The trauma triad of death
The lethal triad of trauma has historically been seen as the cause of ATC, however, based on extensive research it is now seen as a contributory factor in the development of coagulopathy. Trauma-induced hypothermia as a result of cellular hypoperfusion has a negative effect on the production of activated thrombin which further compounds the intrinsic and extrinsic coagulation system. Hypothermia also impairs platelet function however its inhibitory effects have been shown to be more prevalent at very low-temperature levels. The effect of a temperature <30°C in relation to ATC however is not seen as a significant contributory factor as temperatures this low are not normally associated with the trauma patient.
Additional research has however shown that trauma patients with a temperature of <35.8°C are seen as an independent risk factor in the development of ATC. It is therefore apparent that hypothermia does have an effect on the coagulation cascade but its significance when managing the trauma patient requires further research. Current guidance does however indicate the need for patients to be actively warmed utilising blankets, heat pads, and/or warmed blood products or fluids to correct or prevent hypothermia.
The role of acidosis and ATC appears to be significant with clotting factor reduction, reduced platelet activity, and increased coagulation time all being affected by acidaemia. Studies have also indicated that when acidosis is accompanied by hypothermia an increase in coagulation time is observed, furthermore any correction of acidosis alone does not guarantee an improvement in clotting times. Acidosis and subsequent coagulopathy can be further impaired by the use of crystalloid fluid resuscitation due to sodium chloride and ringer’s lactate being acidic. The aggressive use of fluid resuscitation has also correlated with a dilution of clotting factors and a subsequent increase in coagulation times. Furthermore, this can result in higher blood pressures (BP) and a subsequent increase in hydrostatic pressures resulting in clot disruption and further bleeding with research and randomised clinical controlled trials confirming these findings. As a consequence of this research it is recommended that fluid resuscitation should be limited to fluid challenges of 250ml in the prehospital environment and endeavour to achieve a state of permissive hypotension in order to achieve cellular perfusion but at a lower than normal BP. Current paramedic UK guidance for penetrating trauma to the torso suggests a target SBP of 60mmHg and a Systolic BP of 90mmHg for blunt trauma in order to facilitate this delicate balance between cellular perfusion and permissive hypotension.
The primary mechanism for acidosis however appears to be cellular hypoperfusion due to reduced oxygen saturation and or reduced Systolic BP. Cells that are not oxygenated sufficiently are required to produce energy via glycolysis or anaerobic metabolism as opposed to aerobic metabolism which utilises oxygen. The anaerobic metabolism of cells is far less efficient and effective in producing energy, and when its use is prolonged as in a patient who has experienced significant trauma, harmful by-products are produced. The acidic by-products of CO2 and lactic acid increase the content of hydrogen ions in the circulation system and as such, decrease the pH. As the blood becomes more acidic its compensatory mechanism begins to fail due to renal hypoperfusion and exhaustion of bicarbonate reserves. It is therefore recommended that the management of patients with significant trauma who are critically injured are administered high flow oxygen irrespective of their oxygen saturations in order to facilitate an increase in cellular perfusion in an attempt to reduce anaerobic metabolism requirements. However, for patients who are not critically injured oxygen administration should be titrated to achieve saturations of 94-98%.