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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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Surgical Treatment: Evidence-Based and Problem-Oriented.

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Prophylaxis and management of stress ulceration

, M.D. and , M.D.

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Stress-related gastric mucosal damage or stress ulceration has been documented to occur after many major physiologic insults, including trauma, major operative procedures, burn injury, CNS injury and during critical illness. The development of clinically significant upper gastrointestinal bleeding due to stress ulceration is uncommon, however when it manifests, it adds markedly to the complexity of care in an already compromised patient. The physician must have some mechanism to identify those at high risk for stress ulceration so that prophylaxis may be appropriately utilized, as well as an approach to management should clinically significant bleeding become manifest.


Depending on patient disease and severity of illness, stress ulceration can be demonstrated in 70–100% of critically ill patients if followed by serial endoscopic examination (1, 2). Presently, the extent of the clinical problem is difficult to quantify due to variable definitions of bleeding, marked heterogeneity in the populations studied and to the almost uniform implementation of stress ulcer prophylaxis in published studies. In a recent prospective cohort study involving over 2200 patients the incidence of clinically significant upper gastrointestinal bleeding was only 1.5% (3). Approximately one half of these patients were admitted after cardiovascular surgery and only 5% had either major head injury, trauma, or sepsis, the subpopulations traditionally thought to be at highest risk for bleeding. Further, 30% of the patients received some form of prophylaxis. As a result, these data may underestimate the risk of bleeding related to stress ulceration in other ICU populations. In this cohort, multivariate analysis demonstrated that only the need for mechanical ventilation or the presence of coagulopathy were independently associated with clinically relevant bleeding (table I). The mortality in the entire cohort was only 9%. By contrast, in those patients developing clinically significant bleeding, mortality approached 50%. The mortality directly attributable to stress ulceration is unclear. It may simply represent a surrogate marker for severity illness rather than play a causal role in the patients' demise.

Table I. Risk factors for clinically important bleeding a (from: Cook et al (1994) Risk factors for gastro-intestinal bleeding in critically ill patients. N Engl J Med 330: 377–381).

Table I

Risk factors for clinically important bleeding a (from: Cook et al (1994) Risk factors for gastro-intestinal bleeding in critically ill patients. N Engl J Med 330: 377–381).

In a subsequent study in a more homogeneous critically ill population of 33,000 major trauma patients, the incidence of clinically significant events related to stress ulceration was evaluated in a retrospective analysis (4). A significant proportion of these patients received some form of prophylaxis. Only 0.05% of all trauma patients had a clinically significant bleeding event. In a univariate analysis, several factors were clearly identified as risk factors for the development of clinically significant stress ulceration (bleeding or perforation) (table II). Although these two analyses have limitations due to either methodology or generalizability, they do suggest that there exist certain high-risk groups that may benefit from prophylaxis.

Table II. Risk factors for clinically significant stress ulceration (bleeding or perforation) in trauma (adapted from Simons et al (1995) A risk analysis of stress ulceration after trauma. J Trauma 39: 289–293).

Table II

Risk factors for clinically significant stress ulceration (bleeding or perforation) in trauma (adapted from Simons et al (1995) A risk analysis of stress ulceration after trauma. J Trauma 39: 289–293).


The precise mechanism by which gastric stress ulceration develops remains a matter of controversy. Excessive gastric acid production is probably not the principle factor leading to its development, as a pH greater than 3.5–4.0 is evident in 20–60% of critically ill patients (5, 6). Further, there appears to be a relatively poor relationship between occult upper GI bleeding and gastric pH. In view of these data, an acute loss of mucosal barrier protection is probably the most important factor leading to ulceration. In turn, the loss of barrier protection is probably related to a marked reduction in perfusion of the gastric submucosa during critical illness. Splanchnic vasoconstriction represents an early response to a reduction in global oxygen delivery as blood is diverted to the vital organs such as the heart and brain. The reduction in splanchnic blood volume is disproportionately greater than that seen in other vascular beds (7). In human volunteers, a 15% reduction in circulating blood volume may result in a 40% reduction in splanchnic blood volume while heart rate, blood pressure and cardiac output remain unchanged (8). Recognition of this phenomenon and more aggressive and timely resuscitation has probably led to the reduction in overall incidence of stress ulceration over the last two decades (9).


