Subarachnoid Haemorrhage (SAH)
Subarachnoid haemorrhage (SAH) is an extra-axial intracranial haemorrhage occurring between the arachnoid and pia mater.
This updated UKMLA guide to SAH is based on NICE NG228, which covers causes, risk factors, symptoms, complications, diagnosis, and management.
Disclaimer:
This article focuses primarily on spontaneous aneurysmal subarachnoid haemorrhage, as this is the main form covered by NICE NG228 and international guidelines (e.g. AHA/ASA 2023 guideline). Non-aneurysmal causes are briefly mentioned for completeness, but detailed management depends on the underlying cause. Traumatic SAH is NOT the focus of this article.
Definition and Anatomy
Intracranial haemorrhage is a broad term referring to any bleeding within the skull (cranial vault). It can be categorised into:
| Extra-axial haemorrhage = bleeding outside the brain parenchyma | Intra-axial haemorrhage = bleeding within the brain parenchyma |
Which includes:
|
Which includes:
|
Overview of Intracranial Extra-Axial Haemorrhage
The 3 main extra-axial haemorrhages:
| Haemorrhage type | Location | Typical cause / source | Classic CT appearance | High-yield clinical presentation |
|---|---|---|---|---|
| Extradural haemorrhage (EDH) | Between the skull and dura | Middle meningeal artery | Biconvex / lens-shaped hyperdense mass | Head injury followed by a possible lucid interval, then rapid deterioration |
| Subdural haemorrhage (SDH) | Between the dura and arachnoid | Bridging veins | Crescent-shaped mass (hyperdense in acute; hypodense in chronic) | Confusion, focal neurology, reduced GCS, esp. in elderly, alcohol excess, anticoagulation use |
| Subarachnoid haemorrhage (SAH) | Between the arachnoid and pia | Ruptured aneurysm | Hyperdense signal in the sulci, fissures, or basal cisterns | Thunderclap headache, meningism, reduced GCS |
Causes and Risk Factors
Most spontaneous SAHs are caused by ruptured intracranial aneurysms [Ref]
Key risk factors include: [Ref]
- Hypertension and smoking – most important modifiable risk factors
- Non-modifiable factors
- Females
- >55 y/o
- Family history of cerebral aneurysms
- Presence of existing aneurysms
SAH can also be caused by other factors (but is not the focus of this article as explained above): [Ref]
- Vascular malformations
- Trauma
- Tumours (haemorrhage-prone tumours like glioblastoma)
Clinical Features
Classic and most prominent red-flag feature: thunderclap headache [Ref]
- An acute, severe headache that is sudden in onset, and
- Immediately reaches its maximal intensity (typically within 1-5 min)
Other features: [Ref]
- Warning / “sentinel” headache preceding the actual presentation
- Symptom onset during exertion
- Neck pain
- Neck stiffness / limited neck flexion
- Nausea and vomiting
- Photophobia
- Loss of consciousness
- Fever (often refractory to antipyretics)
Atypical presentations: [Ref]
- Primary neck pain
- Syncope
- Seizures
- New focal neurological deficits
SAH can overlap with meningitis clinically because blood in the subarachnoid space irritates the meninges, causing meningism.
SAH may present with “meningitis-like” features like neck stiffness, photophobia, nausea / vomiting.
