Cases reported "Hepatic Encephalopathy"

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1/41. hepatic encephalopathy--a physostigmine-reactive central anticholinergic syndrome?

    This report describes an association between hepatic encephalopathy and central anticholinergic syndrome (CAS). A 60-year-old anaemic woman was admitted unconscious and with a delayed reaction to pain but with no focal neurological deficits. She had signs of portal hypertension and a history of non-alcoholic liver cirrhosis grade child B. Suspecting upper gastro-intestinal bleeding, she was intubated for gastro-duodenoscopy and a fibrin-covered ulcer was revealed. Raised intra-abdominal pressure resulting from ascites caused cardiopulmonary failure, which required mechanical ventilation for 24 h, but extubation was possible after drainage of the ascites and blood volume replacement therapy. However, her neurological state remained unchanged despite normal blood ammonia concentration and no sedation. CAS was considered and physostigmine injected with immediate effect. The patient opened her eyes immediately and was fully orientated to personal and medical history. We suggest that hepatic encephalopathy may trigger CAS, although the significance of physostigmine in the treatment of hepatic encephalopathy remains to be addressed by controlled investigations.
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2/41. Case report: intrahepatic portal-hepatic venous shunts associated with a huge pelvic leiomyoma.

    We present a case of portal-systemic encephalopathy due to intrahepatic multiple portal-hepatic venous shunts. A 71-year-old woman was admitted to our hospital because of recurrent episodes of disturbed consciousness. She showed no clinical signs of portal hypertension. Liver function was normal, except for an indocyanine green retention rate of 34% at 15 min and blood ammonia level of 282 microg/dL. Portal venography revealed dilatation of the portal vein and multiple portal-hepatic venous shunts, and a liver biopsy specimen revealed almost normal liver. Further clinical examination revealed a huge pelvic tumour. At laparotomy, two dilated veins were seen to arise from the pelvic tumour with blood flow into the mesentery. The tumour was resected successfully and a histological diagnosis of leiomyoma was made. The blood ammonia concentration decreased to the normal range postoperatively. A follow-up portal venogram demonstrated decreased portal vein dilatation and minor portal-hepatic venous shunts, considered to be congenital in origin. It is concluded that hepatic encephalopathy was produced in this patient due to an excess portal blood flow from the huge pelvic leiomyoma via the mesentery, with portosystemic shunting through pre-existent (probably congenital) intrahepatic anastomoses.
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3/41. Long-term extracorporeal bilirubin elimination: A case report on cascade resin plasmaperfusion.

    Acute hepatic failure develops as a disease entity of rather diverse origin. With disease progression, toxic bilirubin levels may cause severe complications which include AV-nodal blockage, cardiac arrhythmia, impaired consciousness, generalized seizures, and status epilepticus. Treatment choices to prevent clinical deterioration comprise of costly and limited available orthotopic liver transplantation, utilization of extracorporeal bioartificial liver support devices and haemoperfusion/plasmaperfusion treatment with activated charcoal/anion exchange filters. Here, we present a patient with acute drug-induced cholestatic hepatitis. Excessively elevated bilirubin levels were accompanied by cardiac and cerebral complications. Extracorporeal resin perfusion treatment (Plasorba, BR-350) was successfully performed over a 50-day period without activation of the coagulation system or side effects. bilirubin levels were lowered to a minimum of 225 micromol/l, with concurrent clinical improvement. In conclusion, extracorporeal anion exchange plasmaperfusion may be a viable long-term treatment for hyperbilirubinaemic side effects in overt cholestatic hepatitis.
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4/41. Portal-systemic encephalopathy due to a congenital extrahepatic portosystemic shunt: three cases and literature review.

    Extrahepatic portal-systemic encephalopathy due to congenital extrahepatic portosystemic shunt has so far been rarely reported in the literature. We herein report 3 such cases without liver cirrhosis or portal hypertension which were presented with the chief complaint being disturbance of consciousness and abnormal behavior. In all cases the brain computed tomography scan revealed no pathological findings, while electroencephalogram showed a diffuse slow activity with triphasic waves. The laboratory data revealed a high serum ammonia level. Percutaneous transhepatic portography demonstrated portosystemic shunts. After these shunts were surgically occluded, the serum ammonia level reached a normal range and encephalopathy disappeared. A liver biopsy also revealed neither fibrosis nor cirrhosis in any of the cases. The 23 previously reported cases are also discussed.
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5/41. Type II (adult onset) citrullinaemia: clinical pictures and the therapeutic effect of liver transplantation.

    OBJECTIVE: adult onset type II citrullinemia is an inherited disorder of amino acid metabolism caused by a deficiency of liver specific argininosuccinate synthetase activity. Most of the patients with this disease were reported in japan and therefore, this disease has not been well recognised outside this country. The detailed clinical pictures of the patients with type II citrullinaemia are reported and their outcomes after liver transplantation referred to. methods: Ten patients with this disease were evaluated. Seven of them underwent liver transplants using a graft obtained from a healthy family member. RESULTS: There were six men and four women; the age of onset of encephalopathy ranged from 17 to 51 years. The initial symptom in nine patients was sudden onset disturbance of consciousness, and one patient had long been regarded as having a chronic progressive psychotic illness. High concentrations of plasma citrulline and ammonia were commonly seen on admission. Although brain CT or MRI lacked any consistent findings, the EEG was abnormal in all patients, showing diffuse slow waves. Additionally, in five patients chronic pancreatitis preceded the onset of encephalopathy. After liver transplantation the metabolic abnormalities, including abnormal plasma concentrations of citrulline and ammonia, were immediately corrected and all neuropsychic symptoms soon disappeared, except for impaired cognitive function in one patient. Six out of these seven patients returned to their previous social lives, including work. CONCLUSIONS: The clinical concept of adult onset type II citrullinaemia coincides well with the range of hepatic encephalopathy, and liver transplantation is a very promising therapeutic approach.
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6/41. Complete recovery from fulminant hepatic failure with severe coma by living donor liver transplantation.

