1/73. Hypercalcaemia secondary to hepatocellular carcinoma.Many syndromes reflecting impaired metabolism have been described in association with primary neoplastic diseases. Hypercalcaemia secondary to malignancy without bone metastases and with normal parathyroid glands has been described as "pseudohyperparathyroidism". Differentiation from primary hyperparathyroidism is difficult and care should be taken to exclude an occult malignancy prior to surgical exploration for a parathyroid adenoma. Hypercalcaemia associated with hepatocellular carcinoma is not uncommon. Nevertheless, we describe a rare case of coma with persistent hypercalcaemia in a cirrhotic patient not previously known to have hepatocellular carcinoma.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
2/73. Fatal hepatitis and renal failure during treatment with nimesulide.A healthy 70-year-old woman who took nimesulide for 5 days, presented 2 weeks later with jaundice for which no other cause was found. Laboratory evidence of coagulopathy, hypoalbuminaemia and hypoglycaemia were present on admission, and liver biopsy showed massive necrosis of hepatocytes and severe inflammatory infiltrate. Despite supportive and corticosteroid treatment, her jaundice deepened and progressive acute renal failure developed, characterized by a 'prerenal' profile changing into irreversible acute tubular necrosis pattern, coma, occult Gram-negative sepsis and death. Although rare, nimesulide-associated hepatotoxicity and nephrotoxicity may occur and should be recognized as early as possible, to ensure immediate drug withdrawal and treatment.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
3/73. Primary hypothyroidism masquerading as hepatic encephalopathy: case report and review of the literature.A 74 year old woman with hepatitis c of long duration was admitted to hospital in hyperammonaemic coma. Despite aggressive treatment of hepatic encephalopathy, there was no clinical improvement. As part of her evaluation for other causes of altered mental status, she was found to be profoundly hypothyroid. Treatment with thyroid replacement hormone was accompanied by prompt normalisation of her mental status and hyperammonaemia. hypothyroidism may exacerbate hyperammonaemia and portosystemic encephalopathy in patients with otherwise well compensated liver disease. Hyopthyroidism should be considered in the differential diagnosis of encephalopathy in patients with liver disease.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
4/73. Chronic renal failure and portal hypertension--is portosystemic shunt indicated?We report two girls with histories of recessive polycystic kidney disease. Both were on maintenance hemodialysis. They had undergone surgical distal portocaval shunt because of portal hypertension. Later, bilateral nephrectomy was performed, and they presented with hepatic encephalopathy (HE) and evolution towards irreversible hepatic coma and death. Portosystemic shunt is the treatment of choice of portal hypertension. The kidney plays a pivotal role in ammonia disposal during portosystemic shunt. Thus, we stress the risk of HE after portosystemic shunt followed by bilateral nephrectomy in patients with end-stage renal failure and suggest that combined liver-kidney transplantation should be considered.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
5/73. Case studies in orthotopic liver transplantation for hepatitis B: a panel discussion.Five cases that were referred to the Division of Transplantation at NYU School of medicine for consideration for liver transplantation were discussed among a panel of hepatitis B and liver transplant experts. Opinions were obtained on the management at every stage of treatment of patients with the following initial information: Case one: young Asian woman in stage IV hepatic coma; intubated; prothrombin time (PT): 30 s; serum glutamic oxaloacetic transaminase (SGOT): 8,000 IU; total bilirubin: 25 mg/dL; hepatitis B surface antigen (HBsAg) positive. Case two: 70-yr-old woman, native of greece; decompensated cirrhosis with encephalopathy; child-Pugh Class C; HBsAg positive; hepatitis B surface antibody (HBsAb) negative; hepatitis B e antigen (HBeAg) positive; hepatitis B e antibody (HBeAb) negative; hepatitis b virus (HBV) dna titer: 10,000. Case three: Muscular detective working full-time; cirrhosis; child Pugh Class B; ascites controlled with spironolactone and furosemide; PT: 19s; HBsAg positive; HBsAb negative; HBV dna titer: 50,000; low platelet count. Case four: 45-yr-old baker; cirrhosis and resectable 4-cm hepatoma; child-Pugh Class B; PT: 16 s; Blood type O; United Network for Organ Sharing (UNOS) 2B; HBV dna titer: 3,000. Case five: 40-yr-old Indian man; 300 pounds with massive ascites; child Pugh Class C; PT: 17 s; HBsAg positive; HBV dna titer: 22,000; transplanted with intra-operative hypotension; tacrolimus; graft functioning; HBIg 10,000 IU intra-operative and around the clock during the first post-operative week; required huge doses of hepatitis B immune globulin (HBIg) to maintain adequate HBsAb level; daily loss of 5 6 L of ascites fluid; post-operative day 8: anuric, blood urea nitrogen (BUN) 127, creatinine 3, mental status changes.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
6/73. Acute hepatic encephalopathy with diffuse cortical lesions.Acute hepatic encephalopathy is a poorly defined syndrome of heterogeneous aetiology. We report a 49-year-old woman with alcoholic cirrhosis and hereditary haemorrhagic telangiectasia who developed acute hepatic coma induced by severe gastrointestinal bleeding. Laboratory analysis revealed excessively elevated blood ammonia. MRI showed lesions compatible with chronic hepatic encephalopathy and widespread cortical signal change sparing the perirolandic and occipital cortex. The cortical lesions resembled those of hypoxic brain damage and were interpreted as acute toxic cortical laminar necrosis.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
