Current guideline developed by the Chinese Society of Hepatology on the management of hepatic encephalopathy in cirrhosis is grounded on the published evidences and panelists' consensus. This guideline presents recommendations for diagnosis and management of covert and overt hepatic encephalopathy, and underline the importance of screening minimal hepatic encephalopathy in patients with end-stage liver diseases. In addition, it also stresses that early identification and timely treatments are the means to know the prognosis. The principles of treatment are primary and secondary prevention, prompt removal of the cause, and recovery of acute neuropsychiatric abnormalities to baseline status.
Consensus ; Disease Management ; Gastroenterology ; Gastrointestinal Agents/therapeutic use* ; Hepatic Encephalopathy/drug therapy* ; Humans ; Liver Cirrhosis ; Practice Guidelines as Topic ; Prognosis

OBJECTIVETo investigate the potential effects on cognitive function, prognosis, and neuropeptide levels of patients in response to combination therapy with ornithine aspartate plus naloxone for hepatic encephalopathy.

METHODSEighty-four consecutive patients diagnosed with hepatic encephalopathy were randomly divided into two equal groups. The control group (n = 42) received traditional medical treatment, and the research group (n = 42) received the traditional medical treatment as well as the combination therapy with ornithine aspartate plus naloxone. The supplemental treatment was comprised of daily intravenous injection of 10-15 g ornithine aspartate in 250 ml of 5% glucose plus intravenous drip of 3 mg naloxone in 100 ml of 5% glucose, and was given in 7-day cycles for one or two cycles. The cognitive function of patients was assessed by Hasegawa Intelligence Scale (HDS) and Mini-Mental State Examination (MMSE) questionnaires. The effective rate and time duration from coma to consciousness were recorded. Changes in blood ammonia level, markers of liver function, and neuropeptide levels were measured by standard biochemical assays. Intergroup differences were assessed by the Chi-squared test.

RESULTSThe HDS and MMSE scores of the research group were significantly higher than those of the control group after therapy. The effective rate, time duration from coma to consciousness, blood ammonia, the liver function markers alanine aminotransferase, gamma-glutamyl-transpeptidase and total bilirubin, and the neuropeptides arginine vasopressin and beta-endorphin were remarkably improved after treatment in the research group, as compared with that in the control group.

CONCLUSIONSupplementing the traditional treatment for hepatic encephalopathy with ornithine aspartate plus naloxone combination therapy provides better therapeutic outcome than traditional treatment alone.

Adult ; Dipeptides ; therapeutic use ; Female ; Hepatic Encephalopathy ; drug therapy ; metabolism ; psychology ; Humans ; Male ; Middle Aged ; Naloxone ; therapeutic use ; Neuropeptides ; metabolism ; Prognosis

An eight-month-old female infant with severe dengue disease, who was repeatedly given therapeutic paracetamol for severe dengue, developed fulminant liver failure with encephalopathy, gastrointestinal haemorrhage and severe coagulopathy. She responded to supportive measures and N-acetylcysteine infusion. This case highlights the potential danger of administering repeated therapeutic doses of paracetamol in childhood severe dengue disease with hepatitis.
Acetaminophen ; adverse effects ; therapeutic use ; Antipyretics ; adverse effects ; therapeutic use ; Blood Coagulation ; Female ; Hepatic Encephalopathy ; drug therapy ; Humans ; Infant ; Liver Failure, Acute ; chemically induced ; Severe Dengue ; drug therapy ; Treatment Outcome

OBJECTIVETo summarize the incidence of various adverse reactions in the clinical application of L-asparaginase (L-Asp), and to analyze the cause of hepatic encephalopathy in three cases.

METHODSThe complete data of 23 patients in our department from December 2009 to December 2010 were collected. Their blood ammonia levels, transaminase, serum albumin and blood coagulation function before, during and after the L-Asp application were assayed.

