Nutrisi in Gastric Ulcer

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Nutrition in Clinical Practicehttp://ncp.sagepub.com/

When to Feed the Patient With Gastrointestinal Bleeding

Stephen A. McClave and Wei-Kuo ChangNutr Clin Pract 2005 20: 544

DOI: 10.1177/0115426505020005544

The online version of this article can be found at:http://ncp.sagepub.com/content/20/5/544

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The American Society for Parenteral & Enteral Nutrition

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Clinical Dilemma

When to Feed the Patient With Gastrointestinal Bleeding

Stephen A. McClave, MD*; and Wei-Kuo Chang, MD*Departments of Medicine, University of Louisville School of Medicine, Louisville, Kentucky; and Tri-Service

General Hospital, National Defense Medical Center, Taipei, Taiwan

ABSTRACT: Whether to provide artificial enteral nutri-tion therapy to a patient with evidence ofgastrointestinalbleeding (GIB) creates a difficult clinical dilemma.Con-cern that enteral feeding may contribute to themorbidityassociated with GIB leads to delays in initiating enteral

therapy or to cessation of feeding in the patient inwhomartificial nutrition support has already been started. Sur-prisingly, evidence of GIB is not an automaticcontraindi-cation to further enteral feeding. Depending on theetiol-ogy of the GIB, enteral nutrition may protect thegutmucosa and reduce further bleeding in somepatients,actually increase risk for rebleeding in other patients,

or

serve as a moot point with no relation to furtherbleeding

or morbidity in still other patients. In many cases,anendoscopic evaluation is needed to distinguish thediffer-ential etiology of the GIB. The nutrition support specialist

needs a full understanding of the physiology behindthevarying diagnoses for GIB to know whether feedingscanbe initiated or continued or whether enteral feedingsneedto be withheld for 48-72 hours until risk for

rebleeding and further morbidity is minimized.

Evidence of gastrointestinal bleeding (GIB) is a

common fear factor for nutrition supportspecialists,causing them to stop enteral feeding orwithholdinitiation of feedings in the first place. Theclinical

significance of GIB is variable, ranging frominnoc-uous guaiac-positive coffee-ground gastric

aspirateto clinically significant GIB with hemodyncom-promise. The decision to start entfeeding orcontinue feeding once evidence of develops isbased on the etiology of the bleed. In patients,the etiology of the GIB is such that en

feedingmay protect the patient and reducelikelihood forcontinued bleeding. In other patients, theetiology of

Correspondence: Stephen A. McClave, MD, ProfeMedicine, Division of Gastroenterology/HepatologS. Jackson St.,Louisville, Kentucky 40202. Electronic mail may [email protected].

0884-5336/05/2005-0544$03.00/0Nutrition in Clinical Practice 20:544-550, October 2005Copyright 2005 American Society for Parenteral and EnteNutrition


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GIB is different, the volume of bleeding may beater, and providing enteral nutrition may be ality jeopardizing the chances for hemostasis andeasing risk for rebleeding.here are usually 2 distinct scenarios for GIB inintensive care unit (ICU) setting. One scenariolves the critically ill, septic patient receivinghanical ventilation who develops GIB several

s after admission to the ICU. The etiology of thein this setting invariably involves stress gas-athy, and usually results in a fairly low volume

eeding. The lesions in stress gastropathy aretiple diffuse erosions or very shallow ulcers.r 20-30 erosions may be present, tending to

ur proximally in the gastrointestinal tract, mostmonly in the fundus of the stomach. Except forbleeding, these lesions are otherwise asymptom-and are painless clinically. The pathophysio-

c mechanism of these lesions is mucosal isch-a. Because the lesions are so numerous and soerficial throughout the gastric fundus, perform-endoscopy and using hemostasis techniques tothe bleeding are not needed. In fact, usually the

cal conditions and presentation are so typicalendoscopy is not required to confirm the diag-

s (the diagnosis may be assumed and supportiveapy may be initiated).n the other hand, a different scenario involvespatient who presents to the emergency room a massive acute upper GIB, undergoes endo-

pic intervention, and is then admitted directly to

the ICU. In this latter patient, the differentialdiagnosis is wider, involving peptic ulcerdisease,Mallory-Weiss tear, gastritis, esophagitis, oracutevariceal bleeding. The volume of bleeding isusuallygreater in this scenario, hypotension andhemody-namic instability are common, and patientsaremore likely to require blood transfusion. Ofthe

different etiologies, the most common is eitheragastric or duodenal ulcer. These lesions tend tobedistal (the majority occurring in the duodenalbulb,the rest in the body and antrum of thestomach),tend to be solitary and deep, and clinically aremorelikely to be associated with abdominal pain.Thepathophysiologic mechanism in peptic ulcerdisease

involves Helicobacter pylori infection or use ofnon-steroidal antiinflammatory drugs. Thepathophysio-logic mechanism of acute variceal bleedinginvolves

