Nutrition in Clinical Practice

http://ncp.sagepub.com/ When to Feed the Patient With Gastrointestinal Bleeding

Stephen A. McClave and Wei-Kuo Chang Nutr Clin Pract 2005 20: 544 DOI: 10.1177/0115426505020005544

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Clinical Dilem m a
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 nutrition therapy to a patient with evidence of gastrointestinal bleeding (GIB) creates a difficult clinical dilemma. Concern that enteral feeding may contribute to the morbidity associated with GIB leads to delays in initiating enteral therapy or to cessation of feeding in the patient in whom artificial nutrition support has already been started. Surprisingly, evidence of GIB is not an automatic contraindication to further enteral feeding. Depending on the etiology of the GIB, enteral nutrition may protect the gut mucosa and reduce further bleeding in some patients, actually increase risk for rebleeding in other patients, or serve as a moot point with no relation to further bleeding or morbidity in still other patients. In many cases, an endoscopic evaluation is needed to distinguish the differential etiology of the GIB. The nutrition support specialist needs a full understanding of the physiology behind the varying diagnoses for GIB to know whether feedings can be initiated or continued or whether enteral feedings need to be withheld for 48-72 hours until risk for rebleeding and further morbidity is minimized.

aspirate to clinically significant GIB with hemodynamic compromise. The decision to start enteral feeding or continue feeding once evidence of GIB develops is based on the etiology of the bleed. In some patients, the etiology of the GIB is such that enteral feeding may protect the patient and reduce the likelihood for continued bleeding. In other patients, the etiology of

Correspondence: Stephen A. McClave, MD, Professor of Medicine, Division of Gastroenterology/Hepatology, 550 S. Jackson St., Louisville, Kentucky 40202. Electronic mail may be sent to samcclave@louisville.edu.
0884-5336/05/2005-0544$03.00/0 Nutrition in Clinical Practice 20:544-550, October 2005 Copyright 2005 American Society for Parenteral and Enteral Nutrition

5 4 4

Evidence of gastrointestinal bleeding (GIB) is a common fear factor for nutrition support specialists, causing them to stop enteral feeding or withhold initiation of feedings in the first place. The clinical significance of GIB is variable, ranging from innocuous guaiac-positive coffee-ground gastric

the GIB is different, the volume of bleeding may be greater, and providing enteral nutrition may be a liability jeopardizing the chances for hemostasis and increasing risk for rebleeding. There are usually 2 distinct scenarios for GIB in the intensive care unit (ICU) setting. One scenario involves the critically ill, septic patient receiving mechanical ventilation who develops GIB several days after admission to the ICU. The etiology of the GIB in this setting invariably involves stress gastropathy, and usually results in a fairly low volume of bleeding. The lesions in stress gastropathy are multiple diffuse erosions or very shallow ulcers. Over 20-30 erosions may be present, tending to occur proximally in the gastrointestinal tract, most commonly in the fundus of the stomach. Except for the bleeding, these lesions are otherwise asymptomatic and are painless clinically. The pathophysiologic mechanism of these lesions is mucosal ischemia. Because the lesions are so numerous and so superficial throughout the gastric fundus, performing endoscopy and using hemostasis techniques to stop the bleeding are not needed. In fact, usually the clinical conditions and presentation are so typical that endoscopy is not required to confirm the diagnosis (the diagnosis may be assumed and supportive therapy may be initiated). On the other hand, a different scenario involves the patient who presents to the emergency room with a massive acute upper GIB, undergoes endoscopic intervention, and is then admitted directly to

the ICU. In this latter patient, the differential diagnosis is wider, involving peptic ulcer disease, Mallory-Weiss tear, gastritis, esophagitis, or acute variceal bleeding. The volume of bleeding is usually greater in this scenario, hypotension and hemodynamic instability are common, and patients are more likely to require blood transfusion. Of the different etiologies, the most common is either a gastric or duodenal ulcer. These lesions tend to be distal (the majority occurring in the duodenal bulb, the rest in the body and antrum of the stomach), tend to be solitary and deep, and clinically are more likely to be associated with abdominal pain. The pathophysiologic mechanism in peptic ulcer disease involves Helicobacter pylori infection or use of nonsteroidal antiinflammatory drugs. The pathophysiologic mechanism of acute variceal bleeding involves

