Subarachnoid haemorrhage: diagnosis, causes and management

Citation
J. Van Gijn et Gje. Rinkel, Subarachnoid haemorrhage: diagnosis, causes and management, BRAIN, 124, 2001, pp. 249-278
Citations number
292
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
BRAIN
ISSN journal
00068950 → ACNP
Volume
124
Year of publication
2001
Part
2
Pages
249 - 278
Database
ISI
SICI code
0006-8950(200102)124:<249:SHDCAM>2.0.ZU;2-1
Abstract
The incidence of subarachnoid haemorrhage (SAH) is stable, at around six ca ses per 100 000 patient years. Any apparent decrease is attributable to a h igher rate of CT scanning, by which other haemorrhagic conditions are exclu ded, Most patients are <60 years of age. Risk factors are the same as for s troke in general; genetic factors operate in only a minority, Case fatality is <similar to>50% overall (including pre-hospital deaths) and one-third o f survivors remain dependent, Sudden, explosive headache is a cardinal but non-specific feature in the diagnosis of SAH: in general practice, the caus e is innocuous in nine out of 10 patients in whom this is the only symptom. CT scanning is mandatory in all, to he followed by (delayed) lumbar punctu re if CT is negative. The cause of SAH is a ruptured aneurysm in 85% of cas es, non-aneurysmal perimesencephalic haemorrhage (with excellent prognosis) in 10%, and a variety of rare conditions in 5%, Catheter angiography for d etecting aneurysms is gradually being replaced by CT angiography, A poor cl inical condition on admission may be caused by a remediable complication of the initial bleed or a recurrent haemorrhage in the form of intracranial h aematoma, acute hydrocephalus or global brain ischaemia, Occlusion of the a neurysm effectively prevents rebleeding, but there is a dearth of controlle d trials assessing the relative benefits of early operation (within 3 days) versus late operation (day 10-12), or that of endovascular treatment versu s 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, avoidanc e of antihypertensive drugs and administration of nimodipine. Once ischaemi a has occurred, treatment regimens such as a combination of induced hyperte nsion and hypervolaemia, or transluminal angioplasty, are plausible, but of unproven benefit.