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October 2005 FEEDING THE GI BLEEDER 545

Table 1 visible signs of blood. Overt bleeding is defined byDifferentiating those patients who may be fedimmediatelyfrom those for whom feedings should be delayedafter presentation of GIB

May usually be fed immediatelyStress gastropathy

Peptic ulcer disease with clean ulcer base or flatspot Mallory-Weiss tearAngiodysplasiaLower GI bleeds

Feeds should be delayed for 48 hPeptic ulcer disease with adherent clot, visible vessel,

active ooze/spurter, or lesion requiring electrothermalcoagulation therapy

Esophageal or gastric varices

GIB, gastrointestinal bleeding.

cirrhosis and portal hypertension. Endoscopyis

required to establish the diagnosis (from amongthenumerous possibilities) and to achievehemostasisthrough such techniques asthermocoagulation,mechanical hemoclips, injection therapy, orrubberband ligation.

Understanding the difference between these2scenarios is imperative for the clinician toknowwhether or not it is safe to provide nutrition

supportby the enteral route (Table 1). For patients inthefirst scenario involving stress gastropathy,enteralfeeding is safe, its use serves to protect thepatient,and continuing to provide feedings may reducethelikelihood for further bleeding. For patients inthesecond scenario involving massive upperGIB,enteral feeding may be temporarilycontraindicated.

The patient has to be stabilized first with regardtotheir bleed. Continuing to provide feedings inthesepatients may actually increase the likelihoodforrebleeding. The enteral feeding can be startedlateronly when risk from rebleeding has diminished.

Patients Who Develop GIB After Admissionto the ICU

The literature in the past, which was mainly

retrospective, suggested that thedevelopment ofany GIB in the ICU had a profound adverseeffect onoutcome, raising mortality dramatically.1

Concern

over this issue led to excessive use of acireducingagents, providing stress prophylaxis to aanypatient admitted to the ICU. More recentprospec-tive studies have focused on thedifferentiationbetween any evidence of GIB and clinicaimpor-tant hemorrhage and have thus shown tthemorbidity and mortality associated with Gthe

ICU is much less than previously thought.Amaz-ingly, this same body of literature has shthatone of the best strategies for preventing thecritically ill patient is to provide enteralfeeding.

Specific definitions of bleeding in the IChavebecome very important. 2,3 Occult GIBrefers toguaiac-positive stool or gastric aspirate,with no

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presence of hematemesis (bright-red blood oree grounds per nasogastric tube), hematocheziaght-red blood per rectum), or melena (black stoolrectum). Clinically important hemorrhage,

wever, is defined as overt bleeding plus eithermodynamic changes or need for blood transfusion.modynamic changes mean that the patient isotensive, tachycardic, or orthostatic. The needtransfusion usually is defined by a patient

uiring 2 units of blood transfused.2,3

ccording to these definitions, more recent stud-have shown that, whereas the incidence of overtin the ICU ranges from 5% to 25%, the inci-

ce of clinically important hemorrhage rangesy from 3.7% to 6.0%. 2,3 One report showed thatand aggressive volume resuscitation alone

reased the incidence of GIB to 0.6%.3 In a Cana-n multicenter trial (where patients in the ICUd to have greater severity of critical illness thanse patients in the United States), the mortality inse patients with a clinically important hemor-ge was 48.5%, whereas the mortality in thosehout clinically important hemorrhage was only%. 2 In a large study from the United States,rtality in those patients that demonstrated evi-ce of clinically important hemorrhage was 31%.4

prisingly, the deaths in these patients with GIB

e felt to be related to their underlying diseasecess and not to the GIB itself.4

he main factor in the pathophysiology of the GIBhese patients is stress gastropathy and mucosalemia. 3 Reduction of blood flow to the gastric

cosa sets up the injury. The ability to stimulateod flow to the gut explains why ultimately enteralding is such a good stress prophylactic agentinst GIB. Reduction in blood flow to the gastriccosa sets up a vicious cycle. Reduced perfusion togastric mucosa results in a buildup of lacticosis and a drop in the intramural pH of the

tric wall. These factors lead to further reductionastric blood flow. The initial insult of hypoper-on leads to the increased production of nitricde, superoxide radicals, and a reduction in thease of cytoprotective prostaglandins.3

