Stress ulcer

From Wikipedia, the free encyclopedia

This article or section needs to be wikified to meet Wikipedia's quality standards. Please help improve this article with relevant internal links. (May 2007)

This article may require cleanup to meet Wikipedia's quality standards. Please improve this article if you can. (May 2007)

Stress ulcers are single or multiple mucosal defects which can become complicated by upper gastrointestinal bleeding during the physiologic stress of serious illness. Ordinary peptic ulcers are found commonly in the gastric antrum and the duodenum whereas stress ulcers are found commonly in fundic mucosa and can be located anywhere within the stomach and proximal duodenum.

[edit] Risk Factors

Risk factors for stress ulcer formation that have been identified are numerous and varied. However, two landmark studies and one position paper exist that addresses the topic of risk factors for stress ulcer formation:

• Non-critically ill medical patients with 2 or more of the following: respiratory failure, sepsis, heart failure, hepatic encephalopathy, jaundice, renal failure, stroke, hypotension, previous gastrointestinal disease and treatment with corticosteroids, NSAIDS, heparin, or warfarin.

• In surgical critically ill patients, only those patients who are on a mechanical ventilator for more than 48 hours and/or those with a coagulopathy.^[1]

• The American Society of Health-System Pharmacists guideline recommends against the practice of stress ulcer prophylaxis in non-critically ill patients.

[edit] Diagnosis

Stress ulcer is suspected when there is upper gastrointestinal bleeding in the appropriate clinical setting, for example, when there is upper gastrointestinal bleeding in elderly patients in a surgical intensive care unit (ICU) with heart and lung disease, or when there is upper gastrointestinal bleeding in patients in a medical ICU who require respirators.

Stress ulcer can be diagnosed after the initial management of gastrointestinal bleeding, the diagnosis can be confirmed by upper GI endoscopy.

[edit] The site of ulcerations

The ulcerations may be superficial and confined to the mucosa, in which case they are more appropriately called erosions, or they may penetrate deeper into the submucosa. The former may cause diffuse mucosal oozing of blood, whereas the latter may erode into a submucosal vessel and produce frank hemorrhage. ^[2]

[edit] Lesion of stress ulcers

The characteristic lesions may be multiple, superficial mucosal erosions similar to erosive gastroduodenitis. Occasionally, there may be a large acute ulcer in the duodenum (Curling’s ulcer). ^[3]

Generally, there are multiple lesions located mainly in the stomach and occasionally in the duodenum. They range in depth from mere shedding of the superficial epithelium (erosion) to deeper lesions that involve the entire mucosal thickness (ulceration). ^[4]

[edit] Stress Ulcer formation

The pathogenic mechanisms are similar to those of erosive gastritis.” ^[5]

The pathogenesis of stress ulcer is unclear but probably is related to a reduction in mucosal blood flow or a breakdown in other normal mucosal defense mechanisms in conjunction with the injurious effects of acid and pepsin on the gastroduodenal mucosa. ^[6]

[edit] Stress Ulcer Prophylaxis (SUP)

Prevention of this condition is far better than trying to treat it once it occurs. ^[7] Prophylactic agents include antacids, H2-receptor blockers, sucralfate, proton pump inhibitors (PPIs), prostaglandin analogs, and nutrition.

Antacids have been used in SUP. Numerous studies have shown them to be as effective in prevention when compared to H2-receptor blockers. ^[8] However, one study has shown them to be no more effective than placebo. ^[9] Thus, they are not widely used. In contrast, H2-receptor blockers are widely used in SUP. Most trials, but not all, have demonstrated their effectiveness in preventing stress ulcer formation. ^{[10] [11]} Sucralfate has not been shown to effectively decrease the incidence of stress ulcer formation. This was demonstrated in a large randomized, double-blinded, control trial of 1200 patients and compared sucralfate to the H2-receptor blocker, ranitidine. ^[12]

PPIs are also widely used in SUP. "Data regarding the efficacy and potential adverse effects of these drugs in the prevention of stress ulceration are less extensive than for antacids, H2 blockers, or sucralfate." ^[13] In one study looking at omeprazole, patients were given an oral suspension by mouth followed by nasogastric tube and there were no episodes of bleeding or signs of toxicity. ^[14] Similar results were reproduced in another study. ^[15]

Not every patient who enters the hospital needs SUP. Cook et al demonstrated that in surgical critically-ill patients the only risk factors associated with clinically significant bleeding from stress ulcers were mechanical ventilation for more than 48 hours and coagulopathy (OR 15.6 and 4.3, respectively). ^[16]

[edit] Management

The principles of management are the same as for the chronic ulcer. ^[17] The steps of management are similar as in erosive gastritis.^[18]

[edit] Treatment

Endoscopic means of treating stress ulceration may be ineffective and operation required. ^[19] It is believed that shunting of blood away from the mucosa makes the mucous membrane ischaemic and more susceptible to injury. ^[20]

Treatment of stress ulceration usually begins with prevention. Careful attention to respiratory status, acid-base balance, and treatment of other illnesses helps prevent the conditions under which stress ulcers occur. Patients who develop stress ulcers typically do not secrete large quantities of gastric acid; however, acid does appear to be involved in the pathogenesis of the lesions. Thus it is reasonable either to neutralize acid or to inhibit its secretion in patients at high risk. ^[21]

In case of severe hemorrhagic or erosive gastritis and stress ulcers, a combination of antacids and H2-blockers may stop active bleeding and prevent re bleeding. In selected patients, either endoscopic therapy or selective infusion of vasopressin into the left gastric artery may help control the hemorrhage. ^[22]

[edit] Footnote

Bailey & Love's, Short Practice of Surgery (23rd ed.), New York, USA: Arnold, Co-published in the USA by Oxford University press Inc., New York 2000, <http://www.baileyandlove.com> 

[edit] Selected Readings

Cheung, L. Y. Pathogenesis, prophylaxis and treatment of stress gastritis. Am. J. Surg. 156:437, 1988.
Craven, D. E., et al. Risk factors for pneumonia and fatality in patients receiving continuous mechanical ventilation. Am. Rev. Respir. Dis. 133:792, 1986.
Driks, M. R., et al. Nosocomial pneumonia in intubated patients given sucralfate as compared with antacids or histamine type 2 blockers. N. Engl. J. Med. 317:1376, 1987.
DuMoulin, G. C., et al. Aspiration of gastric bacteria in antacid-treated patients: A frequent cause of postoperative colonisation of the airway. Lancet 1:242, 1982.
Lamothe, P. H., et al. Comparative efficacy of cimetidine, famotidine, ranitidine, and Mylanta in postoperative stress ulcers: Gastric pH control and ulcer prevention in patients undergoing coronary artery bypass graft surgery. Gastroenterology 100:1515, 1991.
Priebe, H. J., et al. Antacid versus cimetidine in preventing acute gastrointestinal bleeding: A randomized trial in 75 ill patients. N. Engl. J. Med. 302:426, 1980.
Shuman, R. B., Schuster, D. P., and Zuckerman, G. R. Prophylactic therapy for stress ulcer bleeding: A reappraisal. Ann Intern. Med. 106:562, 1987.
Tryba, M. Stress bleeding prophylaxis with sucralfate: Pathophysiologic basis and clinical use. Scand. J. Gastroenterol. [Suppl. 173] 25:22, 1990.