Sub arachnoid haemorrhage

Question 1

A 20 year old man presents with the sudden onset of a severe occipital headache and transient loss of consciousness an hour ago while at work. He complains now of persistent headache, nausea and photophobia. He has neck stiffness but no focal neurological signs. How would you assess and manage him?

Answer 1

Impression
Likely a SAH given the clinical features of sudden onset ‘thunderclap’ headache, associated neck stiffness, nausea and photophobia (features of raised ICP).

DDX
- Neuro: SOL, ICH, ischaemic stroke
- infective: meningitis, encephalitis (given features of meningism in the stem)
- trauma
- benign causes of headache: tension, migraine

Goals
- senior help and primary survey acutely assess and stabilise
- likely retrieval for neurosurgeon for definitive management with evacuation

Question 2

SAH - Assessment

Answer 2

Assessment
- call for senior help, stroke call, move patient to resus bay
- primary survey approach

A - Tube pending GCS assessment
B -
C - Cushings response to raised ICP, ECG and vitals monitoring. Cannula for bloods including trops (prognostic), VBG, UEC, Coags. Vitals monitoring
- administer labetalol infusion for BP control
D - GCS, PEARL, cranial nerves examination. Non-con CTB (blood in ventricles/sulci and gyri, crosses suture lines - hyper dense if acute, surrounding hypotenuse area of oedema). +/- further angio/pefusion imaging.
E - Temp

Immediate Mx
- Blood pressure control (10mmHg lower than presentation, MAP<110)
- Head up at 30 degrees
- maintain glucose from 8-10mmol/L

Question 3

SAH - History

Answer 3

History
- MIST AMPLE
- Risk factors for SAH: known berry aneurysm, HTN, heavy exertion at work at time of onset, polycystic kidney disease, AV Malformations
- Medications: anticoagulants
- CVD risk factors
- PMHx, FamHx, SNAP

Question 4

SAH - Examination

Answer 4

Examination
- General appearance + vitals
- Neuro exam: PEARL, Cushings triad (HTN, irregular breathing, bradycardia), FAST signs,
- Fundoscopy: venous pulses, papilloedema

Question 5

SAH - Investigations

Answer 5

Investigations
Key/Diagnostic
- non-con CT Brain

• Bloods: Cultures if febrile (meningitis), UEC, LFT, CRP/ESR, Coags, Lipid panel
• Imaging: as in stroke protocol on initial assessment
• Other: LP if negative on imaging but clinical features are suggestive - send for xanthochromia (Red cell break down products)

Question 6

SAH - Management

Answer 6

Management
Supportive
- BP control
- End of bed head up
- Temp homeostasis, Glucose control and monitoring
- electrolytes and fluids as indicated
- telemetry
- DVT prophylaxis with mechanical rather than pharmacological treatment
- analgesia, antiemetics
- prophylactic aontiseizure medications (phenytoin?)

Definitive
- Coiling and clipping of aneurysmal vessels OR craniotomy
- Prevent vasospasm with CCBs (nifedipine)
- Reverse any anticoagulation to limit risk of re-bleeding

Key complications of SAH
- Vasospasm and ischaemic extension
- Re-bleeding
- Hydrocephalus (long-term), epilepsy
o VP shunt, referral to neurosurg

• Neurosurgeon consult for definitive management options
• SAH follows a rule of thirds in terms of prognosis/outcomes.