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Query: UMLS:C0031154 (peritonitis)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Peritonitis was induced in 12 horses by median celiotomy and 1 hour of small intestinal ischemia. Six horses had primary closure of the incision, whereas six horses had a plastic mesh sutured to the ventral abdominal wall leaving the abdomen open for ventral drainage. The mesh was removed after 5 days and the abdominal wall was closed by apposition of the linea alba and subcutaneous tissues and approximation ef the skin edges. Peritoneal fluid was collected and analyzed for nucleated cell count and total protein concentration on days 0 and 5. Serum biochemical profiles, serum electrolyte concentrations, and complete blood counts were performed on days 0, 1, 2, 5, 6, 10, and 14. Body weight, rectal temperature, and physical examination findings were recorded daily for 30 days, then horses were euthanatized and the abdominal cavity was examined for the presence of adhesions. Histological examination was performed to assess the inflammatory response of the healing body wall; inflammation scores were significantly lower in horses that had primary closure of the incision. The mesh was well tolerated by all horses and allowed egress of peritoneal fluid for 5 days. Adhesions were present in four control horses and in two horses that had open peritoneal drainage. All horses that had open drainage developed incisional infections after mesh removal. Abdominal wall herniation did not occur in any of the horses. The mild peritonitis induced in this study was insufficient to establish the efficacy of open peritoneal drainage for an established peritonitis in horses; however, the results of this study indicate that open peritoneal drainage is feasible in horses.
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PMID:Open peritoneal drainage in horses with experimentally induced peritonitis. 901 2

Mesenteric vein thrombosis, an uncommon but important clinical entity, can cause ischemia or infarction of the small intestine. Mesenteric vein thrombosis was first described nearly a century ago, but diagnosis remains difficult because it can affect young individuals without any known predisposing disorder and because patients often present with nonspecific abdominal symptoms. We report 4 cases of small intestinal ischemia secondary to superior mesenteric vein thrombosis. Three were due to hypercoagulable states (protein-S deficiency, factor-VII abnormalities) and one was idiopathic. In recent years, the development of modern imaging techniques (particularly ultrasonography, duplex scanning, and computed tomography) have enabled early recognition of this disease. Anticoagulation is therapeutic acutely unless there are signs of peritonitis which necessitate surgical resection of the infarcted bowel.
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PMID:Mesenteric vein thrombosis. Four cases and review of the literature. 903 Apr 70

The aim of this study was to investigate mucosal pH and lactate production in a porcine model of ischemia/reperfusion and sepsis using both tonometry and a technique for segmental intestinal perfusion. Eighteen pigs (17-23 kg) were anesthetized and mechanically ventilated. They were divided into three groups and followed for 4 h. Group C (n = 6) served as controls. In the ischemia/reperfusion group (I/R; n = 6), the superior mesenteric artery was totally occluded for 60 min. In group P (n = 6), sepsis was induced by fecal peritonitis. Cardiac index (CI) was determined by thermodilution and blood flow in the superior mesenteric artery (QSMA), using a Transonic flow probe. Intramucosal pH (pHi) was calculated using tonometry. A special balloon tube for segmental perfusion was introduced in the midileum for lactate measurement. Lactate and oxygen saturation were measured in arterial blood and in the superior mesenteric vein. CI, QSMA, pHi, and lactate in blood and perfusate remained unchanged in controls. Occlusion of intestinal blood flow induced a fall in pHi from 7.28 +/- .02 to 6.76 +/- .04, a marked rise in lactate in the perfusate, and an increased arteriovenous lactate difference. During reperfusion, pHi tended to return to baseline values. Lactate in the perfusate and the arteriovenous lactate difference decreased. In sepsis there was a continuous reduction in CI and QSMA to 45 +/- 13% and 40 +/- 20% of baseline, respectively. pHi decreased moderately from 7.22 +/- .09 to 6.98 +/- .25. Lactate remained unchanged in blood and perfusate. Microscopic mucosal injury was observed in all animals subjected to ischemia/reperfusion and in three of six pigs in group P. A good association between pHi and lactate production was seen in ischemia/reperfusion. However, in sepsis, lactate in superior mesenteric venous blood or in intestinal perfusate did not increase, despite the fall in pHi. The mechanism causing ischemic mucosal injury has different characteristics in sepsis and in ischemia caused by arterial occlusion.
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PMID:Small intestinal mucosal pH and lactate production during experimental ischemia-reperfusion and fecal peritonitis in pigs. 903 89