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Table 1 Differentiating those patients who may be fed immediately from those for whom feedings should be delayed after presentation of GIB May usually be fed immediately Stress gastropathy Peptic ulcer disease with clean ulcer base or flat spot Mallory-Weiss tear Angiodysplasia Lower GI bleeds Feeds should be delayed for 48 h Peptic ulcer disease with adherent clot, visible vessel, active ooze/spurter, or lesion requiring electrothermal coagulation therapy Esophageal or gastric varices
GIB, gastrointestinal bleeding.

cirrhosis and portal hypertension. Endoscopy is required to establish the diagnosis (from among the numerous possibilities) and to achieve hemostasis through such techniques as thermocoagulation, mechanical hemoclips, injection therapy, or rubber band ligation. Understanding the difference between these 2 scenarios is imperative for the clinician to know whether or not it is safe to provide nutrition support by the enteral route (Table 1). For patients in the first scenario involving stress gastropathy, enteral feeding is safe, its use serves to protect the patient, and continuing to provide feedings may reduce the likelihood for further bleeding. For patients in the second scenario involving massive upper GIB, enteral feeding may be temporarily contraindicated. The patient has to be stabilized first with regard to their bleed. Continuing to provide feedings in these patients may actually increase the likelihood for rebleeding. The enteral feeding can be started later only when risk from rebleeding has diminished.

visible signs of blood. Overt bleeding is defined by retrospective, suggested that the development of any GIB in the ICU had a profound adverse effect on outcome, raising mortality dramatically.1 Concern over this issue led to excessive use of acidreducing agents, providing stress prophylaxis to almost any patient admitted to the ICU. More recent prospective studies have focused on the differentiation between any evidence of GIB and clinically important hemorrhage and have thus shown that the morbidity and mortality associated with GIB in the ICU is much less than previously thought.1,2 Amazingly, this same body of literature has shown that one of the best strategies for preventing GIB in the critically ill patient is to provide enteral feeding. Specific definitions of bleeding in the ICU have become very important. 2,3 Occult GIB refers to guaiac-positive stool or gastric aspirate, with no
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Patients Who Develop GIB After Admission to the ICU

The literature in the past, which was mainly

the presence of hematemesis (bright-red blood or coffee grounds per nasogastric tube), hematochezia (bright-red blood per rectum), or melena (black stool per rectum). Clinically important hemorrhage, however, is defined as overt bleeding plus either hemodynamic changes or need for blood transfusion. Hemodynamic changes mean that the patient is hypotensive, tachycardic, or orthostatic. The need for transfusion usually is defined by a patient requiring 2 units of blood transfused.2,3 According to these definitions, more recent studies have shown that, whereas the incidence of overt GIB in the ICU ranges from 5% to 25%, the incidence of clinically important hemorrhage ranges only from 3.7% to 6.0%. 2,3 One report showed that full and aggressive volume resuscitation alone decreased the incidence of GIB to 0.6%.3 In a Canadian multicenter trial (where patients in the ICU tend to have greater severity of critical illness than those patients in the United States), the mortality in those patients with a clinically important hemorrhage was 48.5%, whereas the mortality in those without clinically important hemorrhage was only 9.1%. 2 In a large study from the United States, mortality in those patients that demonstrated evidence of clinically important hemorrhage was 31%.4 Surprisingly, the deaths in these patients with GIB were felt to be related to their underlying disease process and not to the GIB itself.4 The main factor in the pathophysiology of the GIB in these patients is stress gastropathy and mucosal ischemia. 3 Reduction of blood flow to the gastric mucosa sets up the injury. The ability to stimulate blood flow to the gut explains why ultimately enteral feeding is such a good stress prophylactic agent against GIB. Reduction in blood flow to the gastric mucosa sets up a vicious cycle. Reduced perfusion to the gastric mucosa results in a buildup of lactic acidosis and a drop in the intramural pH of the gastric wall. These factors lead to further reduction in gastric blood flow. The initial insult of hypoperfusion leads to the increased production of nitric oxide, superoxide radicals, and a reduction in the release of cytoprotective prostaglandins.3 When blood flow is restored to the gastric mucosa, the resultant reperfusion hyperemia may facilitate even greater injury. The restoration of blood flow flushes out the vascular bed, releasing a number of superoxide radicals and inflammatory cytokines, which increase the overall inflammatory response. The end result is a defect in the mucosal barrier. Increased permeability between the gastric epithelial cells, reduction in thickness and bicarbonate content of the mucous layer, and decreases in prostaglandin synthesis now afford the opportunity for further injury to the mucosal defect from acid present within the gastric lumen.3 As recent studies have shown that the incidence of clinically important hemorrhage is much less than previously thought, it is not felt to be costby guest on January 26, 2013

