PEPTIC ULCER disease is the most common cause of acute bleeding from the upper gastrointestinal tract, accounting for 50% to 60% of cases. The vast majority of these are attributable to either the use of nonsteroidal anti-inflammatory drugs or chronic infection with Helicobacter pylori. However, any process that affects the primary lines of mucosal defense (ie, mucus and bicarbonate, intrinsic epithelial cell factors, mucosal blood flow) or repair has the propensity to induce such damage. An excellent example of such a process is the physiologic changes that occur in critically ill patients. These patients have visible signs of mucosal ischemia and in some cases increased acid outputs, which are felt to predispose to the breakdown of the integrity of the gastric mucosa and cause ulceration. Given that these documented changes appear to readily explain the pathophysiology of stress ulcer, it is perhaps not surprising that relatively little work has been performed looking at the role of other factors such as H. pylori, and even less on the value of specific therapy. In addition, though up to 5% of critically ill patient stays may be complicated by stress ulcer bleeding, the overall incidence appears to be decreasing with better supportive care and the use of ulcer-specific prophylaxis. Generally, it is rare that this complication is a major factor in a patient’s death. Studies to date have generally had large cohorts with extremely low rates of stress ulcer bleeding (1%–2%). These have failed to show a significant correlation between infection and hemorrhage. Aside from the small number of bleeds, these studies could also be criticized for using serology, a less accurate means of diagnosing active H. pylori infection, as a means of classifying patients. In this issue of the Journal of Critical Care, van der Voort et al use urea breath testing to determine the presence of active H. pylori infection at the time of emergent intensive care unit admission. Though not treated with specific H. pylori eradication nor given specific stress ulcer prophylaxis, all patients were enterally fed and given an aggressive regimen of selective gut decontamination. As with most recently published studies, the rate of clinically significant stress ulcer bleeding was extremely low (1.0%). Though both the number of unevaluable patients was high and the rate of follow-up breath testing disappointingly low because of patient discharges, it is clear from their data that this selective gut decontamination regimen is at least moderately effective in suppressing H. pylori infection. Whether the low rate of stress ulcer bleeding can be attributed to this effect or other factors, such as aggressive hemodynamic support and early enteral feeding, remains questionable. In addition, their data does not distinguish between suppression and eradication of H. pylori, a question that may have a significant impact on future patient management. Good supportive care, early enteral feeding, ulcer-specific prophylaxis, and now perhaps even selective gut decontamination may all be reasonable choices in the prevention of stress ulcer bleeding. Whether we will ever have a prospective randomized study to identify the preferred strategy will depend on the perceived magnitude of the problem and the use of these interventions on other aspects of patient outcome.
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Sep 1, 2003
M.A De Witte + 3
Open Access