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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical course and causes of death in 132 consecutive patients with fulminant hepatic failure and grade III or IV encephalopathy have been reviewed. 105 patients died and in 96 of these an autopsy examination was performed. In 36 patients there was cerebral oedema and the mean age of this group was significantly younger than the other fatal cases. In 28 patients death was attributed to major haemorrhage which originated in the gastrointestinal tract in 25. The prothrombin time ratio was not significantly greater in patients with major bleeding than in those without but they did have a significantly lower platelet count. Sepsis contributed to death in 12 patients. In 25 patients massive hepatic necrosis only was found at autopsy and death was considered to be due solely to hepatic failure. The degree of hepatocyte loss was assessed in 80 fatal cases by a histological morphometric technique on a needle specimen of liver taken immediately post-mortem. The proportion of the liver volume occupied by hepatocytes (hepatocyte volume fraction, HVF) was greatly reduced in all patients (normal 85+/-SD 5 percent) but the mean value was significantly higher in the patients dying with sepsis, cerebral oedema or haemorrhage than in the group in whom death was attributed solely to hepatic failure. There were ten patients in whom liver function was improving at the time of death which was due to cerebral (9) or haemorrhage (1). These observations suggest that many patients presently dying from fulminant hepatic failure may be expected to survive, once more effective therapy is available for the complications of the illness.
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PMID:Causes of death in fulminant hepatic failure and relationship to quantitative histological assessment of parenchymal damage. 17 38

In 75 cases of histologically verified liver cirrhosis the plasma amino acids were determined by ion exchange chromatography and the results were correlated with different liver function tests as prothrombin time, pseudocholinesterase, serum albumin, GOT, bilirubin and venous ammonia. Out of these parameters prothrombin time, pseudocholinesterase and serum albumin significantly correlated with the sum of branched-chain amino acids and with the Fischer's quotient (molar ratio of branched-chain and aromatic amino acids). Methionin and aromatic amino acids inversely correlated with these parameters, additionally methionin positively correlated with bilirubin and GOT. By comparing plasma amino acid levels in cirrhotics without and with hepatic encephalopathy (grade 3 or 4) no significant differences were found. "Fischer's quotient" showed an overlap in patients with and without encephalopathy. Therefore the precipitation of hepatic encephalopathy is not fully explained by the changes in plasma amino acids. Therapeutic administrations of specially mixtures of amino acids with a high content in branched-chain and a low content in aromatic amino acids correct the plasma amino inbalance for a short time and improves hepatic encephalopathy.
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PMID:Plasma amino acids in hepatic encephalopathy. 29 Jul 44

The authors studied four children with Reye's syndrome aged 16 months, 6 years, 8 years and 11 years respectively with severe liver failure and progressive coma. The laboratory investigations in all of them showed a marked elevation of serum transaminases, hyperammoniaemia and a prolongation of the prothrombin time. The electroencephalograms showed a grossly abnormal picture with generalised continuous delta activity. Three children survived with return to normal of the liver function tests whilst the fourth child died. In the last two patients an electroencephalogram carried out every six hours has enabled certain prognostic features to be determined. Improvement in the E.E.G. correlates closely with clinical improvement and vice versa. The authors also advocate serial E.E.G. recordings in Reye's syndrome. The role of hyperammonaemia in the genesis of encephalopathy and the electroencephalographic changed is discussed. The role played by raised intracranial pressure is stressed and the importance of controlling it in order to prevent further damage and improve the prognosis of this serious illness.
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PMID:[Reye's syndrome a clinical and electrophysiological study of four patients (author's transl)]. 61 96

