- Subarachnoid Haemorrhage
Link:ceaccp.oxfordjournals.org/content/13/2/52.full.pdf
- Cause of 5% of strokes, 10/100,000 people per yr - peak incidence 40-60yrs
- 50% mortality, 25% die before reaching hospital. 1/3 of survivors will be dependent ant 1/2 will have cognitive impairment
- Causes
- Aneurysmal in 85% (genetic association with APCKD, Ehlers Danlos)
- Rarer causes include AVMs & trauma
- Contributed to by HT, smoking, cocaine use,
- Clinical features & Ix
- Classic thunderclap headache, neck stiffness, photophobia, LOC, focal neurology, possible cardiac arrest
- CT will pick up 95% of cases on first day
- LP at 12h after onset of symptoms may be indicated if CT is negative and SAH is still suspected to look for xanthochromia
- A CT angio may look for the cause of SAH (most sensitive for >4mm in size) and a DSA may be done if further Ix is needed
- Management
- Initial assessment and management is similar to other forms of acute brain injury (CO2 4.5-5kPa, pO2 >13kPa)
- Extreme hypertension must be managed (aim SBP<160, MAP <110) as well as hypotension (SBP <100 is detrimental)
- Risk of re-bleed is highest in first 72h, and in females, and poor grade haemorrhages
- Risk of re-bleeding reduced by minimising changes in transmural pressure
- Avoid fluctuations in BP
- Avoid rapid rises/falls in ICP
- Smooth anaesthesia
- Coughing
- Vasalva
- ICD insertion
- Clipping versus Coiling
- ISAT trial favoured coiling over clipping
- Slightly higher longer term risk of re-bleeding
- Clipping still necessary for aneurysms with wide neck, or MCA aneurysms
- Non-Neurological Complications
- VTE
- Multidisciplinary decision re: LMWH, all should have mechanical prophylaxis. LMWH usually started after the aneurysm is secure
- Cardiogenic
- Massive catecholamine surge with SAH leads to cardiac involvement in 50% of cases. Can cause ST elevation, AF, TWI, troponin rises, LVF and regional wall movement abnormalities
- Pulmonary complications
- 80% have impaired oxygenation at some time
- Non-cardiogenic pulmaonry oedema, aspiration, ARDS, VAP, and cardiogenic pulmonary oedema are all causes
- Ongoing management focuses on preventing delayed neurological deficit (DND)
- Delayed cerebral ischaemia (DCI)
- Occurs in 60% of patients
- Risk highest on days 4-10
- May be due to vasospasm but can occur independently of it
- Vasospasm risks include poor grade SAH, IVH, smokers, large subarachnoid blood load
- Vasospasm is seen in 70% of patients who have angiography, with 30% having clinical symptoms
- May be asymptomatic or difficult to detect
- Can be diagnosed with TCD, CTA, DSA or CT perfusion imaging
- Treatments
- Nimodipine, an L-type Ca channel antagonist
- Mode of action not understood
- 60mg 4 hourly (enterally when possible) for 3 weeks. Can be given IV on ITU.
- HHH therapy (hypertension, hypervolaemia, haemodilution)
- Not universally accepted as has poor evidence base
- However, keep CPP >70
- Aim for NORMOvolaemia
- Traditional H’ct of 0.3 for haemodilation has also fallen out of favour
- Aim for Hb 8-10
- Magnesium
- Statins
- No good evidence (STASH trial awaited)
- Endovascular therapies
- IA vasodilator therapy & angioplasty have been tried but prophylaxis is not recommended
- Antiplatelets
- Only indicated when a stent is deployed in the treatment of a ruptured aneurysm
- Hydrocephalus
- Occurs in 25% within the first 3 days
- Higher risk in poor grade
- Treatment requires insertion of EVD
- Cerebral oedema
- Medical management and surgical review
- Fever
- Common and associated with a worse outcome => treat
- Seizures
- Uncommon, and seen in 5% - may be a sign of a re-bleed
- Prophylactic anticonvulsants not recommended
- Treat seizures aggressively
- Glucose/electrolyte abnormalities
- Avoid hypoglycaemia, hyperglycaemia associated with a poorer outcome (4.5-11 target)
- `Na disturbance is common due to SIADH, CSW or DI.