The high attendant mortality and morbidity associated with the development of bleeding from stress ulceration has resulted in a variety of strategies designed to prevent its occurrence. In spite of eight well-designed meta-analyses directly addressing this question, the ideal prophylactic regimen remains a matter of controversy (1017). The regimens differ in their mechanism of action, efficacy, adverse effects, ease of administration and cost.

The earliest prophylactic regimens consisted of antacids administered via nasogastric tube and titrated to maintain an intragastric pH > 3.5. Typically, most ICU protocols call for gastric aspirate pH testing with litmus paper every 2 to 4 hours. Antacids are usually given as a 20–40 ml bolus with additional boluses as required to achieve a pH > 3.5. Although relatively inexpensive, the requirement for repeated assessment of gastric pH and the frequency of administration make this a very resource intensive regimen. The large volumes of administered antacids increased the risk of aspiration, particularly in the presence of a nasogastric tube. Finally, the large amount of aluminum or magnesium may result in diarrhea, hypophosphatemia, hypermagnesemia or metabolic alkalosis.

The introduction of H2 antagonists greatly simplified stress ulcer prophylaxis. Their benefits were touted to be relative ease of administration with reliable gastric acid suppression. In initial clinical trials of prophylaxis in the ICU, H2 antagonists were administered by bolus injection. Bolus administration may fail to control acidity consistently, with breakthrough acid production causing low pH in at least 35% of surgical ICU patients. Although there is clear evidence that a continuous infusion of an H2 antagonist provides better gastric pH control than intermittent boluses (5, 18), two randomized controlled trials suggest that infusion therapy offers no clinical benefit (18, 19). The preference for one H2 antagonist over another is related to the relative potency, duration of action, and side effects profile of the various agents. Efficacy appears to be equivalent. Cimetidine is known to cause gynecomastia, hepatotoxicity, and renal toxicity and has a variety of CNS effects (20). In addition, cimetidine has been reported to induce hypotension after bolus infusion. Finally, its effects on microsomal drug metabolism result in altered metabolism and clearance of many commonly used agents in the ICU. Ranitidine has a far better safety profile, with the most significant adverse effect being thrombocytopenia. Famotidine is becoming the preferred agent in many intensive care units. Unlike cimetidine, it has no significant hemodynamic effects nor does it alter hepatic drug metabolism and in preference to ranitidine, it has no adverse effects on platelet production. This favorable safety profile combined with its profound inhibitory effect on gastric acid secretion and its q12h-dosing schedule has made this H2 antagonist exceedingly popular for use as an agent for stress ulcer prophylaxis.

Pirenzipine, an M1-cholinoceptor antagonist, has been shown to decrease gastric acidity during critical illness. Comparison of pirenzipine, 10 mg, with ranitidine demonstrate that both increase the pH of gastric aspirates sufficiently, although ranitidine is slightly more effective (21, 22). One potential problem with its use in critically ill patients is it's relatively low receptor specificity. As a result, rapid infusion leads to a significant tachycardia due to blockade of M2-cholinoceptors. Further, its efficacy in reducing the rate of clinically significant gastrointestinal bleeding has not been assessed to any great extent. For these reasons, it has found only limited utility in stress ulceration prophylaxis.

Omeprazole, a potent proton-pump inhibitor with demonstrated clinical efficacy in chronic acid-peptic disorders, has only recently been evaluated as an agent for stress ulcer prophylaxis. Although the maximal acid inhibition is not obtained for several days, by 24 hours its efficacy in is similar to that of H2 blockers, and beyond 24 hr it has superior acid suppression. Omeprazole is administered 40 mg once daily either orally or via nasogastric tube and achieves adequate acid suppression (pH > 4.0) more than 85% of the time when assessed by intermittent pH monitoring (23). Its potency, long duration of action and ease of administration suggest that it may have a role for use in stress ulcer prophylaxis. However, like pirenzipine, its therapeutic efficacy in critically ill patients remains to be established in large prospective, randomized trials.

