Related Subjects:
|Hypertension
|Subarachnoid Haemorrhage
|Perimesencephalic Subarachnoid haemorrhage
|Haemorrhagic stroke
|Acute Stroke Assessment (ROSIER&NIHSS)
π₯ The main cause of subarachnoid haemorrhage (SAH) is rupture of a berry aneurysm. Any sudden "thunderclap headache" should be considered SAH until proven otherwise. See the SAH management topic for full details.
π§ Introduction
- Berry (saccular) aneurysms are developmental vascular abnormalities of the Circle of Willis and its branches.
- Causes include inherited connective tissue weakness, anatomical defects, and abnormal haemodynamic flow.
- Not present at birth but may appear in early adulthood, enlarge, and rupture later in life.
- Account for ~5% of all strokes but with high mortality and morbidity.
- Most remain asymptomatic lifelong; a minority rupture, causing subarachnoid haemorrhage (SAH).
πΌοΈ Images
β οΈ Presentation
- π₯ Sudden βthunderclapβ headache or collapse due to SAH β emergency referral to neurosurgery.
- 70β80% of non-traumatic SAH cases are from aneurysmal rupture.
- π Sentinel bleeds: up to 50% report a sudden severe headache days/weeks before rupture.
- Pressure effects from large aneurysms may cause cranial nerve palsies (e.g. IIIrd nerve palsy with PCoA aneurysm).
- Asymptomatic aneurysms may be detected incidentally or through family screening.
π Anatomy
- Aneurysms have a neck and dome. Rupture usually occurs from the dome.
- Typically form at arterial bifurcations where the media and internal elastic lamina are deficient.
- Often develop mural thrombus and become irregular with growth.
π Risk Factors
- Smoking π¬ and Hypertension.
- Age >40, female sex, family history of aneurysms.
- Larger aneurysm size and location (posterior circulation, basilar apex, PCoA) increase rupture risk.
π€ Associations
- ADPKD (Autosomal Dominant Polycystic Kidney Disease).
- Ehlers-Danlos type IV, Marfan syndrome.
- Coarctation of the aorta, bicuspid aortic valve.
- NF1, hereditary haemorrhagic telangiectasia, Ξ±1-antitrypsin deficiency.
π Common Sites
| Anterior Circulation (90%) | Posterior Circulation (10%) |
- Anterior communicating artery (ACoA): 30β40%
- Supraclinoid ICA & ICA/PCoA junction: ~30%
- MCA bifurcation (M1/M2): 20β30%
|
- Basilar tip
- Superior cerebellar artery
- Posterior inferior cerebellar artery (PICA)
|
π©» Imaging
- Non-contrast CT: Detects SAH acutely; CTA follows if aneurysm suspected.
- CT Angiography (CTA): First-line in most UK centres; quick and widely available.
- MRI/MRA: Shows aneurysms as flow voids; good for follow-up.
- Digital Subtraction Angiography (DSA): Gold standard for small/complex aneurysms and planning intervention.
π©Ί Treatment & Prognosis
All ruptured aneurysms require urgent treatment (usually within 24h). Small, incidental aneurysms <7mm are often observed unless symptomatic or high-risk. Mortality after aneurysmal SAH is ~30β40% at 1 month.
| π Five-Year Rupture Risk (ISUIA Study) |
| Size | <7 mm | 7β12 mm | 13β24 mm | >24 mm |
| Intracavernous ICA | 0% | 0% | 3% | 6.4% |
| Other ICA, MCA, ACA | 1.5% | 2.6% | 14.5% | 40% |
| Posterior circulation | 3.4% | 14.5% | 18.4% | 50% |
π οΈ Treatment Options
- Endovascular Coiling π: Minimally invasive, avoids craniotomy. Preferred if anatomy is suitable. ISAT trial showed better 1-year outcomes than clipping.
- Surgical Clipping βοΈ: Craniotomy and aneurysm clipping. Effective but carries procedural risk and higher vasospasm rates.
- Supportive: Nimodipine for vasospasm prophylaxis, neurocritical care, BP control.
Other Aneurysms
- Fusiform: Elongated spindle-shaped aneurysms, often basilar artery. Rarely rupture, mainly compressive symptoms.
- Mycotic: Infective emboli (endocarditis). Risk of infarcts/abscess; treat underlying infection.
π References
- ISUIA: International Study of Unruptured Intracranial Aneurysms.
- ISAT Trial: Lancet 2002 β better outcomes with coiling.
- NICE Guidance: Stroke and TIA (NG128, 2019); SAH management pathways.