Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study compared prophylactic administration of either intragastric misoprostol (200 micrograms four times a day), a prostaglandin E1 analog, or bolus intravenous cimetidine (300 mg every 6 hours) in preventing stress lesions and stress bleeding in 127 adult postoperative patients who required mechanical ventilation and also had developed hypotension or sepsis. Both drug treatments were equally effective in preventing the development of diffuse gastritis (greater than 10 gastric hemorrhagic lesions) and in preventing upper gastrointestinal hemorrhage (UGIH). The combined data from both groups showed that for the 44 (35%) patients who died, death was significantly associated with the presence at study entry of renal failure (64% of 25 patients with renal failure died), hepatic failure (57% of 23 patients) or coagulopathy (62% of 29 patients) (p less than 0.02 for each), and with the number of organ system failures at study entry (48% of 69 patients with multiple organ system failures died, p less than 0.001). Death was also significantly associated with the presence of adult respiratory distress syndrome (ARDS) at study entry or the development of ARDS (63% of 24 patients with ARDS died, p less than 0.001), and the development of UGIH (5% of 93 patients with known bleeding outcome died, p less than 0.05). The number of stress lesions that developed was significantly associated with subsequent UGIH (p less than 0.001). Additional organ system failure developed during the study in 31% of the 127 patients, as did diffuse gastritis in 20% of 111 patients who had a follow-up endoscopy. These results demonstrate that postoperative patients who require mechanical ventilation and have hypotension or sepsis are at significant risk for the development of stress gastric lesions and multiple organ system failure even when prophylaxis for stress ulcers is provided. Furthermore, the presence of ARDS, renal failure, hepatic failure, coagulopathy, and UGIH are significantly associated with death.
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PMID:Stress ulcers and organ failure in intubated patients in surgical intensive care units. 155 13

Stress gastritis frequently occurs in association with shock or sepsis. Gastric mucosal ischemia appears to be a key feature in these critically ill patients. The University of Wisconsin cold preservation solution (UWS) is an isoosmolar, nonglucose-based perfusate that minimizes hypothermia-induced cell swelling and prevents intracellular acidosis and oxygen-free radical injury, while providing high energy substrates for donor organs. In a prospective, single-blind study, 18 similar Sprague-Dawley rats were randomly divided to receive only 5 per cent dextrose and water (D5W) (Group 1) or a 50 per cent solution of D5W+UWS (Group 2) for 72 hours. At the end of 72 hours the animals were stressed by the cold-restraint model. The mean number of ulcers for Group 2 was nearly half that of Group 1. Also, Group 2 had a significantly lower mean total ulcer length (P less than 0.005) and ulcer index (P less than 0.05). Most of Group 2 had mild gastritis changes (grade 0 to 1), while more than half of Group 1 had severe gastritis (grade 3). Gastric mucosal pH was similar for both groups. Topically applied UWS appears to reduce the severity and incidence of stress gastritis in this experimental model. Because mucosal pH values were similar, it is thought that UWS may alter the effects of gastric mucosal ischemia at a cellular level.
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PMID:Prevention of stress gastritis with tissue preservation solution. 158 84

