1/251. A case of primary lymphoma of the liver.A case of primary malignant lymphoma of the liver is described. Presenting with epistaxis, he died in hepatic encephalopathy with an intractable bleeding post-bulbar duodenal ulcer.- - - - - - - - - - ranking = 1keywords = encephalopathy (Clic here for more details about this article) |
2/251. Possible response of acute psychosis in hepatic encephalopathy to levodopa.A favorable response to levodopa in two episodes of hepatic encephalopathy, the latter presenting as acute psychosis, is described in a patient with Budd-Chiari syndrome.- - - - - - - - - - ranking = 5keywords = encephalopathy (Clic here for more details about this article) |
3/251. 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.- - - - - - - - - - ranking = 7keywords = encephalopathy (Clic here for more details about this article) |
4/251. Fulminant hepatic failure secondary to congestive heart failure.An elderly female with an acute episode of congestive heart failure, unaccompanied by any periods of hypotension, developed fulminant hepatic failure with an accompanying coagulopathy. Attempts to establish an etiology for her acute hepatic insufficiency, other than cardiac failure, proved negative. Fulminant hepatic failure as a consequence of congestive heart failure, without prolonged periods of hypotension preceding alteration in hepatic function, has not heretofore been described. Liver function is adversely effected in congestive heart failure. Hepatic ammonia clearance is impaired in cardiac failure and may be diminished to the point of resulting in hepatic encephalopathy. Coagulopathy is a frequent concomitant of fulminant hepatic failure. Establishing a clear etiology for a coagulopathy in the face of concomitant liver disease is difficult, thus making any therapeutic intervention fraught with peril.- - - - - - - - - - ranking = 1keywords = encephalopathy (Clic here for more details about this article) |
5/251. Sibling cases of chronic recurrent hepatocerebral disease with hypercitrullinemia.Two sibling cases with chronic recurrent hepato-cerebral syndrome which correspond to the nutritional form of hepato-cerebral disease entitled by Shikata et al. and the data of plasma free aminoacids analyses of these cases were reported. The one case is 27 years old male and the other case is 36 years old female. Their parents were cousins. Both cases have had unbalanced diet, especially liked legumes unusually. Their main symptom was recurrent disturbance of conciousness and convulsive seizures. Slight abnormality of liver function test and hyperammonemia were demonstrated. Electroencephalogram showed the pattern of triphasic wave. Coeliac angiography did not revealed a portal-systemic shunt. Hepatic biopsy specimen revealed liver fibrosis with fatty change in the one case and mild fatty change in the other case. Analyses of plasma free aminoacids showed particurally high level of citrulline in both cases. From the results of plasma free aminoacids analyses, it is considered that pathogenesis of these patients is congenital hereditary urea cycle disorders.- - - - - - - - - - ranking = 9.298144662256E-5keywords = cerebral (Clic here for more details about this article) |
6/251. The basal ganglia and portal-systemic encephalopathy.Despite decades of research, the pathogenesis of portal-systemic encephalopathy (PSE) remains puzzling. Current hypotheses on the pathophysiology of PSE usually deal with metabolic toxins like ammonia or disturbances in neurotransmitter systems, especially glutamatergic or GABA-ergic neurotransmission. With respect to clinical, neuropathological, MRI and PET findings this review advances the hypothesis that the known alterations of neurotransmission and astrocytic function in PSE might impair basal ganglia function in cirrhotics. The symptoms of PSE - whether cognitive, emotional or motor - are proposed to be a consequence of basal ganglia dysfunction.- - - - - - - - - - ranking = 5keywords = encephalopathy (Clic here for more details about this article) |
7/251. 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.- - - - - - - - - - ranking = 2keywords = encephalopathy (Clic here for more details about this article) |
8/251. 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.- - - - - - - - - - ranking = 1.5496907770427E-5keywords = cerebral (Clic here for more details about this article) |
9/251. Reversibility of hyperintense globus pallidus on T 1-weighted MRI follow- ing surgery for a portosystemic shunt in an 8-year-old girl.An 8-year-old Japanese girl with a portosystemic shunt had shown hyperammonaemia since she was 3 years of age. MRI of her brain showed bilateral hyperintense globus pallidus. A portosystemic shunt was evident on US and angiography. She underwent surgical banding of the shunt, after which the lesion and clinical symptoms disappeared.- - - - - - - - - - ranking = 3.7651867418557E-5keywords = brain (Clic here for more details about this article) |
10/251. Control of solitary gastric fundal varices and portosystemic encephalopathy accompanying liver cirrhosis by balloon-occluded retrograde transvenous obliteration (B-RTO): a case report.In a patient with liver cirrhosis complicated by solitary gastric fundal varices and portosystemic encephalopathy, Balloon-occluded retrograde transvenous obliteration (B-RTO) of the varices was performed. The gastric varices were decreased in size 2 weeks after treatment and had not recurred after 1 year. B-RTO successfully occluded the portosystemic shunt (gastrorenal shunt). Accordingly, the patient's blood ammonia levels, total bile acid level, and 15 min retention rate of indocyanine green decreased, and his hepatic encephalopathy improved. However, since consecutive increase in blood flow through the portal collateral vessels except for gastrorenal shunt vessel at 6 months and 1 year after B-RTO was noted, further careful follow-up may be required.- - - - - - - - - - ranking = 6keywords = encephalopathy (Clic here for more details about this article) |
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