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

Because of the inhomogeneous prognosis in fulminant hepatic failure, prognostic criteria are required which help to establish the indication for liver transplantation as a successful therapeutic procedure. In our study of 33 patients with fulminant hepatic failure (94% viral hepatitis, 67% hepatitis B), serum bilirubin > 320 or < 160 mumol/L, serum creatinine > 110 mumol/L, prothrombin time < 15% of the normal value and duration of jaundice until onset of encephalopathy > 7 days indicated a fatal outcome. When criteria described by O'Grady et al. were used, only limited predictability was achieved. This, as well as the frequently contradictory results of the few prognostic studies published so far, is probably due to the regional differences in the etiology and the different clinical courses of fulminant hepatic failure.
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PMID:Prognostic indicators in fulminant hepatic failure. 144 4

To assess the prevalence of spontaneous bacterial peritonitis (SBP), ascitic fluid cell count, and ascitic fluid culture by conventional method and by bedside inoculation in blood culture bottles were performed in 31 consecutive patients of liver cirrhosis. Seven (22.58%) patients had ascitic fluid polymorphonuclear count (PMN) more than 500/mm. Ascitic fluid culture by conventional method was negative in all the patients, while in 4 patients culture was positive by bedside inoculation method. Six of 7 patients with SBP or its variant were in Child class C. Clinical features in these patients were abdominal pain (5 patients), fever (4) and encephalopathy (2); serum bilirubin level was 6.8 +/- 5.5 mg/dl, serum albumin 1.98 +/- 0.2 g/dl, prothrombin index 59.8 +/- 12.2%, ascitic fluid protein 0.78 +/- 0.24 g/dl. Three of 7 patients with SBP or its variant expired during hospital stay; the other 4 patients recovered after appropriate antibiotic therapy. We conclude that SBP is a serious complication in patients of liver cirrhosis with ascites. Ascitic fluid PMN count and bedside inoculation of blood culture bottles with ascitic fluid are sensitive indicators of SBP. Hence they should be performed routinely for early detection of SBP.
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PMID:Prevalence of spontaneous bacterial peritonitis. 145 29

Symptomatic viral hepatitis A usually only requires supportive therapy and the majority of cases are managed in the community. The prodromal symptoms of nausea, anorexia and lethargy tend to improve with the onset of clinical jaundice. Fulminant hepatic failure is said to be an uncommon complication, occurring in only 0.14-0.35% of hospitalized cases. However, an increasing incidence has been documented in some northern European countries where up to 20% of cases of fulminant viral hepatitis is due to hepatitis A. This trend parallels the increasingly delayed exposure to hepatitis A and the increased severity of the illness when contracted in later life. The risk of developing fulminant hepatic failure is best monitored using coagulation factor assays, with the prothrombin time and factor V levels being the most favoured. The diagnosis is established with the onset of encephalopathy. Patients progressing to grade 4 encephalopathy have a reasonably good prognosis compared to other aetiologies and survival rates of up to 67% have been obtained with medical management, despite the co-existence of such complications as cerebral oedema, renal and respiratory failure and the metabolic sequelae of acute liver failure. Nevertheless, some patients require emergency liver transplantation and 10 such patients have been reported to date. Transplantation is especially required in older patients (> 40 years) and those who are jaundiced for > 7 days before the onset of encephalopathy. The serum bilirubin and the prothrombin time complement these parameters in the decision making process.
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PMID:Management of acute and fulminant hepatitis A. 147

