MULTIPLE-SYSTEM ORGAN DAMAGE RESULTING FROM PROLONGED HEPATIC INFLOW INTERRUPTION - ELECTRON-MICROSCOPIC FINDINGS

Background: It has been reported that patients undergoing major hepate ctomy tolerated 90 and 127 minutes of continuous hepatic inflow interr uption with no evidence of permanent damage to the liver. We questione d the safety and feasibility of the interruption beyond 90 minutes in normothermic human beings. We also postulated that, besides injury to the liver per se, extended continuous hepatic inflow interruption woul d cause extrahepatic multiple-system organ damage in subjects exposed to continuous hepatic inflow interruption for 90 or 120 minutes. Desig n: Fifty Sprague-Dawley rats were divided into three groups. Group 1 s erved as controls that had only laparotomy. Group 2 underwent continuo us hepatic inflow interruption for 90 minutes, and group 3 was subject ed to continuous hepatic inflow interruption for 120 minutes. Scanning electron microscopy and transmission electron microscopy were used to evaluate ultrastructural alterations in the liver, lung, heart, and i ntestine. Setting: Lund (Sweden) University Hospital and Top Cancer In stitute, Lund. Interventions: Intraoperative and postoperative infusio n and blood transfusion were given in all experimental animals. Main O utcome Measures: Animal survival and manifestations of multiple-system organ failure. Results: In rats with continuous hepatic inflow interr uption for 90 or 120 minutes, scanning electron microscopy showed a ne crotic surface of the liver cells together with fibrin exudation. Hepa tic sinusoids and intrahepatic nerves also had severe injury. Destruct ion of pulmonary structures and breakdown of microcirculation in the l ung were characterized by thinned and ruptured walls of alveoli and a greatly decreased number of capillaries in the damaged alveolar wall. Transmission electron microscopy showed four types of ultrastructural changes, ie, necrosis of epithelial cells, extremely swollen mitochond ria in intestinal cells, death of mucosal cells, and increased permeab ility of vessels in the injured intestine. The affected heart manifest ed highly enlarged mitochondria in myocardial cells, thickened vascula r walls, and scattered necrotic lesions in myocardial tissue. Conclusi ons: Multiple-system organ failure resulting from ischemia-reperfusion injury and obstacle of portal hemodynamics in a subject subjected to an extended continuous hepatic inflow interruption is an unrecognized new disorder that may cause a high mortality rate. Our preliminary res ults indicated that animals subjected to continuous hepatic inflow int erruption for 90 or 120 minutes developed various injuries to the live r, lung, heart, and gut. Therefore, we believe that continuous hepatic inflow interruption exceeding 90 minutes could also be hazardous in h uman beings.