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Abstract
Hemorrhagic shock (HS) in trauma patients results in liver injury from impaired blood flow and increased mediators of the systemic inflammatory response. These mediators include high-mobility group protein B1 (HMGB1), a marker of hepatocyte necrosis, and toll-like receptor (TLR)-4 and TLR-9, which are thought to initiate early and late inflammation in the liver during resuscitated HS. A new treatment strategy, direct peritoneal resuscitation (DPR), improved liver blood flow, function, and survival after HS.
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