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

Ascites is a complication of chronic liver disease that is associated with decreased survival. The purpose of the present study was to identify some prognostic factors easily obtainable by the clinician in a large group of cirrhotic patients with ascites, possibly useful for first screening of outpatients as candidates for liver transplantation. We studied 134 ambulatory patients with cirrhosis who came to our outpatient clinic between July 1983 and March 1989 because of an episode of ascites. These patients were then followed up for an average period of 31 +/- 23 months and survival was determined. Thirty-one variables determined at the time of inclusion were analyzed with a Cox proportional hazards model to identify predictors of mortality. Cumulative mortality as of June 30, 1991, was 59%. Factors independently correlated with death were: refractory ascites (relative risk, 4.78), low albumin levels (3.77), high Child-Pugh score (3.31), encephalopathy (2.71), high bilirubin levels (2.03), high gamma-glutamyl-transferase levels (1.87), and old age (1.57). The results show that 1) the occurrence of refractory ascites has a prognostic value superior to those of other variables, and 2) simple clinical and biochemical parameters, most of them components of the Child-Pugh score, are useful for a first screening of ascitic cirrhotic patients as candidates for liver transplantation.
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PMID:Survival and prognostic factors of cirrhotic patients with ascites: a study of 134 outpatients. 847 Jun 31

Hepatic encephalopathy is a neuropsychiatric syndrome occurring in patients with acute or chronic liver disease. Its pathogenesis remains unclear; however, it appears to be multifactorial. There are several conventional treatments for this condition, such as lactulose, neomycin, and protein restriction. There is significant controversy regarding the role of branched chain amino acids in the treatment of chronic hepatic encephalopathy. We describe a patient who had hepatic encephalopathy secondary to Budd-Chairi syndrome and a mesoatrial shunt that failed vigorous conventional therapy. She required multiple hospitalizations for severe recurrent encephalopathy. The patient was considered for a colonic exclusion procedure for the management of intractable encephalopathy. However, branched amino acid therapy was instituted as a last measure before the contemplated surgery, and the patient's encephalopathy responded in dramatic fashion, and she remained free from encephalopathy during a prolonged follow-up.
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PMID:Severe recurrent hepatic encephalopathy that responded to oral branched chain amino acids. 865 Nov 89

The syndrome of minimal hepatic encephalopathy is used to describe discrete psychomental and neuro-psychological abnormalities in patients with chronic liver disease (cirrhosis) or portosystemic shunt, in whom classical clinical investigations reveal no evidence of mental or cerebro-neurological disorders, and who cannot be assigned to any of the usual stages of hepatic encephalopathy. Disorders of cerebral function, such as lack of concentration, impaired ability to think logically, loss of comprehension, impairment of space perception and the recognition of numbers and letters can be very reliably detected by simple psychometric tests (number-connection test, line-tracing test, handwriting), and are present in as many as 70% of cirrhotics. This may be expressed in everyday life by an impairment of driving ability, and at work by impaired ability to operate a machine. The use of established means of lowering blood ammonia levels (lactulose, ornithine-aspartate) results in a rapid improvement in the symptoms of encephalopathy.
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PMID:[Hepatic minimal encephalopathy. The most frequently overlooked, clinically occult "metabolic syndrome" on the cirrhosis patient]. 868 29

In the setting of chronic liver disease, portal hypertension and its complications pose major challenges in management. Once it develops, portal hypertension is the source of potentially devastating sequelae, including life-threatening hemorrhage, infection, renal failure, and encephalopathy. Improved understanding of the pathophysiology of these conditions has led to advances in endoscopic, radiologic, medical, and surgical management. The possibility in selected cases of successful amelioration of portal hypertension and its dreaded complications by liver transplantation highlights the importance of timely and careful management of patients with decompensated cirrhosis.
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PMID:Management of portal hypertension and its complications. 880 73

