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Biomedical subjects

M K Mohapatra

Publications and source records attributed to M K Mohapatra.

7 recordsLinked to original sources
PubMed1996

Clinicopathological profile of subacute hepatic failure.

Twenty two patients of subacute hepatic failure (SAHF), diagnosed when jaundice progressed for more than 8 weeks with appearance of ascites, with or without encephalopathy, along with biochemical evidence of hepatocellular damage, were studied. The male and female ratio was 4.5:1 and majority (45.4%) of cases were between the age group of 41-50. The mean biochemical values were: S.bilirubin; 9.2 +/- 3.8 mg/dl SGOT; 94.4 +/- 25.0 I.U./lit., SGPT; 107.8 +/- 32.7 I.U./lit., S.Protein; 5.2 +/- 3.5 secs. Ascitic fluid analysis showed transudate in 16 (72.7%) and exudate in 6 (27.2%) patients. Bacterial peritonitis was found in 5 (22.7%) patients. Liver biopsy showed bridging and submassive necrosis. The complications developed in the hospital were: renal failure (36.3%), infection (27.2%), G.I. bleeding (18.1%) and encephalopathy (13.6%). The mortality was (86.3%). Out of 3 (13.6%) patients who survived, only two recovered completely and one had biochemical evidence of hepatocellular necrosis after 6 months of follow up.

Acute Disease↗
PubMed1995

Acute renal failure associated with freshwater fish toxin.

Clinical observations on toxicity after ingestion of gall bladder of Labeo rohita, a freshwater fish found commonly in India, were recorded from 22 patients between 1985 to 1990. The gall bladder in raw, cooked or desiccated form was swallowed as a traditional method of treatment for various chronic diseases. Patients generally presented with gastrointestinal symptoms such as cramping pain, nausea and vomiting within 12 hours (mean 4.6 +/- 3.7 hours) after ingestion. Subsequently renal failure was observed in all and hepatic dysfunction in some (36.3%) patients. The outcome in general is good. From the clinical course the role of toxic substance(s) is presumed as the causative factor(s), which needs further evaluation.

Acute Kidney Injury↗
PubMed1992

Encephalopathy in patients with extrahepatic obstruction after lienorenal shunts.

Thirty patients with portal hypertension resulting from extrahepatic portal vein obstruction were studied. Evidence of postshunt encephalopathy was sought using neurological and psychometric tests and visual evoked potentials. Eleven patients were studied before and after lienorenal shunt operations and 19 at varying intervals, from 6 to 123 (median 26) months, after the same procedure. All the shunts were patent and none of the patients developed clinical or subclinical encephalopathy. In patients with extrahepatic portal vein obstruction, a lienorenal shunt does not appear to be associated with postshunt encephalopathy.

Adolescent↗