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effective for all patients in the ICU to receive acidreducing medications. In the past, the practice of stress prophylaxis was one of the biggest financial drains on the hospital pharmacy. Adverse events are associated with the use of acid-reducing agents, such as allergic reactions, likelihood for bacterial colonization of the stomach, and increased risk of aspiration pneumonia. Few clinicians, though, regard use of enteral nutrition as an effective stress prophylactic agent. In a recent survey, 0.9% of respondents indicated that they used enteral nutrition as primary agents for stress prophylaxis. However, 51% of respondents indicated that they discontinued primary acid-reducing agents on initiation of enteral nutrition.5 Early on, most of the literature involving enteral nutrition and stress gastropathy focused on control of intragastric pH. Enteral nutrition formulas are alkaline, with a pH in the range of 5.5-7.0. Most of the studies would suggest that, according to the alkalinity of the formulas, the intraluminal pH should rise as a response to infusion of enteral formula. However, their actual effect on intragastric pH is variable. 1 In a recent review by Maclaren et al,1 studies showed that gastric intraluminal pH increased in response to infusion of enteral nutrition. In one study, enteral nutrition was more effective in raising the pH than histamine-2 (H-2) blockers, proton pump inhibitors, or antacid therapy. 6 Two studies, however, showed no change in pH in response to infusion of enteral nutrition, 7,8 and 1 study actually showed a decrease in the pH in response to enteral nutrition (or at least the pH was more difficult to control once enteral nutrition was started).9 This variable effect from infusion of enteral nutrition may be related to the fact that

