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Massive haemorrhage: a current perspective

01 March 2012
Volume 2 · Issue 1

Abstract

Trauma and massive haemorrhage are associated with coagulopathy secondary to tissue injury, hypoperfusion, dilution, and consumption of clotting factors and platelets occurring already at the scene of the accident. Concepts of damage control surgery have evolved prioritizing early control of the cause of bleeding by non-definitive means, while haemostatic control resuscitation seeks early control of coagulopathy. Haemostatic resuscitation provides transfusions with plasma and platelets in addition to red blood cells in an immediate and sustained manner as part of the transfusion protocol for massively bleeding patients and consequently limiting the amount of crystalloids and colloids are crucial for avoiding further impairment of haemostatic competence. Transfusion of red blood cells, plasma and platelets in a similar proportion as in whole blood prevents both hypovolaemia and coagulopathy. Results from recent before-and-after studies in massively bleeding patients indicate that trauma exsanguination protocols involving early administration of plasma and platelets are associated with improved survival. Furthermore, viscoelastic whole blood assays, such as thrombelastography (TEG) appear advantageous for identifying coagulopathy in trauma patients with severe haemorrhage as opposed the conventional coagulation assays. In our view, patients with uncontrolled bleeding, including trauma patients, should be treated with goal-directed haemostatic control resuscitation involving early administration of plasma and platelets and based on the results of TEG analysis. The aim of the goal-directed therapy should be to maintain a normal haemostatic competence until surgical haemostasis is achieved, as this appears to be associated with reduced mortality.

Haemorrhage requiring massive transfusion remains a major cause of potentially preventable deaths. Trauma and massive transfusion are associated with coagulopathy secondary to tissue injury, hypoperfusion, dilution and consumption of clotting factors and platelets. Coagulopathy, together with hypothermia and acidosis, forms a ‘lethal’ triad (Lier et al, 2008). Also, in the last 10–15 years, there has been some paradigm shift regarding optimal resuscitation of bleeding trauma patients before definitive haemorrhage control is achieved. Aggressive fluid resuscitation increases blood pressure, reverses vasoconstriction, dislodges early formed thrombus, causes dilutional coagulopathy and metabolic acidosis and increases blood loss in experimental studies (Stern et al, 1993). According to previous guidelines (American Society of Anesthesiologists Task Force on Perioperative Blood Transfusion and Adjuvant Therapies, 2006), fresh frozen plasma (FFP) and platelets (PLT) should be administered only when a whole blood volume or more has been substituted and then according to conventional coagulation analyses. Yet, this strategy leads to dilutional coagulopathy and compromises haemostatic competence for the most severely bleeding patients (Lier et al, 2008). Instead, limiting fluid resuscitation with the goal of achieving a palpable radial pulse in patients has been advocated, whereas in patients with head injury a systolic blood pressure above 110 mmHg is recommended (Dries, 1996; Krausz, 2003; Soreide and Deakin, 2005).

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