Fig. 1
Pathophysiology of traumatic hemorrhagic shock. a Traumatic hemorrhage five locations. b Traumatic hemorrhagic response. (1) Genomic response. Up-regulated anti-inflammatory genes with rapid recovery. Up-regulated pro- inflammatory genes leads to complications and death. (2) Cellular response. Anerobic metabolism with damage to mitochondria, smooth endoplasmic reticulum (SER) and rough endoplasmic reticulum (RER), leading to cellular homeostasis failure. (3) Tissue response. Local hemostatic plug formation with conversion of fibrinogen to fibrin. Distant coagulopathy with hyperfibrinolysis and diffuse coagulopathy. (4) Organ response. Moderate hemorrhage with end-organ damage and Exsanguination leading to death. aPC activated protein C, CARS compensatory anti-inflammatory response syndrome, DAMPs damage-associated molecular patterns, DNA deoxyribonucleic acid, Pi inorganic phosphate, C3H6O3 lactic acid, MOF multi organ failure, O2–, OH–, oxygen radicals, RE respiratory enzymes, SIRS systemic inflammatory response syndrome, tPA tissue plasminogen activator, ↑ increased