Based on smear morphology and the red blood cell indices (mean cell volume [MCV], mean cell hemoglobin [MCH], mean corpuscular hemoglobin concentration [MCHC]), the patient has a severe microcytic, hypochromic….
Complete replacement of circulating platelets
The prolonged collagen/epinephrine PFA closure time, together with a normal collagen/ADP PFA closure time, is indicative of a platelet-based coagulopathy, namely inhibition by aspirin. However, concurrent type I von Willebrand disease, worsened by aspirin therapy, cannot be fully excluded given the setting of acute trauma causing an acute phase reaction. A diagnostic workup for vWD (including ristocetin cofactor activity, vWF antigen, and factor VI II activity) must wait until the patient is fully convalescent. Since aspirin irreversibly blocks platelet cyclooxygenase function, and the patient has been taking aspirin on a daily basis, nearly all of the platelets in circulation can be assumed to be affected. Depending on the severity of the defect in platelet function, this can lead to excessive bleeding with surgery or trauma and may have exacerbated the subdural hemorrhage. Moreover, the aspirin effect on platelets is irreversible, so that platelet function will only normalize as new platelets, not exposed to aspirin, enter the circulation. This will obviously take several days-a delay which is not tolerable in this patient. The aspirin inhibition must be overcome by increasing the general procoagulant platelet function. This can, in part, be accomplished by increasing the von Wille brand factor concentration in blood through transfusion of vWF product or administration of DDAVP. However, complications of DDAVP include hyponatremia and hypertension, both of which may be problematic in a patient with subdural hematoma. The best option in this patient is the transfusion of normal platelets. Complete replacement of circulating platelets is not necessary. For most surgeries or mild to moderate trauma, a single platelet transfusion will supply at least 10% of circulating platelets, which is enough to normalize the PFA and restore adequate platelet function. For neurosurgery, where bleeding into a closed space can be devastating, transfusion of 2 U of pooled platelets should provide extra insurance against postoperative bleeding. In this case, the patient received 2 U of pooled platelets prior to surgery; the hematoma was successfully evacuated, and there was no further bleeding.