A 39-year-old woman was evaluated for possible liver transplantation due to rapidly developing hepatic failure 4 weeks after initiation of oral minocycline 100 mg twice a day for the treatment of acne. The patient developed a maculopapular rash, malaise, fever, nausea, and vomiting 2 weeks prior to admission to the hospital. On admission, her symptoms rapidly progressed to liver failure characterized by rapidly rising liver enzyme levels, worsening encephalopathy, and coagulopathy. Viral hepatitis serologies and blood cultures were all negative. After intensive supportive care for 2 weeks, the patient's condition gradually improved and she was discharged with mildly elevated liver enzyme levels and pruritus, without need of liver transplantation. Minocycline-induced hepatic injury is an idiosyncratic reaction with a sensitization period that appears to be 3-4 weeks in duration. The characteristic features include rash, fever, lymphadenopathy, and eosinophilia, as well as severe alterations in liver function. The high liver enzyme levels and the significant prolongation of the prothrombin time suggest massive hepatocellular damage. In light of the profound liver damage that occurs with this adverse reaction, care should be taken in administering minocycline to patients who have concomitant liver disease. It is recommended that patients should be instructed as to the possible signs and symptoms of toxicity and be monitored for evidence of idiosyncratic reaction or liver failure.
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PMID:Acute hepatic failure associated with oral minocycline: a case report. 153 50

1. In a retrospective study, we stratified 79 patients with paracetamol hepatotoxicity into two groups according to weekly alcohol consumption below (n = 49) or above (n = 30) Royal College of Physicians' guidelines of 21 units week-1 for males and 14 for females. 2. Survival was lower (33%) and serum creatinine on admission higher (median 207 mumol) in patients whose alcohol consumption was above recommended guidelines than in those whose drank less than this (65.9% and 138 mumol, P less than 0.01 and P = 0.027, respectively). An arterial blood pH less than 7.30 on admission was also more common in those patients with a higher alcohol consumption (30% v 12.2%, P = 0.05). 3. In all patients whose alcohol consumption exceeded the guidelines, paracetamol overdose was fatal if associated with a serum creatinine greater than 300 mumol in conjunction with a prothrombin time over 100 s and grade 3 or 4 encephalopathy or a peak prothrombin time over 180 s. 4. Chronic alcohol intake above suggested limits is an adverse prognostic feature in cases of severe paracetamol overdose. This effect is partly related to increased nephrotoxicity.
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PMID:The effect of chronic alcohol intake on prognosis and outcome in paracetamol overdose. 168 56

Twelve cases of childhood fulminant hepatitis seen over a 4-year period are described. Six had hepatitis A, five hepatitis B and one non-A non-B hepatitis. Encephalopathy, the cardinal feature of fulminant hepatitis, was usually evident within 2 weeks of onset of illness, and the median duration of illness in fatal cases was 19 days. Deep jaundice, prolongation of the prothrombin time and raised serum ammonia were invariable. Eight children died and the four survivors were critically ill before recovering. Acute viral hepatitis is generally a benign illness in childhood. Although infrequently recorded, fulminant hepatitis may, however, ensue and is associated with a high mortality.
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PMID:Fulminant hepatitis in children: report of 12 cases. 171 18

Severe alcoholic hepatitis is still a therapeutic challenge. It has been recently advocated that a 3-wk infusion with insulin and glucagon reduces its short-term mortality rate. A multicenter, randomized, single-blind, sequential trial was designed to compare this treatment with placebo. The triangular boundary was defined with alpha = 0.05, beta = 0.10 and estimated survival at 4 wk of 50% with placebo, 75% with treatment. Patients with biopsy-proven severe alcoholic hepatitis (presence of one or more of three criteria: encephalopathy, prothrombin activity less than or equal to 50%, bilirubinemia greater than or equal to 100 mumol/L) were randomized into two groups; one treatment group received an infusion (12 hr/day) of an association of insulin (30 IU) and glucagon (3 mg), and a control group received an infusion of glucose. Treatments were administered during a 3-wk period, and the mortality rate was noted at 4 wk. The decision to discontinue the trial was reached on the basis of results from the first 44 patients. Overall results were assessed in the 72 patients included at the time of this decision (treatment group: n = 37; control group: n = 35). Fifty-three patients had cirrhosis. No significant differences were noted between the two groups at inclusion on the basis of clinical, laboratory and histological criteria. The mortality rate was not significantly different in the two groups; 10 patients (27%) in the treatment group and 5 patients (14%) in the control group died. Causes of death were similar in the two groups and consisted primarily of gastrointestinal hemorrhage, hepatic failure and infectious events.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of severe alcoholic hepatitis by infusion of insulin and glucagon: a multicenter sequential trial. 172 3

