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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Acute emphysematous gastritis (AEG) is a life-threatening disease in which gas-forming bacteria invade the gastric wall and cause acute inflammation of it. The clinical presentation of the patient with AEG is stormy: severe sepsis which usually leads to an early death. Presented herein is a case of a 16-yr-old boy with AEG. There were no predisposing factors to the condition in this case. Gas invaded the stomach wall and portal venous system, as well as the duodenal wall, a finding that has not been reported previously. The clinical course was very severe but, in contrast to previously reported cases, recovery was very rapid and left no sequelae.
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PMID:Emphysematous gastritis secondary to ingestion of large amounts of Coca Cola. 842 Feb 53

With continuing improvements in the medical therapy of peptic ulcer disease, the incidence of primary upper gastrointestinal bleeding (UGIB) has markedly declined. Nonetheless, in a subset of surgical patients, secondary UGIB following a major operation may still be a source of substantial morbidity. To further elucidate this problem, we reviewed 103 cases of overt UGIB following all major surgical procedures conducted in two hospitals between July 1982 and June 1994. The prevalence of postoperative UGIB during this period was 0.39%. The mean interval between initial operation and UGIB was 16 days (range 1-55 days) and there was a high incidence of associated sepsis (26%). The source of bleeding was defined endoscopically in all cases and included gastritis (69.9%), solitary ulcers (17.5%), and other causes (12.6%). Postoperative UGIB (nonvariceal) was most commonly seen following portacaval shunting operations but mortality rates were highest in patients who developed UGIB after cardiovascular operations. We conclude that: (1) postoperative UGIB has become a relatively uncommon but still formidable clinical problem; (2) erosive gastritis continues to be the major source of UGIB but acute ulcers, varices, and other causes contribute to the total; and (3) postoperative UGIB is most likely to be fatal in cardiovascular patients and those who develop concurrent sepsis and/or multiorgan failure.
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PMID:Upper gastrointestinal bleeding following major surgical procedures: prevalence, etiology, and outcome. 880 77

Thirty-one patients with biliary enteric fistula who were operated on over a 19-year period (1976-1994) with an incidence of 0.74% in all biliary tract operations were reviewed retrospectively to identify etiologic factors, types of fistulas, signs and symptoms, methods of diagnosis, management and prognosis of the cases. Most common symptoms were abdominal pain, nausea, vomiting and jaundice. Two patients had gallstone ileus. The majority of the patients had severe concomitant medical illnesses. The exact preoperative diagnosis of a biliary enteric fistula was established in only five (16%) patients. In 81% of the cases fistula was secondary to chronic calculous biliary tract disease. Postoperative complications included wound infection in six (19%), biliary fistula in two (6%) and erosive gastritis in one (3%) patient. Two patients died of intra-abdominal sepsis and two of cardiac failure, with an operative mortality of 13%. Early elective cholecystectomy is recommended to avoid complications of chronic calculous cholecystitis such as bilioenteric fistulas and their increased mortality and morbidity.
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PMID:Biliary enteric fistulas. 937 75

This review illustrates the changing paradigms in the understanding of the pathogenesis of pneumatosis intestinalis. Although many theories have been evoked, pragmatically there appear to be four major clinical and diagnostic imaging considerations. The most common and most emergent life-threatening cause of intramural bowel gas is the result of bowel necrosis due to bowel ischemia, infarction, necrotizing enterocolitis, neutropenic colitis, volvulus, and sepsis. In the stomach, intramural gas can be caused by emphysematous gastritis or ingestion of caustic agents. These situations represent surgical emergencies. Pneumatosis is found secondary to mucosal disruption presumably due to over-distention from peptic ulcer, pyloric stenosis, annular pancreas, and even to more distal obstruction. Disruption can also be caused by ulceration, erosions, or trauma, including the trauma of child abuse. Disruption can also be iatrogenic from intracatheter jejunal feeding tubes, stent perforation, sclerotherapy, or surgical or endoscopic trauma. In these cases, the gas may be focal or linear. Treatment depends on the extent of the disruption and the underlying cause. A more subtle form of mucosal disruption may occur due to mucosal erosions and also to defects in intestinal crypts secondary to acute and subclinical enteritides that allow intraluminal bacterial gas under pressure to percolate into the bowel wall layers, particularly the submucosa (29). Pneumatosis, often linear or cystic in appearance, is seen with increased frequency in patients who are immunocompromised because of steroids, chemotherapy, radiation therapy, or AIDS. In these cases, the pneumatosis may result from intraluminal bacterial gas entering the bowel wall due to increased mucosal permeability caused by defects in bowel wall lymphoid tissue. Clinical and imaging findings are important in the differentiation of this transient pneumatosis from fulminant life-threatening causes in this subset of patients. A pulmonary cause must still be considered in cases of chronic obstructive pulmonary disease, asthma, and cystic fibrosis. It can occur with barotrauma and after chest tube placement. It may relate to increased intrathoracic pressure associated with retching and vomiting. The possibility remains that occasionally the origin of pneumatosis intestinalis will remain cryptogenic--caused but unexplained.
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PMID:Pneumatosis intestinalis: a review. 953 Feb 94

