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Published on: October 10, 2012
Coagulation disorders and neo-membrane formation in the pathogenesis of chronic subdural haematoma
K Rajeev1, B S Sharma1, N Marwaha1
1Department of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh - 160 012, India.
Haematological investigations in the haematoma fluid and venous blood along with histological changes in the haematoma membrane were studied in twenty five patients of chronic subdural haematoma. Their median age was 60 years with a marked male predominance. Haemoglobin level in the haematoma fluid was unrelated to its age. Prolongation of prothrombin time and activated partial thromboplastin time was observed in all the haematoma fluid samples. Fibrinogen and antithrombin III levels were significantly decreased in haematoma fluid and fibrin degradation products were positive in 44 of these specimens. The neo-membrane showed 'giant' capillaries and abundant eosinophils with an inverse relationship between the presence of inflammatory cells andfibroblasts. These findings suggest a localized consumption coagulopathy and hyperfibrinolysis with reactive formation of a leaky neo-membrane resulting in recurrent haemorrhages and progressive enlargement of chronic subdural haematoma.
Haematological investigations in the haematoma fluid and venous blood along with histological changes in the haematoma membrane were studied in twenty five patients of chronic subdural haematoma. Their median age was 60 years with a marked male predominance. Haemoglobin level in the haematoma fluid was unrelated to its age. Prolongation of prothrombin time and activated partial thromboplastin time was observed in all the haematoma fluid samples. Fibrinogen and antithrombin III levels were significantly decreased in haematoma fluid and fibrin degradation products were positive in 44 of these specimens. The neo-membrane showed 'giant' capillaries and abundant eosinophils with an inverse relationship between the presence of inflammatory cells andfibroblasts. These findings suggest a localized consumption coagulopathy and hyperfibrinolysis with reactive formation of a leaky neo-membrane resulting in recurrent haemorrhages and progressive enlargement of chronic subdural haematoma.
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