Spontaneous bacterial peritonitis (SBP) is a frequent complication of cirrhosis with ascites. As clinical symptoms are often mild or lacking, the condition may not be perceived in otherwise severely ill patients. This study focuses on diagnostic and prognostic aspects in 25 patients with 26 episodes of SBP. A microbiological diagnosis was established in 18 patients by positive culture of ascitic fluid or positive gram stain. In 8 episodes the diagnosis was presumed on the basis of an elevated polymorphonuclear leukocyte (PMN) count in the ascitic fluid (> 250 PMN/microliters). The mean (+/- SD) age of the 11 women and 14 men was 55 +/- 14 years; 16 were attributed to Child grade C, 9 to Child grade B liver dysfunction. In 19 cases, cirrhosis was confirmed histologically. The underlying liver disease was Laennec's cirrhosis in 13 cases, hepatitis-B virus associated chronic liver disease in 7 cases and primary biliary cirrhosis in 2 cases. At the time of diagnosis, 6 of 25 patients had no fever, 13 of 25 patients had no abdominal pain, 10 of 24 patients showed no abdominal tenderness upon palpation and 5 of 26 patients had no fever or abdominal pain. 17 of 26 patients showed signs of portosystemic encephalopathy. The total white blood cell count in the ascitic fluid was 3627 +/- 3978/microliters with 71 +/- 29% polymorphonuclear cells in the group with microbiologically proven peritonitis and 5105 +/- 2860 cells/microliters (80 +/- 13%) in the group with negative ascitic fluid culture, respectively. Gram stains were positive in 8 cases and culture in 16 of 25 patients. E. coli was cultured in 8 episodes and Str. pneumoniae in two. In-hospital mortality was 61% in the group with microbiologically proven peritonitis and 14% in the group with negative ascitic fluid culture (p = 0.062); 6-month mortality rate was 78% and 86% respectively (p = 0.91). Prognosis was worse in patients Child grade C (p = 0.027), in patients lacking symptoms or signs of peritoneal irritation (p = 0.017), in patients with septic shock (p = 0.018) and in patients with elevated serum-creatinin levels at the time of diagnosis (p = 0.05). SBP is a treatable complication with high mortality of advanced liver disease. Clinical manifestations may be non-specific or absent. We recommend that diagnostic paracentesis be performed in all patients with cirrhosis and ascites if their clinical condition is rapidly worsening.
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PMID:[Spontaneous bacterial peritonitis: diagnostic and prognostic aspects]. 884 98

Evidence suggests that liver disease per se may contribute to the cognitive and motor impairments encountered in chronic alcoholics. Neuropathologic studies reveal astrocytic changes (Alzheimer type II astrocytosis) in the brains of alcoholic cirrhotic patients who died in hepatic coma. Pathophysiologic mechanisms responsible for hepatic (portal-systemic) encephalopathy in alcoholics include the loss of neuron-astrocytic metabolic trafficking as well as selective alterations of serotoninergic and dopaminergic function. In addition, there is evidence to suggest that endogenous ligands for both central-type (GABA-related) and "peripheral-type" (astrocytic) benzodiazepine receptors are implicated in the pathogenesis of hepatic encephalopathy in these patients. Chronic liver disease may also interfere with brain thiamine homeostasis and thus contribute to the pathogenesis of the Wernicke-Korsakoff syndrome in chronic alcoholism.
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PMID:Cerebral dysfunction in chronic alcoholism: role of alcoholic liver disease. 897 45

In children, fulminant hepatic failure is a rare multisystem disorder in which severe impairment of liver function, with or without encephalopathy, occurs in association with hepatocellular necrosis in a patient with no recognized underlying chronic liver disease. Recognized etiologies include infections, toxins, metabolic disorders, infiltrative diseases, autoimmune hepatitis, ischemic or irradiation damage; a proportion of cases are cryptogenic. The diagnosis of the cause is essential to institute lifesaving medical treatment, decide if transplantation is indicated, and offer genetic counseling. The maximum International Normalized Ratio *(INR) reached during the course of the illness is the most sensitive predictor of outcome, mortality being 86% with an INR > or = 4, and 27% with an INR < 4 in our own series. Prognosis is worse in children younger than 2 years. Thus, urgent transplantation should be considered when the INR reaches 4, particularly in very young children. Survival after transplantation is 60% to 68%. Children with fulminant hepatic failure must be treated in specialized centers with facilities for liver transplantation.
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PMID:Fulminant hepatic failure: pediatric aspects. 902 48

