton a hypoallergenic formula, such asNutramigen or Pregestimil, in gradu-ally increasing strengths until their

diarrhea stops and normal weightgain and growth develop.

Some infants with intractable diar-rhea from formula intolerance mayeven require the use of parenteralnutrition as a means of providing thenecessary nutrients and fluids thatwill allow the intestinal mucosa toheal and bleeding to stop. Patientswho have cow milk or soy proteinintolerance first should be tested withthe appropriate disaccharide in theformula to show that the small intes-tinal mucosal lining has healed andcan tolerate the sugar present in theformula. If the tolerance test for sugaris passed without any malabsorption,the complete formula may be fed tothe patient. Stools should be free ofoccult blood and white cells beforeformal testing is done. A baselinewhite blood count and differentialcount should also be obtained beforethe challenge.

If the infant shows tolerance to thesugar in the formula to be tested, andif the stools are free of occult bloodand white cells, the patient is usuallygiven 3 to 4 ounces of the presumedoffending formula. If the patient isintolerant of the protein in the for-mula, within a period of 24 hours heor she should become symptomaticwith vomiting or diarrhea, or both. Ifthe patient develops vomiting or diar-rhea, a white blood cell count anddifferential should be obtained at thatpoint. If the patient is truly protein-intolerant to the formula, leukocytosiswith neutrophilia or neutrophilia alonewill be found. The stools in that 24hours will typically become eitherHemoccult positive or grossly posi-tive for blood, and white cells willappear in the stool.

Malabsorption also may occur.Eighty percent of those who havecow milk protein intolerance will alsohave soy protein intolerance. Gener-ally, the intolerance to formula pro-teins does not endure beyond the ageof 1 to 2 years, and at this pointpatients should be retested to see ifthey have developed tolerance.

INFANTS AND CHILDREN

Gastritis or Stress Ulcerations

Erosions of the gastric mucosamay occur acutely after any major

trauma, burn, shock, or sepsis.These lesions are typically superficialand multiple and occur mainly in thefundus of the stomach. Deeper le-sions may involve the esophagus,stomach, or duodenum and morecommonly develop after intracranialsurgery and head injuries. The path-ogenesis of all of these lesions isunknown, but it appears that the nor-mal buffering ability of the gastric mu-cosa is interfered with by the complexpathophysiology that is the commonpathway after trauma, burn, shock,or sepsis. Furthermore, reflux into thestomach of duodenal contents withcaustic bile salts may be a contribut-ing factor. lschemia and bile salts,with their subsequent damage to theesophageal, gastric, and duodenalmucosa, lead to back-diffusion of hy-drogen ions, which in the presence ofnormal acidification leads to break-down of the mucosa.

Patients who experience any of theabove conditions should be treatedprophylactically to avoid stress le-sions and bleeding. Either antacidtherapy or H2 blockers should beadministered. Both have proven to beefficacious in preventing stress-re-lated lesions if administered in ade-quate volumes to maintain an intra-gastric pH level above 4.5. Antacidsshould be administered at least every3 hours to ensure that the intragastricpH level is kept above 4.5. Shouldthe dosage chosen be insufficient,the volume or the neutralizing capac-ity, or both, of the antacid chosenshould be increased. The most effec-tive antacids for the treatment of thiscondition are the magnesium-con-taming antacids. Those that are dou-ble strength are probably the best.However, the problems associatedwith them are those of diarrhea andpalatability. If diarrhea becomes aproblem for the patient, the antacidscan be alternated with those that aremore constipating, such as the alu-minum-containing ones.

An alternative approach is to useH2 blockers.11 H2 blockers are bestadministered intravenously by contin-uous infusion. The dosage used iseither 20 to 30 mg/kg per day forcimetidine or 7.5 mg/kg per day forranitidine. The dosage chosen shouldbe monitored for its effectiveness bychecking the intragastric pH level



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every hour to see that the intragastricpH level remains �4.5. Becausesome tachyphylaxis occurs with pro-longed usage and because there aresome patients in whom it is not pos-sible to suppress acid secretion to-tally with H2 blockers, supplementaltherapy with other medications maybe necessary. There are, therefore, alimited number of patients who mayrequire the benefits of both an H2blocker and antacid therapy to keepgastric acid production suppressedor neutralized so that mucosal break-down does not occur.