When blood flow is restored to the gastric mucosa,resultant reperfusion hyperemia may facilitaten greater injury. The restoration of blood flowhes out the vascular bed, releasing a number oferoxide radicals and inflammatory cytokines,ch increase the overall inflammatory response.end result is a defect in the mucosal barrier.

eased permeability between the gastric epithe-cells, reduction in thickness and bicarbonatetent of the mucous layer, and decreases in pros-

andin synthesis now afford the opportunity forher injury to the mucosal defect from acidsent within the gastric lumen.3

s recent studies have shown that the incidencelinically important hemorrhage is much lessn previously thought, it is not felt to be cost-

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546 MCCLAVE AND CHANG Vol. 20, No. 5

effective for all patients in the ICU to receive acid-reducing medications. In the past, the practiceofstress prophylaxis was one of the biggestfinancialdrains on the hospital pharmacy. Adverse eventsare

associated with the use of acid-reducingagents,such as allergic reactions, likelihood forbacterialcolonization of the stomach, and increased riskofaspiration pneumonia. Few clinicians,though,regard use of enteral nutrition as an effectivestressprophylactic agent. In a recent survey, 0.9%ofrespondents indicated that they used enteralnutri-

tion as primary agents for stress prophylaxis.How-ever, 51% of respondents indicated that theydiscon-tinued primary acid-reducing agents on initiationof enteral nutrition.5

Early on, most of the literature involvingenteralnutrition and stress gastropathy focused oncontrolof intragastric pH. Enteral nutrition formulas arealkaline, with a pH in the range of 5.5-7.0. Mostofthe studies would suggest that, according to

thealkalinity of the formulas, the intraluminal pH

should rise as a response to infusion ofenteralformula. However, their actual effect onintragastricpH is variable.1 In a recent review by Maclaren et

al,1 studies showed that gastric intraluminal pHincreased in response to infusion of enteralnutri-tion. In one study, enteral nutrition was moreeffec-tive in raising the pH than histamine-2 (H-2)block-ers, proton pump inhibitors, or antacidtherapy. 6

Two studies, however, showed no change in pHinresponse to infusion of enteral nutrition, 7,8 and1study actually showed a decrease in the pHinresponse to enteral nutrition (or at least the pHwasmore difficult to control once enteral nutrition

wasstarted).9This variable effect from infusion ofenteral nutrition may be related to the fact that

onone hand, the alkaline formula may bgastricacid, whereas on the other hand, the lunutri-ents may stimulate further productiongastricacid.

What is clear is that if the managemestress prophylaxis was solely focuseraising the pH, infusion of enteral formuthe stomach is more effective than indistal to the pylorus. In one study, infusformula into the duodenum kethe pH 4.5 in 32% of 143 aspiratescontrast,infusion into the stomach held the pH4.5 inof196 aspirates (p .001).10 However, thedifferencein the effect of postpyloric enteral nutritintra-

gastric infusion was clinically negligibleregardto preventing clinically imphemorrhage.10

What may be much more importapreventingstress-induced gastropathy is the effeenteralnutrition on intestinal blood flow. In a stu257patients operated on for cancer, at wtime anoxygen probe was placed in the cecaBraga et

al11 showed that mean intestinal tissuoxygentension was significantly higher in the gran-domized to enteral nutrition comparedthose randomized to parenteral nutritiomm Hg vs31 mm Hg, respectively, p .001). Insecond



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dy, Revelly et al12 studied postoperative cardio-cular patients who received a balloon pump forgestive heart failure after surgery. With sophis-ted monitoring systems, hemodynamic changese monitored as patients began receiving enteralding. Mean systemic blood pressure decreasedm 75 mm to 70 mm Hg with the infusion oferal nutrients. Cardiac output was essentiallyhanged. Splanchnic blood flow, however, increasedificantly.12 With mucosal ischemia as the main

hophysiologic mechanism for stress-induced gas-athy, this effect of enteral nutrients on increasing

nchnic blood flow may be a much bigger factorn its effect on pH in explaining its ability to preventeding in the critically ill patient.