Six patients with end-stage emphysema (age 44 +/- 2 years) underwent double lung transplantation (Tx) from June 1988 through May 1990. All suffered from severe inanition and required oxygen therapy. The ischemic time was 193 +/- 28 minutes. Post-Tx immune suppression was OKT3 (14 days), cyclosporine (trough levels of 150 +/- 25 ng/ml), azathioprine to keep WBC at 3,000 to 5,000/cu mm (1 to 3.0 mg/kg/day) and following OKT3, a tapering prednisone regimen. Two rejection episodes that occurred in two patients on post-Tx day 5 and 10 were treated with bolus doses of methylprednisolone. The mean hospital stay was 32 +/- 7 days (range, 20 to 69 days). Four patients required treatment of cytomegalovirus (CMV) infection: gastritis (+donor, +recipient) in one and CMV pneumonia in two (+donor, -recipient). A fourth (+donor, -recipient) had right-sided Candida empyema six weeks post-Tx, developed CMV and staphylococcal sepsis, and died 64 days post-Tx. One patient required pyloroplasty eight weeks post-Tx and one patient underwent tracheal suture line repair at eight weeks. During a follow-up of 81 patients months (range, 8 to 24 months), one patient had developed Epstein-Barr viral (EBV) induced lymphoproliferative disease in the lung and one patient had developed EBV lymphoma. Three patients are at work, one is continuing rehabilitation, and one is at home. Double lung Tx offers a definitive benefit to patients with emphysema; however, a prolonged postoperative course can be expected. Viral infections remain serious but treatable problems.
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PMID:Treatment of end-stage chronic obstructive pulmonary disease with double lung transplantation. 184 23

True stress ulcers are primarily superficial gastric fundic lesions that occur in the clinical setting of severe shock, trauma, burns, and sepsis, especially peritonitis. They are to be clearly differentiated from Cushing's ulcers, exacerbation of pre-existent chronic ulcers, and drug-induced gastritis, all of which have completely different pathogenetic mechanisms. The etiology of true stress ulcers is most importantly related to ischemia and tissue acidosis, although luminal acid and pepsin are requisite for ulceration to occur. The sole clinical manifestation of stress ulcers is hemorrhage. Prophylaxis with antacids alone, or with a combination of antacids and H2 receptor antagonists is highly efficacious if luminal pH is carefully monitored. The treatment of exsanguinating hemorrhage, once established, carries with it an extremely high morbidity and mortality.
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PMID:The clinical problem of stress ulcers. 288 24

The gastromucosal barrier (GMB) can be disrupted by a number of aggressive factors or by a decrease in mucosal defense factors. If there is back diffusion of hydrogen ions into the mucosa, mucosal damage ranging from an erythematous gastro-duodenitis to erosive and ulcerative gastritis or life-threatening hemorrhage may ensue. The pathogenesis of stress-related mucosal damage seen in critically ill patients suffering from burns, sepsis, head trauma, respiratory insufficiency, or multisystem disease is also related to a decrease in mucosal resistance. Early studies of cimetidine in animals and in humans demonstrated its ability to increase gastric transmucosal potential difference, indicating an enhancement of the integrity of the GMB. Several studies show that cimetidine protects the stomach from aspirin-induced mucosal damage; increases gastric mucus production and mucus glycoprotein content, which contributes to the protective action of mucus; increases mucosal secretion of bicarbonate; increases gastric mucosal blood flow, which prevents mucosal hypoxia seen in patients in shock or otherwise critically ill patients; increases endogenous mucosal prostaglandin synthesis; and increases the rate of epithelial cell renewal, a factor important to mucosal healing. Since cimetidine suppresses acid secretion and enhances mucosal defense, it is an important therapeutic tool in the management of acid-related disorders, particularly stress-related mucosal damage.
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PMID:Gastric acid secretion and mucosal defense mechanisms with special reference to the role of cimetidine in critically ill patients. 353 48