Vol. 20, No. 5 on one hand, the alkaline formula may buffer gastric acid, whereas on the other hand, the luminal nutrients may stimulate further production of gastric acid. What is clear is that if the management for stress prophylaxis was solely focused on raising the pH, infusion of enteral formula into the stomach is more effective than infusion distal to the pylorus. In one study, infusion of formula into the duodenum kept the pH 4.5 in 32% of 143 aspirates.10 In contrast, infusion into the stomach held the pH4.5 in 88% of 196 aspirates (p .001).10 However, the difference in the effect of postpyloric enteral nutrition to intragastric infusion was clinically negligible with regard to preventing clinically important hemorrhage.10 What may be much more important in preventing stress-induced gastropathy is the effect of enteral nutrition on intestinal blood flow. In a study of 257 patients operated on for cancer, at which time an oxygen probe was placed in the cecal wall, Braga et al11 showed that mean intestinal tissue oxygen tension was significantly higher in the group randomized to enteral nutrition compared with those randomized to parenteral nutrition (43 mm Hg vs 31 mm Hg, respectively, p .001). In a second
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study, Revelly et al12 studied postoperative cardiovascular patients who received a balloon pump for congestive heart failure after surgery. With sophisticated monitoring systems, hemodynamic changes were monitored as patients began receiving enteral feeding. Mean systemic blood pressure decreased from 75 mm to 70 mm Hg with the infusion of enteral nutrients. Cardiac output was essentially unchanged. Splanchnic blood flow, however, increased significantly.12 With mucosal ischemia as the main pathophysiologic mechanism for stress-induced gastropathy, this effect of enteral nutrients on increasing splanchnic blood flow may be a much bigger factor than its effect on pH in explaining its ability to prevent bleeding in the critically ill patient. A surprisingly large volume of studies in the literature would suggest that enteral nutrition is a very effective stress prophylactic agent.1 In the recent review by Maclaren et al, 1 5 prospective randomized trials that compared acid-reducing agents to placebo showed no clinical benefit. Interestingly, a large percentage of the controls in these studies (4.8%-72.8%) who were randomized to receive placebo in fact received enteral nutrition. Protection from the enteral feeding in controls may explain why there was no difference in incidence of GIB compared with study patients who received drug. In the 1 prospective randomized trial that did show a benefit of acid-reducing agents to placebo, the fewest number of controls (3.8%) received enteral nutrition. 1 In a large prospective study of 1200 ICU patients, post hoc analysis showed that continuous enteral nutrition was associated with a 70% reduction in the rate of GIB.13 In a prospective study of 166 patients with spinal cord injury initially receiving a H-2 receptor blocking agent, the timing of initiation of enteral nutrition affected the incidence of GIB. Reducing the time to initiation of enteral nutrition from 15.5 to 4.6 days was associated with a decrease in the incidence of GIB from 7.6% to 2.0% (p .05).14 In a prospective randomized controlled trial of 181 burn patients, there was no significant difference in the incidence of GIB between 3 groups of patients, those receiving acidreducing therapy, those receiving enteral nutrition, and those receiving both.15,16 In a large retrospective study over a 2-year period in burn patients, patients received an IV H-2 receptor blocker agent for stress prophylaxis while in the ICU.17 Subsequently, over the next 2 years, no acid-reducing therapy was used, and enteral nutrition was used instead as the primary agent for stress prophylaxis for patients while hospitalized in the unit. In a total of 562 patients, the incidence of upper GIB was reduced from 8.3% during the first 2 years to 3.3% for the subsequent 2 years with conversion from the acid-reducing therapy to enteral feeding (p .05), and the incidence of serious upper GIB was decreased to one-third (from 1.98% to 0.73%, p NS) from the first to the second time period as well. 17 The most impressive study was a
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prospective, multicenter trial by the Canadian Critical Care Trials Group which looked at 1770 critically ill patients in the ICU in an effort to identify those factors that increased the risk of GIB vs those factors that decreased risk.18 Two factors were found to decrease risk of bleeding: use of IV ranitidine and enteral tube feeding. According to the relative risk, confidence intervals, and p values, enteral feeding was at least as good, if not better, at reducing risk of bleeding as the IV ranitidine.18 It is not surprising then that in 2 recent surveys, interesting trends have been demonstrated over the past few years between use of acid-reducing therapy and use of enteral nutrition for stress prophylaxis. In a retrospective analysis over a 4year period in a medical ICU involving almost 3000 patients, Devlin et al 19 showed that the use of pharmacologic acidreducing agents was reduced significantly from 71% to 21% ( p .001). Use of enteral nutrition during this period increased from 51.1% to 79.1%. Interestingly, the incidence of stress ulceration remained unchanged. 19 In a prospective analysis in trauma patients after the introduction of an ICU protocol, the same investigator showed that the use of pharmacologic agents decreased from 70% to 26% (p .001).20 As use of enteral nutrition was substituted for the decreasing use of acid-reducing agents, the rate of GIB was shown to decrease from 25.3% to 19.3%(although the difference did not meet statistical significance).20 In the majority of critically ill patients, use of EN alone should provide adequate protection or prophylaxis against GIB. In a certain subset of patients in the ICU, risk of GIB is significantly greater according to the presence of well-defined risk factors. In these patients, provision of EN alone may not give sufficient protection against stress gastropathy and GIB, and consideration should be made to adding an acid-reducing medication. In a landmark study, Cook et al 2 identified 2 major risk factors that

547 increase risk of bleeding in the ICU. Mechanical ventilation for 48 hours is associated with a 16fold increase in bleeding (p .001), and coagulopathy is associated with a fourfold increase in bleeding (p .001). A third risk factor, clinical shock, just missed statistical significant as a factor associated with increased risk of bleeding (p .08).2 In 847 patients with at least 1 positive risk factor, the incidence of clinically important hemorrhage was 3.7%. In the 1405 patients with no risk factors, the incidence of bleeding was only 0.1%.2 Thus, a general recommendation based on this study would be that stress prophylaxis provided by EN should be supplemented with an acid-reducing agent (preferably a proton-pump inhibitor) in the critically ill patient who has both evidence of coagulopathy and is receiving mechanical ventilation, or the patient who shows signs of overt GIB. One other group of patients that may require the combination of EN and acid-reducing agents is those patients with burns or head injury. Critically ill
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patients who have sustained burns or a head injury may have the additional component of a hypersecretory state and excessive acid production. The Curlings ulcers that develop in burn patients and the Cushings ulcers that develop in head-injury patients tend to be deep solitary lesions (as opposed to the multiple, superficial erosions that occur in critically ill patients without burns and head injuries). In these patients, stress prophylaxis with enteral feeding alone may be insufficient, and an acid-reducing agent may be required in addition to provide adequate protection.

