Pathophysiology of Hemorrhage as It Relates to the Warfighter

Abstract

Saving lives of wounded military warfighters often depends on the ability to resolve or mitigate the pathophysiology of hemorrhage, specifically diminished oxygen delivery to vital organs that leads to multiorgan failure and death. However, caring for hemorrhaging patients on the battlefield presents unique challenges that extend beyond applying a tourniquet and giving a blood transfusion, especially when battlefield care must be provided for a prolonged period. This review describes these challenges and potential strategies for treating hemorrhage on the battlefield in a prolonged casualty care situation.

Keywords: battlefield; hemorrhage; prolonged casualty care; trauma.

FIGURE 1.

A comparison of casualty care management challenges during recent conflicts and future near-peer conflicts The table at bottom represents effects of these situational challenges on the development of pathophysiology.

FIGURE 2.

Flow diagram of early compensation of vital organ perfusion after hemorrhage Activation is represented by solid black lines, and inhibition is represented by dashed red lines. Therapeutic interventions and their targets are shown in green. CO, cardiac output; MAP, mean arterial pressure; SNS, sympathetic nerve system; TPR, total peripheral resistance.

FIGURE 3.

Forward and reversed electron transport in shock The forward flow of electrons through the electron transport chain (orange arrows) is decreased by shock, which causes a loss of O₂ delivery and a loss of ATP synthesis, leading to reverse electron transport (red arrows) at the flavin mononucleotide (FMN) and Qi site of complex I and the Qo site of complex III. These reversed electrons generate reactive oxygen species (ROS), which can be both destructive (complex I) and adaptive (complex III). Potential therapeutic interventions and their targets are suppressors of site 1Q electron leak (S1QEL) and Szeto-Schiller peptides. HIF-1α, hypoxia-inducible factor 1 alpha. Figure modified from Sabiston Textbook of Surgery (21st ed.) (162) with permission.

FIGURE 4.

Flow diagram of ischemia-induced cell death Therapeutic interventions and their targets are shown in green. Ca, calcium; ER, endoplasmic reticulum; H, hydrogen; IL-1, interleukin-1; K, potassium; mPTP, mitochondrial permeability transition pore; Na, sodium; NCX, sodium/calcium exchanger; NOX; nicotinamide adenine dinucleotide phosphate oxidases; ROS, reactive oxygen species; SNA, sympathetic nerve activation; TNF-α, tumor necrosis factor-alpha; VDAC, voltage-dependent anion channel.