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

Sixty-five abdominal computed tomography (CT) scans of 54 systemic lupus erythrematosus (SLE) patients were retrospectively evaluated together with their clinical records. This was to assess the spectrum of CT findings and to determine the value of abdominal CT in this group of patients. Over a 3.5-year period, abdominal CT scans had been requested for suspected renal vein or inferior vena cava thrombosis (n = 52, 80%), sepsis, mesenteric ischaemia, Conn's syndrome, evaluation of hepatosplenomegaly, portal hypertension and hydronephrosis. The most frequent indication for CT was suspected renal vein thrombosis (RVT). An SLE patient with previously stable renal function who rapidly develops nephrotic syndrome with deteriorating renal function has an increased risk of thromboembolic phenomenon. Also, renal vein thrombosis is difficult to diagnose clinically and prompt anticoagulation can help preserve remaining renal function. Of these with suspected RVT, two had RVT only and five had thrombosis in both renal veins and inferior vena cava. Two patients had CT features strongly suggestive of mesenteric ischaemia, one had bilateral hydronephrosis thought to be secondary to lupus cystitis and CT confirmed two abdominal abscesses. Other incidental CT findings were: subscapular renal haematoma, overall enlargement or diminution of renal size, serositis, bowel wall thickening, splenic, hepatic and pancreatic enlargement and mild para-aortic lymphadenopathy. Abdominal CT revealed many diverse findings and aided the management of these SLE patients.
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PMID:Abdominal computed tomography in systemic lupus erythematosus. 911 46

Extrahepatic portal vein thrombosis (EHPVT) is the leading cause of variceal hemorrhage in patients with healthy livers; however, in an era of dynamic imaging, the incidental discovery of EHPVT places a special burden on the surgeon to understand the surgical implications of the disease in this setting. During the period 1989 to 1995, 23 patients (12 males and 11 females) were found to have EHPVT. In 20 (87%), this was an unexpected finding on ultrasound (11 of 23), abdominal CT scan (9 of 23), or both (9 of 23). In two patients, the diagnosis was suspected and confirmed with angiography, whereas in the other, the lesion was discovered at surgery. Only seven (30%) had hemorrhage as a presenting complaint. More typically (61%), abdominal pain alone or pain with sepsis was the indication for evaluation. In 20 patients (87%), there was an identifiable etiology for the EHPVT. A total of 15 operations were performed on 12 patients (52%), in 7 (4, variceal hemorrhage, and 3, bowel ischemia) as a direct consequence of the EHPVT and in five, for conditions not directly related to the EHPVT. Three of the 23 patients (13%) died, two (17%) following surgery and one (9%) from advanced malignant disease. No patients with hemorrhage (seven), even those who required a shunt for decompression (three) or devascularization (one), died. We found that the diagnosis of EHPVT is usually not related to variceal hemorrhage, but rather, abdominal symptoms that serve as an indication for the imaging study. Three subsets of patients emerged: (1) those requiring no surgery (11 patients), (2) those requiring surgery related to hemorrhage (4 patients), and (3) those requiring surgery for conditions other than varices (8 patients). In any of these circumstances, mortality (13%) was related to the underlying disease process rather than EHPVT. Given the earlier recognition of EHPVT, the natural history of the disease has been altered, with outcome reflecting the underlying disease rather than the sequelae of portal hypertension.
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PMID:Portal vein thrombosis in the adult: surgical implications in an era of dynamic imaging. 924 33

Our aim was to evaluate gastric emptying and orocecal transit in patients with end-stage liver disease and portal hypertension undergoing evaluation for liver transplantation. Although gastric emptying half-times for both liquid and solid emptying were similar in patients with chronic liver disease and control subjects, orocecal transit, as measured by a scintigraphic technique, was significantly prolonged in the patients with liver disease (transit time, minutes, mean +/- SEM, patients versus controls: 127 +/- 10.5 versus 80 +/- 9.5, P < .003). Serum levels of progesterone and estradiol were similar in patients and controls. We conclude that small intestinal transit is delayed in patients with advanced liver disease and portal hypertension and may contribute to gastrointestinal symptoms and promote sepsis of enteric origin in this patient population.
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PMID:Gastric emptying and orocecal transit in portal hypertension and end-stage chronic liver disease. 937 56

