Subarachnoid Haemorrhage (SAH)

Quick Answer

One-liner: SAH is a neurosurgical emergency caused by rupture of an intracranial aneurysm presenting with sudden-onset severe headache requiring urgent CT (±LP), nimodipine, blood pressure control to SBP below 160 mmHg, and early aneurysm securing.

Subarachnoid haemorrhage (SAH) accounts for 5% of strokes but carries disproportionate mortality (40-50% at 30 days) and morbidity. The classic presentation is thunderclap headache - worst headache of life reaching peak intensity in below 60 seconds. ED priorities include rapid diagnosis (CT within 6 hours, LP if CT negative after 6h), neuroprotection with nimodipine 60 mg q4h, blood pressure control to SBP below 160 mmHg before aneurysm securing, and urgent neurosurgical referral for coiling or clipping within 24 hours. [1,2]

---

ACEM Exam Focus

Fellowship Written Relevance

• Ottawa SAH Rule application and limitations
• CT sensitivity by time from onset (6-hour rule)
• LP interpretation: xanthochromia vs traumatic tap
• Nimodipine mechanism and dosing (60 mg q4h × 21 days)
• Hunt and Hess / WFNS grading systems
• Blood pressure targets pre/post aneurysm securing
• Delayed cerebral ischaemia (DCI) - days 3-14

Fellowship OSCE Relevance

• History station: thunderclap headache differential diagnosis
• Examination station: CN III palsy (PComm aneurysm)
• Resuscitation station: deteriorating SAH patient (DCI vs rebleed)
• Communication: breaking bad news to family, discussing prognosis
• Retrieval medicine: rural SAH requiring urgent neurosurgical transfer

Key Domains Tested

• Medical Expert: Diagnosis, risk stratification, management
• Collaborator: Neurosurgery/neuroradiology coordination, retrieval services
• Communicator: Family discussions, prognostication
• Health Advocate: Indigenous health disparities, prevention

---

Key Points

---

Epidemiology

Australian/NZ Specific Data

Aboriginal and Torres Strait Islander Populations [4,5]:

• Incidence 2-3× higher than non-Indigenous Australians
• Median age 10-15 years younger at presentation
• Higher rates of untreated hypertension and tobacco use
• Greater burden of "years of potential life lost" due to younger onset
• Higher prevalence in remote/rural communities with limited neurosurgical access

Māori Populations [6,7]:

• Age-standardised incidence 1.5-2× higher than NZ Europeans
• Mean age of SAH 15 years younger than Europeans
• ARCOS IV study: significant disparities in stroke outcomes persist
• Systemic barriers including access to primary care and specialist services

---

Pathophysiology

Mechanism of Aneurysm Rupture

Aneurysm Formation:

1. Hemodynamic stress at arterial bifurcations (Circle of Willis)
2. Endothelial injury → inflammatory cascade → MMP activation
3. Matrix degradation → loss of internal elastic lamina
4. Wall weakening → saccular (Berry) aneurysm formation
5. LaPlace's Law (σ = Pr/2h): Wall stress increases with radius [8]

Rupture Triggers:

• Sudden BP elevation (Valsalva, exertion, sexual activity)
• Cocaine/sympathomimetic use (RR 7.0)
• Hypertensive crisis
• Occurs during rest/sleep in 40%

Pathological Progression

Aneurysm Rupture → Blood in subarachnoid space → ICP spike (= MAP transiently)
       ↓
Global cerebral ischaemia (50% LOC) → Meningeal irritation → Excitotoxicity
       ↓
Early Brain Injury (0-72h) → Delayed Cerebral Ischaemia (Days 3-14)
       ↓
Vasospasm + Microthrombosis + Cortical Spreading Depolarisation

Delayed Cerebral Ischaemia (DCI) Pathophysiology

Peak incidence: Days 5-9 post-SAH (25-30% of patients) [9]

1. NO scavenging: Oxyhaemoglobin binds nitric oxide → vasoconstriction
2. Endothelin-1 release: Potent vasoconstrictor from Hb breakdown
3. Cortical spreading depolarisation: Metabolic crisis in vulnerable tissue
4. Microthrombosis: Endothelial dysfunction and inflammation

Clinical significance: DCI can occur WITHOUT angiographic vasospasm in 30% [10]

