Article Text

Download PDFPDF
  1. P J Kirkpatrick
  1. Correspondence to:
 Mr PJ Kirkpatrick, Academic Neurosurgery Unit, Level 4, A Block, Box 167, Addenbrooke’s Hospital, Hills Road, Cambridge CB2 2QQ, UK;

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

The incidence of stroke caused by subarachnoid haemorrhage (SAH) remains constant, with intracranial aneurysm rupture causing SAH in up to 5000 patients in the UK per annum. Although this represents less than 5% of all strokes, recognition is of crucial importance since intervention can radically alter outcome. The combined mortality and morbidity for aneurysm rupture reaches 50%; since the condition can affect individuals at any age, long term morbidity in survivors can be substantial.1 Failure to diagnose SAH exposes a patient to the fatal effects of a further bleed, and also to complications which can now be avoided or successfully treated.2,3


SAH refers to a leakage of blood into the subarachnoid spaces (fig 1A) which is a continuous space between the supratentorial and infratentorial compartments. A greater concentration of blood products around the site of the bleed is usual, but SAH originating from a focal source can be more diffuse and spread throughout wider aspects of the subarachnoid space. Haemorrhage can extend into adjacent parenchymal structures (fig 1B) and ventricular system, with associated high morbidity and mortality (fig 1C).

Figure 1

(A) Computed tomographic (CT) scan with diffuse subarachnoid blood maximum in the left Sylvian fissure (arrow). (B) CT scan showing collection of blood in the right Sylvian fissure. A giant aneurysm is seen in this location (arrow). (C) CT scan showing extensive intraventricular blood from rupture of anterior communicating aneurysm.

Inflammatory processes (table 1), excited by the presence of red cell breakdown products, affect the large vessels of the circle of Willis and smaller vessels within the subpial space.4 These processes are complex, but combine to impair the adequate distribution of blood to affected territories. Cerebral ischaemia, often delayed by several days, is a common occurrence and major source of cerebral injury (fig 2).

View this table:
Table 1

Inflammatory consequences of …

View Full Text