Patients Who Present With Acute GIB and Then Are Admitted to the ICU
In the second scenario where a patient presents the emergency room with an acute upper GIB, is evaluated by endoscopy, and then admitted to the ICU, the potential etiologic factors are more variable. Endoscopic surveys in the past have shown that 75% of these patients have lesions that are acid related, with equal distribution between gastritis, gastric ulcer, and duodenal ulcer.21 The other 25% of patients usually present with bleeding esophageal varices, Mallory-Weiss tear, or esophagitis.21 Often when these patients are placed in the ICU, factors that complicate their course are present, such as coagulopathy and splanchnic ischemia. With bleeding peptic ulcer disease, the pathophysiologic mechanism most often is H pylori infection in 85% of cases, with use of nonsteroidal antiinflammatory agents accounting for the remaining 10%-15% of cases.22 Less than 1% of these patients with upper GIB and ulcer disease will involve other factors such as Zollinger-Ellison syndrome, Crohns disease, systemic lupus erythematous, or viral infection. These lesions tend to be solitary, and the risk of rebleeding is related to the presence or absence of a visible vessel. The concept of a visible vessel refers to the situation where the ulcer has eroded down to an actual blood vessel (usually an artery) and that the presence of this vessel protruding up through the bed of the ulcer is associated with a high likelihood for rebleeding. Endoscopic therapy, which provides injection of vasoconstrictive agents and electrocautery thermocoagulation, achieves hemostasis in 90% of these cases.22 It is important for nutritionists to understand the concept of visible vessel or bleeding stigmata, to appreciate the risk of further bleeding, and to know how to differentiate those patients who can be fed immediately from those for whom feeding should be delayed. An ulcer with a clean base is associated with a 5% risk of rebleeding, whereas an ulcer with a flat spot (whether it be red, black, or blue) is associated with a 10% risk of rebleeding.22 An adherent clot attached to the ulcer bed is associated with a 22% risk of bleeding, whereas a visible vessel that involves an actual knee or elbow of the vessel sticking up through the bed is associated with a 43% rebleeding rate. An active ooze is associated with a
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55% rebleeding rate, whereas an active arterial spurter is associated with 65%-85% chance of continued bleeding. In general, 62% of cases will present with either a clean ulcer base or a flat spot.22 These lesions have such a low risk of rebleeding that they do not require electrocoagulation therapy. These patients can be fed immediately after the endoscopic procedure. The remaining patients will have an adherent clot, visible vessel, or active bleeding; have a much higher rate of rebleeding; and thus require endoscopic therapy. The period immediately after endoscopic therapy is somewhat tenuous and risky, the likelihood for rebleeding is still significant, and thus feedings may need to be withheld for 48 hours. The risk of rebleeding after endoscopic therapy is about 20%.21 Control of gastric acid, and increasing the pH to 6 becomes important in stabilizing the clot over the visible vessel and reducing risk of further bleeding. Clotting is adversely affected by low pH and the presence of acid. 3 Clotting is optimized if the pH can be increased to a range of 5.0-7.0. Pepsin, secreted by the stomach, has a tendency to lyse the clots. Pepsin is inactivated by a pH of 4.5, and maintaining the pH 5 neutralizes almost all of the acid present in the stomach. Raising the pH 6 is required to assure maintenance of the clot over a lesion once the bleeding has stopped.3 The ability of various acid-reducing medications to maintain a high pH is variable. In one study, Netzer et al 23 showed that there is a rapid, very early development of tachyphylaxis to H-2 receptor blocking agents. Although the pH in response to IV H-2 blockers is 5.0 on day 1, it decreases to 3.0 on day 2, and then 2.7 by day 3. In contrast, aggressive therapy with an IV proton-pump inhibitor

