2000 Volume 28 Issue 4 Pages 243-247
Intracranial hemorrhage is a common, potentially lethal complication of anticoagulant therapy including warfarization. Anticoagulant-related intracranial hemorrhage propounds a difficult clinical selection: maintaining anticoagulant therapy may extend the volume of the hematoma, early resumption of anticoagulation therapy may cause recurrence of hemorrhage, and correction of the coagulopathy may put patients at risk for thromboembolism involving the brain. Particularly, the risk of thromboembolic events may also be greater for patients with mechanical valves prosthesis in the mitral portion with atrial fibrillation. This dilemma on treatment of the patients exists because of a lack of data for a large series. We examined the medical records and CT scan findings for a consecutive group of patients admitted with non-traumatic anticoagulant-related intracerebral hematoma. We reviewed neurological presenting data, cardiac risk factors for systemic thromboembolism, and hospital management. We analyzed the management of warfarin-related intracerebral hemorrhages in 32 patients with cardiac disease, evaluating the degree of anticoagulation via the thrombotest. Anticoagulants were discontinued immediately after diagnosis of intracerebral hematoma was established by CT scan.
Patients with mechanical valve prosthesis patients, who required intensive long-term anticoagulant therapy, constituted the majority of our series (53.1%). Five patients had experienced previous transient ischemic attacks or minor strokes, and 19 had hypertension. The type of intracerebral hematoma was subcortical hematoma (n=13), thalamic hemorrhage (n=11), putaminal hemorrhage (n=4), pontine hemorrhage (n=3), or cerebellar hemorrhage (n=1). Vitamin K was administered in all patients and 3 who demonstrated low thrombotest values received FFP intraoperatively. Seven patients underwent evacuation of hematoma, and in 4 patients with thalamic hemorrhage accompanied by ventricular rupture ventricular drainage was carried out. Intraoperative hemostasis was brought under control at the time of surgery. However, in 1 patient, thalamic hematoma enlarged postoperatively with a fatal outcome within 6 days of surgery even without resumption of anticoagulant therapy. Early resumption of anticoagulant therapy (within 3 days) did not cause intracerebral rebleeding in any operative patients. Only 1 patient developed vertebrobasilar system infarction and died despite early resumption of anticoagulant therapy. Some of the subcortical hematoma patients had a good outcome.
Temporary interruption of anticoagulant therapy within 3 days seems safe for patients with intracerebral hematoma. Aggressive surgical intervention should particularly be performed in patients with anticoagulant-related subcortical hematoma, as in the case of anticoagulant-unrelated parenchymal hematoma.
