Management Of Coagulopathy

Coagulopathy is common in the brain injured potential organ donor. Disseminated intravascular coagulation (DIC) or fibrinolysis may occur after penetrating or severe closed head injury. This results from the release into the circulation of tissue thromboplastin and plasminogen. Hypothermia and catecholamines both affect platelet function further contributing to coagulopathy. Resuscitation may also result in a dilutional coagulopathy resulting from decreased numbers of platelets.

In the massively transfused patients a number of considerations are important which will exacerbate coagulopathy. Packed red cells contain no active platelets. The platelet count should be measured. Banked blood greater than 3 weeks old contains only 10-15% of normal levels of clotting factors V and VIII. Obviously in a brain dead organ donor, spontaneous CNS hemorrhage is significant only insofar as it may further contribute to donor instability. The severely coagulopathic organ donor may, however, become unstable during multiorgan procurement due to excessive blood loss.

To avoid intraoperative blood loss that might adversely affect multiorgan recovery in the severely coagulopathic patient, replacement of clotting factors should be considered. This can be accomplished with either fresh frozen plasma or cryo-precipitate. Platelets should be transfused if the count is less than 50,000/mm3. Red cell replacement should be considered to keep the hemoglobin greater than 10 g/dl. If the potential organ donor has been massively transfused, citrate, an anticoagulant in banked blood can produce hypocalcemia and cardiac arrest. Calcium chloride, 1 mg/kg IV every 15-20 minutes during periods of rapid transfusion will obviate hemodynamic compromise. Ionized calcium and the Q-T interval of the ECG can be monitored if there are concerns.

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