Vol. 20, No. 5 (omeprazole) keeps the pH 6.0 for a full 3 days after initiation of the drug. 23 In a large prospective multicenter trial, there was no effect from H-2 blockers on reducing risk of morbidity from rebleeding.24 In contrast, the impact of proton-pump inhibitors on reducing rate of rebleeding was significant in a different study by Lau et al, 25 when given aggressively in high enough doses. The proton-pump inhibitor omeprazole was given as an 80-mg IV bolus dose, followed by a continuous infusion at 8 mg/h for 72 hours (after which 20 mg a day were given for the next 18 days).25 Compared with placebo, use of this aggressive dosing of a proton-pump inhibitor was associated with a reduction in the rebleeding rate at 7 days from 5.8% down to 1.7% ( p .001), a significant decrease in the hospital length of stay from 5.0 to 4.0 days, and a significant reduction in the mean units of blood transfused from 3.5 to 2.7 units (p .04).25 It is important for the nutritionist to understand these concepts in order to know when it is safe to refeed the patient with a bleeding peptic ulcer. Providing enteral nutrition during the first 4872 hours after endoscopic therapy may interfere with the ability of these acid-reducing medications to
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control intragastric pH and continue to stabilize the clot over the visible vessel. Although theoretically, intragastric feedings might have less effect on decreasing pH through stimulation of gastric acid secretion than intrajejunal feedings (because of a buffering effect from the alkaline formulas), the effect by either route has not been studied well, specifically in patients with GIB due to peptic ulcer disease. Thus, most experts recommend waiting at least 48 hours after endoscopic therapy before initiating enteral feeding. In a small study of 26 patients with upper GIB who underwent injection therapy for peptic ulcer disease, de Ledinghen et al 26 randomized patients to early refeeding the day after endoscopic therapy vs delayed feeding to begin 3 days after injection therapy. Surprisingly, the number of units of blood transfused was less in the early refeeding group (2.6 vs 3.3 units, p NS), and hospital length of stay was reduced significantly in the early refeeding group (6.8 days vs 9.0 days, p .01) compared, respectively, with the group receiving delayed refeeding.26 Only 1 patient in the delayed feeding group developed recurrent GIB (vs none in the early refeeding group). Although this study would suggest that it is not only safe but actually beneficial for patients to receive enteral feeding soon after endoscopic therapy, the study is small and experts are reluctant to make widespread recommendations based on its results. Thus, conservative recommendations would be to start enteral feedings immediately in the patient with peptic ulcer disease who is found on endoscopy to have a clean ulcer base or flat spot. In those patients with ulcer disease and a visible vessel who have undergone endoscopic hemostasis therapy, it is prudent to wait 48 hours before restarting feeding. Other etiologies that account for patients with acute upper GIB include angiodysplasia and Mallory-Weiss tear. Angiodysplasias tend to be lowervolume venous bleeds (as compared with largervolume arterial bleeds associated with peptic ulcer disease), and these lesions do not always require endoscopic therapy. Risk of rebleeding after electrocautery therapy is fairly low, and there is no need to delay refeeding in these patients. Mallory-Weiss tears involve retching and vomiting, with a tear of the mucosa usually in the area of the gastroesophageal junction. Up to 95% of these lesions stop bleeding spontaneously, and endoscopic therapy is rarely required.25 These patients also may resume enteral feeding as soon as tolerated. In contrast, patients who present with upper GIB from esophageal varices, cirrhosis, and portal hypertension tend to have large-volume bleeds with an associated high morbidity and mortality. Esophageal varices develop because of difficulty in venous drainage through a scarred cirrhotic liver. The portal venous system, which is normally a low-pressure compliant system, develops into a higher-pressure system with dilated, tortuous veins. Varices bleed because of a buildup of pressure in the splanchnic
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circulation above 12 mm Hg. Above this pressure, the varices will literally burst at a single point and lead to significant high-volume bleeding. The varices tend to bleed from 1 site on 1 varix, as the largevolume bleed that ensues decompresses the system. Endoscopic management involves band ligation of these varices. A banding device placed on the end of an endoscope flips a rubber band over the varix. Over a matter of days, the compression of the rubber band causes fibrosis and scarring at the site of the varix. Eventually, the banded varix falls off, scar tissue is left behind, and the varices are obliterated. Again, the nutritionist needs to be familiar with these issues to know whether it is safe to feed the patient with acute variceal bleeding. One small study, again by de Ledinghen et al, 27 studied 22 patients over a year period that presented with acute variceal bleeding, who underwent sclerotherapy or band ligation (followed by infusion of octreotide). Patients were randomized after endoscopic therapy to either early refeeding 1 day after banding or late refeeding in which feedings were not started until 3 days after banding. Although numbers were too small to reach statistical significance, the rate of rebleeding was shown to be higher in the early group compared with the late group (33% vs 10%, p NS), hospital length of stay was delayed 2 days (14.5 vs 12.9 days, p NS), and mortality was slightly higher in the early group than the late group (25% vs 20%, p NS). 27 Of concern was the fact that the rebleeding in the early-fed group occurred earlier, closer to the time of banding than the rebleeding that occurred in the late-refeeding group. Also, mor-