    In japan, living donor liver transplantation has been established as a therapeutic strategy for the rescue of terminal liver disease, including fulminant hepatic failure that shows no signs of recovery. We performed living donor liver transplantation for a subacute type fulminant hepatic failure patient, who had developed a hepatic coma of grade V (no right reflex, no response to pain stimuli). The electroencephalogram indicated almost flat waves. However, cranial computed tomography revealed that brain edema was not severe in this case. The recipient did not have hepatitis virus and had not taken medication that had been determined to cause hepatitis. The recipient was a 12-year-old boy, 165.5 cm in height and 45.5 kg in weight. The donor was his mother, who was 42 years old; her blood type, type B, was identical to that of the boy. The mother's right hepatic lobe was transplanted to her son (the recipient). The post-transplantation condition of recipient was quite excellent. He recovered consciousness 3 days after liver transplantation, and rapidly attained normal hepatic function. The donor was discharged on the 20th postoperative day without any problems. The recipient was discharged on the 79th postoperative day without any neurological deficits. This case suggests that deep coma without electroencephalogram waves may not be a contraindication for living donor liver transplantation in fulminant hepatic failure patients, if the brain edema is not severe.
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7/41. Spontaneous closure of intrahepatic portovenous shunt in a noncirrhotic patient with recurrent encephalopathy.

    A 70-year-old man was admitted to our hospital with recurrent encephalopathy. liver function tests, abdominal computerized tomography, ultrasonography, angiography, and laparoscopy revealed an intrahepatic portovenous shunt in a noncirrhotic liver. During follow-up, the intrahepatic portovenous shunt closed spontaneously. Subsequent liver function tests were markedly improved, with resolution of the patient's previously disturbed consciousness. In the elderly, intrahepatic portovenous shunt that can be managed with conservative therapy may spontaneously close, suggesting that management options should include watchful waiting.
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8/41. neostigmine and polyethylene glycol electrolyte solution for the therapy of acute hepatic encephalopathy with liver cirrhosis and ascites.

    We treated a 75-year-old man who had non-B and non-C, and child's class C liver cirrhosis and acute hepatic encephalopathy with neostigmine and polyethylene glycol electrolyte solution. He received repeated transcatheter artrial embolization and percutaneous ethanol injection combination therapy for multiple hepatocellular carcinomas, which controlled his disease for 25 months from the first treatment. He was admitted in a state of hepatic coma after being found unresponsive at his home. With the consent of the patient's family, we gave him 1.0 mg of neostigmine intramuscularly to improve his peristaltic movement, and 2 L of polyethylene glycol electrolyte solution through a nasogastric tube for 4 hours to reduce the production and absorption of gut-derived toxins of nitrogenous compounds. Using these treatments, the blood ammonia level decreased to the normal range within 8 hours, and the coma disappeared after 2 days. We suggest that a combination approach of neostigmime and polyethylene glycol electrolyte solution may be one of the most effective treatments for acute hepatic encephalopathy associated with liver cirrhosis and ascites.
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9/41. Obliteration of portal systemic shunts as therapy for hepatic encephalopathy in patients with non-cirrhotic portal hypertension.

    The effects of obliteration of portal systemic shunts (PSS) in 5 patients with non-cirrhotic hepatic encephalopathy is reported. All patients had a history of disturbance of consciousness for several years, and examinations revealed large PSS, most of which connecting the left gastric vein to the left renal vein. After the obliteration of PSS, portal vein pressure elevated, the shunt ratio of the portal blood flow decreased, the indocyanine green disappearance rate increased, and serum albumin increased. Blood ammonia (NH3) decreased significantly accompanied by disappearance of hepatic encephalopathy. This treatment may open a way to improve the quality of life in patients with large PSS without severe hepatic injury.
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10/41. Hemodialysis-related portal-systemic encephalopathy.

    The authors encountered a case of portal-systemic venous shunt newly diagnosed after initiation of hemodialysis. A 68-year-old Japanese woman began hemodialysis because of symptoms of uremia including loss of appetite and pulmonary edema. Loss of consciousness occurred suddenly after her ninth session of hemodialysis. No hepatic functional abnormality was found other than hyperammonemia (314 microg/dL [184 micromol/L]). Loss of consciousness subsequently occurred often after hemodialysis. color Doppler ultrasonography and magnetic resonance angiography depicted a large shunt between the left gastric vein and left renal vein resulting in portal flow entering the systemic circulation via the renal vein. Because the shunt was large, ligation of it was performed surgically. Results of histologic examination of a liver biopsy specimen obtained intraoperatively were normal. The patient became well postoperatively. This patient's encephalopathy appeared to be caused by the flow of ammonia-rich portal venous blood into the systemic circulation via the large shunt owing to a decrease in intravenous pressure after rapid hemodialysis. Portal-systemic shunt encephalopathy should be recognized as a "new" neuropsychiatric disorder characteristic of patients undergoing hemodialysis.
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