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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiple organ failure continues to be the primary cause of death after trauma and sepsis. This clinical syndrome follows shock and resusitation and the transition from a hypermetabolic response to a syndrome of progressive organ failures and death. Risk factors include: perfusion deficits, persistent foci of dead or injured tissue, an uncontrolled focus of infection, the presence of the respiratory distress syndrome, and preexisting fibrotic liver disease. The imitation of the syndrome represents the clinical manifestation of hepatic failure. It is hypothesized that this hepatic failure results from paracrine amplification with Kupffer cell induced hepatocyte cytotoxicity. The best treatment remains prevention and rapid control of risk factors including restoration of oxygen transport and aggressive nutrition support. There seems to be no treatment "magic bullet" either experimentally or clinically once the syndrome has occurred.
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PMID:Hepatic dysfunction in multiple systems organ failure as a manifestation of altered cell-cell interaction. 267 63

We reviewed in retrospect the records of all patients at our institution in whom peritoneovenous shunts were placed to manage refractory ascites due to chronic liver disease from 1977 through 1986. There was a wide spectrum of underlying liver disease in these 23 patients; most frequent was alcoholic cirrhosis. Five were in modified Child's class A, 14 were in class B, and four were in class C. Fourteen of 23 patients had some complication associated with peritoneovenous shunt placement; clinical consumptive coagulopathy, infection, and gastrointestinal hemorrhage while hospitalized were most frequent. Fifteen of 23 died, 12 while hospitalized or within 1 month of hospitalization. Death in eight patients appeared to be related to shunt placement and was due to sepsis in five, hepatorenal syndrome with an obstructed shunt in one, consumptive coagulopathy in one, and pulmonary edema in one. All modified Child's class C patients, six of seven patients with clinical consumptive coagulopathy, and all patients with a preshunt total bilirubin greater than 3.7 mg/dl died while hospitalized or within 1 month of hospitalization. This review supports studies showing that placement of peritoneovenous shunts for refractory ascites has a high morbidity and mortality in patients with advanced liver disease, and does not support their use in the management of refractory ascites.
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PMID:Poor outcome from peritoneovenous shunts for refractory ascites. 271 11

Plasma or serum extrinsic pathway inhibitor (EPI) activity was measured in 24 patients with disseminated intravascular coagulation (DIC) and in 23 patients with severe hepatocellular disease. EPI was measured as activity in a test sample that inhibited factor VIIa/tissue factor (TF)-catalyzed activation of 3H-factor IX (activation peptide release) in the presence of factor X. Of the 24 patients with DIC, 13 had sepsis and five had metastatic carcinoma, disorders in which tissue factor is believed to initiate DIC. EPI activity ranged from 68% to 300% (mean 134% +/- 50%). Serial measurements in nine patients failed to show depletion of EPI activity coincident with worsening DIC. DIC induced by tissue factor or other activating materials may progress despite normal EPI levels. In the patients with liver disease, of whom 15 had decompensated chronic hepatocellular disease (two fatal cases) and eight had acute fulminant liver failure (seven fatal cases), plasma or serum EPI activity varied from less than 20% to 194%. Values were distributed in a bimodal fashion. EPI activity could not be correlated with either the etiology of the liver disease or the degree of prolongation of the prothrombin time. Patients with chronic hepatocellular disease who survived had normal or elevated EPI activity. Patients with fatal hepatic dysfunction had low, normal, or high values for EPI activity. This must mean that secretion of EPI from cells other than hepatocytes can maintain normal plasma EPI levels.
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PMID:Human plasma extrinsic pathway inhibitor activity: II. Plasma levels in disseminated intravascular coagulation and hepatocellular disease. 278 83