Among 134 patients with chronic active liver disease, selected by identical clinical, biochemical and morphologic criteria, assigned to standard treatment programs and followed at regular intervals, 21 of 105 failed treatment with standard regimens containing steroids. Treatment failure was more common in patients whose serum contained hepatitis B surface antigen, those with more severe liver disease as judged by liver function tests (prothrombin time) and hepatic morphology (subacute hepatitis or cirrhosis). Early diagnosis of treatment failure, based on changes in liver function tests rather than on clinical features of deterioration, coupled with the immediate administration of higher doses of prednisone with or without higher doses of azathioprine, resulted in disappearance of clinical and biochemical features of disease activity in the majority of patients. These results were greatly superior to those earlier reported by us from patients chosen by identical criteria but treated by conventional measures. However, when endogenous encephalopathy developed the outlook was grave, regardless of previous or subsequent therapy. We recommend that patients at risk for failing conventional treatment be identified early, followed carefully with serial liver function tests, and be treated promptly with higher doses of medication when deterioration occurs.
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PMID:Failure of customary treatment in chronic active liver disease: causes and management. 79 99

We report Reye syndrome in an 11-year-old boy whose first symptoms were generalized convulsions and coma without clinical or laboratory evidence of liver disease. Serum glutamic oxaloacetic transaminase and lactate dehydrogenase (LDH) values increased strikingly on the third day after the onset of coma. These enzymatic changes were associated with prolongation of prothrombin time. A rise in blood ammonia concentrations began on the fourth day of coma. The diagnosis of Reye syndrome was confirmed by a liver biopsy and at autopsy. This case demonstrates that encephalopathy in Reye syndrome can develop prior to detectable hepatic involvement, and suggests that factors unrelated to generalized liver damage may occasionally play a role in the pathogenesis of this obscure disorder.
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PMID:Reye syndrome without initial hepatic involvement. 84 16

The intrasplenic injection of 99mTc-labeled albumin microspheres, followed 30 sec later by an injection of 99mTc-labeled red blood cells with recording of the progression of the two tracers, were performed in 110 patients. This also enabled the plotting of activity versus time curves on splenic, hepatic, cardiac, and pulmonary areas of interest, there by giving access to several hemodynamic variables. Scintillation image demonstrated splenoportal obstruction in 8 cases. Intrahepatic obstruction with reflux via collaterals were observed in 53 cases, 14 with umbilical reflux. In 13 cases, the patency of surgical portacaval anastomoses were verified. The splenoportal blood flow velocity was not significantly different in patients with cirrhosis (V = 10.1 cm per sec +/- 3.0 SD) and in normal subjects (V = 13.2 cm per sec +/- 5.8 SD). The fraction of shunted splenic flow in the case of cirrhosis varied from 0 to 100%; there was no relationship between this percentage and the seriousness of the clinical status. In 3 cases, the presence of intrahepatic shunts was detected. There was a very significant difference between mean transit time (MTT) of red blood cells in patients with cirrhosis (t = 12.2 sec +/- 4.4 SD) and those without cirrhosis (t = 19.9 sec +/- 3.7 SD). Among patients with cirrhosis, those with a history of jaundice had a shorter MTT than those without such a history. On the other hand, the MTT was not significantly different whether the patients with cirrhosis had or did not have hemorrhage, ascites or encephalopathy. There was a positive correlation (P less than 0.01) between MTT and plasma albumin concentration,and between MTT and prothrombin (P less than 0.01). Finally, there was a high negative correlation (P less than 0.001) between MTT and total serum bilirubin. Scintillation splenoportography is a useful technique for assessing hepatic hemodynamics and for demonstrating abnormalities of the intrahepatic circulation.
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PMID:Scintillation splenoportography: hemodynamic and morphological study of the portal circulation. 98 35

In 31 patients with cirrhosis of the liver undergoing porta-caval shunt surgery, the prognostic value of some liver function tests was studied. The surgical mortality was not correlated with the test results. Serum concentrations of bilirubin, albumin, and prothrombin were not correlated with postoperative encephalopathy, but the mutually correlated preoperative galactose elimination capacity and age of patients were correlated with encephalopathy development. Incapacitating encephalopathy mainly occurred in patients above 60 years of age, and when the galactose elimination capacity was at or less than an arbitrary limit of 225 mg/min. The liver function decreased significantly following operation.
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PMID:Preoperative liver function tests correlated with encephalopathy after porta-caval anastomosis. 107 89

