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.

Signs and symptoms[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] People 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.

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.

Mechanisms[edit]

Location[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]

Lesions[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]

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]

Prevention[edit]

The need for medications to prevent stress ulcer among those in the intensive care unit is unclear as as of 2014 the quality of the evidence is poor.[7] It is unclear which agent is best or it prevention is needed at all.[8] Benefit may only occur in those who are not being feed.[9]

Possible agents include antacids, H2-receptor blockers, sucralfate, and proton pump inhibitors (PPIs). Tentative evidence supports that PPIs may be better than H2 blockers.[10]

Concerns with its use include increased rates of pneumonia and Clostridium difficile colitis.[9]

Treatment[edit]

The principles of management are the same as for the chronic ulcer.[11] The steps of management are similar as in erosive gastritis.[4]

Endoscopic means of treating stress ulceration may be ineffective and operation required.[11] 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.[12]

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.[13]

Epidemiology[edit]

Among those in the intensive care unit, ulceration resulting in bleeding is very rare.[9]

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. ^ Krag, M; Perner, A; Wetterslev, J; Wise, MP; Hylander Møller, M (2014 Jan). "Stress ulcer prophylaxis versus placebo or no prophylaxis in critically ill patients. A systematic review of randomised clinical trials with meta-analysis and trial sequential analysis.". Intensive care medicine 40 (1): 11–22. PMID 24141808. 
  8. ^ Krag, M; Perner, A; Wetterslev, J; Møller, MH (2013 Aug). "Stress ulcer prophylaxis in the intensive care unit: is it indicated? A topical systematic review.". Acta anaesthesiologica Scandinavica 57 (7): 835–47. PMID 23495933. 
  9. ^ a b c Marik, PE; Vasu, T; Hirani, A; Pachinburavan, M (2010 Nov). "Stress ulcer prophylaxis in the new millennium: a systematic review and meta-analysis.". Critical care medicine 38 (11): 2222–8. PMID 20711074. 
  10. ^ Alhazzani, W; Alenezi, F; Jaeschke, RZ; Moayyedi, P; Cook, DJ (2013 Mar). "Proton pump inhibitors versus histamine 2 receptor antagonists for stress ulcer prophylaxis in critically ill patients: a systematic review and meta-analysis.". Critical care medicine 41 (3): 693–705. PMID 23318494. 
  11. ^ a b Bailey & Love’s SHORT PRACTICE OF SURGERY 23rd Edition ISBN 0-340-75949-6 page 916
  12. ^ Manual of Gastroenterology priyank sinha Gregory L. Eastwood, M.D. & Canan Avunduk, M.D., Ph.D.(1994)
  13. ^ 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