Managing exsanguination: what we know about damage control/bailout is not enough

Juan A. Asensio, MD, Patrizio Petrone, MD, Gloria O'Shanahan, MD, and Eric J. Kuncir, MD

From the Division of Trauma Surgery and Surgical Critical Care, Department of Surgery, University of Southern California Keck School of Medicine, Los Angeles County and University of Southern California Medical Center, Los Angeles, California.

Presented at surgical grand rounds, Baylor University Medical Center, August 28, 2002.

Corresponding author: Juan A. Asensio, MD, Division of Trauma Surgery and Surgical Critical Care, Department of Surgery, University of Southern California Keck School of Medicine, Los Angeles County and University of Southern California Medical Center, 1200 North State Street, Room 10-750, Los Angeles, California 90033-4525 (e-mail: asensio@hsc.usc.edu).

Exsanguination awaits better definition, not only clinically but also physiologically and biochemically. Asensio (1–4) has described it as the most extreme form of hemorrhage, with an initial blood loss of >40% and ongoing bleeding that, if not surgically controlled, will lead to death. Although trauma surgeons recognize exsanguination as a syndrome (1–19), its multifactorial effects on the cell, microcirculation, inflammatory cascades, and temperature-dependent enzymatic functions of both platelets and the coagulation pathways remain to be defined (1–7).