Hematological consequences of profound hypothermic circulatory arrest and aortic dissection

The lower temperatures utilized during profound hypothermic circulatory arrest (PHCA) surgery may exacerbate the hypothermia associated platelet and clotting factor dysfunction observed in conventional cardiopulmonary bypass (CPB) procedures. Hypothermia has been shown to impair the activity of the enzymes involved in the platelet activation pathways and to reduce the enzymatic activity of clotting factors upon coagulation activation. The resulting retardation of the generation of fibrin/platelet clot compounded by the presence of heparin may contribute significantly to a bleeding tendency. Excessive fibrinolytic activity may disrupt surgical wound thrombi and exacerbate haemorrhage. There is good evidence that the fibrinolytic activity, mediated predominantly by tissue plasminogen activator (tPA), is a secondary response to thrombin generated by coagulation activation, which is ongoing during CPB despite full heparinization. The effects of hypothermia on the fibrinolytic response remain to be clarified and the extent to which the lower temperatures and blood stasis associated with PHCA moderate this response is unknown. Despite impairment of coagulation activation by hypothermia there appears to be a shift in the hemostatic balance towards thrombosis presumably as a consequence of endothelial cell injury by both hypothermia and stasis induced ischemia. There is evidence that widespread microvascular thrombus deposition may occur as a consequence of stasis in patients undergoing PHCA and that this might result in vascular occlusion and end organ damage. Although it is not uncommon to find laboratory evidence of disseminated intravascular coagulation (DIC) in patients presenting with aortic aneurysm rupture or dissection, the incidence of clinically overt DIC resulting in bleeding is low. The underlying hemostatic disturbance however may contribute to the surgery-associated bleeding diathesis.