HEMATOLOGICAL CONSEQUENCES OF PROFOUND HYPOTHERMIC CIRCULATORY ARRESTAND AORTIC DISSECTION

The lower temperatures utilized during profound hypothermic circulator y arrest (PHCA) surgery may exacerbate the hypothermia associated plat elet and clotting factor dysfunction observed in conventional cardiopu lmonary bypass (CPB) procedures. Hypothermia has been shown to impair the activity of the enzymes involved in the platelet activation pathwa ys and to reduce the enzymatic activity of clotting factors upon coagu lation activation. The resulting retardation of the generation of fibr in/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 i s good evidence that the fibrinolytic activity, mediated predominantly by tissue plasminogen activator (tPA), is a secondary response to thr ombin generated by coagulation activation, which is ongoing during CPB despite full heparinization. The effects of hypothermia on the fibrin olytic response remain to be clarified and the extent to which the low er temperatures and blood stasis associated with PHCA moderate this re sponse is unknown. Despite impairment of coagulation activation by hyp othermia 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 w idespread microvascular thrombus deposition may occur as a consequence of stasis in patients undergoing PHCA and that this might result in v ascular occlusion and end organ damage. Although it is not uncommon to find laboratory evidence of disseminated intravascular coagulation (D IC) in patients presenting with aortic aneurysm rupture or dissection, the incidence of clinically overt DIC resulting in bleeding is row. T he underlying hemostatic disturbance however may contribute to the sur gery-associated bleeding diathesis.