BACKGROUND: Hypothermia, acidosis and coagulopathy have long been considered critical combinations after severe injury. The aim of this review was to give a clinical update on this triad in severely injured patients. METHODS: A non-systematic literature search on hypothermia, acidosis and coagulopathy after major injury was undertaken, with a focus on clinical data from the past 5 years. RESULTS: Hypothermia (less than 35 °C) is reported in 1·6-13·3 per cent of injured patients. The occurrence of acidosis is difficult to estimate, but usually follows other physiological disturbances. Trauma-induced coagulopathy (TIC) has both endogenous and exogenous components. Endogenous acute traumatic coagulopathy is associated with shock and hypoperfusion. Exogenous effects of dilution from fluid resuscitation and consumption through bleeding and loss of coagulation factors further add to TIC. TIC is present in 10-34 per cent of injured patients, depending on injury severity, acidosis, hypothermia and hypoperfusion. More expedient detection of coagulopathy is needed. Thromboelastography may be a useful point-of-care measurement. Management of TIC is controversial, with conflicting reports on blood component therapy in terms of both outcome and ratios of blood products to other fluids, particularly in the context of civilian trauma. CONCLUSION: The triad of hypothermia, acidosis and coagulopathy after severe trauma appears to be fairly rare but does carry a poor prognosis. Future research should define modes of early detection and targeted therapy.
BACKGROUND:Hypothermia, acidosis and coagulopathy have long been considered critical combinations after severe injury. The aim of this review was to give a clinical update on this triad in severely injured patients. METHODS: A non-systematic literature search on hypothermia, acidosis and coagulopathy after major injury was undertaken, with a focus on clinical data from the past 5 years. RESULTS:Hypothermia (less than 35 °C) is reported in 1·6-13·3 per cent of injured patients. The occurrence of acidosis is difficult to estimate, but usually follows other physiological disturbances. Trauma-induced coagulopathy (TIC) has both endogenous and exogenous components. Endogenous acute traumatic coagulopathy is associated with shock and hypoperfusion. Exogenous effects of dilution from fluid resuscitation and consumption through bleeding and loss of coagulation factors further add to TIC. TIC is present in 10-34 per cent of injured patients, depending on injury severity, acidosis, hypothermia and hypoperfusion. More expedient detection of coagulopathy is needed. Thromboelastography may be a useful point-of-care measurement. Management of TIC is controversial, with conflicting reports on blood component therapy in terms of both outcome and ratios of blood products to other fluids, particularly in the context of civilian trauma. CONCLUSION: The triad of hypothermia, acidosis and coagulopathy after severe trauma appears to be fairly rare but does carry a poor prognosis. Future research should define modes of early detection and targeted therapy.