7/73. Typhoid, hepatitis e, or typhoid and hepatitis e: the cause of fulminant hepatic failure--a diagnostic dilemma.OBJECTIVE: To report a case of hepatitis e-induced fulminant hepatic failure associated with typhoid fever, diagnosed with the Widal test. DESIGN: Case report. SETTING: Eight-bed medical/surgical intensive care unit of a university hospital. PATIENT: A 15-yr-old, 50-kg male with grade IV hepatic encephalopathy was admitted to the intensive care unit for ventilatory support. On admission to the intensive care unit he had had fever associated with loss of appetite and nausea for 15 days, jaundice for 4 days, and altered sensorium for 2 days. INTERVENTION: He was intubated and kept on elective ventilation. Tracheal aspirate, blood, urine, and stool were sterile. Anti-coma measures were instituted in the form of 20 degrees head elevation; mannitol, lactulose, and ampicillin through a nasogastric tube; and bowel wash. The mainstay of fluid therapy was 20% dextrose. Viral marker was positive for hepatitis e. He showed a favorable recovery but continued to have high-grade fever (39-40 degrees C). On investigation, peripheral blood smear was negative for malarial parasite, and Widal was positive. Fever responded to treatment with ceftazidime. RESULT: The patient recovered with anti-coma and anti-typhoid therapy. CONCLUSION: In viral hepatitis, fever is usually present in the prodromal phase but subsides before appearance of the icteric phase. In endemic areas, if fever is present in the icteric phase of hepatitis, typhoid also should be considered in the differential diagnosis of fever, even in the absence of positive cultures for salmonella typhi. The Widal test may be helpful in reaching a diagnosis.- - - - - - - - - - ranking = 2keywords = coma (Clic here for more details about this article) |
8/73. Intensive therapy for hepatic coma.Of 45 patients observed in the ICU with severe acute hepatic insufficiency, 15 patients were in hepatic coma. All patients received combined treatment consisting of standard conservative methods (drug therapy) and surgical methods for temporary support of liver function (hemodialysis, exchange blood transfusion, pig liver perfusion). Intensive therapy which began during the early phase of hepatic coma enabled us to bring six patients out of the coma, four of whom completely recovered. These studies showed that of the diseases causing hepatic coma, the worst results were obtained with viral hepatitis. This may be explained both by the extensive liver damage and marked metabolic disturbances, which led to failure of other vital organs and systems. At present, the combined therapy contributes to a greater percentage of recovery of patients with hepatic failure and coma.- - - - - - - - - - ranking = 9keywords = coma (Clic here for more details about this article) |
9/73. A case of acute hepatic insufficiency treated with novel plasmapheresis plasma diafiltration for bridge use until liver transplantation.A patient with acute hepatic insufficiency induced by a drug presented to our institution, and we performed a novel plasmapheresis that we call plasma dia-filtration (PDF). The patient was a 36 year old woman. She underwent 11 sessions of PDF for a duration of about 9 h for each procedure using the Evacure EC-2A filter together with 20 units of fresh frozen plasma and dialysate simultaneously. serum levels of total bilirubin and prothrombin time were significantly improved after she underwent each procedure. However, after the third procedure the levels returned to the same level as on the previous day. Encephalopathy improved after the first procedure, and this improvement was maintained until the ninth procedure. The patient prepared to undergo liver transplantation after the tenth procedure because of the development of hepatic coma, but she died of respiratory insufficiency before undergoing the procedure. Accordingly in this case, PDF worked to maintain liver function in acute liver failure and may act as bridge therapy until the patient can undergo liver transplantation.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
10/73. status epilepticus as a manifestation of hepatic encephalopathy.OBJECTIVES: seizures have been described as a rare manifestation of hepatic encephalopathy. MATERIAL AND methods: We present a 54-year-old female, with 6-year history of decompensated, hepatitis B liver cirrhosis, admitted with generalized seizures. She reported a history of recurrent episodes of hepatic encephalopathy, spontaneous bacterial peritonitis, tense ascites and variceal hemorrhage. neurologic examination revealed a comatose patient, without papilledema. Laboratory examinations were suitable with cirrhosis and mild renal failure. Blood gas examination revealed severe metabolic acidosis and hypoxemia. Plasma NH3 levels upon admission were twice normal. brain computed tomography and magnetic resonance imaging were normal. Electroencephalogram showed diffuse sharp waves, consistent with hepatic encephalopathy, grades III-IV. RESULTS: status epilepticus was refractory to continuous antiepileptic treatment. However, it was resolved after 24-h therapy with lactulose. Blood NH3 levels were simultaneously normalized with clinical improvement. CONCLUSIONS: We consider the status epilepticus of our patient to be a rare manifestation of hepatic encephalopathy.- - - - - - - - - - ranking = 1keywords = coma (Clic here for more details about this article) |
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