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. 2023 May 24;31:25. doi: 10.1186/s13049-023-01088-8

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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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, P_i 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