B Depreitere1, F Van Calenbergh, J van Loon. 1. Department of Neurosurgery, University Hospital Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium. bart.depreitere@uz.kuleuven.ac.be
Abstract
BACKGROUND: Non-traumatic acute subdural haematomas enable study of the morbidity and mortality due to the haematoma without the effect of trauma. Whereas it is known that coagulation disorders worsen the outcome of spontaneous intracerebral haematomas, this has not been studied in non-traumatic acute subdural haematomas. METHODS: In a series of 13 non-traumatic acute subdural haematomas admitted to our department between January 1995 and March 2002, we had 9 coagulopathy associated haematomas and 3 haematomas corresponding to the syndrome of 'spontaneous acute subdural haematoma of arterial origin'. Both groups were compared. FINDINGS: Age and gender distribution were comparable. The bleeding source was a cortical artery in 2 of the 2 non-coagulopathy related haematomas operated on, but also in 2 of the 4 coagulopathy associated haematomas that underwent surgery. The average haematoma thickness was higher in the coagulopathy related haematomas. The mean Glasgow Coma Score on admission was 7.7 and the mortality rate was 55.6% in the coagulopathy related group. In the non-coagulopathy related haematomas the mean Glasgow Coma Score was 12.0 and the mortality rate 33.3%. The latter mortality rate corresponds well to that of a historical group of 'spontaneous acute subdural haematomas of arterial origin' collected from the literature. INTERPRETATION: The outcome was worse in the non-traumatic acute subdural haematomas that were associated with a coagulation deficiency. While in all non-traumatic acute subdural haematomas the interval to surgery should be minimized, early recognition and urgent correction of coagulation deficiencies is certainly indicated.
BACKGROUND:Non-traumatic acute subdural haematomas enable study of the morbidity and mortality due to the haematoma without the effect of trauma. Whereas it is known that coagulation disorders worsen the outcome of spontaneous intracerebral haematomas, this has not been studied in non-traumatic acute subdural haematomas. METHODS: In a series of 13 non-traumatic acute subdural haematomas admitted to our department between January 1995 and March 2002, we had 9 coagulopathy associated haematomas and 3 haematomas corresponding to the syndrome of 'spontaneous acute subdural haematoma of arterial origin'. Both groups were compared. FINDINGS: Age and gender distribution were comparable. The bleeding source was a cortical artery in 2 of the 2 non-coagulopathy related haematomas operated on, but also in 2 of the 4 coagulopathy associated haematomas that underwent surgery. The average haematoma thickness was higher in the coagulopathy related haematomas. The mean Glasgow Coma Score on admission was 7.7 and the mortality rate was 55.6% in the coagulopathy related group. In the non-coagulopathy related haematomas the mean Glasgow Coma Score was 12.0 and the mortality rate 33.3%. The latter mortality rate corresponds well to that of a historical group of 'spontaneous acute subdural haematomas of arterial origin' collected from the literature. INTERPRETATION: The outcome was worse in the non-traumatic acute subdural haematomas that were associated with a coagulation deficiency. While in all non-traumatic acute subdural haematomas the interval to surgery should be minimized, early recognition and urgent correction of coagulation deficiencies is certainly indicated.
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