Intracranial Aneurysm & Subarachnoid Haemorrhage
Berry Aneurysm · Thunderclap Headache · Clipping vs Coiling · Vasospasm
An intracranial aneurysm is a focal outpouching of an arterial wall at bifurcation points of the Circle of Willis, due to a defect in the internal elastic lamina. Rupture causes subarachnoid haemorrhage (SAH) — blood entering the subarachnoid space. SAH carries 30-day mortality of ~45%; ~30% die before reaching hospital. Survivors face vasospasm (days 4–14), rebleeding, and delayed ischaemia.
"Worst headache of my life" reaching peak intensity within 60 seconds. No other diagnosis acceptable until: CT head within 6h (sensitivity 97–99%) + LP at 12h if CT negative. Do NOT dismiss as "just a tension headache."
Hunt & Hess Grade (Prognosis)
| Grade | Clinical Features | Surgical Risk | Expected Outcome |
|---|---|---|---|
| Grade I | Asymptomatic or mild headache | Low | 70% good outcome |
| Grade II | Moderate-severe headache, meningism, no deficit | Low-moderate | 60% good outcome |
| Grade III | Drowsy, confusion, mild focal deficit | Moderate | 50% good outcome |
| Grade IV | Stupor, moderate-severe hemiparesis | High | 20% good outcome |
| Grade V | Deep coma, decerebrate posturing | Very high | <10% good outcome |
Microsurgical clipping places a permanent titanium clip across the aneurysm neck, permanently excluding it from circulation. Offers durable, complete obliteration.
- Craniotomy + sylvian fissure dissection + Yasargil clip placement under Zeiss microscope
- Complete obliteration rate: 95–99% for well-placed clips
- Preferred for: young patients (<45 years), middle cerebral artery (MCA) aneurysms, large/wide-neck aneurysms, anterior communicating artery with complex anatomy
- ISAT trial: coiling superior for PICA/posterior circulation; equally good for MCA at experienced centres
- At BVH: Yasargil clip systems available; Zeiss microscope operational; clipping performed for all accessible aneurysms
- Endovascular coiling — platinum coils deployed through microcatheter into aneurysm sac via femoral artery approach; no craniotomy
- ISAT trial showed coiling superior to clipping for ACoA aneurysms: 7.4% vs 10.1% dependency/death at 1 year
- Flow diverter (Pipeline) — for fusiform/large/giant aneurysms; parent artery covered stent
- Limitations: higher recanalization rate (20% at 5 years); requires repeat angiogram surveillance
- Available in Lahore/Karachi (NIHD, AKUH); refer for endovascular if coiling preferred
- Nimodipine 60mg PO q4h × 21 days — Calcium channel blocker; reduces vasospasm risk, improves neurological outcome (Level I evidence). Do not delay
- Normovolaemia — Previously triple-H (hypertension, hypervolaemia, haemodilution) abandoned; euvolaemia now recommended
- Antifibrinolytic therapy — Tranexamic acid 1g IV q6h × 72h reduces rebleeding if surgery delayed; discontinue once aneurysm secured
- ICP management — EVD for hydrocephalus (40% of SAH patients); target ICP <20mmHg
- Antiepileptic — Levetiracetam 500mg BD; phenytoin avoided (worse cognitive outcomes)
- BP management — Target SBP <160mmHg pre-treatment; avoid hypotension post-clipping
Cerebral vasospasm: arterial narrowing days 4–14 post-SAH causing delayed cerebral ischaemia (DCI). Clinically: new focal deficits, declining consciousness. TCD monitoring for velocity rise.
- Induced hypertension — Once aneurysm secured: norepinephrine to SBP 160–200mmHg for clinical vasospasm
- Endovascular treatment — Intra-arterial verapamil or papaverine; balloon angioplasty for refractory severe vasospasm
- Statins — Simvastatin 80mg/day during admission may reduce vasospasm (mixed evidence; some centres use routinely)
- Clazosentan — Endothelin-1 antagonist; reduces angiographic vasospasm (Phase III), not yet widely available
Management of incidentally discovered unruptured intracranial aneurysms (UIA) depends on size, location, morphology, patient age, and comorbidities.