surprisingly large volume of studies in theature would suggest that enteral nutrition is a

y effective stress prophylactic agent.1 In theent review by Maclaren et al, 1 5 prospectivedomized trials that compared acid-reducingnts to placebo showed no clinical benefit. Inter-ngly, a large percentage of the controls in thesedies (4.8%-72.8%) who were randomized toeive placebo in fact received enteral nutrition.ection from the enteral feeding in controls maylain why there was no difference in incidence ofcompared with study patients who received

g. In the 1 prospective randomized trial that didw a benefit of acid-reducing agents to placebo,fewest number of controls (3.8%) received

eral nutrition. 1 In a large prospective study of0 ICU patients, post hoc analysis showed thattinuous enteral nutrition was associated with a

% reduction in the rate of GIB.13 In a prospectivedy of 166 patients with spinal cord injury initiallyeiving a H-2 receptor blocking agent, the timingnitiation of enteral nutrition affected the inci-ce of GIB. Reducing the time to initiation oferal nutrition from 15.5 to 4.6 days was associ-

d with a decrease in the incidence of GIB from% to 2.0% (p .05).14 In a prospective random- controlled trial of 181 burn patients, there was

significant difference in the incidence of GIBween 3 groups of patients, those receiving acid-ucing therapy, those receiving enteral nutrition,those receiving both.15,16

n a large retrospective study over a 2-year periodurn patients, patients received an IV H-2 recep-blocker agent for stress prophylaxis while in the17 Subsequently, over the next 2 years, no-reducing therapy was used, and enteral nutri-was used instead as the primary agent for

ss prophylaxis for patients while hospitalized in

unit. In a total of 562 patients, the incidence ofer GIB was reduced from 8.3% during the first 2rs to 3.3% for the subsequent 2 years withversion from the acid-reducing therapy to enteralding (p .05), and the incidence of serious upperwas decreased to one-third (from 1.98% to

3%, p NS) from the first to the second timeod as well.17 The most impressive study was a

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prospective, multicenter trial by the Canadian Crit-ical Care Trials Group which looked at 1770 criti-cally ill patients in the ICU in an effort to identifythose factors that increased the risk of GIB vsthose factors that decreased risk.18Two factorswerefound to decrease risk of bleeding: use of IV

raniti-dine and enteral tube feeding. According totherelative risk, confidence intervals, and pvalues,enteral feeding was at least as good, if not better,atreducing risk of bleeding as the IV ranitidine.18

It is not surprising then that in 2 recent surveys,interesting trends have been demonstrated overthe past few years between use of acid-reducingtherapy and use of enteral nutrition for stressprophylaxis. In a retrospective analysis over a 4-year period in a medical ICU involving almost

3000 patients, Devlin et al19

showed that the useof pharmacologic acid-reducing agents was reduced significantly from71%to 21% (p .001). Use of enteral nutrition duringthis period increased from 51.1% to 79.1%.Interest-ingly, the incidence of stress ulcerationremainedunchanged.19 In a prospective analysis intraumapatients after the introduction of an ICUprotocol,the same investigator showed that the use of

phar-macologic agents decreased from 70% to 26%(p.001).20 As use of enteral nutrition wassubstitutedfor the decreasing use of acid-reducing agents,therate of GIB was shown to decrease from 25.3%to19.3%(although the difference did not meetstatis-tical significance).20

In the majority of critically ill patients, use of EN

alone should provide adequate protection orprophy-laxis against GIB. In a certain subset of patients in

the ICU, risk of GIB is significantly greater accord-ing to the presence of well-defined risk factors.Inthese patients, provision of EN alone may notgivesufficient protection against stress gastropathyandGIB, and consideration should be made to addingan

acid-reducing medication. In a landmarkstudy,Cook et al 2 identified 2 major risk factors that

increase risk of bleeding in the Mechanicalventilation for 48 hours is associated withfoldincrease in bleeding (p .001), and coagulisassociated with a fourfold increase in blee(p .001). A third risk factor, clinical shock,missed statistical significant as a factorassociated withincreased risk of bleeding (p .08).2 In 847patientswith at least 1 positive risk factorincidence of clinically important hemorrhage was 3.7the1405 patients with no risk factorsincidence of bleeding was only 0.1%.2 Thus, a grecommen-dation based on this study would be thstress

prophylaxis provided by EN shouldsupple-mented with an acid-reducing a(preferably aproton-pump inhibitor) in the criticalpatientwho has both evidence of coagulopathy receiv-ing mechanical ventilation, or the pawhoshows signs of overt GIB.