L-carnitine administration prevents the neurological symptoms of acute ammonia toxicity. To further evaluate its efficacy in the prevention of hepatic encephalopathy in hyperammonemic conditions, L-carnitine (16 mmol/kg, intraperitoneally [i.p.] was administered 1 hour before ammonium acetate (NH4OAc) (8.5 mmol/kg, subcutaneously) to portacaval shunted (PCS) rats. Cerebrospinal fluid (CSF) ammonia, lactate, and amino acid levels were measured in relation to deteriorating neurological status in these animals. None of 35 L-carnitine-treated animals showed neurological deterioration after NH4OAC administration compared with saline-treated controls; the latter manifested severe encephalopathy progressing through loss of righting reflex to coma. Survival rate was 100% in the L-carnitine-treated group compared with 5% in saline-treated controls. Following NH4OAC administration to PCS rats, CSF ammonia increased to 0.93 +/- 0.15 mmol/L and 1.24 +/- 0.15 mmol/L at precoma and coma stages of encephalopathy (P < .01) respectively. Treatment with L-carnitine reduced CSF ammonia at both precoma and coma stages; the time-course of this protective effect paralleled blood and CSF L-carnitine accumulation. CSF alanine and lactate increases following NH4OAC administration to PCS rats were significantly attenuated following L-carnitine treatment. However, L-carnitine treatment did not lead to significant reductions in plasma ammonia nor CSF or brain glutamine in these animals. These findings show the therapeutic efficacy of L-carnitine in ammonia-precipitated coma in PCS rats and suggest that this protective effect is centrally mediated involving improved mitochondrial respiration. L-carnitine could be of therapeutic benefit in the prevention of hepatic encephalopathy precipitated by ammoniagenic conditions in humans with chronic liver disease.
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PMID:Protective effect of L-carnitine in ammonia-precipitated encephalopathy in the portacaval shunted rat. 904 97

We studied the outcome of 436 patients with primary biliary cirrhosis (PBC) or primary sclerosing cholangitis (PSC) who underwent orthotopic liver transplant (OLT) at three major liver transplant centers. Univariate predictors of outcome included age, Karnofsky score, Child's class, Mayo risk score, United Network for Organ Sharing (UNOS) status, nutritional status, serum albumin, serum bilirubin, international normalized ratio, and the presence of ascites, encephalopathy, renal failure (serum creatinine > 2 mg/dL), and edema refractory to diuretics. Using these predictors, we developed a four variable mathematical prognostic model to help the liver transplant physician predict the following: 1) the amount of intraoperative blood loss; 2) the number of days in the intensive care unit (ICU); and 3) severe complications after surgery. The model uses age, renal failure, Child's class, and United Network for Organ Sharing status. This study is the first to model the outcome of liver transplant in patients with a specific etiology of chronic liver disease (PBC or PSC). The model may be used to help select patients for OLT and to plan the timing of their transplantation.
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PMID:A prognostic model for the outcome of liver transplantation in patients with cholestatic liver disease. 904 17

Numerous studies suggest that modifications in concentrations of both excitatory and inhibitory amino acids are implicated in the pathophysiology of portal-systemic encephalopathy (PSE), a neuropsychiatric disorder associated with chronic liver disease in humans. In this study, amino acid levels were measured by High Performance Liquid Chromatography (HPLC) in Cerebrospinal Fluid (CSF) of 10 dogs (age range: 3 mo.- 3 yr 4 mo.) exhibiting a congenital portal-systemic shunt, either intra or extra-hepatic, and 8 age-matched control dogs who showed no signs of hepatic or neurologic disorders. Dogs with congenital shunts manifested signs of encephalopathy such as disorientation, head pressing, vocalization, depression, seizures and coma. CSF from dogs with congenital shunts contained significantly increased amounts of glutamate (2 to 3-fold increase, p<0.01), glutamine (6-fold increase, p<0.05) and aromatic amino acids (phenylalanine, tyrosine and tryptophan) compared to CSF of control dogs. Concentrations of GABA and branched chain amino acids (valine, leucine, isoleucine) were within normal limits. Modifications of brain glutamate (an excitatory amino acid) as well as tryptophan (the precursor of serotonin) could contribute to the neurological syndrome characteristic of congenital PSE in dogs.
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PMID:Selective alterations of cerebrospinal fluid amino acids in dogs with congenital portosystemic shunts. 947 3


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