Plasma and serum from patients with liver disease and elevated fibrin(ogen) degradation product (FDP) levels as measured by latex agglutination were analyzed by immunoblotting to characterize the FDP in these patients. An antihuman fibrinogen antibody was used that recognizes fibrinogen, fibrin monomer, soluble high molecular weight fibrinogen and fibrin polymers, as well as high molecular weight cross-linked degradation fragments, and the smaller fragments X, Y, D-dimer, D, and E. The analytic procedures were validated with plasma and serum from patients known to have intravascular fibrinolysis associated either with disseminated intravascular coagulation (DIC) or with thrombolytic therapy. The samples demonstrated a spectrum of plasmin degradation fragments on the immunoblots. Twenty-eight of 35 patients with liver disease (80%) had no evidence of plasmin degradation fragments in their plasma or serum. The cause of the elevated FDP levels as measured by latex agglutination was thought to be fibrin monomer or unclottable fibrinogen that was retained in the sera of some of these patients. Seven patients (20%) were found to have circulating plasmin degradation fragments. In addition to liver disease, however, these patients all had an illness (sepsis, shock, and pancreatic carcinoma) independently associated with intravascular coagulation and fibrinolysis. Three patients who lacked plasmin fragments also had pancreatic carcinoma or sepsis. The two groups of liver disease patients could not be clearly differentiated on the basis of clinical or laboratory evidence, but the blotting procedure proved to be a useful discriminator.
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PMID:Analysis of elevated fibrin(ogen) degradation product levels in patients with liver disease. 293 48

The purpose of this study was to identify which of the biochemical, immunological, or functional parameters derived before surgery as part of a systemic evaluation were helpful in predicting the frequency of rejection episodes, the chance of survival, and the cause risk of death (should death occur) of patients after orthotopic liver transplantation (OLTx). Ninety-eight adult patients who had an extensive preoperative protocol evaluation were studied before OLTx. The biochemical parameters assessed were albumin, prothrombin time, bilirubin, and ICG clearance. The immunologic parameters assessed included total lymphocytes, T3 cells, T4 cells, T8 cells, and the T4/T8 ratio. The degree of histocompatibility antigen (HLA) matching between the donor and the recipient was also evaluated in 80 of the 98 patients studied. Most postoperative deaths occurred within 12 weeks of the procedure (24%; 24 of 98 patients); 13 patients (13%) died within the first 6 postoperative weeks, of either bacterial or fungal sepsis. An additional 14 patients (14%) died after the initial 6 postoperative weeks due, primarily of an acquired viral and/or protozoan infection (p less than 0.01). During the first 6 weeks, survival was better for patients with cholestatic liver disease (ChLD, 93%, n = 45) and miscellaneous liver diseases (MISC, 100%, n = 10) than it was for those with parenchymal liver diseases (PLD, 77%, n = 43). Although albumin, prothrombin time, T4/T8 ratios, and per cent T8 cells were statistically different in patients with PLD as compared with those with ChLD, these parameters, as well as the per cent T4 cells, serum bilirubin level, per cent retention of ICG at 15 minutes, and the plasma ICG disappearance rate were not found to be of substantial help in predicting patient survival or non-survival. Moreover, neither the degree of HLA matching nor the number of rejection episodes differed between surviving and nonsurviving patients. The results of this study suggest that patients with PLD are at increased risk of early postoperative death after OLTx because of bacterial and/or fungal sepsis, as compared with patients operated upon for ChLD. Better pre-, intra-, and postoperative predictors of risk of death and complications are needed to reduce the early mortality observed after orthotopic liver transplantation.
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PMID:Relationship between the diagnosis, preoperative evaluation, and prognosis after orthotopic liver transplantation. 304 26

Variceal hemorrhage is frequently a lethal event. Mortality among patients who have bled is high, with survival over the short term of only 25% to 50%. We retrospectively reviewed the records of 177 patients in whom variceal bleeding was treated with variceal sclerosis during a 5-year period from 1981 to 1986. All patients were treated by freehand injection of 25% sodium morrhuate with 35% dextrose, 4 ml per injection, through a fiberoptic endoscope. Of this group, 46 patients were treated with sclerosis followed by liver transplantation (group 1). These were compared to 36 nonalcoholic Child's class B and C patients treated with sclerosis alone (group 2). Survival at 4 years was poor in group 2 (17%). Liver failure and continued gastrointestinal bleeding were the most frequent causes of death. Survival among the liver-transplant group was significantly better (73%, p less than 0.001). Causes of death in this group were primarily due to sepsis, often in the setting of acute graft rejection. Group 1 patients were younger (39.8 +/- 10.8 vs 49.8 +/- 16.5 years, p less than 0.01); this difference is influenced by the deliberate selection of younger patients for liver transplantation. We conclude that sclerotherapy followed by liver transplantation significantly improves survival compared to conventional therapy in selected patients with advanced liver disease and portal hypertension. Donor organ availability will seriously limit the applicability of this approach to patients with bleeding esophageal varices.
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PMID:Bleeding esophageal varices: treatment by sclerotherapy and liver transplantation. 305 93