All of the previously mentioned agents used for stress ulcer prophylaxis act on increasing gastric pH. By contrast, sucralfate is an orally administered aluminum salt of sucrose and octasulfate that exerts its effects through several mechanisms, none of which have any effect on pH. Initially, the protective effect was thought to be that of a direct barrier to diffusion of hydrogen ions but current evidence suggests that sucralfate may increase release of cytoprotective PGE2 from the gastric mucosa, which enhances mucosal blood flow. Sucralfate also increases mucus output and enhances the mucosal proliferative zone in areas of ulceration through its binding of angiogenic factors and growth factors, which aid in the repair of injury (24). Sucralfate has minimal side effects in the ICU setting. Access to the stomach is required and this necessitates either a nasogastric tube, or preferably a small bore feeding tube. This agent is minimally absorbed from the GI tract and there are essentially no local or systemic side effects. The lack of any effect on pH obviates the requirement for repeated assessment of gastric pH. Therapy consists of 1 gm of sucralfate suspension delivered via feeding tube or orally q6h.

The choice of a prophylactic regimen has been simplified by the availability of several meta-analyses evaluating the efficacy of different regimens. The most recent meta-analysis incorporated data from 57 randomized controlled trials involving over 7000 patients (table III) (13). It is evident from this analysis that H2 antagonists reduce the incidence of clinically important gastrointestinal bleeding (requiring transfusion or resulting in hemodynamic instability) compared to placebo by greater than 50%, and all other regimens are equally efficacious. However, these data conflict with a recent prospective randomized controlled trial of comparing sucralfate versus ranitidine in 1200 high-risk patients. In this study, the rate of clinically relevant bleeding was significantly lower (odds ratio 0.44) in patients receiving ranitidine (25). Inferences from these data are difficult, however, as in over half of the cases the source of bleeding was never identified.

Table III. Randomized trials and summary effects of stress ulcer prophylaxis (adapted from Cook et al (1996) Stress ulcer prophylaxis in critically ill patients: resolving discordant meta-analyses. JAMA 275: 308–314).

Table III

Randomized trials and summary effects of stress ulcer prophylaxis (adapted from Cook et al (1996) Stress ulcer prophylaxis in critically ill patients: resolving discordant meta-analyses. JAMA 275: 308–314).

If one assumes that all available regimens have similar efficacy the decision regarding the optimal prophylactic regimen depends on other advantages or disadvantages of the individual regimens. In this regard there has been accruing evidence that gastric acid inhibition or neutralization increases the incidence of nosocomial pneumonia. Normally, low gastric pH prevents bacterial overgrowth of pathogenic organisms. The increase in gastric pH associated with the neutralization or inhibition of gastric acid results in significant bacterial overgrowth. Aspiration of these colonized gastric secretions is a frequent occurrence and has been associated with the development of nosocomial pneumonia (2630). Based on these considerations, it follows that stress ulcer prophylaxis using an agent without any effect on gastric pH may be optimal. In this regard, data from the meta-analysis suggests a very strong trend favoring sucralfate with a 20% reduction in the rates of nosocomial pneumonia and an almost equivalent mortality benefit (13). No such benefit was identified in a subsequent large randomized controlled trial comparing ranitidine to sucralfate, thus a clear answer to the ideal regimen remains elusive (25).

A detailed cost-effectiveness analysis evaluated the differential costs associated with the use of cimetidine, the most inexpensive H2 blocker versus sucralfate. The cost-effectiveness ratio for sucralfate prophylaxis was $1100 per bleeding dose averted. By contrast if cimetidine were the agent of choice, the cost effectiveness ratio was over $7500 per bleeding episode averted (31). Apart from the clear benefit of sucralfate from a cost standpoint, this cost-effectiveness analysis emphasized the importance of prophylaxis only in high risk patients, as the costs associated with prophylaxis of all intensive care unit patients is prohibitive.

Early enteral nutrition may represent an additional cost-effective strategy for stress ulcer prophylaxis. In one retrospective analysis, early enteral nutrition significantly reduced the incidence of clinically significant stress ulceration (32). The mechanism for its effect may relate to buffering of gastric acid, stimulation of mucosal blood flow, or increasing the turnover of the gastric epithelium. Although there are no good randomized prospective trials of the effect of early enteral nutrition and stress ulceration, the cost of this intervention coupled with its other putative benefits suggests this may be a reasonable prophylactic strategy (33).


