l c t i t z i U o t l r p g a d c t r istorical perspective lthough anecdotal reports of liver trauma such as that f Hellwig and Orr alluded to the effect of shock on the iver, the first large clinical review of liver ischemia was ublished by Bywaters in 1946. Forty-two patients dyng from blunt trauma were presented and autopsy maerial was examined. Twenty-seven (64%) patients in his group were hypotensive, as defined in this study by systolic blood pressure less than 90 mmHg, from 1 to ore than 10 hours. Histologically, some degree of liver ecrosis was found in eight of these patients, particularly n those with more prolonged periods of shock. The attern of necrosis was noted to be midzonal or paracenral, sparing the periportal and, many times, the central egions of the lobule. The earliest necrotic changes were een as soon as 24 hours after injury. Bywaters concluded hat the most likely explanation for this phenomenon as liver anoxia from hemorrhagic shock. The role of hock in production of hepatocyte necrosis was eluciated by Ellenberg and Osserman in 1951. Of 34 paients with central liver cell necrosis, 32 (94%) were ssociated with shock. Again, the duration of shock eemed to be a principal determinant of the presence of ecrosis. The midzonal pattern of cell damage, however, as not as clearly seen. Preexisting conditions, such as irrhosis, in many of the patients might have resulted in ore extensive lobular injury than was seen by others. In 967, Kantrowitz and coauthors published a detailed linicopathologic analysis of four patients suffering arked liver impairment after hemorrhagic shock. Hyerbilirubinemia began early, around the third or fourth ostoperative day, and progressed to profound degrees, p to 39 mg/dL by postoperative days 9 to 18. This was ssociated with elevations of alkaline phosphatase, hich gave the impression of cholestatic jaundice de-