RESULTS(1) All patients had elevated blood ammonia level after the L- Asp application. This occurred 2 days after the beginning of treatment and the median time to reach peak level (ranged from 194 to 446 μmol/L, with a median value of 300 μmol/L) was 4 days. It returned to normal level after a median time of 5 days (ranged 3-7 days) with drug withdrawal. Of the 23 patients studied, 3 developed hepatic encephalopathy. (2) All patients appeared lower blood fibrinogen, 10 cases (43.5%) with lower fibrinogen only, while 13 cases (56.5%) with both prolonged APTT and lower fibrinogen. The lowest level of fibrinogen was detected at 1 week after drug application. Of the 23 patients, 14 (60.9%) had mild lower blood fibrinogen (1-2 g/L), and 9 (39.1%) had significantly lower fibrinogen (0-1 g/L). (3) Six cases (26.1%) had slightly elevated level of transaminase (<2 times the upper limits of normal), 8 (34.8%) appeared hypoalbuminemia.

CONCLUSIONAs the incidence of elevated blood ammonia levels was high in the application of L-Asp, the level of blood ammonia should be closely monitored to avoid the occurrence of hepatic encephalopathy, especially in elderly patients and patients with previous liver disease or long-term heavy drinking. L-Asp can also lead to low fibrinogen level, hypoalbuminemia and abnormal transaminase. Monitoring the blood coagulation function and liver function is required and, if necessary, plasma infusion and liver protection therapy are required.

Adolescent ; Adult ; Aged ; Ammonia ; blood ; Asparaginase ; adverse effects ; therapeutic use ; Female ; Hepatic Encephalopathy ; chemically induced ; Humans ; Male ; Middle Aged ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; blood ; drug therapy ; Young Adult

No abstract available.
Antiviral Agents/therapeutic use ; Ascites/diagnosis/prevention & control/therapy ; Cholagogues and Choleretics/therapeutic use ; Fatty Liver/diagnosis/diet therapy ; Fatty Liver, Alcoholic/diagnosis/drug therapy ; Hemorrhage/prevention & control/therapy ; Hepatic Encephalopathy/diagnosis/prevention & control/therapy ; Hepatitis B, Chronic/diagnosis/drug therapy ; Hepatitis C, Chronic/diagnosis/drug therapy ; Humans ; Liver Cirrhosis/*diagnosis/drug therapy/pathology/*therapy ; Liver Cirrhosis, Biliary/drug therapy ; Vasodilator Agents/therapeutic use

Encephalopathy is a disorder characterized by altered brain function, which can be attributed to various causes. Encephalopathy associated with metronidazole administration occurs rarely and depends on the cumulative metronidazole dose, and most patients with this condition recover rapidly after discontinuation of therapy. Because metronidazole is metabolized in the liver and can be transported by the cerebrospinal fluid and cross the blood-brain barrier, it may induce encephalopathy even at a low cumulative dose in patients with hepatic dysfunction. We experienced a patient who showed ataxic gait and dysarthric speech after receiving metronidazole for the treatment of hepatic encephalopathy that was not controlled by the administration of lactulose. The patient was diagnosed as metronidazole-induced encephalopathy, and stopping drug administration resulted in a complete recovery from encephalopathy. This case shows that caution should be exercised when administering metronidazole because even a low dose can induce encephalopathy in patients with liver cirrhosis.
Anti-Infective Agents/*adverse effects/therapeutic use ; Brain Diseases/*chemically induced/diagnosis ; Hepatic Encephalopathy/*drug therapy/etiology ; Humans ; Liver Cirrhosis/*complications ; Magnetic Resonance Imaging ; Male ; Metronidazole/*adverse effects/therapeutic use ; Middle Aged ; Tomography, X-Ray Computed

Ascites, hepatic encephalopathy and variceal hemorrhage are three major complications of portal hypertension. The diagnostic evaluation of ascites involves an assessment of its etiology by determining the serum-ascites albumin gradient and the exclusion of spontaneous bacterial peritonitis. Ascites is primarily related to an inability to excrete an adequate amount of sodium into urine, leading to a positive sodium balance. Sodium restriction and diuretic therapy are keys of ascites control. But, with the case of refractory ascites, large volume paracentesis and transjugular portosystemic shunts are required. In hepatorenal syndrome, splanchnic vasodilatation with reduction in effective arterial volume causes intense renal vasoconstriction. Splanchnic and/or peripheral vasoconstrictors with albumin infusion, and renal replacement therapy are only bridging therapy. Liver transplantation is the only definitive modality of improving the long term prognosis.
Anti-Bacterial Agents/therapeutic use ; Ascites/complications/*diagnosis/therapy ; Bacterial Infections/*diagnosis ; Hepatic Encephalopathy/complications ; Hepatorenal Syndrome/complications/*diagnosis/therapy ; Humans ; Hypertension, Portal/*complications ; Liver Transplantation ; Peritonitis/*diagnosis/drug therapy/etiology ; Serum Albumin/administration & dosage

