Introduction

A subarachnoid haemorrhage (SAH) is an intracranial haemorrhage that is defined as the presence of blood within the subarachnoid space, i.e. deep to the subarachnoid layer of the meninges.

Epidemiology

  • Incidence: 8.00 cases per 100,000 person-years
  • Peak incidence: 40-50 years
  • Sex ratio: more common in females 2:1
Condition Relative
incidence
Subarachnoid haemorrhage1
Idiopathic intracranial hypertension0.25
Central venous thrombosis0.11
<1 1-5 6+ 16+ 30+ 40+ 50+ 60+ 70+ 80+

Aetiology

The most common cause of SAH is head injury and this is called traumatic SAH . In the absence of trauma, SAH is termed spontaneous SAH . The rest of this note focuses on spontaneous SAH.

Causes of spontaneous SAH include:
  • Intracranial aneurysm* (saccular ‘berry’ aneurysms): this accounts for around 85% of cases. Conditions associated with berry aneurysms include adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta
  • Arteriovenous malformation
  • Pituitary apoplexy
  • Arterial dissection
  • Mycotic (infective) aneurysms
  • Perimesencephalic (an idiopathic venous bleed)

Clinical features

Classical presenting features include:
  • Headache: typically sudden-onset (‘thunderclap’ or ‘baseball bat’), severe (‘worst of my life’) and occipital
  • Nausea and vomiting
  • Meningism (photophobia, neck stiffness)
  • Coma
  • Seizures
  • Sudden death
  • ECG changes including ST elevation may be seen

Investigations

Confirmation of SAH:
  • Computed tomography (CT) head Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system. CT is negative for SAH (no blood seen) in 7% of cases.
  • Lumbar puncture (LP) Used to confirm SAH if CT is negative. LP is performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown). Xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure)
  • Referral to neurosurgery to be made as soon as SAH is confirmed

After spontaneous SAH is confirmed, the aim of investigation is to identify a causative pathology that needs urgent treatment:
  • CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM)
  • +/- digital subtraction angiogram (catheter angiogram)

Management

Treatment
  • The treatment in spontaneous SAH is in accordance with the causative pathology
  • Intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours
  • Most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
  • Until the aneurysm is treated, the patient should be kept on strict bed rest, well controlled blood pressure and should avoid straining in order to prevent a re-bleed of the aneurysm
  • Vasospasm is prevented using a 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature) and treated with hypervolaemia, induced-hypertension and haemodilution**
  • Hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculo-peritoneal shunt

Complications

Complications of aneurysmal SAH:
  • Re-bleeding (in around 30%)
  • Vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
  • Hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
  • Seizures

Prognosis

If SAH is untreated the prognosis is often poor: around 50% within 1 month of the
haemorrhage, and of those who survive the first month, 50% will remain dependent for help with activities of daily living. However, survival improves to 85% in patients with confirmed SAH admitted to a specialist neurosurgical unit.