Trauma induced coagulopathy

Relatively recently, coagulation abnormalities have been observed soon after injury in trauma patients, with the working title of trauma induced coagulopathy. It may present on admission, or during early treatment, and at least one factor is activation of the C-reactive protein pathway. Hypoperfusion is part of the problem.

Coagulopathy either may develop, or not be corrected, by less than optimal fluid resuscitation. There is a trend away from resuscitation with pure crystalloid such as saline or Ringer's lactate, but considerable debate on the proper approach to blood and blood products. A number of trauma specialists have noted that the blood product subset is more of a U.S. problem, as only whole blood is available for transfusion in many countries. Component transfusions with packed red blood cells, for example, are efficient in restoring oxygen-carrying capacity, but do not provide the coagulation components present in fresh-frozen plasma or other specialized components.

Evolving views

A 2008 consensus conference in Chicago agreed on "Trauma Induced Coagulopathy - TIC" which is the multifactorial clinical entity of disordered coagulation seen in trauma patients. The mechanisms involved in TIC include:

• Dilution
• Acute Traumatic Coagulopathy (ATC) - the "endogenous" shock-induced coagulopathy
• Acidemia
• Hypothermia
• Hyperfibrinolysis
• Inflammation
• Platelet dysfunction
• Underlying genetic factors
• Pre-morbid conditions
• Therapeutic anticoagulant medications

While these tend to lead to inadequate coagulation, there is also may be a hypercoagulability phenomenon. "The early "hypercoagulable state" appears to be a normal response to injury. Patients with late hypercoagulability who are at risk of deep venous thrombosis or pulmonary embolism etc are the ones who are hypocoagulable on arrival. Hypercoagulability is not considered part of TIC or a clinically relevant coagulopathy in the acute phase.

An informal prepublication report from a participant in the January 2010 and the April 2010 Department of Defense/National Heart, Lung and Blood Institute has a more complex view. The first meeting suggested reduction in crystalloid and increase in colloid replacement in field medicine. While this is an informal consensus, especially the latter conference began to hold the opinion that there are three parts to the phenomenon; it was questioned if what has been called TIC is the entire system, or only the second part:

1. Dilutional - This was secondary to loss of clotting factors and was best addressed by replacement of the lost factors be with through use of plasma itself or the individual components such as factor VII, PCC or other factors that may become available
2. Tissue damage factors - This is the least understood. There seem to be multiple factors incriminated such as protein C or fibrinolysis.
3. Hypercoagulopathy - This is possible a rebound phenomenum but also may b secondary to a specific component produced by the trauma. This is an area that will require some research funding as well.

CRASH II

The large multicenter CRASH-2 trial, in 2010, has shown striking mortality reductions after trauma and elective surgery after administration of tranexamic acid. This was reflected in the new European guidelines.

Work in the CRASH trial is prompting reexamination of the broader clinical implications of antifibrinolysis.

At low concentration, tranexamic acid, which binds to the Kringle domain of plasminogen, is a competetive inhibitor of plasminogen activation into plasmin (fibrinolysin), an enzyme that degrades fibrin clots, fibrinogen, and procoagulant plasma proteins such as factor V and factor VIII. At higher concentrations it is a noncompetetive inhibitor of plasmin. It binds to the strong and weak receptor sites of plasminogen with affnities about 10 times greater than aminocaproic acid.