Experimental Hepatic Coma

Abstract

While experimenting with ischemia of the liver in dogs, we observed 4 animals in comatose states which closely resembled hepatic coma in man. Two of these were fatal, 2 non-fatal. After many attempts to induce these comatose states at will, we found that a graded production of liver ischemia might result in the clinical manifestations of coma. If the increasing ischemia of the organ can be coped with by the gradually developing blood flow from collateral circulation, the animal may recover from coma.

Ischemia of the liver can be induced by gradually tying the vessels in the hepatic-duodenal ligament and diverting the blood flow from the portal vein into the vena cava (classical Eck fistula). The collateral circulation will then develop from the reversed flow in the gastro-duodenal, left gastric and phreni-co-abdominal arteries (1).

Six 9 to 15 kg dogs were operated upon under nembutal anesthesia (35 mg/kg body weight) in a 2-stage procedure: 1st stage: Portalcaval anastomosis and ligation of the portal vein in the hepato-duodenal ligament (Eck fistula). 2nd stage: 24 to 48 hours later under nembutal anesthesia (only half the previous dose is now necessary) ligation of the common hepatic artery. Intensive treatment with penicillin and streptomycin was started immediately after the first stage and continued for about 7 days post-operatively. Four of the dogs were infused continuously with saline-glucose solution in order to avoid the complicating factor of hypoglycemia. Of the 2 dogs which did not receive glucose, one died in hypoglycemic convulsions. The other dog was in a subcomatose state for 36 hours and recovered. Of the 4 dogs infused with glucose, three had a non-fatal liver coma. One dog died 33 hours after the second state operation in a deeply comatose state.