Another maneuver that can beused in such patients is the place-ment of a nasogastric tube to aspi-rate gastric contents in response tothe secretion by the mucosa. Somepatients will certainly benefit fromhaving their stomachs decompressedand what little acid they make aspi-rated at the same time that acid pro-duction is being inhibited by the H2blockers. Other modalities that havebeen used have included the admin-istration of sucralfate, but there arenot nearly as many data on its use-fulness for preventing stress-associ-ated lesions as on the other thera-pies.12 Intravenous administration ofomperazole, a benzimidazole, may inthe future offer the best alternative toinhibition of acid secretion because itcan suppress virtually all acid secre-tion for up to 24 hours, but an intra-venous form is not yet available.13

Acid Peptic Disease

Children with peptic ulcer diseaseduring the school years typically havesymptoms similar to those of adultpatients. Abdominal pain with or with-out associated vomiting and night-time awakening is the most typicalpattern. Unfortunately, in the pre-school child, lesions both in the stom-ach and the duodenum are morelikely to be associated with compli-cations. Of pediatric patients with idi-opathic peptic ulcer, nearly 70% willhave family members with associatedulcer disease. Most pediatric patientswith idiopathic peptic ulcers aremales, and their fathers have the dis-ease. Of preschool children with idi-opathic ulcers, most have either gas-trointestinal bleeding (hematemesisor melena), obstruction, or perfora-

tion. Bleeding is the most commonsymptom. Gastric ulcers more com-monly cause hematemesis, whereasduodenal ulcers more often causemelena. However, a characteristicmode of manifestation for one typeof ulcer does not exclude the possi-bility of the other type.

Since physicians have becomeaware of the dangers of aspirin inges-tion, there has been a marked reduc-tion in the use of aspirin for the con-trol of fever and for the relief of symp-toms associated with respiratoryinfection. This has resulted in a re-markable reduction in the number ofinfants and children admitted forbleeding following ingestion of aspi-rin. Whereas in the past those chil-dren who bled from gastritis or fromaspirin-associated lesions made upnearly one third of all of the patientswith bleeding in our practice, cur-rently they make up less than i 0%.

TREATMENT OF BLEEDINGULCER

Once the ulcer has been identifiedas the source of the bleeding, treat-ment should be initiated. Patientsshould receive nothing by mouth forat least 48 hours and should be man-aged with intravenous fluids and elec-trolytes. Patients who undergo en-doscopy and are found to have bleed-ing secondary to either a gastric orduodenal ulcer should be treated in-tensely to see if the bleeding can beprevented from recurring. Antacidsshould be started routinely and givenevery 1 or 2 hours around the clockto ensure that the intragastric pHlevel is maintained at more than 4.5.The intragastric pH level can be mon-itored using a nasogastric tube in thestomach. Before each dose of ant-acid is given, gastric contents shouldbe aspirated to determine the intra-gastric pH level. If the pH level ismaintained consistently at more than4.5, the dosage of antacids is appro-priate. Should the pH level decreaseto less than 4.5, the dosage volumeshould be increased.

H2 receptor antagonists in the formof cimetidine, ranitidine, or famotidinemay also be used. Although they maynot help in controlling the actualbleeding, they may prevent the secre-tion of acid, which is a contributing

factor to the production of the ulcer.Initially, they should be used intrave-nously for a period of 48 hours andgiven by continuous infusion. If bleed-ing does not recur within a period of48 hours, H2 receptor antagonistscan be an given orally. Sucralfate,which is a topical agent used to coatulcers and to treat gastritis, may alsobe used, despite the fact that it is notan agent specifically for stoppingbleeding. This agent is typically takenfour times per day and may be givenas a tablet or as a suspension.

Newer Agents for the Treatmentof Bleeding

Prostaglandin and synthetic pros-taglandin analogues are potent inhib-itors of gastric acid secretion thatexert a cytoprotective effect on theintegrity of the gastric mucosa.14These agents have proven to be ofvalue in the treatment of patients whohave gastritis when all other forms oftherapy have failed. In two infantswho had idiopathic hemorrhagic gas-tritis, and in whom for months noother form of therapy had been effec-tive in resolving the lesions, use ofprostaglandins prevented recurrenceof bleeding. These agents, which aretaken orally or given topically fourtimes per day, may have the greatestbenefit in hemorrhagic gastritis. Anew and unproven agent, syntheticsomatostatin, has been shown to de-crease gastric acid secretion and in-crease production of gastric mucus.15However, its effectiveness as a ther-apeutic agent has yet to be estab-lished. Endoscopic treatment ofbleeding via coagulation using theNd:YaG laser or the heater probe, orboth, has been shown to be safe andeffective for the treatment of bleedingulcers in adults.16 The use of thesemethods in pediatric patients hasbeen quite limited, however. The bi-cap heater probe is the safest andpossibly cheaper of the two methods.