Between 1972 and 1993 a total of 90 patients were operated on for acute mesenteric ischemia at Hanover Medical School, Department of Abdominal- and Transplantation Surgery. As causes of mesenteric ischemia, arterial embolism (23%), arterial thrombosis (30%), venous thrombosis (33%), and non-occlusive disease (14%) were differentiated. The overall hospital mortality was 66%. The hospital mortality after venous thrombosis was 37%, significantly lower than after arterial (79%) and functional (83%) types of mesenteric ischemia. Besides the pathogenesis of mesenteric infarction, a multivariate analysis revealed age and presence of peritonitis and intestinal perforation to be independent prognostic factors of hospital lethality. Patients with venous thrombosis had a mean age of 48 years and were significantly younger than the remaining patients who had an average age of over 60 years. Surgical procedures comprised solitary bowel resection (60%), isolated embolectomy and/or thrombectomy (10%), a combination of embolectomy/thrombectomy and bowel resection (4%), and exploratory laparotomy only (21%). Vascular reconstruction was associated with a significantly better survival rate than bowel resection only. While hospital mortality was dependent on the type of mesenteric ischemia, long-term survival after exclusion of hospital deaths proved independent of the original pathogenesis. Of the patients who survived the acute attack of mesenteric ischemia, 70% were alive 2 years later and 50% 5 years later. The survival probability of these patients was not determined by recurrence of mesenteric ischemia, but was mainly related to their cardiovascular comorbidity and a high incidence and prevalence of malignancies.
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PMID:[Surgical therapy of acute mesenteric ischemia]. 906 67

The successful use of a combination of "patch, drain, and wait" (PDW) and home total parenteral nutrition (TPN) in the management of a case of acute, catastrophic midgut volvulus in a 2-year-11-month-old boy with near-total ischemia/necrosis of his small intestine is reported. The PDW approach to the highly effective management of acute midgut ischemia/necrosis in infancy and childhood (necrotizing enterocolitis and midgut volvulus) involves maximum gut salvage by avoidance of resection, stoma formation, or both through the use of extensive peritoneal cavity drainage by Penrose drains, TPN, and broad-spectrum antibiotics. The extensive peritoneal drainage fosters capture of enteric fistulas with the formation of enterostomies at drain exit sites, while adhesions and ischemia/inflammation-induced hypervascular obliteration of the peritoneal cavity diminish the potential for peritonitis (no peritoneal cavity, no peritonitis) and facilitate impressive salvage of seemingly hopelessly lost ischemic/necrotic gut (a simulation of the in utero ischemic gut process leading to atresias and some varying, but generally mild, gut loss) while simultaneously contributing to the resorption of absolutely non-salvageable gut and the creation of a remarkably clean and adhesion-free peritoneal cavity resembling that of a newborn infant with midgut intestinal atresia.
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PMID:Combination of "patch, drain, and wait" and home total parenteral nutrition for midgut volvulus with massive ischemia/necrosis 906 40

MVT is an uncommon form of visceral ischemia. Symptoms and signs of MVT are usually nonspecific and should not be relied on for accurate diagnosis. A simple, logical diagnostic algorithm can be used to manage most of these patients (Fig. 6). CT or MRI appears to be the most sensitive diagnostic test and should be obtained early for any patient suspected of harboring MVT. Patients with peritonitis require prompt abdominal exploratory laparotomy to rule out ischemic bowel. Once the diagnosis of acute MVT is confirmed, the patient should be anticoagulated with heparin. During operation, all nonviable bowel should be resected with intent for a second-look laparotomy after 24 hours if there is any question of ongoing ischemia. We recommend using fluorescein-assisted evaluation of marginally viable bowel intraoperatively. After the operation, anticoagulation is continued with heparin and then oral warfarin sodium when the patient's bowel function returns. For those patients without peritonitis, we recommend prompt anticoagulation followed by at least a 48- to 72-hour period of close observation. All patients who have had an episode of acute MVT and do not have a contraindication to anticoagulation should be anticoagulated on a life-long basis with warfarin sodium. Despite our increased awareness of acute MVT, the 30-day mortality rate remains high. Acute MVT typically has a more insidious and unpredictable course than do other forms of visceral ischemic syndromes, with a mortality rate as high as that of its arterial counterpart. Although there has been a slight improvement in survival during the last 20 years, the recurrence rate remains high and the long-term prognosis is poor in this group of patients. Survival of patients with chronic MVT is better than that of those with acute MVT and appears to be determined by the underlying disease.
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PMID:Mesenteric venous thrombosis. 914 16