A retrospective study of 1068 patients who had operations for peptic ulcer disease in the 12-year period from January 1, 1974, to January 1, 1986, permits these conclusions: The number of patients admitted to the Massachusetts General Hospital (MGH) has declined steadily in the years of this study--1974-1986. The average number of patients admitted with a diagnosis of peptic ulcer disease in precimetidine years--1974, 1975, and 1976--and in recent years--1982, 1983, and 1984--shows a decline of 39.3% in admissions. In the same periods, the average number of operations per year has declined from 92 in precimetidine years to an average of 71 (16.5%) recently. The decline has been greatest in patients operated on electively for duodenal ulcer. Operations for massive hemorrhage and acute perforations and the number of deaths have remained nearly constant. The overall mortality rate was 10.3%. The mortality following elective operations for pain was 0.5%; for urgent operations, including those for obstruction, 4.5%, and for bleeding other than massive, 7.5%; and for emergency operations, including those for acute perforation, 20.9%, and for massive hemorrhage, 22.1%. The main causes of death were organ failure (most commonly of the lungs) and sepsis. Early complications were documented 345 times and were followed by reoperation in 84 cases, or 7.4% of the total. Delayed stomal function was noted in 63 cases and required reoperation in 14. It was most common after Roux anastomoses and required operative intervention most commonly after gastric resection, Billroth I (GRBI). Delay was three times as common when vagotomy (V) was added to GR. Early postoperative hemorrhage was a serious complication when it occurred after operations for acute perforations or massive hemorrhage. The incidence was 3.7% after suture of a perforation; after operations for acute massive hemorrhage, it was 4.3% after pyloroplasty and vagotomy, with or without arterial ligation [PV(L)], and 0.3% after GR, with or without arterial ligation [GR(L)]. Late complications led to reoperation in 66 cases (6.2%). The most important were recurrent ulceration and alkaline gastritis. Recurrence rates after a minimum follow-up of 5 years (based on survivors of initial procedures and a second operation, both in the MGH) were 20.5% after suture of a perforation, 6.2% after PV, 2.3% after GRBII, and 0.4% after GRVBII. These figures are lower than expected; incomplete follow-up and improved medical care are factors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A thousand operations for ulcer disease. 376 81

To investigate the patterns of interaction between vascular graft complications and the gastrointestinal (GI) tract, the incidence, pattern, and cause of GI bleeding among patients treated for secondary aortoenteric fistula (AEF) or chronic perigraft infection (PGI) was reviewed. Among 110 patients with infected grafts, there were 39 with secondary AEF and 71 chronic PGI. GI hemorrhage occurred in 24 AEF patients (61.5%), five PGI patients (9.4%) with aortoiliofemoral grafts (PGI-AIF), and in no PGI patients with peripherally located grafts (PGI-Other). The incidence of acute and chronic bleeding patterns was the same in both AEF and PGI patients. All GI bleeding in PGI patients was from the upper GI tract, whereas lower GI hemorrhage predominated slightly among AEF patients. Endoscopy was often negative among AEF patients (10 of 17) but always diagnosed the etiology of bleeding in PGI patients (gastritis in four; duodenal ulcer in one). Fifteen AEF patients (38%) had no evidence of GI bleeding at any time during evaluation. Acute hemorrhage among AEF patients was usually associated with an anastomotic fistula (10 of 14), while paraprosthetic fistulas often did not bleed (6 of 10) or bled chronically (12 of 15). Sepsis occurred significantly more often among AEF patients (8 of 39, 21%) than among PGI patients (2 of 71, 3.0%). However, there was no significant difference in the incidence of sepsis or systemic infection between PGI-AIF patients and PGI-Other patients. In summary, gastrointestinal involvement by prosthetic graft infection may be either direct (fistula formation), indirect (sepsis/infection induced stress gastritis or ulceration), or silent. No absolute correlation exists between GI hemorrhage and the presence or absence of a graft-enteric fistula. Endoscopic demonstration of nonfistula GI pathology does not exclude the presence of graft infection. Recognition of these patterns of GI tract involvement by vascular graft infection may facilitate prompt diagnosis and improve treatment results.
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PMID:Gastrointestinal tract involvement by prosthetic graft infection. The significance of gastrointestinal hemorrhage. 387 83