Surgery for the treatment of ableeding peptic ulcer should be re-served for the small group of patientswho do not respond to medical ther-apy or coagulation, and for cases inwhich the loss of blood is significant.If surgery is needed, bleeding ulcersshould be oversewn and a pyloro-plasty and vagotomy performed. An-





trectomy and gastrectomy should beavoided, if possible, because of thepotential consequences regardingweight gain and growth. Becausegastrectomy in adults is associatedwith major malabsorption and in-creased risk of cancer in the long run,its use should be minimized.

Esophagitis. Hematemesis sec-ondary to gastroesophageal reflux isuncommon. It is typically seen in pa-tients who are severely symptomaticwith vomiting or aspiration. The pres-ence of esophagitis severe enough tocause hematemesis is an indicationthat medical therapy for gastroesoph-ageal reflux is unlikely to be benefi-cial.

Foreign Bodies and Caustic Inges-tions. Since the development ofsafety caps for both medicines andcaustic household cleaning products,there has been a reduction in thefrequency of caustic ingestions withsecondary hematemesis. Bleedingfrom caustic ingestion is usually notmassive. Edema with secondary dys-phagia and obstruction is more likely.

Foreign body ingestion rarely is as-sociated with upper gastrointestinalbleeding as a major presenting symp-tom. Surprisingly, swallowed glassand pins may not cause significantblood loss.

Esophageal and Gastric Tumors.Polyps in the esophagus and stom-ach of infants and children are ex-ceedingly rare and more typically areassociated with dysphagia, odyno-phagia, and abdominal pain with vom-iting. Hematemesis may occur, butthis is not the typical manifestation.

Adenocarcinoma of the gastro-esophageal junction or gastric mu-cosa is extremely rare in individualsless than 18 years of age and com-monly exhibits obstructive symptomsand pain, not hematemesis.

Portal Hypertension andEsophageal Gastric Varices

Intrahepatic and extrahepatic por-tal venous obstruction leads to portalvein hypertension with subsequentesophageal or gastric varices andsplenomegaly with hypersplenism.Extrahepatic portal vein obstructionmost commonly occurs as a result ofomphalitis in the neonatal period,either secondary to catheterization of

the umbilical vein or secondary to aspontaneous inflammatory processof the umbilical blood vessels. Intra-hepatic obstruction in the pediatricpopulation is secondary to cirrhosisfrom previously diagnosed liver dis-ease. Patients with idiopathic portalhypertension may first be recognizedat routine physical examination whenthey are discovered to have spleno-megaly in the presence of a liver ofnormal size and functioning. Patientswith portal vein thrombosis and portalhypertension and with secondarysplenomegaly typically have corn-pletely normal liver function tests.They may have an associated leuko-penia or thrombocytopenia, or both,depending on the degree of trappingof these blood elements in the spleen.

Variceal bleeding may be the firstevidence of cirrhosis. The most com-mon causes of variceal bleeding inchildren and adolescents with liverdisease are secondary to biliary atre-sia that has been operated either suc-cessfully or unsuccessfully using theKasai procedure. Other causes maybe secondary to cirrhosis developingfrom neonatal hepatitis, congenitalhepatic fibrosis, and cystic fibrosis.Bleeding from vances is uncommonin the first year of life but can anddoes occur in patients with biliaryatresia who have not been success-fully decompressed by the Kasai pro-cedure. Two thirds of patients withportal hypertension hemorrhage be-fore 5 years of age, and 85% do soby 1 0 years of age. The most com-mon reason for bleeding to occur inthose with portal vein hypertension isprogressive and increasing elevationof portal vein pressure. There havebeen no longitudinal studies in chil-dren on the use of propranolol for theprevention of variceal hemorrhage.There are only short-term data toshow the usefulness of this medica-tion. On the other hand, in the adultliterature, there is controversy overthe use of the medication in dosessufficient to reduce the pulse rate.

If a variceal hemorrhage occurs,maintenance of hemodynamic stabil-ity is extremely important. Physiciansmust expand the blood volume withcare because of the risk that exces-sive expansion could result in furtherbleeding, or a recurrence of it. Mostchildren respond to the preshock

state with vasoconstriction and ces-sation of bleeding. Preshock state in-cludes mild tachycardia, without or-thostatic changes, associated with adecreasing hematocnt of at least30%. If bleeding persists or multipletransfusions are needed, more spe-cific therapeutic intervention may benecessary.