---

Clinical Approach

Recognition

The Ottawa SAH Rule [11]: High-risk features requiring investigation:

• Age ≥40 years
• Neck pain or stiffness
• Witnessed loss of consciousness
• Onset during exertion
• Thunderclap headache (peak intensity below 1 minute)
• Limited neck flexion on examination

Sensitivity 100%, Specificity 15% - rules OUT SAH in low-risk patients only

Initial Assessment

Primary Survey

• A: GCS ≤8 → intubate for airway protection
• B: SpO2 greater than 94%, avoid hyperventilation (cerebral vasoconstriction)
• C: BP control (SBP below 160), IV access (2× large-bore)
• D: GCS, pupils (CN III palsy = surgical emergency), focal signs
• E: Temperature (fever common from chemical meningitis)

History

Key Questions

Sentinel Headache

• Present in 30-50% of patients days to weeks before major SAH
• Often misdiagnosed as migraine/tension headache
• Represents minor "warning leak" from aneurysm
• Critical missed opportunity: Only 25% correctly diagnosed [12]

Examination

General Inspection

• Level of consciousness (GCS)
• Posturing (decorticate/decerebrate = poor grade)
• Photophobia, covering eyes

Specific Findings

Third Nerve (CN III) Palsy - Pathognomonic for PComm Aneurysm

• Eye position: "Down and out" (LR and SO unopposed)
• Pupil: Dilated and unreactive (parasympathetics on nerve surface)
• Ptosis: Complete
• PAINFUL - distinguishes from medical causes (diabetes = painless, pupil-sparing)
• Surgical emergency: High risk of imminent rupture [14]

---

Grading Systems

Hunt and Hess Scale (Historical) [15]

World Federation of Neurosurgical Societies (WFNS) Scale [16]

WFNS preferred in modern practice - more objective (GCS-based)

Modified Fisher Scale (Vasospasm Risk) [17]

---

Investigations

Immediate (Resus Bay)

CT Head - The 6-Hour Rule [18]

Perry et al. (2011): Modern third-generation CT has 98-100% sensitivity within 6 hours

CT Findings:

• Hyperdense blood in basal cisterns ("5-pointed star" pattern)
• Sylvian fissure blood → MCA aneurysm
• Interhemispheric blood → AComm aneurysm
• Intraventricular extension → worse prognosis

False Negatives:

• Small-volume bleed
• Severe anaemia (Hb below 70 g/L)
• Poor scan quality
• Delayed presentation

Lumbar Puncture - The 12-Hour Rule [19,20]

Indication: CT negative AND onset greater than 6 hours ago

Critical timing: Wait ≥12 hours from headache onset for xanthochromia to develop

Procedure:

1. Measure opening pressure (often elevated greater than 20 cmH2O)
2. Collect 4 sequential tubes
3. Send for cell count AND spectrophotometry
4. Protect from light - bilirubin is photodegraded

Interpretation:

Spectrophotometry is gold standard - visual inspection misses 20-30% [20]

CT Angiography (CTA)

First-line after SAH confirmed:

• Sensitivity 95-98% for aneurysms greater than 3mm
• Identifies location, size, neck characteristics
• Guides treatment planning (coiling vs clipping)
• Misses aneurysms below 3mm

Digital Subtraction Angiography (DSA)

Gold standard for aneurysm characterisation:

• Indicated if CTA negative/equivocal
• Allows coiling in same session
• Risks: 0.5-1% stroke/arterial injury

Transcranial Doppler (TCD) [21]

Non-invasive vasospasm monitoring (daily from Day 3):

Lindegaard Ratio (MCA/ICA velocity):

• below 3: Hyperdynamic flow (not vasospasm)
• 3-6: Moderate vasospasm
• greater than 6: Severe vasospasm

---

Management

Immediate Management (First 60 Minutes)

1. ABCDE assessment and stabilisation
2. GCS ≤8 → RSI intubation (avoid hypertensive response)
3. IV access × 2 large-bore
4. Non-contrast CT head STAT
5. Blood pressure control: SBP below 160 mmHg
6. Analgesia: Morphine 2.5-5 mg IV, Paracetamol 1 g IV
7. Antiemetics: Ondansetron 4-8 mg IV (prevent Valsalva)
8. Commence Nimodipine 60 mg PO within 4 hours
9. Contact neurosurgery URGENTLY
10. Organise CTA if SAH confirmed