The key difference is onset:
- SAH: sudden onset, severe thunderclap headache (maximal at onset or within minutes)
- Meningitis: usually more gradual headache with fever, systemic illness and infective symptoms
Complications
Key acute complications:
- Acute re-rupture and re-bleeding – highly fatal
- Hydrocephalus – common (seen in 15-87% cases)
- Delayed cerebral vasospasm and ischaemia – mostly occurs 4-14 days post-haemorrhage
- Seizures
- Cerebral oedema and raised ICP
- The acute phase is also highly associated with systemic medical complications
- Hyponatraemia and hypovolaemia
- ARDS and respiratory failure
- VTE
- Cardiac arrhythmias, neurogenic myocardial stunning (→ cerebral T waves: widespread, inverted T waves)
Key chronic complications:
- Persistent hydrocephalus
- Seizure and epilepsy
- Cognitive impairment and dementia
- Psychological disorders (e.g. depression, anxiety, PTSD)
Investigation and Diagnosis
The diagnostic pathway can be split into 2 steps:
- Confirming SAH
- Assess whether SAH is aneurysmal or non-aneurysmal (i.e. whether an aneurysm caused the SAH)
1. Confirming SAH
1st line test: non-contrast CT head to be performed ASAP
- Typical CT findings → diagnose SAH with no further tests
- Inconclusive CT → subsequent actions depend on the timing of the scan
Typical CT head findings in SAH: hyperdense signal (blood) in the cerebral sulci and basal cisterns (esp. around the circle of Willis)
If the initial CT is inconclusive (i.e. not diagnostic of SAH):
- If the scan is done within 6 hours → consider alternative diagnosis (SAH unlikely)
- If the scan is done after 6 hours → perform a lumbar puncture at least 12 hours after symptom onset
- If lumbar puncture is +ve → diagnose SAH
- If lumbar puncture is -ve → consider alternative diagnosis (SAH unlikely)
Lumbar puncture findings in SAH: elevated bilirubin (xanthochromia) in the CSF, on spectrophotometry
Why should the lumbar puncture be performed 12 hours after? It takes time for blood to be broken down into bilirubin to give xanthochromia in the CSF
3 tubes of CSF are collected to assess for SAH vs traumatic tap
- SAH is diagnosed by the presence of xanthochromia
- Traumatic tap is suggested by declining RBC count across tube 1 to 3
Note that CSF RBC counts CANNOT be used to diagnose SAH, as no RBC cut-offs reliably diagnose SAH.
In short, SAH can be diagnosed in the following scenarios:
- Initial CT head showing typical SAH findings
- Inconclusive initial CT head that is performed >6 hours after symptom onset PLUS a +ve lumbar puncture (xanthochromia), that is performed >12 hours after symptom onset
Rationale:
- The diagnostic accuracy of non-contrast CT head for SAH is highest within 6 hours of symptom onset.
- After 6 hours, CT is less reliable in diagnosing SAH, therefore a lumbar puncture is needed
2. Detecting an Aneurysm
Once diagnosed with SAH, urgently discuss with a specialist neurosurgical centre the need for transfer of care.
The following should be performed without delay once SAH is confirmed:
- 1st line: CT angiography
- 2nd line: MR angiography / digital subtraction angiography
Purpose: to identify an underlying ruptured intracranial aneurysm and guide treatment planning.
It is important to determine whether SAH is secondary to a ruptured aneurysm or not, as it would affect management.
Management
As noted above, this article focuses only on SAH secondary to ruptured intracranial aneurysm, in line with NICE and major international guidelines.
Pharmacological Management
- Ensure sufficient analgesia (opioids might be necessary)
- Consider nimodipine
- A calcium channel blocker that aims to prevent delayed cerebral vasospasm and ischaemia
- Oral route preferred over IV
Do not offer pharmacological VTE prophylaxis until the lesion has been secured or the condition has stabilised.
Definitive Aneurysm Management
Options to manage the underlying aneurysm:
| Management | Description | Indications [Ref] |
|---|---|---|
| Endovascular coiling (accounts for ~75% of interventions in current practice) | A minimally invasive procedure performed by an interventional neuroradiologist.
A catheter is passed through the blood vessels to reach the aneurysm, and small coils are deployed into the aneurysm sac. This promotes thrombosis within the aneurysm, helping to seal it off from the circulation and reduce the risk of rebleeding. |
Preferred in:
|
| Neurosurgical clipping | An open neurosurgical procedure performed via craniotomy.
A clip is placed across the neck of the aneurysm to exclude it from the circulation while preserving flow through the parent artery. |
Preferred in:
|
| No interventional procedure | Regular monitoring to check for clinical improvement and reassess treatment options | When the patient suffered irreversible and devastating neurological injury and is deemed unsalvageable, indicators include:
|
If interventional treatment is planned, it should be carried out ASAP to prevent rebleeding, as the risk is highest within 24 hours of onset.
Disclaimer:
Regarding the choice between endovascular coiling and neurosurgical clipping, NICE does not explicitly state a preferred approach. Instead, it recommends that the treatment options should be discussed by an interventional neuroradiologist and a neurosurgeon, taking into account the aneurysm characteristics, patient-specific factors, and local availability of expertise.
The information in the “indications” column is based on the AHA/ASA guideline and is included to provide additional context and completeness. [Ref]
Complication Management
Management of key complications: [Ref]
| Complication | Management |
|---|---|
| Hydrocephalus | Acute symptomatic cases:
Chronic symptomatic cases:
|
| Delayed cerebral vasospasm and ischaemia | Prevention:
Active treatment:
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