If a variceal hemorrhage persists,the first line of therapy is vasopres-sin.17 Vasopressin reduces splenicblood flow, decreases portal pres-sure, and is effective in controllingvariceal bleeding. Intravenous infu-sion of vasopressin is as effective asintra-arterial infusion. A dosage of 0.1to 0.4 units of vasopressin per minuteis effective. This hormone may causevisceral infarction and decreasedpulses secondary to its systemicvasoconstriction. A synthetic ana-logue called glypressin is also an ef-fective vasoconstrictor that has ad-vantages over vasopressin of alonger period of pharmacologic activ-ity with reduced toxicity. It is, how-ever, not widely used. Somatostatin,a hypothalamic extract, decreasessplenic blood flow and may be moreeffective than vasopressin in control-ling acute variceal hemorrhage with-out inducing serious side effects. Thisagent, however, has not been widelyused in children.15

Another mode of therapy that canbe used for the patient with varicealbleeding is the Sengstaken-Blake-more tube. Patients who are havingmassive bleeding from either gastricor esophageal varices can have aSengstaken-Blakemore tube placedin the stomach and esophagus as ameans of compressing the bleedingvarices. If the patient undergoes en-doscopy and no esophageal varicesare seen, there is a strong probabilitythat the bleeding is from a gastricvarix, and the gastric balloon only ofthe Sengstaken-Blakemore tube maybe inflated until it is shown that thebleeding has stopped. In this case, itis not necessary to inflate the esoph-ageal balloon. If, however, there isbleeding from the esophageal var-ices, both balloons should be inflated.The balloons should be insufflatedand their position checked radio-graphically. The balloons should re-mained fully insufflated for 12 hours.At the end of that time, the balloons



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may be deflated to reduce mucosalischemia. The balloons may then bereinsufflated for another 1 2 hours, atthe end of which time they may againbe deflated. If bleeding does not recurin the following 24 hours, the instru-ment may be removed. Should be-leeding recur, the patient could betreated with the use of sclerosis ofvarices.

Injection sclerotherapy, using asclerosing agent such as 5% sodiummorrhuate injected into or next to thevarices via endoscope, has been ex-tremely useful as a means of stoppingactive bleeding from varices, as wellas preventing varices from bleed-ing.18 This method, we believe, isbest used under elective conditions,although it certainly can be used inan emergency situation. When doneas an emergency procedure, the en-doscopist faces the dilemma ofwhether or not the patient should beintubated to reduce the risk of aspi-ration if bleeding is brisk, while anattempt is made to inject the bleedingvarices. In any one setting, it probablyis unwise to use more than 4 to 5 mLof sclerosing agent. Sclerosis can berepeated every second or third dayuntil the suspected varices are scle-rosed. The risks of sclerosis are ul-ceration of the esophageal mucosa,stricture of the esophagus, and per-foration. The risks are directly pro-portional to the experience of thephysicians as well as the volume ofsclerosing agent used. There is noquestion that injection sclerotherapymay be the best means to managebleeding secondary to extrahepaticportal hypertension, particularly inchildren less than i 0 years of age. Inyounger children, shunting proce-dures fail in the majority of cases.They should only be contemplated ifsclerotherapy is a failure and if con-ditions are extreme.

For patients who have varices it isalways wise, when possible, to do anendoscopy rather than presume thatthe bleeding is coming from varicesbecause, in a large portion of cases,gastritis or ulcers and not the varicesthemselves may be the source of thebleeding.

Mallory-Weiss Tear

A Mallory-Weiss tear consists of alaceration of the posterior wall of the

gastroesophageal junction, whichmay extend through the esophagealmucosa.19 This tear, which is moreoften seen on the gastric mucosalrather than the esophageal side, fol-lows forceful emesis or repeatedretching. Typically, the patient willhave two or three forceful emeses inwhich there is no blood, followed bymassive hematemesis. These lesionsmay be difficult to diagnose unless avery careful upper intestinal endos-copy is performed. They sometimeshave to be defined by selective celiacarteriography. Mallory-Weiss tearshave been reported in children asyoung as i 6 weeks of age. Theselesions usually stop bleeding spon-taneously and surgery is rarely mdi-cated. A patient with the diagnosis ofa Mallory-Weiss tear should receivenothing by mouth, and his or herstomach should be kept decom-pressed. He or she should be givenH2 blockers or antacids, or both, fora period of at least 48 to 72 hoursbefore the tube is withdrawn. If, afterthe nasogastnc tube is withdrawn,there has been no evidence of recur-rent bleeding in the following 24hours, feeding can be commenced.The chance of bleeding recurring isgreatest in the first 48 hours after thefirst hemorrhage.