| Aneurysm Size | Location | Annual Rupture Risk | Recommendation |
|---|---|---|---|
| <5mm | Anterior circulation | <0.5%/year | Observation + risk factor modification |
| 5–10mm | Any | 1–2%/year | Shared decision-making; consider treatment if young patient |
| >10mm or posterior circulation | PCA, basilar, PICA | 3–6%/year | Treatment recommended |
| Any with "daughter dome" | Any | Higher risk morphology | Treatment strongly recommended |
References — Aneurysm
- ISAT 2002 Molyneux A et al. International subarachnoid aneurysm trial. Lancet 2002;360:1267–74
- Barrow Brain Aneurysm Program. barrowneuro.org
- Mayo Clinic Brain aneurysm. mayoclinic.org
Cerebral Venous Sinus Thrombosis (CVST)
Dural Venous Sinus Occlusion · Post-Partum High Risk · Anticoagulate Even with Haemorrhage
CVST is thrombosis of the cerebral dural venous sinuses (superior sagittal sinus most commonly), causing venous hypertension, cerebral oedema, venous infarction, and haemorrhage. Young women in the postpartum period (up to 6 weeks post-delivery) represent the highest risk group. Annual incidence: 3–4 per million. Prognosis is favourable with early anticoagulation — even in the presence of haemorrhage.
CVST with haemorrhagic venous infarct: anticoagulation is STILL recommended and improves outcomes. The haemorrhage is a consequence of venous hypertension — treating the clot prevents further haemorrhage. This counterintuitive principle is supported by Level B evidence (EFNS Guidelines, Coutinho et al).
Signs & Symptoms
Diagnosis
May show hyperdense sinus ("cord sign"), haemorrhagic venous infarct, cerebral oedema. Normal CT does NOT exclude CVST.
MRI demonstrates parenchymal changes; MRV (magnetic resonance venography) directly visualises sinus occlusion. Best sequence: T1 with contrast + TOF MRV. Sensitivity >95%.
D-dimer elevated but non-specific. Full thrombophilia workup: antiphospholipid antibodies, factor V Leiden, prothrombin G20210A, protein C/S, antithrombin III. Ideally draw before starting anticoagulation.
Postpartum, OCP use, dehydration, infections (mastoiditis → sigmoid sinus thrombosis), malignancy, IBD, haematological disorders.
Anticoagulation is the cornerstone of CVST management — even in the presence of haemorrhagic infarction (Level IIa, AHA/ESO).
- Acute: LMWH (Clexane/Enoxaparin) — 1mg/kg SC BD (therapeutic dose). Start immediately on diagnosis. Safe in haemorrhagic CVST. Monitor anti-Xa levels. Continue until transition to oral anticoagulation
- Oral maintenance: Warfarin — Target INR 2.0–3.0. Duration: 3–6 months for provoked CVST; 6–12 months for unprovoked; indefinite for recurrent thrombosis or thrombophilia
- Warfarin preferred over DOACs for breastfeeding — Warfarin does not transfer significantly into breast milk; safe for breastfeeding mothers (BNF, WHO recommendation). DOACs (rivaroxaban, dabigatran, apixaban) are not recommended during breastfeeding
- DOAC alternative (non-breastfeeding) — Dabigatran (RE-SPECT CVST trial) shows non-inferiority to warfarin; avoids INR monitoring. Use after acute LMWH phase
- Seizure prophylaxis: Levetiracetam 500–1000mg BD for all CVST with cortical involvement or haemorrhage
- Duration: typically 3–6 months; EEG guidance for discontinuation
- Valproate: effective but avoid in women of childbearing potential (teratogenicity)
- Status epilepticus: IV lorazepam → IV levetiracetam → anaesthetic agents if refractory
- Catheter-directed thrombolysis — For rapidly deteriorating patients despite anticoagulation; urokinase or tPA into affected sinus. Rescue therapy only; significant haemorrhage risk
- Mechanical thrombectomy — Thrombectomy devices for large sinus occlusion; emerging evidence
- Decompressive craniectomy — For large haemorrhagic venous infarct with herniation; life-saving in extremis
- ICP management — Acetazolamide 250mg BD for papilloedema; CSF drainage (LP) for severe ICP; avoid ventriculostomy if large venous infarct
Post-partum CVST is a recurring presentation at BVH. Superior sagittal sinus thrombosis with haemorrhagic venous infarct is the most common pattern. Anticoagulation with Clexane (Sanofi/Hoechst Pakistan Limited) initiated immediately, transitioned to warfarin for breastfeeding safety. INR monitoring every 2 weeks initially. Full thrombophilia workup sent to Chughtai Lab or AKUH.