The successful use of a combination of "patch, drain, and wait" (PDW) and home total parenteral nutrition (TPN) in the management of a case of acute, catastrophic midgut volvulus in a 2-year-11-month-old boy with near-total ischemia/necrosis of his small intestine is reported. The PDW approach to the highly effective management of acute midgut ischemia/necrosis in infancy and childhood (necrotizing enterocolitis and midgut volvulus) involves maximum gut salvage by avoidance of resection, stoma formation, or both through the use of extensive peritoneal cavity drainage by Penrose drains, TPN, and broad-spectrum antibiotics. The extensive peritoneal drainage fosters capture of enteric fistulas with the formation of enterostomies at drain exit sites, while adhesions and ischemia/inflammation-induced hypervascular obliteration of the peritoneal cavity diminish the potential for peritonitis (no peritoneal cavity, no peritonitis) and facilitate impressive salvage of seemingly hopelessly lost ischemic/necrotic gut (a simulation of the in utero ischemic gut process leading to atresias and some varying, but generally mild, gut loss) while simultaneously contributing to the resorption of absolutely non-salvageable gut and the creation of a remarkably clean and adhesion-free peritoneal cavity resembling that of a newborn infant with midgut intestinal atresia.
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PMID:Combination of "patch, drain, and wait" and home total parenteral nutrition for midgut volvulus with massive ischemia/necrosis. 915 65

Gangrene of the stomach is a rare and catastrophic event, usually attributed to local pathologic conditions. Although there are no cases documented in the literature, non-occlusive arterial ischemia is sometimes listed among the causes of necrotizing gastritis. We report a case of necrotizing gastroenteritis associated with a low flow state secondary to an episode of fulminant colitis, fecal peritonitis and septic shock. The patient recovered after staged resection of the involved segments of the gastrointestinal tract.
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PMID:[Necrotizing gastroenteritis associated with inflammatory bowel disease]. 944 44

Abdominal compartment syndrome develops whenever the mean intraperitoneal pressure rises above the physiological pressure, leading to renal and mesenteric ischemia and respiratory decompensation due to pressure on the diaphragm. Abdominal compartment syndrome may occur after conditions such as peritonitis, intestinal obstruction, laparoscopic procedures, or abdominal tumors. Leakage from the urinary tract may cause accumulation of urine in the peritoneal cavity which commonly manifests as single or multiple urinomas, or urinary ascites. The case of a patient who had delayed identification of a ureteral perforation following the abdomino-perineal resection of a rectal carcinoma is presented. Massive urinary leakage into the peritoneal cavity led to the abdominal compartment syndrome. Peritoneal drainage and ureteral stenting improved her condition. A high index of suspicion is necessary in order to diagnose this rare condition.
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PMID:Abdominal compartment syndrome due to delayed identification of a ureteral perforation following abdomino-perineal resection for rectal carcinoma. 947 95

On the basis of results of complex treatment of 427 patients with acute small bowel obstruction the authors of the article have established five stages of the clinical course of the disease. The stage of ischemia was diagnosed in 26.9% of the patients, the stage of water-electrolytic disturbances--in 26.2% the peritonitis stage--in 15.9%, the stage of multiple organ insufficiency at the postoperative period--in 8.9%. The stage of chronic intestinal insufficiency at the remote postoperative period was diagnosed in 41.1% of the patients operated upon. The amount of lethal outcomes was found to depend on the stage of the clinical course of the acute small bowel obstruction in which complex treatment had been started.
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PMID:[Differentiated approach to choice of strategy in the treatment of patients with acute obstruction of the small intestine depending on the stage of the clinical course of disease]. 950 81


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