GENERAL COMMENTS

The most important aspect of theevaluation of any patient who hasgastrointestinal bleeding is to deter-mine the degree of blood lost andrapidity with which the loss occurred.Establishing vital signs when the pa-tient is first seen is critical to deter-mining the extent of the loss. Patientswho have stable blood pressures inthe erect and supine positions, andhave no significant alteration in pulsewith the changes of position, can beconsidered to have less serious bloodloss or minimal loss. Patients whohave orthostatic changes in bloodpressure warrant a more aggressiveapproach to management. It is mostimportant in those patients who haveevidence of hemodynamic instabilityto treat the hypotension first and laterto determine the cause and specifictreatment. Patients such as theseneed rapid placement of intravenouslines to administer fluids and bloodproducts, rapid expansion of blood

volume, and careful monitoring of vi-tal signs, urinary output, and hema-tocrit. Once the patient has been sta-bilized with adequate replacement ofvolume expanders, logical diagnosticevaluation should be performed sothat specific treatment may be estab-lished.

REFERENCES

1 . Runciman WB, Skowronski GA. Patho-physiology of haemorrhagic shock. An-aesth. Intensive Care. 1984;1 2:193-205

2. Collins JA. Hemorrhage, shock and burns:pathophysiology and treatment. In: PetzLD, Swisher SN, eds. Clinical Practice ofBlood Transfusion. New York: ChurchillLivingstone; 1981:425-453

3. Silverstein FE, Gilbert DA, Tedesco FJ.The National ASGE Survey on Upper Gas-trointestinal Bleeding. Gastrointest En-dosc. 1981 27:73-102

4. Ponsky JL, Hoftman M, Swayngim OS.Saline irrigation in gastric hemorrhage: theeffect of temperature. J Surg Res.1980;28:204-205

5. Sherman NJ, Clathworthy HW. Gastroin-testinal bleeding in neonates: a study of94 cases. Surgery. 1967;62:61 4-620

6. Cox K, Ament ME. Upper gastrointestinalbleeding in children and adolescents. Pe-diatrics. 1979:63:408-413

7. Ament ME, Berquist WE, Vargas J, PerisicV. Fiberoptic upper intestinal endoscopyin infants and children. Pediatr Clin NorthAm. 1988;35:141 -155

8. Szasi lJ, Morrison RT, Lyster OM. Tech-netium-99m-labelled red blood cell scan-ning to diagnose occult gastrointestinalbleeding. Can J Surg. 1985;28:51 2-518

9. Silber G, Klish WJ. Hematochezia in in-fants less than six months of age. Am JDis Child. 1986:140:1097-1098

10. Powell GK. Milk and soy induced entero-colitis of infancy. Clinical features andstandardization of challenge. J Pediatr.1978:93:553-561

11. More OG, Raper RF, Munro IA, et al.Randomized, prospective trail of cimeti-dine and ranitidine for control of intragas-tric pH in the critically ill. Surgery.1985;97:21 5-222

12. Borrero E, Margolis lB. Bank S. A random-ized trial of sucralfate vs. antiacid in pre-venting acute gastrointestinal bleeding in1 00 critically ill patients. Am J Surg.1984;148:809-814

1 3. Sharma BO, Walt RP, Pounder RE, et al.Optimal dose of oral omperazole for max-imal 24 hour decrease of intragastric ac-idity. Gut. 1984:25:957-963

14. Oeakin M, Ramage J. Paul A, et al. Effectof enprostil, a synthetic prostaglandin E2on 24 hour intragastric acidity, nocturnalacid and pepsin secretion. Gut.1986:27:1054-1082

15. Mulvihill 5, Pappas TN, Passaro E, OebasHT. The use of somatostatin and its ana-logs in the treatment of surgical disorders.Surgery. 1987:100:467-473



EDUCATIONAL OBJECTIVE

54. The pediatrician should havean appropriate recognition of thereasons for excessive school ab-sence cited by adolescent pa-tients. (Recent Advances, 90/91)


