Triad of Death
Triad of Death
Injured patients presenting with hypothermia, acidosis and coagulopathy have been identified at very high risk of death ,hence the term ‘triad of death’. The triad can develop rapidly in the exsanguinating trauma patient, and is the result of the primary trauma and the secondary systemic response. Once established, it forms a vicious circle that may be impossible to overcome .Hypothermia is both a marker of profound injury and is by itself deleterious, promoting this vicious cycle in the bleeding patient. Hypothermia can occur in the field and subsequently in the various hospital environments, due to exposure and heat loss, transfusion of cold fluids and impaired thermogenesis (use of muscle relaxants, for example). It develops more rapidly in infants and children due to their small body mass and large surface area to volume ratio. Hypothermia induces multiple adverse effects: It causes cardiac dysfunction (arrhythmias, decreased contractility) and
increased inotropic requirement. It shifts the oxyhaemoglobin dissociation curve to the left and impairs oxygen delivery, thereby aggravating tissue hypoxia in the trauma patient with a preexisting ‘oxygen debt’. Hypothermia suppresses enzymatic activity, induces endotheliopathy and increases
fluid leak, and promotes platelet dysfunction and coagulopathy.Although metabolic acidosis has been considered not harmful per se in this setting, but rather a marker of tissue hypoxia , recent studies indicate that low pH by
itself severely impairs thrombin generation and accelerates fibrinogen degradation.Tissue hypoxia may be due to direct tissue damage,hypotension or impairment of the microcirculation by hypovolemia, disseminated coagulation, intravascular sludging and endothelial damage. Tissue hypoxia leads to anaerobic metabolism and lactic acid production that may be aggravated by abundant glucose supply and by hepatic function impairment. In pediatric trauma, the probability of mortality increases precipitously in children with a base deficit less than -8 mEq/L .Coagulopathy after major trauma is a multifactorial, global failure of the coagulation system to sustain adequate hemostasis . Derangements in coagulation are detectable already in the hyperacute phase following severe trauma, driven by the combination of tissue trauma and systemic hypoperfusion, and are characterized by global anticoagulation and hyperfibrinolysis . Subsequently, coagulopathy proceeds due to continued blood loss, hemodilution and consumption of platelets and clotting factors, and is exacerbated by hypothermia and acidemia .Studies analyzing the effects of the ‘triad of death’ on mortality in pediatric trauma patients are lacking. Mortality in adult trauma patients presenting with this triad approximates 50 % . Hypothermia contributes to mortality over and above the mortality associated with multiple severe injuries, independent of hypotension, fluid requirements, age, or duration of surgery . Coagulopathy on presentation has been associated with a fourfold increase in overall mortality .The presence of all three conditions not only adds to mortality, but they further potentiate each other, forming a “vicious cycle resulting in death” . Continuing attempts to stop hemorrhage and repair the injury in the hypoperfused patient result in deepening hypothermia and coagulopathy. SIRS is evolving, further lowers blood pressure, worsens tissue acidosis and enhances capillary leak. The intravascular hypovolemia requires further transfusion and crystalloids volume infusion, resulting in dilution of coagulation factors and enhanced SIRS. The patient is now “oozing” extensively and the vicious cycle spirals down, often resulting in the patient’s death in the OR.Even if the bleeding can be eventually stopped, the patient
will arrive at the ICU with massive fluid overload and ongoing capillary leak and is at high risk of developing MODS, MOF and abdominal compartment syndrome. If he also has a significant TBI, the previously incurred hypoperfusion and generalized edema will negatively impact on the brain’s ability to recover and on the development of cerebral edema.The recognition of the poor outcome of these multiply injured, bleeding patients, had led in the early 1990s to a paradigm shift – to the ‘damage control surgery’ and subsequently to the ‘damage control resuscitation’ paradigms.
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