Stress ulcer
| Stress ulcer | |
|---|---|
| Specialty | Gastrointestinal |
A stress ulcer is a single or multiple mucosal defect which can become complicated by upper gastrointestinal bleeding or physiologic stress. 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
Stress ulcers, as defined by overt bleeding and hemodynamic instability, decreased hemoglobin, and/or need for transfusion, were 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 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 low blood pressure, sepsis, and respiratory failure to the mortality independently of the stress ulceration cannot be ignored.[citation needed]
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, kidney failure, stroke, hypertension, 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.
Mechanisms
Location
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
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
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]
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.[citation needed]
Stress ulcer can be diagnosed after the initial management of gastrointestinal bleeding, the diagnosis can be confirmed by upper GI endoscopy.[citation needed]
Prevention
The need for medications to prevent stress ulcer among those in the intensive care unit is unclear. As of 2014, the quality of the evidence is poor.[7] It is unclear which agent is best or if prevention is needed at all.[8] Benefit may only occur in those who are not being fed.[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 the use of stress ulcer prophylaxis agents include increased rates of pneumonia and Clostridium difficile colitis.[9]
Treatment
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 help 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
Among those in the intensive care unit, ulceration resulting in bleeding is very rare.[9]
References
- ^ a b Cook DJ, Fuller HD, Guyatt GH, et al. (1994). "Risk factors for gastrointestinal bleeding in critically ill patients". N Engl J Med. 330 (6): 377–81. doi:10.1056/NEJM199402103300601. PMID 8284001.
- ^ Cook DJ, Griffith LE, et al. (Dec 2001). "The attributable mortality and length of intensive care unit stay of clinically important gastrointestinal bleeding in critically ill patients". Critical Care. 5 (6): 368–75. doi:10.1186/cc1071. PMC 83859. PMID 11737927.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Manual of Gastroenterology by Gregory L. Eastwood, M.D. &Canan Avunduk, M.D., Ph.D. (1994)
- ^ a b c Hai, A.A. & Shrivastava, R.B. (2003). Textbook of Surgery. Tata/McGraw-Hill. ISBN 0074621491, page 409
- ^ a b Robbins PATHOLOGIC BASIS OF DISEASE 6TH Edition ISBN 81-7867-052-6 page 796
- ^ Manual of Gastroenterology. Gregory L. Eastwood, M.D.& Canan Avunduk, M.D., Ph.D. (1994)
- ^ Krag, M; Perner, A; Wetterslev, J; Wise, MP; Hylander Møller, M (Jan 2014). "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. doi:10.1007/s00134-013-3125-3. PMID 24141808. S2CID 24990932.
- ^ Krag, M; Perner, A; Wetterslev, J; Møller, MH (Aug 2013). "Stress ulcer prophylaxis in the intensive care unit: is it indicated? A topical systematic review". Acta Anaesthesiologica Scandinavica. 57 (7): 835–47. doi:10.1111/aas.12099. PMID 23495933.
- ^ a b c Marik, PE; Vasu, T; Hirani, A; Pachinburavan, M (Nov 2010). "Stress ulcer prophylaxis in the new millennium: a systematic review and meta-analysis". Critical Care Medicine. 38 (11): 2222–8. doi:10.1097/CCM.0b013e3181f17adf. PMID 20711074. S2CID 17819100.
- ^ Alhazzani, W; Alenezi, F; Jaeschke, RZ; Moayyedi, P; Cook, DJ (Mar 2013). "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. doi:10.1097/CCM.0b013e3182758734. PMID 23318494. S2CID 8138473.
- ^ a b Bailey & Love’s SHORT PRACTICE OF SURGERY 23rd Edition ISBN 0-340-75949-6 page 916
- ^ Manual of Gastroenterology priyank sinha Gregory L. Eastwood, M.D. & Canan Avunduk, M.D., Ph.D. (1994)
- ^ A Practical Approach to Emergency Medicine by Robert J. Stine, M.D., Carl R. Chudnofsky, M.D., Cynthia K. Aaron, M.D. (1994)