PIR 116 pediatrics in review #{149} vol. 12 no. 4 october 1990

16. Matthewson K, Swain CP, Bland M, et al.Randomized comparison of Nd YaG laser,heater probe (HP) and no endoscopic ther-apy for bleeding peptic ulcer. Gastroenter-ology. 1987:92:1522. Abstract

17. Johnson WC, Widrich WC, Ansell JE, etal. Control of bleeding varices by vaso-pressin: a prospective randomized study.Ann Surg. 1977;186:369-374

18. Hassall E, Berquist WE, Vargas J, AmentME, Dorney S. Sclerotherapy for extra-hepatic portal hypertension in childhood.J Pediatr. 1989;115:69-74

19. Lamiell JM, Beyandt TB. Mallory-Weisssyndrome in two children. J Pediatr.1978:92:583-586

Self-Evaluation Quiz

6. Acidosis due to blood loss is determinedprimarily by:

A. Gastric hypersecretion.B. Tissue anoxia.C. Transfer of fluid and electrolyte from the

intracellular to the extracellular compart-ment.

0. Renal compensatory mechanisms.

7. In monitoring the clinical response of apatient with acute hemorrhage, the mostvaluable measurement among the followingis:A. Hematocrit.

B. Hemoglobin.C. Volume of blood lost.0. Vital signs.

8. In patients with upper gastrointestinalbleeding of uncertain origin, the most usefuldiagnostic procedure among the followingis:A. Radiographic study using barium.B. Angiography.C. Endoscopy.0. Radionuclide scan.

9. Among the following, the most commoncause of rectal bleeding in patients in whom

proctosigmoidoscopy, colonic endoscopyand air-contrast barium studies give nega-tive results is:A. Intussusception.

B. Meckel diverticulum.C. Small bowel tumor.0. A vascular lesion of the intestine.

10. Stress ulcers in children most com-monly involve the:

A. Ouodenum.B. Pyloric antrum.C. Lesser curvature of the stomach.0. Fundus of the stomach.

11. Agents that may be appropriately usedin the management of peptic ulcer diseaseinclude each of the following except:

A. Corticosteroids.B. Prostaglandins.C. H2 blockers.0. Antacids.

School Absenteeism

High-Risk Youth and Health: The Case of Excessive School Absence. WeitzmanM, Alpert JJ, Klerman, LV, et al. American Academy of Pediatrics. Pediatrics.

� 1 986;78:31 3-322.Medical Examination of School Entrants: Later School Problems and Absenteeismof Attenders and Non-attenders. Am J Public Health. 1985;75:395-396.

I Children at Risk: Current Social and Medical Challenges. Zuckerman B, WeitzmanM, Alpert JJ. Pediatr C/in North Am. 1 988;35:1 253-1269.

� How Do I Value You? Let Me Count the Ways. Montemayor AM. Newsletter.� Intercultural Development Research Association. 1989;1 6:1 -1 1.

Children aged 6 to 17 years (kindergarten through twelfth grade) average 5 days

of school missed per school year for health or health-related conditions that are mostoften acute and self-limited or need minimal medical intervention. Rarely is chronicillness the cause of excessive absence from school but, when it does occur, itbecomes the responsibility of parent and pediatricians to initiate measures to keepthe educational experience intact for such children to the extent possible consideringthe condition and other circumstances.

There is a significant association between lack of motivation, inappropriate lag ingrade for chronological age, repeated school absence, and subsequent school failureand “drop out.” This most often has a variety of social, psychological, and perhapseconomic causes. In some families, it is important to recognize that minor healthproblems superimposed on a complex psychosocial environment and parental anxietymay facilitate excessive absences.

In recent years, it has been recognized that excessive school absence, withoutcontributing physical health problems, is an indicator of risk-taking or deviant behaviorthat can lead to health and social problems during adolescent or young adult years.Recognition by physicians of the pattern of repeated absence may allow for earlyinterventions that could prevent such conditions as early sexual activity, substanceabuse (especially smoking and alcohol use), and delinquent behavior.

Comment: Awareness by physicians and educators of repeated school absence asa symptom that requires some creative strategies for intervention may allow for thedevelopment of relevant community-based models that integrate the needs of the “atrisk” student and family with community resources, including the health and educa-tional system that ultimately must respond. (Fernando A. Guerra, MD, Editorial Board)



DOI: 10.1542/pir.12-4-1071990;12;107Pediatrics in Review

Marvin E. AmentPatient

Diagnosis and Management of Upper Gastrointestinal Tract Bleeding in the Pediatric

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