- Avoid dehydration, restrict OCP use post-recovery
- Future pregnancies: LMWH prophylaxis throughout pregnancy and 6 weeks post-partum
- Recurrence risk in subsequent pregnancy: ~1–2% with LMWH prophylaxis
References — CVST
- EFNS 2010 Einhaupl K et al. EFNS Guideline on CVST. Eur J Neurol 2010;17:1229–35
- RE-SPECT Ferro JM et al. Dabigatran vs Warfarin in CVST. NEJM 2019;380:1820–29
- Cleveland Clinic Cerebral Venous Thrombosis. my.clevelandclinic.org
Ischaemic Stroke & Malignant MCA Infarction
FAST Assessment · tPA · Thrombectomy · Decompressive Hemicraniectomy
Ischaemic stroke is caused by thrombotic or embolic occlusion of cerebral arteries. MCA territory infarction is most common (80%). "Malignant" MCA infarction (complete MCA territory) causes massive cerebral oedema, herniation, and 80% mortality without surgical intervention. Decompressive hemicraniectomy within 48h reduces mortality by ~50% and improves functional outcomes in patients <60 years.
Face drooping · Arm weakness · Speech slurring · Time to call emergency. tPA window: 4.5 hours from onset. Thrombectomy: up to 24h for selected patients. Every 15 minutes of delay = 2 million neurons lost.
- IV tPA (Alteplase 0.9mg/kg, max 90mg) — Within 4.5h of onset in selected patients (no haemorrhage, BP <185/110, no recent major surgery). Absolute contraindications: haemorrhage, recent surgery, anticoagulation with therapeutic INR
- Mechanical thrombectomy — Stent retriever or aspiration; superior to tPA alone for large vessel occlusion (LVO). Available at NIHD Karachi, AKUH; Lahore centres developing capacity
- Antiplatelets — Aspirin 300mg immediately if tPA not given; loading dose followed by 75–100mg OD. Dual antiplatelet (aspirin + clopidogrel) × 21 days for minor stroke/TIA (POINT trial)
- BP management — <185/110 before tPA; <220/120 if no thrombolysis (permissive hypertension maintains penumbra); aggressive lowering increases infarct
DESTINY II / HAMLET trials: Decompressive hemicraniectomy within 48h of malignant MCA infarction reduces mortality from 78% to 29% (NNT = 2). Strong evidence for patients ≤60 years.
- Large (≥10cm) hemicraniectomy removing temporal bone for temporal lobe swelling accommodation
- Duraplasty with pericranial graft to allow brain expansion
- Cranioplasty (bone flap replacement) 8–12 weeks later after brain swelling resolved
- Age limit: <60 years (strong evidence); 60–80 years (informed consent for increased survival with dependency)
- Available at BVH; performed using Hudson brace + Gigli saw (manual technique) pending craniotome restoration
- Aspirin 75mg OD — Long-term antiplatelet. Add dipyridamole MR (Aggrenox) for additional 22% relative risk reduction (ESPS-2)
- Clopidogrel (Plavix Plus) — Sanofi; for aspirin intolerance or combined aspirin+clopidogrel after high-risk TIA/minor stroke × 21 days then monotherapy
- Anticoagulation — For cardioembolic stroke (AF): warfarin INR 2–3 or DOAC (apixaban/dabigatran). Start 1–2 weeks post-stroke after haemorrhagic transformation risk declines
- Statin therapy — High-intensity statin (atorvastatin 80mg) regardless of baseline LDL; reduces recurrent stroke 25–30%
- BP control — Target <130/80mmHg; ACE inhibitor + thiazide diuretic combination most evidence (PROGRESS trial)
- Glycaemic control — Hyperglycaemia worsens stroke outcomes; target normoglycaemia 6–10 mmol/L in acute phase
- Early mobilisation (within 24h if haemodynamically stable) — reduces DVT, pneumonia, depression
- Physiotherapy: gait retraining, spasticity management, constraint-induced movement therapy (CIMT)
- Speech and language therapy: for dysphasia and dysphagia (swallowing assessment mandatory before oral feeding)
- Occupational therapy: ADL retraining, home modification assessment
- Botulinum toxin for post-stroke spasticity: effective for focal upper limb spasticity
References — Stroke
- DESTINY II Juttler E et al. Hemicraniectomy in older patients. NEJM 2014;370:1091–1100
- MGH Stroke Center. massgeneral.org
- AHA/ASA 2019 Powers WJ et al. 2019 AHA/ASA Stroke Guidelines. Stroke 2019