Histiocytosis X describes a disease characterized by histiocytic infiltration of the reticuloendothelial system, skin, bones, and pituitary gland. The disseminated form frequently occurs in infants and children. Chemotherapy has significantly improved the prognosis in this disorder. Sixty-three per cent of survivors, however, have some residual disability related to fibrosis of tissues previously infiltrated by histiocytes. In instances of liver involvement, healing by fibrosis may result in cirrhosis with portal hypertension and bleeding esophageal varices. Clinical findings include hepatosplenomegaly, jaundice, ascites, hypoalbuminemia, prolonged prothrombin time, and Bromsulphalein retention. Histologic examination of the liver shows a characteristic dense "macronodular" periportal cirrhotic pattern. Three children with portal hypertension and bleeding varices due to healed histiocytosis X were sucessfully managed by portosystemic shunt procedures. Portacaval, mesocaval, and central splenorenal shunts were equally effective in relieving poral hypertension. These children had neither recurrence of bleeding nor evidence of encephalopathy. Two children remain well whereas in one patient a primary hepatoma developed fourteen years posthung and he died of pulmonary metastases. Portosystemic shunt procedures effectively relieve the threat of potentially fatal variceal hemorrhage and improve the opportunity for long-term survival in children with cirrhosis and portal hypertension due to healed histiocytosis X.
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PMID:Portal hypertension in infants and children with histiocytosis X. 108 50

The Child-Turcotte classification, as modified by Pugh et al., was recorded on diagnosis in 598 completely followed patients with cirrhosis of the liver. The variables that comprise the Pugh classification are ascites, encephalopathy, serum albumin, serum total bilirubin, and prothrombin time. The Pugh score categorized in three classes (class A = score 5 or 6, class B = score 7 to 11, class C = score 12 to 15) separates the series into three groups of approximately equal size with significant differences in median survivals (p less than 0.005) and in survival curves (p less than 0.0001). The characteristics of simplicity, availability, low cost and good discrimination power make the Pugh classification a very useful method to estimate prognosis in patients with cirrhosis of the liver.
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PMID:Prognostic value of Pugh's modification of Child-Turcotte classification in patients with cirrhosis of the liver. 140 30

Variceal haemorrhage in cirrhotic patients carries a high early mortality even when balloon tamponade or emergency sclerotherapy are applied. The aim of this study to identify patients dying within six weeks of their first variceal haemorrhage. One hundred and twenty one patients with parenchymal cirrhosis presenting with the first variceal bleeding episode between June 1983 and December 1988 were studied. Nineteen patients were excluded for various reasons. Emergency sclerotherapy was carried out in cases of active bleeding or where there were endoscopic signs of recent bleeding, and then regularly repeated afterwards. Of the 24 variables studied and included in a multivariate analysis using a logistic regression model, three had an independent prognostic value: encephalopathy, prothrombin time, and the number of blood units transfused within the 72 hours of time zero. The subsequent regression equation was able to predict 89% of the patients who will die and 97% of the patients who will still be alive six weeks after their first variceal haemorrhage treated by sclerotherapy. Pugh score was less discriminatory than these last three variables in terms of accuracy of adjustment, goodness of fit to the model, receiver operating characteristic curves, and percentage correct prediction. To measure the accuracy of the prediction rule, our model was applied to another series of 28 cirrhotic patients admitted with their first variceal bleeding during the next period (January 1989 to May 1990). Death and survival were correctly predicted in respectively 82% and 94% of the cases. The use of this score is recommended for the selection of patients with high early mortality after variceal bleeding despite sclerotherapy, and for the design of new therapeutic trials.
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PMID:Factors related to early mortality in cirrhotic patients bleeding from varices and treated by urgent sclerotherapy. 144 64


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