Pacific herring Clupea pallasi populations in Prince William Sound, Alaska, USA, declined from an estimated 9.8 x 10(7) kg in 1992 to 1.5 x 10(7) kg in 1994. To determine the role of disease in population decline, 233 Pacific herring from Prince William Sound were subjected to complete necropsy during April 1994. The North American strain of viral hemorrhagic septicemia virus (VHSV) was isolated from 11 of 233 fish (4.7%). VHSV was significantly related to myocardial mineralization, hepatocellular necrosis, submucosal gastritis, and meningoencephalitis. Ichthyophonus hoferi infected 62 of 212 (29%) fish. I. hoferi infections were associated with severe, disseminated, granulomatous inflammation and with increased levels of plasma creatine phosphokinase (CPK) and aspartate aminotransferase (AST). I. hoferi prevalence in 1994 was more than double that of most previous years (1989 to 1993). Plasma chemistry values significantly greater (p < 0.01) in males than females included albumin, total protein, cholesterol, chloride, glucose, and potassium; only alkaline phosphatase was significantly greater in females. Hypoalbuminemia was relatively common in postspawning females; other risk factors included VHSV and moderate or severe focal skin reddening. Pacific herring had more than 10 species of parasites, but they were not associated with significant lesions. Two of the parasites have not previously been described: a renal intraductal myxosporean (11% prevalence) and an intestinal coccidian (91% prevalence). Transmission electron microscopy of a solitary mesenteric lesion revealed viral particles consistent with lymphocystis virus. No fish had viral erythrocytic necrosis (VEN). Prevalence of external gross lesions and major parasites was not related to fish age, and fish that were year-lings at the time of the 1989 'Exxon Valdez' oil spill (1988 year class) had no evidence of increased disease prevalence.
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PMID:Viral hemorrhagic septicemia virus, Ichthyophonus hoferi, and other causes of morbidity in Pacific herring Clupea pallasi spawning in Prince William Sound, Alaska, USA. 967 59

An effective locoregional therapy is needed for adenocarcinomas of the pancreas, stomach, and gastroesophageal junction. Paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) may enhance the effect of radiation therapy (RT). Paclitaxel synchronizes cells at G2/M, a relatively radiosensitive phase of the cell cycle. We have shown that response to paclitaxel and concurrent RT (paclitaxel/RT) was not affected by p53 mutations in non-small cell lung cancer. This finding suggested that paclitaxel/RT was a rational treatment approach for other malignancies that frequently harbor p53 mutations, such as upper gastrointestinal malignancies. We completed a phase I study of paclitaxel/RT for locally advanced pancreatic and gastric cancer. The maximum tolerated dose of paclitaxel was 50 mg/m2/wk for 6 weeks with abdominal RT. The dose-limiting toxicities were abdominal pain within the radiation field, nausea, and anorexia. Phase II studies are now under way. Twenty-five patients with locally advanced pancreatic cancer have been entered at the phase II dose level of paclitaxel 50 mg/m2/wk with concurrent RT (total dose, 50 Gy). Thus far, the only grade 3/4 toxicities have been hypersensitivity reactions (n = 2), asymptomatic grade 4 neutropenia (n = 3), and nonneutropenic biliary sepsis (n = 1). Of the first 18 assessable patients with pancreatic cancer treated on the phase II study, six obtained a partial response, for a preliminary response rate of 33%. In the phase II study for locally advanced gastric cancer, 20 patients have been enrolled. Of the first 19 patients who have completed treatment, nine (47%) had grade 3/4 toxicities, including nausea, anorexia, esophagitis, and gastritis. Of the first 16 patients with gastric cancer, complete and partial responses have been observed in one and eight patients, respectively, for a preliminary response rate of 56%. We have also completed treatment on 24 patients with potentially resectable adenocarcinomas of the gastroesophageal junction with neoadjuvant paclitaxel 60 mg/m2 and cisplatin 25 mg/m2, weekly for 4 weeks, with concurrent RT (total dose, 40 Gy) followed by surgical resection. Ten patients (41%) had grade 3/4 toxicities, including neutropenia, nausea, and dehydration. Of 24 patients, four complete responses (17%) and 14 partial responses (58%) were observed, for an overall response rate of 75%. Severe esophagitis was uncommon, making this a well-tolerated outpatient regimen for adenocarcinomas of the distal esophagus. These findings demonstrate that paclitaxel-based chemoradiation for locally advanced upper gastrointestinal malignancies is well-tolerated with substantial activity.
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PMID:Paclitaxel and concurrent radiation therapy for locally advanced adenocarcinomas of the pancreas, stomach, and gastroesophageal junction. 1021 May 40


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