One other group of patients that may rethecombination of EN and acid-reducing age

thosepatients with burns or head injury. Criticill



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ents who have sustained burns or a head injuryy have the additional component of a hypersecre- state and excessive acid production. The Curl-s ulcers that develop in burn patients and thehings ulcers that develop in head-injury patientsd to be deep solitary lesions (as opposed to thetiple, superficial erosions that occur in critically illents without burns and head injuries). In theseents, stress prophylaxis with enteral feeding aloney be insufficient, and an acid-reducing agent mayequired in addition to provide adequate protection.

ients Who Present With Acute GIB anden Are Admitted to the ICU

n the second scenario where a patient presentsemergency room with an acute upper GIB, isuated by endoscopy, and then admitted to the the potential etiologic factors are more vari-

e. Endoscopic surveys in the past have shown75% of these patients have lesions that are acid

ted, with equal distribution between gastritis,tric ulcer, and duodenal ulcer.21 The other 25% ofents usually present with bleeding esophagealces, Mallory-Weiss tear, or esophagitis.21 Often

en these patients are placed in the ICU, factorst complicate their course are present, such asgulopathy and splanchnic ischemia.

With bleeding peptic ulcer disease, the patho-siologic mechanism most often is H pylori infec-in 85% of cases, with use of nonsteroidal anti-

ammatory agents accounting for the remaining%-15% of cases.22 Less than 1% of these patientsh upper GIB and ulcer disease will involve otherors such as Zollinger-Ellison syndrome, Crohnsase, systemic lupus erythematous, or viral infec-. These lesions tend to be solitary, and the risk ofeeding is related to the presence or absence of a

ble vessel. The concept of a visible vessel refershe situation where the ulcer has eroded down toactual blood vessel (usually an artery) and thatpresence of this vessel protruding up throughbed of the ulcer is associated with a high likeli-d for rebleeding. Endoscopic therapy, which pro-es injection of vasoconstrictive agents and elec-autery thermocoagulation, achieves hemostasis0% of these cases.22

is important for nutritionists to understand thecept of visible vessel or bleeding stigmata, toreciate the risk of further bleeding, and to know

w to differentiate those patients who can be fedmediately from those for whom feeding should be

ayed. An ulcer with a clean base is associatedh a 5% risk of rebleeding, whereas an ulcer withat spot (whether it be red, black, or blue) isociated with a 10% risk of rebleeding.22 Anerent clot attached to the ulcer bed is associated

h a 22% risk of bleeding, whereas a visible vesselt involves an actual knee or elbow of the vesselking up through the bed is associated with a 43%eeding rate. An active ooze is associated with a

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55% rebleeding rate, whereas an active arterialspurter is associated with 65%-85% chance ofcontinued bleeding. In general, 62% of caseswillpresent with either a clean ulcer base or a flatspot.22

These lesions have such a low risk of rebleeding

thatthey do not require electrocoagulationtherapy.

These patients can be fed immediately aftertheendoscopic procedure. The remaining patientswillhave an adherent clot, visible vessel, or activebleed-ing; have a much higher rate of rebleeding; andthusrequire endoscopic therapy. The periodimmediatelyafter endoscopic therapy is somewhat tenuous

andrisky, the likelihood for rebleeding is still signifi-cant, and thus feedings may need to be withheldfor48 hours.

The risk of rebleeding after endoscopic therapyis about 20%.21 Control of gastric acid, andincreasingthe pH to 6 becomes important in stabilizingtheclot over the visible vessel and reducing riskoffurther bleeding. Clotting is adversely affectedby

low pH and the presence of acid. 3 Clotting isopti-mized if the pH can be increased to a rangeof5.0-7.0. Pepsin, secreted by the stomach,has atendency to lyse the clots. Pepsin is inactivated byapH of 4.5, and maintaining the pH 5 neutralizesalmost all of the acid present in the stomach.Rais-ing the pH 6 is required to assure maintenanceofthe clot over a lesion once the bleeding hasstopped.3

The ability of various acid-reducingmedicationsto maintain a high pH is variable. In one study,

