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I Buhac

Publications and source records attributed to I Buhac.

36 records · Page 2Linked to original sources

Histology of the intestinal peritoneum in patients with cirrhosis of the liver and ascites.

Portal hypertension and hypoalbuminemia are usually incriminated in the development of ascites in liver cirrhosis, and altered peritoneal permeability is considered only as a hypothetical possibility. Jejunal postmortem specimens were studied in 15 control patients and 16 patients dying with cirrhosis of the liver and ascites. In decompensated cirrhosis a fibrous thickening of the peritoneum was found, 159.0 +/- 96.4 micrometer (mean +/- SD) compared to 24.5 +/- 10.6 micrometer in controls (P less than 0.001). An increase in the size and number of blood vessels, lymphangiectasiae, and mononuclear cell infiltration were invariably present. These histological changes are consistent with a nonspecific chronic peritonitis. The findings indicate there is increased blood perfusion and lymph flow within the intestinal peritoneum in patients with decompensated cirrhosis of the liver and support the existence of an intestinal peritoneal factor in the pathogenesis of cirrhotic ascites.

Aged↗

Diabetic visceral neuropathy: treatment with bethanechol chloride.

An 86-year-old diabetic man developed nausea, emesis, abdominal distention, and decreased gastrointestinal motility. A Hollander test confirmed incomplete vagal dysfunction. Treatment with bethanechol chloride resulted in marked improvement which was reproducible after withdrawal and reinstitution of therapy. We believe that treatment with bethanechol chloride deserves further investigation in selected patients with diabetic visceral neuropathy.

Aged↗

Septicemia as a complication of percutaneous liver biopsy.

Three cases of septicemic shock after liver biopsy are reported. Escherichia coli was cultured in 2 patients and in 1 E. coli was cultured with Streptococcus viridans. All 3 patients were afebrile and had normal WBC counts before the procedure. Two had cholangitis and the 3rd had primary hepatoma and cirrhosis of the liver. Septicemic shock should be recognized as a rare complication of liver biopsy in patients with biliary obstruction.

Aged↗

Bacteremia after upper gastrointestinal endoscopy.

During 24 months, 200 upper gastrointestinal endoscopies were performed on 193 patients. Blood cultures were obtained before and five and 30 minutes after the procedure using thiol (50 ml) and trypticase soy broth (100 ml) media. The mean endoscopic time was 34 minutes. Sixteen patients developed bacteremia (8%). Twelve groups of microorganisms were detected in positive blood cultures: Streptococcus (5 species), Lactobacillus sp, Veillonella alcalescens, Staphylococcus aureus, Staph epidermidis, Propioni-bacterium acnes, Corynebacterium acnes, and Bacillus subtilis. Seven patients had positive blood cultures at five and 30 minutes, eight at five minutes, and one at 30 minutes only. There was no clear correlation of bacteremia with the age or previous history of the patient, biopsy, active bleeding, endoscopic time, or findings. A follow-up study of all patients for six months to two years indicated no complications related to endoscopy and/or bacteremia.

Adult↗

Spontaneous hepatic artery thrombosis with infarction of the liver.

Extensive infarction of the liver, initially thought to be halothane hepatitis, is described. The patient developed severe right upper quadrant abdominal pain and abnormal liver function tests after amputation of the leg. The correct diagnosis was made by percutaneous needle biopsy of the liver which demonstrated a large area of avascular necrosis. The patient recovered, indicating the remarkable ability of the liver to maintain function despite ischemic injury. The patient died later from an acute myocardial infarction, and at autopsy thrombosis of the hepatic artery and multiple hepatic infarcts were confirmed.

Aged↗

Abnormal metabolism of secondary bile acids in patients with cirrhosis.

The composition of bile acids in human bile was determined in bile-rich duodenal fluid on four consecutive days in a group of seven patients with cirrhosis and eight control patients with no liver disease. There was a marked reduction of secondary biliary bile acids in cirrhotic patients. Possible mechanisms for these changes are discussed.

Bile↗