Pathophysiology

In most cases of SAH, the bleed is arterial with free communication between blood at arterial pressure and the subarachnoid space resulting in the characteristic abrupt onset of symptoms especially headache and loss of consciousness.

It has been proposed that perimesencephalic bleeds may be venous [20], the lower pressures causing a slower onset of symptoms and a smaller haemorrhage thus resulting in a better clinical picture and outcome.

The spread of blood in the subarachnoid space can lead to:

• Meningism
• Hydrocephalus
• Intraventricular haemorrhage
• Cerebral oedema
• Raised intracranial pressure (ICP)

In those patients who survive the initial insult, rebleeding and vasospasm are the major causes of morbidity and mortality. Attempts to prevent rebleeding (that is often catastrophic) are primarily directed at the timely identification and treatment of the cause of the SAH (usually an aneurysm).

Vasospasm can be apparent radiologically or clinically [21] and is a difficult phenomenon to understand. Though many theories have been postulated the only consistent predictor is that the severity of the vasospasm is related to the size of the haemorrhage [21].

Learning Bite

In patients who survive the initial haemorrhage the primary complications are rebleeding and vasospasm [14].

Other frequent complications of SAH include neurogenic cardiac dysfunction and electrolyte problems, particularly hyponatraemia, hyperglycaemia and hypomagnesaemia. Though these can be treated individually, the primary goal should always be the treatment of the anatomical cause for the SAH [11].