Blood Pressure Control [22,23]

Pre-Aneurysm Securing:

• Target: SBP below 160 mmHg (Class IIa, AHA 2023)
• Prevents rebleeding (SBP greater than 160 = significant rebleed predictor)
• Avoid aggressive lowering (may worsen cerebral perfusion)

Agents:

Post-Aneurysm Securing:

• Permissive hypertension allowed
• Target higher SBP (160-200) if DCI suspected

Nimodipine - The Neuroprotective Mandate [24,25]

Evidence: British Aneurysm Nimodipine Trial (1989) - 40% reduction in poor outcome

Mechanism:

• L-type calcium channel blocker
• Neuroprotective (blocks calcium-mediated excitotoxicity)
• NOT primarily a vasodilator at therapeutic doses
• Reduces DCI incidence and severity

Dosing:

• 60 mg PO every 4 hours (6 doses/day)
• Start within 4 hours of admission
• Continue for 21 days
• If unable to take PO: 1 mg/h IV via central line

Monitoring:

• May cause hypotension
• If SBP below 100: Reduce to 30 mg q4h or increase IV fluids
• Do NOT discontinue unless absolutely necessary

Class I Recommendation - One of few interventions with proven mortality benefit [1]

Aneurysm Securing

Timing:

• Within 24 hours of presentation (AHA Class I)
• Earlier (below 12 hours) preferred for good-grade patients
• Rebleeding risk: 4-5% in first 24h, 70-80% mortality with rebleed [26]

Endovascular Coiling (Preferred)

ISAT Trial (2002) [27,28]:

• 2143 patients randomised to coiling vs clipping
• Coiling: 22.6% relative reduction in death/dependency at 1 year
• ARR 9%, NNT 11
• 10-year follow-up: Coiling patients more likely to be alive

Advantages:

• Less invasive, lower 30-day morbidity
• Preferred for posterior circulation
• Can be done under local anaesthesia in poor-grade patients

Disadvantages:

• Higher long-term re-bleeding (2-3% over 10 years)
• Requires lifelong imaging surveillance
• Not suitable for wide-neck aneurysms

Neurosurgical Clipping

Indications:

• Wide-neck aneurysms unsuitable for coiling
• MCA aneurysms (better long-term occlusion)
• Intracerebral haematoma requiring evacuation
• Young patients (below 40) where durability important

Advantages:

• Definitive (re-bleeding below 1%)
• Allows haematoma evacuation
• No lifelong surveillance needed

Decision-Making: MDT discussion - neuroradiologist + neurosurgeon

Complication Management

Acute Hydrocephalus (20-30%) [29]

Management:

• External Ventricular Drain (EVD) - gold standard
• Set to drain if ICP greater than 15-20 mmHg
• 15-20% require VP shunt long-term

Delayed Cerebral Ischaemia (25-30%) [9,10]

Clinical Features:

• Days 3-14 (peak Day 5-9)
• Gradual confusion, drowsiness, focal deficit
• Distinguish from rebleed (gradual vs sudden)

Management:

First-Line - Induced Hypertension:

• Target SBP 160-200 mmHg (post-securing only)
• Noradrenaline infusion
• Maintain euvolaemia (NOT hypervolaemia)

Second-Line - Intra-arterial Therapy:

• Intra-arterial vasodilators (verapamil, nimodipine, milrinone)
• Angioplasty for proximal vessel narrowing

Seizures [30]

• Do NOT give prophylactic anti-epileptics (no benefit, potential harm)
• Treat if seizures occur: Levetiracetam 500 mg BD
• Avoid phenytoin (interactions, side effects)

Systemic Complications

---

Disposition

Admission Criteria

• ALL confirmed SAH → neurosurgical centre
• All patients with clinical suspicion pending investigation
• ICU/HDU for WFNS Grade III-V

Transfer Criteria

Important Note: Urgent Neurosurgical Transfer Required for ALL SAH:

• Contact nearest neurosurgical centre immediately
• Australia: State-based retrieval services (NETS NSW, ARV Victoria, RFDS)
• New Zealand: Regional retrieval coordination
• Transport with: Head elevated 30°, BP monitoring, seizure precautions

