Summary Improvements in the control of haemorrhage after trauma have resulted in the survival of many people who would otherwise have died from the initial loss of blood. However, the danger is not ...over once bleeding has been arrested and blood pressure restored. Two-thirds of patients who die following major trauma now do so as a result of causes other than exsanguination. Trauma evokes a systemic reaction that includes an acute, non-specific, immune response associated, paradoxically, with reduced resistance to infection. The result is damage to multiple organs caused by the initial cascade of inflammation aggravated by subsequent sepsis to which the body has become susceptible. This Series examines the biological mechanisms and clinical implications of the cascade of events caused by large-scale trauma that leads to multiorgan failure and death, despite the stemming of blood loss. Furthermore, the stark and robust epidemiological finding—namely, that age has a profound influence on the chances of surviving trauma irrespective of the nature and severity of the injury—will be explored. Advances in our understanding of the inflammatory response to trauma, the impact of ageing on this response, and how this information has led to new and emerging treatments aimed at combating immune dysregulation and reduced immunity after injury will also be discussed.
Haemorrhage control in severely injured patients Gruen, Russell L, Prof; Brohi, Karim, Prof; Schreiber, Martin, Prof ...
The Lancet (British edition),
09/2012, Letnik:
380, Številka:
9847
Journal Article
Recenzirano
Most surgeons have adopted damage control surgery for severely injured patients, in which the initial operation is abbreviated after control of bleeding and contamination to allow ongoing ...resuscitation in the intensive-care unit. Developments in early resuscitation that emphasise rapid control of bleeding, restrictive volume replacement, and prevention or early management of coagulopathy are making definitive surgery during the first operation possible for many patients. Improved topical haemostatic agents and interventional radiology are becoming increasingly useful adjuncts to surgical control of bleeding. Better understanding of trauma-induced coagulopathy is paving the way for the replacement of blind, unguided protocols for blood component therapy with systemic treatments targeting specific deficiencies in coagulation. Similarly, treatments targeting dysregulated inflammatory responses to severe injury are under investigation. As point-of-care diagnostics become more suited to emergency environments, timely targeted intervention for haemorrhage control will result in better patient outcomes and reduced demand for blood products. Our Series paper describes how our understanding of the roles of the microcirculation, inflammation, and coagulation has shaped new and emerging treatment strategies.
Abstract Background Tranexamic acid (TXA) in traumatic haemorrhage reduces death from bleeding. However, its effect on the coagulation system after trauma is unclear. We aimed to assess the effect of ...TXA on functional clotting dynamics in patients with suspected traumatic haemorrhage. Methods Adult trauma patients for whom the major haemorrhage protocol was activated within a single major trauma centre were prospectively recruited. Blood was drawn on admission to the emergency department and during the acute bleeding phase (after transfusion of 4, 8, and 12 red blood cell RBC units) for thromboelastometry. Patients who received TXA before admission blood draw (TXA group) were compared with patients who did not (no TXA group). Proteins of coagulation and fibrinolysis were measured in a subset of patients. Findings 222 patients were included (109 TXA group, 113 no TXA group) for functional clotting analysis, and 162 patients were included (60 TXA, 102 no TXA) for protein analysis. The proportion of patients with trauma-induced coagulopathy was lower in the TXA group than in the no TXA group throughout the acute bleeding phase (after 12 RBC units 67% 6/9 vs 100% 9/9 with coagulopathy, p=0·21). TXA abolished the functional hyperfibrinolysis of trauma-induced coagulopathy on admission (0% 0/109 vs 20% 23/113, p<0·0001) and during bleeding (after 12 RBC units 0% 0/9 vs 22% 2/9, p=0·47). Despite massive blood transfusion, clot strength was protected in the TXA group compared with the no TXA group (after 12 RBC units, median maximum clot firmness 53 mm IQR 48–56 vs 44 29–48, p=0·008). TXA switched off functional lysis even in the presence of extremely high concentrations of plasmin-antiplasmin complex. Patients treated with TXA had lower D-dimer levels after massive haemorrhage (after 12 RBC units 12·1 μg/mL 5·8–16·8 vs 30·4 22·7–55·0, p=0·005). 24 h mortality was lower in the TXA group than in the no TXA group (7% 8/109 vs 23% 21/90, p=0·002) but not 28 day mortality. Interpretation Our study shows that early TXA is associated with augmented clot strength, avoidance of hyperfibrinolysis, reduced trauma-induced coagulopathy, and lower 24 h mortality in patients with traumatic haemorrhage. Funding None.
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