Total parenteral nutrition (TPN)-induced liver disease develops in 40-60% of infants who require long-term TPN for intestinal failure. The clinical spectrum includes cholestasis, cholelithiasis, hepatic fibrosis with progression to biliary cirrhosis, and the development of portal hypertension and liver failure in a significant number of children who are totally parenterally fed. The pathogenesis is multifactorial and is related to prematurity, low birth weight, and duration of TPN. The degree and severity of the liver disease is related to recurrent sepsis including catheter sepsis, bacterial translocation, and cholangitis. Lack of enteral feeding leading to reduced gut hormone secretion, reduction of bile flow, and biliary stasis may be important mechanisms in the development of cholestasis, biliary sludge, and cholelithiasis. Although it is unlikely that modern TPN solutions have a major role in the etiology of TPN liver disease, manganese toxicity recently has been recognized in children with hepatic dysfunction on TPN. Although there is a definite relationship with the degree of manganese toxicity and hepatic decompensation, it is not yet clear whether this is a primary mechanism or whether the high levels are related to reduced biliary excretion of manganese. The management strategies for the prevention of TPN-induced liver disease include early enteral feeding, a multidisciplinary approach to the management of parenteral nutrition, and aseptic catheter techniques to reduce sepsis. The administration of ursodeoxycholic acid may improve bile flow and reduce gall bladder and intestinal stasis. As survival from isolated intestinal transplantation improves, this therapeutic option should be considered before TPN liver disease becomes irreversible and combined liver and small bowel transplantation is required.
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PMID:Liver complications of pediatric parenteral nutrition--epidemiology. 943 2

Budd-Chiari syndrome (BCS) is an uncommon form of portal hypertension caused by obstruction of the hepatic venous outflow. From 1969 to 1997 we treated 19 patients (7 men, 12 women; mean age 37.6 years) affected by primary BCS. In most of the cases no etiologic factors were identified; in the remaining cases the etiology was associated with polycythemia vera, use of oral contraceptives, presence of endoluminal membranes, and repeated episodes of sepsis. Three patients with membranous occlusion of the major hepatic veins were treated by percutaneous placement of a self-expanding metallic stent inserted via a transjugular or transhepatic approach. The remaining 16 patients underwent a side-to-side portacaval shunt, which required interposition of a graft in five cases. In two patients with a significant caval obstruction, a metallic vascular stent was placed in the narrowed tract of the inferior vena cava, before shunting, by means of a transfemoral venous approach. One patient died within the first 30 postoperative days. The 18 survivors were followed for a mean of 66.7 months. The 5-year survival was 83%. Primary BCS requires different therapies depending on the stage of the disease. The fulminant or chronic forms with irreversible hepatic damage require definitive treatment, such as orthotopic liver transplantation. For the acute or subacute forms, characterized by reversible hepatic injury, a portasystemic shunt represents the most effective treatment. The patients at poor hepatic risk can be treated by interventional radiology. In both cases preliminary caval stenting is necessary if the syndrome is complicated by significant obstruction of the inferior vena cava.
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PMID:Surgical and radiologic treatment of primary Budd-Chiari syndrome. 946 61

A 27-year-old woman with chronic renal failure, who had been treated with chronic ambulatory peritoneal dialysis and had developed sclerosing peritonitis, was admitted to the hospital with intra-abdominal sepsis. In spite of antibiotic therapy, sepsis recurred and was associated with intrahepatic cholestasis. In addition, over a period of about 4.5 weeks she developed hepatomegaly and portal hypertension unassociated with occlusion of the portal vein or one of its main extrahepatic branches. A wedge biopsy of the liver revealed extensive thick fibrosis of the liver capsule, intrahepatic cholestasis, diffuse swelling of hepatocytes, central veins that were difficult to visualize and small portal tracts. It is suggested that the sepsis was responsible for the intrahepatic cholestasis, swelling of hepatocytes and hepatomegaly. It is also suggested that the rigidity of the fibrotic liver capsule provided resistance to the development of hepatomegaly, with the result that intrahepatic pressure increased (compressing intrahepatic branches of the portal vein as well as portal tracts and central veins) and portal hypertension developed.
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PMID:Sclerosing peritonitis complicated by sepsis: a potential cause of portal hypertension. 951 60

The transjugular intrahepatic portosystemic shunt (TIPS) represents an important advance in the treatment of complications of portal hypertension. The results from the first 10 TIPS procedures in Arhus are reported. We found, as also documented in other clinical series, that TIPS is more effective in controlling acute haemorrhage than treatment with sclerotherapy and specific medical treatment. Seven out of 10 were treated for acute haemorrhage, and two patients were treated for recurrent variceal bleeding in spite of at least 20 procedures of sclerotherapy and pharmaceutical therapy. One patient was treated with TIPS due to refractory ascites. All 10 TIPS procedures were satisfactory, in four patients it was necessary to embolize collaterals. There were no acute complications associated to the TIPS procedures, but one patient developed stenosis of the shunt within one year, and another chronic encephalopathy. Two patients died, one because of sepsis with Candida albicans, and the other of intracerebral bleeding 16 months after the TIPS procedure.
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PMID:[Transjugular intrahepatic portosystemic shunt in the treatment of portal hypertension]. 952 55

