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PubMed1997

Hepatic coma recovered after interventional obliteration for ileocecal-inferior vena cava shunt--report of one case.

We performed interventional angiography (IVA) in a patient with liver cirrhosis (LC) and hepatoma (HCC) who experienced repeated attacks of unconsciousness due to hyperammonemia caused by ileocecal-inferior vena cava (IC-IVC) shunt and succeeded in the treatment. We report the results below. The patient, 53-year-old male, underwent endoscopic injection sclerotherapy for esophageal varix due to LC followed by splenectomy for pancytopenia in 1986. He made good progress. However intraarterial anticancer therapy was conducted for HCC in 1994. From that time hepatic coma began to appear and its frequency gradually increased. Hepatic coma occurred once every 3 weeks from June 1996. He was thus admitted to our hospital. Hematobiochemical testes showed that ammonia level was 297 mcg/dl. Albumin 2.8d/dl, and Total-Bilirubin 10.78 mg/dl. Arterioportography from superior mesenteric artery showed most of portal blood flowed away from the liver though the ileocolic vein to IVC. We decided to conduct IVA for treatment. Specially, a 6Fr balloon catheter was inserted from the right inguinal region into a shunt to the portal vein though IVC by the Seldinger technique. The balloon was inflated in the shunt to close the shunt. Six ml of 5% ethanolamime oleate with iopamidol was injected because retrograde angiography showed that iopamidol was flowed out via testicular vein to IVC. The balloon catheter was retained for 24 hours. Angiography, conducted from the catheter again 24 hours later, showed that the shunt was occluded, blood ammonia level was 71 mcg/dl after occlusion. Hepatic coma was not observed after treatment. We encountered a very rare case who repeated hepatic comas due to IC-IVC shunt and recovered dramatically after IVA.

Angiography↗
PubMed1985

Hepatic coma and amino acids in the nerve endings of the central nervous system.

The levels of amino acids in the cerebral cortex and synaptosomes of 6 autopsied patients who had died of chronic liver diseases with portasystemic shunt were examined and compared with those of controls. The level of threonine in the cerebral cortex and synaptosomes of the 6 patients, who had developed hepatic coma before death, was significantly higher than that of 9 patients without hepatic coma. However, the levels of the neurotransmitters, aspartate, glutamate, and glycine, showed no significant difference between the two groups. In animal experiments, threonine uptake into the synaptosomes was enhanced by an increase of threonine concentration in the cerebral cortex, and at the same time ammonia further promoted threonine uptake. The high level of threonine in the synaptosomes was released just like a neurotransmitter on potassium stimulation in the patients with hepatic coma. Since threonine has no post-synaptic action, it is thought that threonine released in this way somehow interferes with brain action. This phenomenon may play an important role in the development of hepatic coma.

Amino Acids↗