Search

Introduction: The place of platelet antiaggregants in the aetiology of intracerebral hemorrhage (IH) has not been extensively studied., Objective: To analyze the characteristics of IH in patients treated with platelet antiaggregants and the possible clinical and prognostic differences from other primary IH., Patients and Methods: A retrospective study of patients admitted to hospital with primary IH from 1985 to 1997. The cases were IH patients while being treated with platelet antiaggregants. For each case we selected two controls with IH and similar age and IH risk factors. The following data was analyzed: start of clinical condition; type, dose, indication and duration of treatment with antiaggregants; mortality, localization, volume and extension of IH to the ventricles. The last four variables were compared with the control group using the ji squared test (chi 2) and the t student test., Results: 21one patients had a primary IH while being treated with antiaggregants: 20 with salicylates (17 aspirin and 3 riflusal) and one with ticlopidine. The dose of aspirin was 500 mg or less in 90% of the cases. In the group treated with salicylates, this was given for more than 20 months in 90% of the cases. Initially there was no clinical progression in any case. No significant differences were observed between the variable compared, although there was a tendency to greater volume, extension to the ventricles and mortality in the group treated with antiaggregants., Conclusions: More studies with larger numbers of patients are necessary to be able to confirm the tendencies observed.

The presence of intracranial hemorrhage with a fluid-blood level in patients receiving anticoagulant medication or with coagulopathy is an infrequent but well-documented complication. We reported a patient with a fluid-blood level with normal haemostasis. A 62-year-old-man was admitted with a left putaminal hemorrhage containing a fluid-blood level, but without abnormal haemostasis. Five months later the patient returned to the hospital because of a transient ischemic attack. A cranial CT demonstrated a hypodensity in the left putamen nucleus and corona radiata. Electrocardiogram revealed atrial fibrillation and a cardiac ultrasonographic examination showed mitral annulus calcification and left atrial enlargement. The finding of intracranial fluid-blood level has been seen in patients with arteriovenous malformations, primary and metastatic neoplasm, radiation-induced necroses, cerebral amyloid angiopathy, intrainfarct hematoma and without any identified aetiology. We suggest that in our patient this disorder was due to a intrainfarct hematoma.