Clinically significant bleeding occurs infrequently, however its consequences can be catastrophic in an already critically ill patient. The first priorities in management should be directed toward volume resuscitation, blood transfusion and correction of coagulopathy. It is critical to re-evaluate the patient and ensure that supportive care is optimized. A diligent search should be undertaken for sepsis, the most frequent cause of deterioration in any critically ill patient.

Once appropriate resuscitation is under way, gastric lavage through a large bore orogastric tube with room temperature saline will break down and remove clots and reduce gastric distention, thus minimizing the risk of aspiration. By removing the clot, lavage also reduces local fibrinolytic activity and shift the balance toward hemostasis. Ice cold saline is no more effective than room-temperature saline and may worsen hemostasis through a detrimental effect on the coagulation cascade (34). If bleeding persists, then one of two approaches may be used to reduce gastric submucosal blood flow to increase the likelihood of hemostasis. Intravenous vasopressin (0.5–1.0 units/min) has been advocated but is associated with significant complications including cardiac arrhythmias and myocardial ischemia. If available, the preferred agent is an intravenous somatostatin infusion (250 μg/hour), which has similar efficacy with minimal risk (35). At the same time, H2 antagonists or omeprazole should be administered to raise the gastric pH to greater than 5.0. There are no controlled studies of the effectiveness of such an approach in this clinical scenario but given the limited risk and the potential for benefit, the balance favors aggressive control of gastric pH.

With adequate resuscitation and gastric lavage, hemorrhage will cease in approximately 80–95% of all cases (1, 36). Ongoing hemorrhage requires a more aggressive diagnostic and therapeutic approach. The first step in this process is urgent upper gastrointestinal endoscopy. Endoscopy can rule out the possibility of other sources of upper gastrointestinal bleeding such as chronic peptic ulcer, Mallory-Weiss tear, or esophageal varices. Although stress ulceration is a diffuse process, active bleeding may be localized to one or a few sites. In this scenario, endocoscopic electrocoagulation, laser coagulation or heat-probe methods may offer some benefit in arresting hemorrhage. If bleeding is diffuse or therapeutic endoscopy is unsuccessful then alternative treatment using therapeutic angiography or surgery may be required.

Angiography may be useful in identifying the site of bleeding when endoscopy has failed as a result of retained clot or poor visualization. If the source of bleeding is identified then intra-arterial vasopressin infused via the celiac axis or the left gastric artery will result in a reduction of mucosal blood flow and attenuation or cessation of hemorrhage. Local infusion of 0.2–0.4 units/min obviates the adverse effects of larger systemic doses. A continuous infusion for 48–72 hrs may be effective in over 70–80% of cases (37, 38). If the exact bleeding site can be identified then angiographic embolization using autologous clot, gelfoam or coils may be considered. Ischemic ulceration with persistent hemorrhage, full thickness necrosis or perforation are potential complications, thus this approach should only be considered when other methods have failed and experienced interventional radiologists are available.

The need for surgical intervention for massive hemorrhage related to stress ulceration is extremely rare. A number of surgical procedures have been used to control hemorrhage, ranging from suture ligation of the bleeding sites alone to total gastrectomy. All procedures appear to control bleeding initially, but rebleeding rates range from 9% to 67% for procedures less extensive than total gastrectomy (39, 40). There are neither controlled studies nor recent figures attesting to the efficacy of one procedure over another. The endoscopic and angiographic findings provide important guidance for the surgeon. If preoperative investigations demonstrate identifiable sites of bleeding then the optimal operation is gastrotomy and oversewing of the bleeding sites accompanied by truncal vagotomy and a drainage procedure. There is no evidence that subtotal gastric resection (with or without vagotomy) is any better than this more conservative approach. Both approaches appear to prevent recurrent bleeding in 50–80% of patients and have similar mortality rates (40). If the bleeding is diffuse then the options are either a total gastrectomy or gastric devascularization. Although the former is clearly the most effective technique, it carries with it a mortality of close to 100% (1, 40), an outcome related to both the severity of illness and the magnitude of the procedure. Gastric devascularization, accomplished by ligation of the left and right gastric and gastroepiploic arteries while preserving the short gastric vessels, is associated with a 100% initial control of bleeding and has a 9% rebleeding rate and a mortality rate of 38%. A second look procedure should be considered given the potential for gastric necrosis. The choice of total gastrectomy versus gastric devascularization will depend on the stability of the patient and the experience of the surgeon.


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Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6992


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