Portal cavernomatosis consists in the substitution of the portal vein by many fine, twisting venules leading to the liver. This phenomenon is produced as a consequence of anterior thrombosis of the portal vein and is associated with chronic pancreatitis, cancer of the pancreas, intraabdominal sepsis and cholelithiasis. The symptomatology may be nul or present as obstructive jaundice or portal hypertension. Diagnosis is made by Doppler echography. The treatment is portal shunt when symptomatology is produced. In patients with cholelithiasis requiring surgery, the shunt is advised prior to biliary surgery since perioperative hemorrhage, if present, may be incoercible as in the case herein described. We present a 84-year-old woman with portal cavernomatosis the etiology of which was a hydatidic cyst located in the hepatic bifurcation and treated with mebendazol 10 years previously. This etiology has not been previously reported.
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PMID:[Hydatid cyst in the hepatic hilum causing a cavernous transformation in the portal vein]. 964 76

Portal hypertension hemorrhage (PHH) due to esophageal varices (EV) rupture in nearly 80% of cases, or gastric varices (GV) in the remaining 20%, account for one-fifth of the GI tract bleedings in a general hospital. Its frequency, but more importantly, its magnitude, that causes up to one-third of the cirrhotic casualties, deserves constant update in its management. Diverse inherent patient factors influence the course of any PHH, i.e., a) remaining liver function, which is determinant; b) variceal size; c) sepsis, and d) alcohol intake. Mortality due to PHH is 27% during the first week, 41% within 6 weeks and 75% by one year of follow-up after the index hemorrhage. Time of intervention is then of utmost importance. All these key circumstances determine the ultimate course of the bleeding event, in many cases to a greater degree than the opportunity and quality of the specific treatment itself. This diversity of influential factors also jeopardizes adequate patient randomization in trials designed to compare treatment modalities. During the last decade, EV sclerosis, when compared to conventional medical treatment (non-beta blockers), has proved useful to stop active bleeding in 71 vs. 31% of cases, decreasing early and late recurrence from 70 to 40%, and direct bleeding-related mortality from 24 to 9%, even when global mortality remains around 14% per year. Disappointing as it seems, remaining liver function is the determinant issue, but a biased underestimation factor may also play a role, due to greater surgical rescue of patients in the medical branch compared to EV sclerosis, 6 vs. 28%. Minor morbidity in 14% of sclerosis treatment has given way to endoscopic ligation with similar results and less morbidity. Prophylactic EV sclerosis was prohibited by prospective controlled trials, which demonstrated significant increase in bleeding and mortality, even though there might be a subgroup of patients with large varices or endoscopic prognostic signs of bleeding that decrease by 10% their incidence expected 35%/year bleeding. GV bleeding remains a challenge; where cyanoacrylate may be needed to improve immediate control and prevent recurrence of PHH. These patients, as well as those failures to endoscopic treatment are candidates for intrahepatic portosystemic shunt (TIPS), although long-lasting control is achieved, in most cases, by liver transplant.
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PMID:[Therapeutic endoscopy in portal hypertension. When, how and how far in 1998]. 1006 21

The present study investigates clinical factors associated with decreased survival following Transjugular Intrahepatic Portosystemic Stent Shunt (TIPSS). Sixty-seven patients underwent TIPSS for bleeding related to portal hypertension, 42 (63%) on an urgent basis. TIPSS was successfully placed in 65 (97%) patients with no fatal procedural complications. Thirty day mortality was 21%, there being several predictive factors: transfer from another institution, urgency of procedure, sepsis, encephalopathy, higher mean serum bilirubin and low serum albumin. However, using regression analysis, 30 day mortality was predicted independently only by severe liver disease (Child-Pugh C, P= 0.003) and older age (P= 0.003). When stratified by Child-Pugh class, cumulative survival rates at 1 year for class A, B and C were 100, 90 and 34%, respectively. Only three of 25 patient deaths were due to variceal rebleeding. Thirty (46%) patients had a total of 41 rebleeding episodes, with mean time to first rebleed of 4.8 months (range, 3 days-38 months). Cumulative rebleeding rate at 1 year was 25%. Log-rank analysis did not reveal a significant difference in overall survival between rebleeders and non-rebleeders (P= 0.125). When investigated, shunt abnormalities (stenosis, occlusion) were identified in all cases of rebleeding. Our findings confirm TIPSS can be safe and effective in the control of refractory variceal haemorrhage. However, prognosis remains poor for patients with advanced liver disease, particularly if older and in the emergency setting. Vigilant surveillance and high rate of intervention is necessary to maintain shunt patency. Consideration could be given to elective shunt surgery instead of TIPSS for patients with recurrent bleeding and good prognosis liver disease.
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PMID:Mortality and rebleeding following Transjugular Intrahepatic Portosystemic Stent Shunt for variceal haemorrhage. 1022 18


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