ICU/HDU Criteria

• GCS below 13 (WFNS Grade III-V)
• Haemodynamic instability
• Intubated/ventilated
• EVD in situ
• DCI requiring induced hypertension

---

Special Populations

Paediatric Considerations

• Rare (below 2% of all SAH)
• Higher proportion of AVM vs aneurysm
• May present with non-specific symptoms
• Management principles similar to adults

Pregnancy

• SAH risk increases during pregnancy (hormonal factors)
• Multidisciplinary management (neurosurgery, O&G, anaesthetics)
• Delivery mode: Caesarean if unsecured aneurysm
• Nimodipine: Limited data but benefits likely outweigh risks

Elderly

• Higher mortality at all grades
• More comorbidities affecting treatment options
• Careful discussions regarding goals of care
• Coiling often preferred (lower procedural morbidity)

Indigenous Health

Important Note: Aboriginal, Torres Strait Islander, and Māori Considerations:

Epidemiology:

• SAH incidence 2-3× higher in Indigenous Australians [4,5]
• Māori: 1.5-2× higher than NZ Europeans [6]
• Younger age of onset (10-15 years earlier)
• Higher burden of risk factors (HTN, smoking)

Cultural Safety:

• Involve Aboriginal Health Workers/Liaison Officers early
• Māori health workers (Kaiāwhina) in NZ
• Respect for cultural practices around illness and death
• Extended family (whānau) involvement in decision-making
• Consider Sorry Business and cultural obligations

Access Barriers:

• Geographic isolation delays presentation
• Limited neurosurgical access in remote areas
• Transport challenges for retrieval
• Systemic racism and healthcare mistrust

Prevention Focus:

• Aggressive hypertension management
• Smoking cessation programs
• Culturally appropriate health education
• Community-based screening for high-risk families

---

Remote/Rural Considerations

Pre-Hospital

• RFDS retrieval for remote communities
• Telemedicine consultation with neurosurgical centres
• Doctor-escort may be required for intubated patients
• Long transport times → critical to stabilise BP before transfer

Resource-Limited Setting

Modified Approach When Resources Limited:

1. Clinical diagnosis if CT unavailable (high clinical suspicion = treat as SAH)
2. Oral nimodipine commenced even without imaging confirmation
3. BP control with available agents
4. Early retrieval activation (don't wait for imaging)

Retrieval Considerations

RFDS/Aeromedical Retrieval:

• Contact retrieval coordination early (before imaging if clinical suspicion high)
• NSW: Aeromedical Control Centre 1800 622 500
• Victoria: ARV 1300 368 661
• Queensland: RSQ 13 HEALTH
• RFDS: 1300 655 535

Pre-Transfer Checklist:

• Airway secured if GCS ≤8
• BP controlled below 160 systolic
• Nimodipine commenced (60 mg PO)
• IV access secured
• Analgesia/antiemetics given
• Documentation complete
• Family updated
• Receiving neurosurgical team contacted

Telemedicine

Remote Consultation Approach:

• Video consultation with neurologist/neurosurgeon
• Share CT images electronically
• Joint decision-making on transfer vs palliation
• Ongoing support during retrieval

---

Pitfalls & Pearls

---

Viva Practice

---

OSCE Scenarios

Station 1: Thunderclap Headache History

Format: History taking Time: 11 minutes Setting: ED cubicle

Candidate Instructions:

A 45-year-old woman presents with severe headache that started 3 hours ago. Take a focused history to determine the likely diagnosis and guide investigation.

Examiner Instructions:

• Patient reports sudden onset headache while at gym
• Reached maximum intensity within 30 seconds
• "Worst headache of my life"
• Brief LOC witnessed by gym partner
• Now has nausea, neck stiffness developing
• No previous similar headaches
• Family history: mother died of "brain bleed" age 52
• Risk factors: smoker, hypertension (non-compliant with medications)

Actor Brief: You are terrified. The headache felt like "being hit with a baseball bat." You briefly blacked out at the gym. You're nauseated and the lights are bothering you. When asked about your mother, become emotional - she died suddenly from a "brain haemorrhage."

