Brain, Vol. 124, No. 2, 249-278,
February 2001
© 2001 Oxford University Press
Invited review |
Subarachnoid haemorrhage: diagnosis, causes and management
Department of Neurology, University Medical Centre, Utrecht, The Netherlands
Correspondence to:
J. van Gijn, MD, Department of Neurology, University Medical Centre Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands E-mail: J.vanGijn{at}neuro.azu.nl
The incidence of subarachnoid haemorrhage (SAH) is stable, at around six cases per 100 000 patient years. Any apparent decrease is attributable to a higher rate of CT scanning, by which other haemorrhagic conditions are excluded. Most patients are <60 years of age. Risk factors are the same as for stroke in general; genetic factors operate in only a minority. Case fatality is ~50% overall (including pre-hospital deaths) and one-third of survivors remain dependent. Sudden, explosive headache is a cardinal but non-specific feature in the diagnosis of SAH: in general practice, the cause is innocuous in nine out of 10 patients in whom this is the only symptom. CT scanning is mandatory in all, to be followed by (delayed) lumbar puncture if CT is negative. The cause of SAH is a ruptured aneurysm in 85% of cases, non-aneurysmal perimesencephalic haemorrhage (with excellent prog nosis) in 10%, and a variety of rare conditions in 5%. Catheter angiography for detecting aneurysms is gradually being replaced by CT angiography. A poor clinical condition on admission may be caused by a remediable complication of the initial bleed or a recurrent haemorrhage in the form of intracranial haematoma, acute hydrocephalus or global brain ischaemia. Occlusion of the aneurysm effectively prevents rebleeding, but there is a dearth of controlled trials assessing the relative benefits of early operation (within 3 days) versus late operation (day 10–12), or that of endovascular treatment versus any operation. Antifibrinolytic drugs reduce the risk of rebleeding, but do not improve overall outcome. Measures of proven value in decreasing the risk of delayed cerebral ischaemia are a liberal supply of fluids, avoidance of antihypertensive drugs and administration of nimodipine. Once ischaemia has occurred, treatment regimens such as a combination of induced hypertension and hypervolaemia, or transluminal angioplasty, are plausible, but of unproven benefit.
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