Netzer et al 23 showed that there is a rapid,veryearly development of tachyphylaxis to H-2receptorblocking agents. Although the pH in response toIVH-2 blockers is 5.0 on day 1, it decreases to 3.0on

day 2, and then 2.7 by day 3. In contrast,aggressivetherapy with an IV proton-pump inhibitor

(omepra-zole) keeps the pH 6.0 for a full 3 afterinitiation of the drug.23 In a large prospmul-ticenter trial, there was no effect fromblockerson reducing risk of morbidity rebleeding.24 Incontrast, the impact of proton-pinhibitors onreducing rate of rebleeding was significain adifferent study by Lau et al, 25 when aggres-sively in high enough doses. The proton-inhib-itor omeprazole was given as an 80-mgbolusdose, followed by a continuous infusionmg/h for72 hours (after which 20 mg a day were

for thenext 18 days).25 Compared with placebof thisaggressive dosing of a proton-pump inhwasassociated with a reduction in the reblerate at7 days from 5.8% down to 1.7% ( p .asignificant decrease in the hospital lengtstayfrom 5.0 to 4.0 days, and a signreduction inthe mean units of blood transfused fro

to 2.7units (p .04).25

It is important for the nutritioniunderstandthese concepts in order to know whensafe torefeed the patient with a bleeding pepulcer.Providing enteral nutrition during the firs72hours after endoscopic therapy may intewiththe ability of these acid-reducmedications to



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trol intragastric pH and continue to stabilize theover the visible vessel. Although theoretically,

agastric feedings might have less effect onreasing pH through stimulation of gastric acidretion than intrajejunal feedings (because of afering effect from the alkaline formulas), thect by either route has not been studied well,cifically in patients with GIB due to peptic ulcer

ease. Thus, most experts recommend waiting att 48 hours after endoscopic therapy before initi-g enteral feeding. In a small study of 26 patients

h upper GIB who underwent injection therapy

peptic ulcer disease, de Ledinghen et al 26 ran-mized patients to early refeeding the day after

oscopic therapy vs delayed feeding to begin 3

s after injection therapy. Surprisingly, the num-of units of blood transfused was less in the earlyeding group (2.6 vs 3.3 units, p NS), andpital length of stay was reduced significantly inearly refeeding group (6.8 days vs 9.0 days, pcompared, respectively, with the group receiv-delayed refeeding.26 Only 1 patient in the

ayed feeding group developed recurrent GIB (vse in the early refeeding group). Although this

dy would suggest that it is not only safe butually beneficial for patients to receive enteralding soon after endoscopic therapy, the study isll and experts are reluctant to make widespread

ommendations based on its results. Thus, conser-ve recommendations would be to start enteral

dings immediately in the patient with pepticer disease who is found on endoscopy to have a

n ulcer base or flat spot. In those patients wither disease and a visible vessel who have under-e endoscopic hemostasis therapy, it is prudent tot 48 hours before restarting feeding.ther etiologies that account for patients with

te upper GIB include angiodysplasia and Mal--Weiss tear. Angiodysplasias tend to be lower-ume venous bleeds (as compared with larger-ume arterial bleeds associated with peptic ulcerease), and these lesions do not always requireoscopic therapy. Risk of rebleeding after electro-tery therapy is fairly low, and there is no need toay refeeding in these patients. Mallory-Weissrs involve retching and vomiting, with a tear ofmucosa usually in the area of the gastroesoph-al junction. Up to 95% of these lesions stop

eding spontaneously, and endoscopic therapy isely required.25 These patients also may resumeeral feeding as soon as tolerated.

n contrast, patients who present with upper GIBm esophageal varices, cirrhosis, and portal hyper-sion tend to have large-volume bleeds with anociated high morbidity and mortality. Esopha-l varices develop because of difficulty in venousnage through a scarred cirrhotic liver. The por-

venous system, which is normally a low-pressurempliant system, develops into a higher-pressuretem with dilated, tortuous veins. Varices bleedause of a buildup of pressure in the splanchnic

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circulation above 12 mm Hg. Above thispressure,the varices will literally burst at a single point and

lead to significant high-volume bleeding. Thevaricestend to bleed from 1 site on 1 varix, as the

large-volume bleed that ensues decompresses thesystem.Endoscopic management involves band ligationofthese varices. A banding device placed on the endofan endoscope flips a rubber band over thevarix.Over a matter of days, the compression of therubberband causes fibrosis and scarring at the site ofthevarix. Eventually, the banded varix falls off,

scartissue is left behind, and the varices areobliterated.