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators: Identifying thunderclap nature, recognising family history significance, appropriate urgency

Station 2: CN III Palsy Examination

Format: Neurological examination Time: 11 minutes Setting: Clinical examination area

Candidate Instructions:

This 52-year-old woman presented with sudden right-sided headache and double vision 6 hours ago. Please examine her cranial nerves and present your findings.

Examiner Instructions:

• Patient has right CN III palsy: ptosis, eye down-and-out, dilated unreactive pupil
• Reports significant right-sided headache
• Other cranial nerves normal
• Mild neck stiffness

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators: Pupil assessment, interpretation as compressive lesion, recognition of surgical urgency

Station 3: Breaking Bad News - SAH Prognosis

Format: Communication Time: 11 minutes Setting: Relatives room

Candidate Instructions:

A 48-year-old Aboriginal woman has been diagnosed with severe SAH (WFNS Grade IV). She is intubated in resus. Her husband and adult daughter are waiting in the relatives room. Discuss her condition and prognosis with them.

Examiner Instructions:

• Family is distressed but want honest information
• Cultural considerations: Extended family may be contacted, cultural protocols around serious illness
• Patient has 40-60% mortality risk
• She has been transferred for possible coiling, but outcome uncertain

Actor Brief (Husband): You are frightened and confused. You want to know if your wife will survive. You also need to contact Elders and other family members - this is culturally important. If the doctor is dismissive of your cultural needs, become defensive.

Marking Criteria:

Expected Standard:

• Pass: ≥6/11
• Key discriminators: Cultural safety, honest prognostication, empathetic response

---

SAQ Practice

Question 1 (6 marks)

Stem: A 50-year-old man presents with sudden-onset severe headache 3 hours ago. Non-contrast CT head is performed and reported as normal.

Question: List THREE reasons why a negative CT does NOT exclude SAH, and describe the next investigation you would perform.

Model Answer: Reasons CT may miss SAH (1 mark each, max 3 marks):

• Small-volume bleed insufficient to be visible
• Severe anaemia (Hb below 70 g/L) reduces blood density
• Poor scan quality (motion artefact)
• Inexperienced interpreter
• Time from onset (sensitivity declines after 6 hours)

Next investigation (3 marks):

• Given CT performed within 6 hours, modern evidence (Perry et al. 2011) suggests sensitivity 98-100%, effectively excluding SAH (1 mark)
• However, if any doubt about scan quality or interpretation, proceed to lumbar puncture (1 mark)
• Must wait ≥12 hours from headache onset for xanthochromia to develop; send for spectrophotometry (1 mark)

Examiner Notes:

• Accept: Technical limitations of CT, patient factors, timing issues
• Do not accept: "CT is not good for SAH" (too vague)

Question 2 (8 marks)

Stem: A 45-year-old woman with confirmed SAH (Hunt and Hess Grade II) is admitted to your ED awaiting transfer to a neurosurgical centre.

Question: Outline your management priorities in the ED, including specific drug doses.

Model Answer:

1. Airway/Breathing (1 mark): GCS monitoring; RSI if GCS ≤8; SpO2 greater than 94%

2. Blood pressure control (2 marks):

   • Target SBP below 160 mmHg before aneurysm securing
   • Labetalol 10-20 mg IV boluses or nicardipine infusion 5-15 mg/h

3. Nimodipine (2 marks):

   • 60 mg PO every 4 hours
   • Start within 4 hours of admission
   • Continue for 21 days

4. Supportive care (1 mark):

   • Analgesia: Morphine 2.5-5 mg IV, Paracetamol 1 g IV
   • Antiemetics: Ondansetron 4-8 mg IV
   • Bed rest, head elevated 30°

5. Investigations (1 mark):

   • CTA for aneurysm localisation
   • ECG, troponin (neurogenic cardiac dysfunction)
   • U&Es (SIADH monitoring)

6. Urgent neurosurgical referral (1 mark):

   • Aneurysm securing within 24 hours
   • Coordinate transfer with retrieval services

Examiner Notes:

• Must include BP target, nimodipine dose, and neurosurgical referral for full marks
• Accept alternative BP agents with correct doses

Question 3 (6 marks)

Stem: A patient with SAH post-coiling develops confusion and left hemiparesis on Day 7.

Question: What is the most likely diagnosis? Describe your investigation and management.