We have established an improved model of fulminant hepatic failure in dogs. Buthionine sulfoximine is used to inactivate glutathione synthesis, and small increments of acetaminophen are given intravenously to maintain the plasma level at approximately 200 micrograms/ml for 20 hr. This regimen produces severe liver injury along with many of the features seen in humans with acetaminophen poisoning. The first sign of impending liver failure is hypoglycemia. This occurs about 15 hr into the experiment and requires treatment with a continuous infusion of glucose. Between 15 and 20 hr, serum ALT activity begins to rise, indicating the onset of liver necrosis. Over the following 15 to 20 hr ALT activity continues to rise and is accompanied by an increase in bilirubin, a prolongation of the prothrombin time and the development of fetor hepaticus. Thirty to 48 hr after the initial acetaminophen dose, the animals begin to exhibit symptoms of encephalopathy and progress from lethargy to the inability to maintain posture and then coma, seizures and death. Liver biopsy specimens obtained at several stages throughout the study showed progressive necrosis, ultimately resulting in the complete destruction of zones 2 and 3.
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PMID:An improved model of acetaminophen-induced fulminant hepatic failure in dogs. 173 38

Despite consistent improvement in its treatment, amatoxin poisoning still extolls an elevated overall mortality, ranging between 10 and 15%, which approaches 100% when severe (grade 3-4 encephalopathy) hepatic failure supervened. Therefore, the proper treatment of intoxication by amatoxin containing mushrooms, and particularly of its complications, remains a challenge in emergency medicine. Klein and coworkers reviewed the role of liver transplantation in amatoxin poisoning as a useful therapeutic tool for patients with severe impairment of liver function. Their indication for intervention is the presence of any of the following signs: grade 2 encephalopathy or higher; prothrombin time twice than normal, despite fresh frozen plasma infusion; hypoglycemia requiring hypertonic glucose infusion; hyperbilirubinemia (greater than 25 mg/dl). During the past autumn two patients with fulminant hepatic failure due to amatoxin poisoning were referred to our institutions as candidates for liver transplantation, since both satisfied Klein's criteria. However, due to shortage of organ donors it was impossible to transplant them over the following days. Despite they did not receive liver transplantation, both patients wakened from coma, their liver function improved, and they recovered from terminal amatoxin poisoning. After one year, both patients are long-term survivors, in good health and without any sequelae either in brain or liver function.
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PMID:[Recovery after serious mushroom poisoning (grade IV encephalopathy) with intensive care support and without liver transplantation. Clinical case]. 175 80

The value of the aminoterminal procollagen-III-peptide (P-III-P) in predicting death or survival was evaluated in a group of 43 patients with proven postnecrotic or alcoholic cirrhosis. Patients were followed-up prospectively for 2 years. The prognostic value of P-III-P was compared with the Child classification, fasting and postprandial serum bile acids, and standard laboratory tests such as bilirubin, prothrombin index, pseudocholinesterase, albumin, GOT, GPT, gamma-GT, and clinical findings such as ascites, encephalopathy (assessed with the number connection test = NCT), and nutritional status. Between patients who died and those who survived the following 2 years, there were significant differences in the following parameters at the time of inclusion in the study: encephalopathy judged by NCT (p = 0.001), serum albumin (p = 0.0012), postprandial serum bile acids (p = 0.0024), fasting serum bile acids (p = 0.0025), pseudocholinesterase (p = 0.0044), GOT (p = 0.015), bilirubin (p = 0.016), and prothrombin index (p = 0.01). None of the other parameters investigated, including SP-III-P (p = 0.46), revealed any statistically significant differences between patients who died and survivors. The prognostic significance of laboratory tests and recorded clinical findings was evaluated, either alone or in combination with life-table analysis using the Cox model. SP-III-P, alone or in combination with other parameters, failed to improve prediction of mortality in patients with cirrhosis. In comparison to the Child classification (p = 0.0004) the combination of NCT and postprandial serum bile acids showed a similar ability (p = 0.0003) to predict patient survival.
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PMID:Predictive value of serum procollagen-III-peptide for the survival of patients with cirrhosis. 180 22


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