Initial management of all patients with headache should include adequate analgesia, and antiemetics, if required. However, once a diagnosis of aneurismal SAH is established, the priorities shift to ensuring timely definitive treatment of the causative lesion. Meticulous attention is paid to resuscitation principles, in particular airway protection with rapid sequence induction if requiredand fluid resuscitation to euvolaemia with intravenous crystalloid, whilst trying to prevent the development of complications, particularly rebleeding and vasospasm
Aneurismal SAH has been demonstrated to have a rebleed rate of 2-4% in the first 24 hours and 15-20% in the first two weeks . After rebleeding the prognosis is very poor with many dying or permanently disabled.
Medical prevention of rebleeding
The administration of antifibrinolytics can reduce rebleeding but clinical outcomes are not affected and their use is not recommended following SAH . Though most clinicians would ensure bed rest, there is no good evidence that this practice reduces the rate of rebleeding. The AHA/ASA management guidance suggests that a systolic BP of >160mmHg should be controlled with a titratable agent to balance the risk of hypertension-related rebleeding and maintain cerebral perfusion pressure, however this should be discussed with your local neurosciences centre .
Surgical and endovascular prevention of rebleeding
The decision regarding definitive treatment of a ruptured aneurysm is taken with reference to the clinical grade of the patient, the presence of co-morbidities and relevant clinical anatomy. Where possible, aneurysm occlusion by endovascular coil embolisation or microsurgical aneurysm clipping is undertaken as soon as practicable (ideally within 72 hours) to prevent rebleeding.
For aneurysms amenable to both treatments, endovascular coiling is superior and has replaced surgical clipping in most cases (ARR 7% for dependency and death with sustained benefit at 7 years, NNT 14 (95%CI 9-25) [85,86].
When SAH is diagnosed, patients should be transferred promptly to a neurosciences centre with both endovascular and neurosurgical capabilities as clinical outcomes are better [80,81].
Vasospasm is a common but poorly understood entity that occurs with greatest frequency at 5-14 days  after the primary SAH. It may be asymptomatic and visible only as an angiographic phenomenon but in one third of patents  it is clinically apparent as delayed cerebral ischaemia (DCI) manifesting as focal neurological deficits or a reduction in level of conscious level . Unlike a thromboembolic stroke, clinical signs usually present gradually  and can occur across vascular territories . The main independent predictors of the development of vasospasm are the size of the SAH  and initial loss of consciousness .
A Cochrane review has demonstrated calcium channel antagonists, i.e. nimodipine 60 mg 4 hourly orally, to be effective in the prevention and treatment of cerebral vasospasm. Its use is associated with a significant improvement in clinical outcome . Magnesium sulphate may also have benefits  though further work is needed [18,46].
The role of antiplatelet agents  and statins  in the treatment of vasospasm is not clear and Cochrane reviews on the use of volume expansion , endothelin receptor antagonists  and corticosteroids  demonstrated no benefit.
The only medical treatment for vasospasm with proven clinical benefit is the administration of oral nimodipine 60 mg 4-hourly .
Other neurological complications
Other neurological complications include hydrocephalus which, if symptomatic, is best treated by ventriculostomy .
Sander Connolly, E et al. Guidance for the Management of Aneurysmal Subarachnoid Haemorrhage: A guideline for Healthcare professionals from the American heart Assosciation/American Stroke Association. Stroke. 2012;43:1711-1737