549 tality in the early-fed patients was related to rebleeding (and aspiration and encephalopathy).27 Early refeeding may cause a shift in blood flow to the splanchnic circulation, which could lead to increases in pressure and increased risk of rebleeding from the varices. For these reasons, feeding should be delayed for at least 48 hours after endoscopic therapy for bleeding esophageal varices. If a TIPS (transjugular intrahepatic portosystemic shunt) were placed, one would probably wait at least 48 hours in these high-risk patients (although there are no data in this specific situation). NG tubes have to be removed to perform banding. There is reluctance to replace tubes right away for fear of knocking off the bands prematurely (but nasogastric tubes nonetheless may be placed gingerly at approximately 48 hours). Cirrhotic patients are usually thrombocytopenic due to hypersplenism, and although risk for rebleeding is increased, platelets are not routinely given before endoscopic intervention. If bleeding recurs and platelets are 25,000, then platelet transfusion may be used. Withholding enteral nutrition is rarely an issue for patients who present with lower GIB. The clinical presentation of lower GIB invariably involves hematochezia, and only in rare circumstances, melena. In a prospective study of 235 patients who presented with severe hematochezia, thought to
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have a lower GIB, a definitive colonic source for the bleed was found in 75%. 22 The etiologies for the colonic bleeds included diverticulosis, ischemia, hemorrhoids, rectal ulcer, polyps, cancer, and angiomas.22 Providing enteral nutrition to these patients rarely affects the risk for rebleeding, and the decision to continue or withhold enteral nutrition usually depends on issues related to the patient preparation required before colonoscopy. With respect to the lower GIB itself, enteral feeding is usually a moot point.

Conclusions
Evidence of GIB in the intensive care setting has variable clinical significance. The evidence of a clinically important hemorrhage may warrant endoscopic evaluation, especially if the clinician is prone to withhold enteral nutrition in response to signs of any GIB. The decision to initiate, continue, or withhold enteral nutrition is dependent on the specific etiology of the GIB. It is appropriate to continue enteral feeding in the patient suspected to have stress gastropathy or in that patient found to have peptic ulcer disease with a clean ulcer base or flat spot. For most lower GI bleeds, it is appropriate to continue enteral nutrition as long as it does not interfere with the patient preparation for colonoscopy. Patients with GIB for whom enteral nutrition should be held for at least 48 hours include those patients who present with an upper GIB and are found to have a peptic ulcer disease with visible vessel or those patients who present with esophageal varices.

References
1. MacLaren R, Jarvis CL, Fish DN. Use of enteral nutrition for stress ulcer prophylaxis. Ann Pharmacother. 2001;35:1614-1623. 2. Cook DJ, Fuller HD, Guyatt GH, et al. Risk factors for gastrointestinal bleeding in critically ill patients: Canadian Critical Care Trials Group. N Engl J Med. 1994;330:377-381. 3. Fennerty MB. Pathophysiology of the upper gastrointestinal tract in the critically ill patient: rationale for the therapeutic benefits of acid suppression. Crit Care Med. 2002;30(6 suppl):S351-S355. 4. Ben-Menachem T, Fogel R, Patel RV, et al. Prophylaxis for stress-related gastric hemorrhage in the medical intensive care unit: a randomized, controlled, single-blind study. Ann Intern Med. 1994;121:568-575. 5. Levy MJ, Seelig CB, Robinson NJ, Ranney JE. Comparison of omeprazole and ranitidine for stress ulcer prophylaxis. Dig Dis Sci. 1997;42:1255-1259. 6. Bonten MJM, Gaillard CA, Van Tiel FH, Van Der Geest S, Stobberingh EE. Continuous enteral feeding counteracts preventative measures for gastric colonization in intensive care unit patients. Crit Care Med. 1994;22:934-944. 7. Bonten MJM, Gaillard CA, Van der Geest S, Van Tiel FH, Beysens AJ, Smeets HGW, et al. The role of intragastric acidity and stress ulcer prophylaxis on colonization and infection in mechanically ventilated ICU patients. Am J Respir Crit Care Med. 1995;152:1825-1834. 8. Pingelton SK, Hinthorn DR, Liu C. Enteral nutrition in patients receiving mechanical ventilation. Am J Med. 1986;80:827-832. 9. Rigaud D, Chastre J, Accary JP, Bonfils S, Gilbert C, Hance AJ. Intragastric pH profile during acute respiratory failure in patients with chronic obstructive pulmonary disease. Effect of ranitidine and enteral feeding. Chest. 1986;90:58-63.
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