An analysis was made of the causes of death in 22 of 50 patients receiving consecutive orthotopic liver transplants. A close look at the fatal course of these patients revealed three major patterns: surgical complications (27%), pathology of the hepatic artery anastomosis (23%), and cholestasis (32%). Technical factors were the major reasons for excessive peroperative blood loss, and not the coagulopathy accompanying the liver disease. The etiology of hepatic artery thrombosis is not known. It leads to irreversible damage of the graft, causing death due to acute hepatic failure or to cholangitis and sepsis. The only way to treat patients with this complication is retransplantation. Several factors can induce cholestasis. Retrospectively, it appears that this was mostly due to inappropriate immunosuppression, often a result of the difficult differential diagnosis between rejection and viral infection. Recognition of these three basic patterns should enable us to anticipate their subsequent complications. This may lead to a reduction in morbidity and mortality after liver transplantation.
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PMID:Mortality after orthotopic liver transplantation. An analysis of the causes of death in the first 50 liver transplantations in Groningen, The Netherlands. 307 83

The branched-chain amino acids (BCAAs)--leucine, isoleucine, and valine--share unique biochemical properties that may make them useful in altered physiologic states. They can be metabolized independently of liver function to provide energy, other amino acids, or small nitrogenous compounds. This unique ability makes the BCAAs a desirable supplement in liver disease with encephalopathy and, to a lesser extent, in sepsis with hepatic dysfunction. Furthermore, the BCAAs play a role in the regulation of protein synthesis, suggesting beneficial effects in catabolic states such as postoperative stress, trauma, renal failure, and burns. However, initial studies in these areas have presented equivocal results.
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PMID:Clinical use of branched-chain amino acids in liver disease, sepsis, trauma, and burns. 308 Sep 79

Four patients with hemophilia A have undergone liver transplantation in our institution, three successfully. The first was a 21-year-old man with chronic active hepatitis (CAH) in whom the effects of previous abdominal operations prevented the satisfactory technical insertion of the new liver. He died intraoperatively. The second patient was a 15-year-old boy with CAH who began to synthesize factor VIII coagulant activity (F VIII:C) within 18 hours of successful liver transplantation and has continued to do so for almost 2 years (F VIII:C range 0.89 to 3.20 U/mL). The first 2 months of his postoperative course were complicated by infections, but since that time he has done well and has returned to school. The third patient was a 48-year-old man with portal fibrosis and severe ascites. He synthesized F VIII:C (range 0.96 to 1.50 U/mL) within six hours after reestablishment of circulation through the new liver. His postoperative course was complicated by numerous infections, and he died with sepsis and an acquired immunodeficiency-like syndrome 4 months after transplantation. The fourth patient was a 47-year-old mild hemophiliac with CAH who produced adequate factor VIII:C levels following transplantation (range 0.79 to 2.80 U/mL). These patients demonstrate that liver transplantation in hemophiliacs with end-stage liver disease may be lifesaving and results in correction of the F VIII:C deficiency and associated hemorrhagic tendency.
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PMID:Liver transplantation in hemophilia A. 1947 Apr 40

We evaluated the effect of total parenteral nutrition (TPN) on abnormalities of hepatic histology. Liver biopsies of 93 patients who were concurrently receiving TPN were compared with a control group of 35 patients. The control patients were matched for extent of preexisting liver disease and degree of illness. The liver biopsy specimens were blindly graded on 19 histopathologic findings, including fatty change, portal inflammation, and cholestasis. Twenty-seven clinical variables, such as preexisting liver disease, the presence or absence of sepsis or shock, and number of days receiving TPN before biopsy, were recorded. Individual and partial correlations were established between the clinical variables and histopathologic findings. The control and TPN groups proved to have been closely matched regarding the extent of risk factors for hepatic histopathologic features. Positive correlations were repeatedly found between abnormal hepatic histologic features and preexisting liver disease, abdominal sepsis, renal failure, and blood transfusion but not with the administration of TPN. We conclude that clinical phenomena, such as existing liver disease, renal failure, and abdominal sepsis, rather than administration of TPN, had a predominant effect on histopathologic features in this group of patients.
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PMID:Effect of total parenteral nutrition on hepatic histology. 313 13


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