[Post-traumatic jaundice--its mechanism from a view point of hepatic mitochondrial function]

It has been proposed that post-traumatic jaundice was the result of increased hemolysis, absorption of hematoma, effects of drugs, and so on. We considered that hepatic impairment in the bilirubin metabolism as a result of hepatic hypoperfusion might also be an important factor of the jaundice. Patients who developed jaundice after trauma were divided into two groups according to the maximum total bilirubin level; groups H (greater than 8 mg/dl) and L (less than 5 mg/dl). Severity of shock, levels of serum hepatic enzyme, and blood ketone body ratio were compared between the groups. Minimum systolic pressure, H 58, L 82 mmHg (p = 0.003); duration of shock (less than 80 mmHg), H 225, L 20 min (p less than 0.001); blood transfusion, H 9188, L 2914 ml (p less than 0.001); direct/total bilirubin, H 0.66, L 0.43 (p less than 0.001). Although no significant difference was noted in serum hepatic enzyme levels, blood ketone body ratios were significantly lower in group H throughout the first week. From these facts, it is considered that an impairment in the most energy requiring process of bilirubin metabolism, excretion of conjugated bilirubin from cytosol to capillary bile duct, due to post-traumatic hepatic mitochondrial dysfunction, followed by the reabsorption of conjugated bilirubin into the blood stream, would be one of factors of post-traumatic jaundice.