Again, the nutritionist needs to be familiar with

these issues to know whether it is safe to feedthepatient with acute variceal bleeding. Onesmallstudy, again by de Ledinghen et al, 27 studied22patients over a year period that presentedwithacute variceal bleeding, who underwent

sclerother-apy or band ligation (followed by infusion ofoct-reotide). Patients were randomized afterendoscopictherapy to either early refeeding 1 day afterbandingor late refeeding in which feedings were notstarteduntil 3 days after banding. Although numbersweretoo small to reach statistical significance, the rateof

rebleeding was shown to be higher in the earlygroupcompared with the late group (33% vs 10%, pNS),hospital length of stay was delayed 2 days (14.5vs12.9 days, p NS), and mortality was slightlyhigher in the early group than the late group (25%vs20%, p NS).27 Of concern was the fact thattherebleeding in the early-fed group occurredearlier,closer to the time of banding than the

rebleedingthat occurred in the late-refeeding group. Also,mor-

tality in the early-fed patients related torebleeding (and aspiration encephalopathy).27

Early refeeding may cause a shift in blooto thesplanchnic circulation, which could leincreasesin pressure and increased risk of reblefrom thevarices. For these reasons, feedshould bedelayed for at least 48 hours after endosther-apy for bleeding esophageal varices. If a(trans-jugular intrahepatic portosystemic swereplaced, one would probably wait at leahours inthese high-risk patients (although there adata

in this specific situation). NG tubes havto beremoved to perform banding. Thereluctance toreplace tubes right away for fear of knooff thebands prematurely (but nasogastric nonethe-less may be placed gingerly approximately 48hours). Cirrhotic patients are uthrombocyto-penic due to hypersplenism, and althougfor

rebleeding is increased, platelets areroutinelygiven before endoscopic interventionbleedingrecurs and platelets are 25,000, platelettransfusion may be used.

Withholding enteral nutrition is rareissuefor patients who present with lower GIBclini-cal presentation of lower GIB invarinvolveshematochezia, and only in circumstances,melena. In a prospective study of 235 pawhopresented with severe hematocthought to



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e a lower GIB, a definitive colonic source for theed was found in 75%. 22 The etiologies for theonic bleeds included diverticulosis, ischemia,morrhoids, rectal ulcer, polyps, cancer, and angi-as.22 Providing enteral nutrition to these patientsely affects the risk for rebleeding, and the deci-n to continue or withhold enteral nutrition usu-

depends on issues related to the patient prepa-on required before colonoscopy. With respect tolower GIB itself, enteral feeding is usually a

ot point.

nclusionsvidence of GIB in the intensive care setting hasable clinical significance. The evidence of a clin-y important hemorrhage may warrant endo-

pic evaluation, especially if the clinician is pronewithhold enteral nutrition in response to signs of

GIB. The decision to initiate, continue, or with-d enteral nutrition is dependent on the specificlogy of the GIB. It is appropriate to continueeral feeding in the patient suspected to havess gastropathy or in that patient found to havetic ulcer disease with a clean ulcer base or flatt. For most lower GI bleeds, it is appropriate to

tinue enteral nutrition as long as it does notrfere with the patient preparation for colonos-y. Patients with GIB for whom enteral nutritionuld be held for at least 48 hours include thoseents who present with an upper GIB and are

nd to have a peptic ulcer disease with visiblesel or those patients who present with esopha-l varices.

erencesacLaren R, Jarvis CL, Fish DN. Use of enteral nutrition fortress ulcer prophylaxis. Ann Pharmacother. 2001;35:1614-1623.ook DJ, Fuller HD, Guyatt GH, et al. Risk factors for gastroin-estinal bleeding in critically ill patients: Canadian Critical Carerials Group. N Engl J Med. 1994;330:377-381.ennerty MB. Pathophysiology of the upper gastrointestinal tract the critically ill patient: rationale for the therapeutic benefits ofcid suppression. Crit Care Med. 2002;30(6 suppl):S351-S355.en-Menachem T, Fogel R, Patel RV, et al. Prophylaxis fortress-related gastric hemorrhage in the medical intensive carenit: a randomized, controlled, single-blind study. Ann Interned. 1994;121:568-575.

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