Stress ulcer

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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.

Incidence/Significance[edit]

Stress ulcers, as defined by overt bleeding and hemodynamic instability, decreased hemoglobin, and/or need for transfusion, was seen in 1.5% of patients in the 2252 patients in the Canadian Critical Care Trials group study.[1] Patients with stress ulcers have a longer ICU length of stay (up to 8 days) and a higher mortality (up to 4 fold) than compared to patients who do not have stress ulceration and bleeding.[2] While the bleeding and transfusions associated with the stress ulcerations contribute to the increased mortality, the contribution of factors like hypotension, sepsis and respiratory failure to the mortality independently of the stress ulceration cannot be ignored. Ulcers are commonly caused by stress, alcohol,and spicy foods.

Risk Factors[edit]

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:

Diagnosis[edit]

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.

The site of ulcerations[edit]

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.[3]

Lesion of stress ulcers[edit]

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).[4]

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).[5]

Stress Ulcer formation[edit]

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]

Stress Ulcer Prophylaxis (SUP)[edit]

Prevention of this condition is far better than trying to treat it once it occurs.[7] Significant bleeding associated with the ulcers and bleeding is associated with increased morbidity and mortality.

Who should be on stress ulcer prophylaxis?[edit]

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).[8]

Drug classes and options available[edit]

Prophylactic agents include antacids, H2-receptor blockers, sucralfate, proton pump inhibitors (PPIs), prostaglandin analogs, and nutrition.

Proton pump inhibitors[edit]

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."[9] 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.[10] Similar results were reproduced in another study.[11]

H2 Receptor antagonists[edit]

In contrast, H2-receptor blockers are widely used in SUP. Most trials, but not all, have demonstrated their effectiveness in preventing stress ulcer formation.[12][13]

Sucralfate[edit]

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.[14]

Prostaglandin analogues[edit]

This class includes Misoprostol and the likes. Significant side effects including diarrhea, drug interactions, lack of overall efficacy and availability of much better alternatives preclude its use in current medical practice.

Antacids[edit]

Antacids are not effective treatment for SUP. It is not recommended that antacids be used due to increased risk of hemorrhage and mortality.

Treatment[edit]

The principles of management are the same as for the chronic ulcer.[7] The steps of management are similar as in erosive gastritis.[4]

Endoscopic means of treating stress ulceration may be ineffective and operation required.[7] It is believed that shunting of blood away from the mucosa makes the mucous membrane ischaemic and more susceptible to injury.[4]

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.[15]

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.[16]

Footnotes[edit]

  1. ^ a b Cook, DJ, Fuller, HD, Guyatt, GH, et al. Risk factors for gastrointestinal bleeding in critically ill patients. N Engl J Med 1994; 330:377.PMID 8284001
  2. ^ Cook DJ, Griffith LE et al. The attributable mortality and length of intensive care unit stay of clinically important gastrointestinal bleeding in critically ill patients. Critical Care 2001 Dec;5(6):368-75. Epub 2001 Oct 5 PMID 11737927
  3. ^ Manual of Gastroenterology by Gregory L. Eastwood, M.D. &Canan Avunduk, M.D., Ph.D.(1994)
  4. ^ a b c Hai, A.A. & Shrivastava, R.B. (2003). Textbook of Surgery. Tata/McGraw-Hill. ISBN 0074621491, page 409
  5. ^ a b Robbins PATHOLOGIC BASIS OF DISEASE 6TH Edition ISBN 81-7867-052-6 page 796
  6. ^ Manual of Gastroenterology Gregory L. Eastwood, M.D.& Canan Avunduk, M.D., Ph.D.(1994)
  7. ^ a b c Bailey & Love’s SHORT PRACTICE OF SURGERY 23rd Edition ISBN 0-340-75949-6 page 916
  8. ^ Cook, DJ, Fuller, HD, Guyatt, GH, et al. Risk factors for gastrointestinal bleeding in critically ill patients. N Engl J Med 1994; 330:377.
  9. ^ [1]
  10. ^ Phillips, JO, Metzler, MH, Palmieri, MT, et al. A prospective study of simplified omeprazole suspension for the prophylaxis of stress-related mucosal damage. Crit Care Med 1996; 24:1793.
  11. ^ Lasky, MR, Metzler, MH, Phillips, JO. A prospective study of omeprazole suspension to prevent clinically significant gastrointestinal bleeding from stress ulcers in mechanically ventilated trauma patients. J Trauma 1998; 44:527.
  12. ^ Shuman, RB, Schuster, DP, Zuckerman, GR. Prophylactic therapy for stress ulcer bleeding: A reappraisal. Ann Intern Med 1987; 106:562.
  13. ^ Messori, A, Trippoli, S, Vaiani, M, et al. Bleeding and pneumonia in intensive care patients given ranitidine and sucralfate for prevention of stress ulcer: meta-analysis of randomised controlled trials. BMJ 2000; 321:1103.
  14. ^ Cook, D, Guyatt, G, Marshall, J, et al. A comparison of sucralfate and ranitidine for the prevention of upper gastrointestinal bleeding in patients requiring mechanical ventilation. N Engl J Med 1998; 338:791.
  15. ^ Manual of Gastroenterology priyank sinha Gregory L. Eastwood, M.D. & Canan Avunduk, M.D., Ph.D.(1994)
  16. ^ A Practical Approach to Emergency Medicine by Robert J. Stine, M.D., Carl R. Chudnofsky, M.D., Cynthia K. Aaron, M.D. (1994)

Bailey & Love's; R.C.G Rusell, MS, FRCS Consulting surgeon, The Middlesex Hospital, UK. N.S Williams,MS, FRCS Professor of Surgery and Director of the Academic Department of Surgery, St Bartholomew's and the Royal London School of Medicine and Dentistry, Royal London Hospital, London, UK. C.J.K Bulstrode, MA, FRCS Professor in Orthopaedic Surgery, John Radcliffe Hospital, Oxford, UK, Short Practice of Surgery (23rd ed.), New York, USA: Arnold, Co-published in the USA by Oxford University press Inc., New York 2000 

Selected Readings[edit]