The critical care environment may be characterized by invasive monitoring, vasoactive drugs, and major interventions which may have adverse effects on gastrointestinal function. Furthermore, conditions such as heart failure or sepsis may compromise oxygen delivery to gastrointestinal organs. Life threatening illness from a variety of causes may produce endoscopically evident gastritis or ulceration in up to 100% of patients, and clinically evident bleeding in 20%. Clinical studies suggest that antacids or H2 receptor blockers may reduce the frequency of this complication. Other conditions are associated with a spectrum of hepatic dysfunction ranging from the cholestatic jaundice of reactive hepatopathy during sepsis to centrilobular necrosis and hepatitis of shock liver. Additionally, many drugs used in the critical care setting may adversely affect mesenteric oxygen delivery and result in ischemia or infarction of the bowel. An increased awareness and understanding of these and other gastrointestinal complications in critically ill patients will, it is hoped, lead to earlier detection and better therapy than is now available.
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PMID:Gastrointestinal complications in critically ill patients: the intensivists' overview. 396 47

Development of acute mucosal ulceration is a complex series of catabolic interactions. Hospitalized patients with duodenal or gastric ulcer, pathologic gastric hypersecretory states (such as Zollinger-Ellison syndrome), gastric outlet obstruction, esophagitis, severe gastritis or duodenitis, sepsis, trauma (particularly head injury or burns), and some patients receiving high-dose corticosteroids are at risk of developing acute stress ulcers. Treatment should be initiated as soon as the patient is identified as being at risk, because measures designed to prevent bleeding or perforation are more effective than those designed to stop bleeding once it supervenes and the cascade of multiple organ failure commences. The presence of acid will trigger the onset of this condition; however, ulceration will not occur if the intraluminal pH can be maintained above 5 by periodic antacid treatment or by H2-receptor blockade. The dosing regimen of antacid or of H2-receptor antagonist should not be fixed, but should be sufficient to keep the gastric pH higher than 5. Antagonists administered via a nasogastric tube are the first line of defense, but 30 to 50 percent of the most ill patients will also be treated parenterally with H2-receptor antagonists. Parenteral H2-receptor blockade therapy is indicated in these patients when the risk of acute or continued ulceration of esophageal, gastric, or duodenal mucosa is high and the oral administration of medication is either not possible or the response to such therapy is unreliable. Parenteral H2-receptor antagonists are rarely administered alone.
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PMID:Indications for the use of parenteral H2-receptor antagonists. 615 Jun 38

The cytoprotective and acid-inhibitory effects of cimetidine and 16,16-dimethyl PGE2 were evaluated in a septic canine erosive gastritis model. In 21 dogs, total gastric fistulas were created, and after a 3-wk recovery period, basal, food-, and pentagastrin-stimulated acid output were measured. Then bacterial peritonitis was created by the intraperitoneal instillation of Pseudomonas, Bacteroides, Streptococcus Fecalis, Klebsiella and canine gallbladder bile. In 5 dogs no drug were given throughout the septic period while in 16 dogs either cimetidine, 6 or 12 mg/kg i.m. every 6 h, or 16,16-dimethyl PGE2, 0.2 or 0.4 microgram/kg i.m. every 6 h, was given 24 h before the induction of peritonitis and continued for 3 days. All 21 dogs had positive blood cultures on the 1st septic day. In the control animals, basal, food-, and pentagastrin-stimulated acid output significantly increased during the first 2 septic days, and gastroscopy demonstrated bleeding acute fundic erosions. Cimetidine decreased basal, food-, and pentagastrin-stimulated acid output in a dose-related manner, and only with the higher dose did it prevent gastric mucosal damage. 16,16-Dimethyl PGE2, 0.4 microgram/kg, significantly decreased acid output and prevented gastric mucosal damage. 16,16-Dimethyl PGE2 0.2 microgram/kg, although having no apparent effect on basal, food-, and pentagastrin-stimulated acid output, prevented the development of acute gastric erosions. Thus, in the canine septic model, acid output significantly increases during sepsis. Cimetidine prevents the development of sepsis-induced gastric erosions by inhibition of acid secretion and 16,16-dimethyl PGE2 by cytoprotection.
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PMID:Prevention of sepsis-induced gastric lesions in dogs by cimetidine via inhibition of gastric secretion and by prostaglandin via cytoprotection. 745 Apr 26


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