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The fluid-blood level in intracranial haematoma due to anticoagulant medication.

Sir: The occurrence of intracranial haemorrhage in patients receiving anticoagulant medication is a well-documented complication.' This complication most commonly occurs in patients with poorly controlled haemostasis. Intracranial haemorrhage may also occur in anticoagulated patients with carefully controlled haemostasis as manifested by coagulation results (bleeding time, prothrombin time, partial thromboplastin time) which are within the accepted therapeutic range. I wish to describe the fluid-blood level in five anticoagulated patients with intracranial haemorrhages. A typical case history is that of a 57 year old normotensive woman with a history of two prior myocardial infarctions and was admitted to hospital because of substernal chest pain. Electrocardiogram was consistent with new acute ischaemic changes. Her blood pressure was 130/70mm Hg. She was neurologically normal. She was treated with a loading dose of intravenously administered streptokinase and heparin. Her prothrombin time (180 seconds with normal of 20 seconds) and partial thromboplastin time (180 seconds with normal of 50 seconds) became markedly elevated. The dose of streptokinase was reduced and the heparin was discontinued. Despite this, 4 hours later she suddenly became unresponsive, right hemiplegic, apnoeic with no response to noxious stimulation, negative dolls head and negative caloric response, fixed and dilated pupils. CT was immediately performed and showed a large left hemisphere intracerebral haemorrhage with a fluid-blood level (fig). The patient died 4 hours later and no necropsy was performed. In patients with normal haemostasis who develop an intracranial haemorrhage, CT showsa homogeneously nonenhancing hyperdense lesion in the acute stage. In certain anticoagulated patients, the appearance of the acute haematoma may be different, with the finding of a fluid-blood interface which is unique for this condition.2 It is believed that the fluid seen above the haematoma represents plasma; the layering is a sedimentation effect. This appearance of layering within the haematoma was seen in all our patients. This fluid-blood interface occurred when there was not adequate hemostasis. When anticoagulant medication was discontinued and coagulation studies returned to normal, CT showed hyperdense hematoma without the fluid-blood interface. This change was seen in two of these patients. J