Traumatic-induced coagulopathy (TIC) is often associated with significant bleeding, transfusion requirements, inflammation, morbidity, and mortality. This review considers TIC as a systems failure, not as a single-event manifestation of trauma. After briefly reviewing the meaning of TIC and the bewildering array of fibrinolysis phenotypes, we will discuss the role of platelets and fibrinogen in coagulopathy. Next, we will review the different TIC hypotheses and drill down to a single mechanistic domain comprising (1) thrombin's differential binding to thrombomodulin, (2) the expression of annexin II-S100A10 complex, and (3) the functional integrity of the endothelial glycocalyx. This triad forms the basis of the “switch” hypothesis of TIC. We will next address the potential limitations of current practice in treating a coagulation or fibrinolytic defect, and the next defect, and so on down the line, which often leads to what U.S. surgeon William C. Shoemaker considered “an uncoordinated and sometimes contradictory therapeutic outcome.” The treat-as-you-go approach using sequential, single-target treatments appears to be a by-product of decades of highly reductionist thinking and research. Lastly, we will present a unified systems hypothesis of TIC involving three pillars of physiology: the central nervous system (CNS)–cardiovascular system, the endothelial glycocalyx, and mitochondrial integrity. If CNS control of ventriculoarterial coupling is maintained close to unity following trauma, we hypothesize that the endothelium will be protected, mitochondrial energetics will be maintained, and TIC (and inflammation) will be minimized. The Systems Hypothesis of Trauma (SHOT) also helps to answer why certain groups of severely bleeding trauma patients are still dying despite receiving the best care. Currently, no drug therapy exists that targets the whole system.

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Our aim was to examine the effect of low-volume 0.9% NaCl adenosine, lidocaine and Mg 2+ (ALM) 'drip' on early immune-inflammatory activation after a single laparotomy with no further manipulation. Male Sprague-Dawley rats were anesthetized and randomly assigned to one of the groups, baseline, 1 h infusion 0.9% NaCl AE ALM and metrics, 1 h infusion and 6-h metrics, and 6 h continuous infusion and metrics. Complete blood count, acid-base balance, systemic levels of IL-6 and IL-10, and coagulation status were measured. After 1 h, there was a disproportionate increase in circulating neutrophils between saline and ALM groups despite an identical 45% fall in lymphocytes. Disproportionate increases also occurred in platelet counts 1 h after surgery, and saline controls had increased respiratory alkalosis at 6 h with higher lactate. Systemic inflammation was also evident after 1 h in both groups (plasma IL-6 increase) and was amplified in saline-controls after 6 h. The ALM group increased anti-inflammatory cytokine IL-10. Surgery was not associated with acute coagulopathy; however, there were significant reductions in fibrinolysis. Following a single laparotomy, ALM infusion appeared to reduce stress-induced release of neutrophils and platelets into the circulation, and reduced acid-base disturbance. After 1 h, both groups had similar IL-6 levels, but ALM animals had increased IL-10, indicating improved inflammatory balance. The uncoupling of inflammation and coagulation activation but not fibrinolysis may offer a unique opportunity to investigate differential activation of innate immunity in response to sterile injury in this model.

Graphical abstract

Introduction An escharotomy is an effective surgical procedure for the rapid decompression of a constricting and unyielding eschar, to permit restoration of blood flow. However, an escharotomy is also a full‐thickness incision, which adds additional scarring to the burn injury area. The cosmetic and functional morbidity of escharotomy scarring in children is poorly characterised. Methods Children who required a burn wound escharotomy at the Queensland Children's Hospital (QCH) between May 2011 and May 2020 were included. Demographics of these children were described. In addition, the number of operations for revision of escharotomy scars was recorded as an indicator of functional or cosmetic concern. Results A total of 19 patients required an escharotomy after a burn injury. Children with 1% to 96% TBSA burns required an escharotomy, with a median of 28% (IQR 10–39%) TBSA. Two patients (81% and 96% TBSA) died. Seventy‐one percent (12/17) of survivors had operative revisions of their escharotomy scars. The median time from burn to first scar intervention was 35 weeks (IQR 19–70 weeks). Conclusion There is substantial morbidity associated with escharotomies in children. Further investigation of the current methods of decompression after burn injury, and the long‐term morbidity of escharotomy, is required.