Acute Disease ; Bacterial Infections ; prevention & control ; Brain Edema ; drug therapy ; etiology ; Critical Care ; Hepatic Encephalopathy ; etiology ; therapy ; Humans ; Intracranial Hypertension ; etiology ; therapy ; Liver Failure, Acute ; etiology ; nursing ; therapy ; Liver Transplantation ; nursing ; standards

OBJECTIVETo evaluate the efficacy and safety of adefovir dipivoxil in treatment of decompensated liver cirrhosis patients with YMDD motif mutation during lamivudine therapy.

METHODSThe disease relapsed in 14 hepatitis B patients with decompensated liver cirrhosis during lamivudine treatment due to the YMDD motif mutation. All 14 patients had positive HVBDNA and active hepatitis, and were evaluated as Child-Pugh Score C (CPS-C). The patients were treated with lamivudine 50 mg/d and adefovir dipivoxil 10 mg/d for 6 months.

RESULTSOne patient signed off due to non-hypoxemic hyperlactacidemia; other 13 patients showed decreased serum HBVDNA. All patients had serum HBVDNA < or =10(5) copies/ml and 7 patients had HBVDNA < or =10(4) copies/ml. Six patients regained normal serum ALT level and Child-Pugh scores decreased in all patients.

CONCLUSIONAdefovir dipivoxil has satisfied efficacy and safety in treatment of decompensated liver cirrhosis patients with YMDD motif mutation during lamivudine treatment.

Adenine ; adverse effects ; analogs & derivatives ; therapeutic use ; Adult ; Aged ; Amino Acid Motifs ; genetics ; Antiviral Agents ; therapeutic use ; DNA-Directed DNA Polymerase ; genetics ; Female ; Hepatic Encephalopathy ; drug therapy ; genetics ; virology ; Hepatitis B virus ; genetics ; Hepatitis B, Chronic ; complications ; drug therapy ; Humans ; Lamivudine ; therapeutic use ; Liver Cirrhosis ; drug therapy ; genetics ; virology ; Male ; Middle Aged ; Mutation ; Organophosphonates ; adverse effects ; therapeutic use ; Protein Structure, Tertiary ; genetics ; Recurrence ; Reverse Transcription ; genetics

We treated a 49-yr-old man with neostigmine, who had liver cirrhosis, acute hepatic encephalopathy, and acute intestinal pseudoobstruction. He was admitted in a state of hepatic confusion. On physical examination, the abdomen was distended; and bowel sound was absent. Plain abdomen film revealed multiple airfluid levels and distention of bowel loops. Initially, we gave him lactulose enemas every 6 hr for one day without improvement in his mental state. Furthermore, he became to a state of coma. Therefore, we gave him 0.5 mg of neostigmine subcutaneously to improve his peristaltic movement, and 2 L of polyethylene glycol electrolyte solution through a nasogastric tube for 4 hr to reduce the production and absorption of gutderived toxins of nitrogenous compounds. After these treatments, the venous ammonia level decreased to the normal range within 12 hr, and the coma disappeared after 2 days. We suggest that neostigmine may be one of the most effective treatments to initiate peristaltic movement and bowel cleansing in cirrhotic patients with acute hepatic encephalopathy and acute intestinal pseudoobstruction.
Air ; Ammonia/metabolism ; Blood Pressure ; Cholinesterase Inhibitors/*pharmacology ; Electrolytes/pharmacology ; Enema ; Fibrosis/*drug therapy ; Hepatic Encephalopathy/*diagnosis/*drug therapy/radiography ; Humans ; Intestinal Pseudo-Obstruction/*diagnosis/*drug therapy/radiography ; Lactulose/pharmacology ; Liver/metabolism ; Male ; Middle Aged ; Neostigmine/*pharmacology ; Peristalsis ; Polyethylene Glycols/pharmacology ; Time Factors