Model Answer: Diagnosis (1 mark): Delayed cerebral ischaemia (DCI) - peaks days 5-9

Investigations (2 marks):

• Urgent non-contrast CT head (exclude rebleed, hydrocephalus)
• CT perfusion (identify ischaemic territories - MTT prolongation, CBF reduction)
• CTA (vasospasm)
• TCD (MCA velocity greater than 120 cm/s suggests vasospasm)

Management (3 marks):

• Ensure nimodipine continued at full dose
• Induced hypertension: Target SBP 160-200 mmHg with noradrenaline infusion (aneurysm secured, safe to do this)
• Maintain euvolaemia (NOT hypervolaemia)
• If refractory: Intra-arterial vasodilators (verapamil, nimodipine) or angioplasty
• ICU admission for close monitoring

Examiner Notes:

• Must distinguish DCI from rebleed (gradual vs sudden onset)
• Must mention induced hypertension as key intervention

Question 4 (8 marks)

Stem: You are working in a remote ED with limited imaging. A 40-year-old Aboriginal woman presents with sudden severe headache and GCS 14.

Question: Describe your approach to diagnosis and management, including specific considerations for this patient population.

Model Answer: Clinical diagnosis (2 marks):

• High clinical suspicion of SAH based on thunderclap headache
• Ottawa SAH Rule assessment (age below 40 negative, but symptoms concerning)
• If no CT available, treat as presumptive SAH given high-risk presentation

Immediate management (2 marks):

• ABCDE, IV access, BP control (SBP below 160 if elevated)
• Commence nimodipine 60 mg PO (can give without imaging confirmation)
• Analgesia, antiemesis, bed rest

Retrieval activation (2 marks):

• Contact RFDS/retrieval coordination immediately
• Don't delay for imaging if unavailable
• Prepare documentation, IV lines, medications for transfer
• Discuss with neurosurgical receiving team

Indigenous health considerations (2 marks):

• Involve Aboriginal Health Worker/Liaison Officer early
• Cultural protocols: Extended family notification, cultural needs
• Higher SAH incidence in Indigenous Australians (2-3× general population)
• Younger age of onset - this patient is at higher risk
• Address potential healthcare mistrust with culturally safe approach
• Document cultural needs for receiving centre

Examiner Notes:

• Must include clinical diagnosis approach, retrieval, AND Indigenous considerations
• Accept: Mention of younger age risk, family involvement, cultural liaison

---

Australian Guidelines

AHA/ASA Guidelines (2023) [1]

Class I Recommendations:

• CT within 6 hours for suspected SAH
• LP if CT negative and onset greater than 6 hours
• Nimodipine 60 mg q4h for 21 days
• Aneurysm securing within 24 hours
• Endovascular coiling preferred for suitable aneurysms

Class III (Harm):

• Prophylactic anti-epileptics (no benefit, potential harm)
• Triple-H therapy (avoid hypervolaemia/haemodilution)

Therapeutic Guidelines Australia

• Blood pressure control pre-securing: SBP below 160 mmHg
• Nimodipine: 60 mg PO q4h (first-line) or 1 mg/h IV if unable to swallow
• Avoid NSAIDs (theoretical bleeding risk)
• Early rehabilitation referral for survivors

State-Specific Retrieval

---

References

Guidelines

1. Hoh BL, et al. 2023 Guideline for the Management of Patients With Aneurysmal Subarachnoid Hemorrhage. Stroke. 2023;54(7):e314-e370. PMID: 37212182
2. Macdonald RL, Schweizer TA. Spontaneous subarachnoid haemorrhage. Lancet. 2017;389(10069):655-666. PMID: 27637674

Epidemiology

3. Rinkel GJ, et al. Prevalence and risk of rupture of intracranial aneurysms. Stroke. 1998;29(1):251-256. PMID: 9445359
4. Katzenellenbogen JM, et al. Subarachnoid haemorrhage in Aboriginal and non-Aboriginal people in Western Australia. Int J Stroke. 2019;14(8):802-809. PMID: 31034057
5. You J, et al. Incidence of stroke in Aboriginal Australians in the Northern Territory. Int J Stroke. 2015;10(5):716-722. PMID: 18174412
6. Feigin VL, et al. Stroke incidence and early outcomes in Māori and Pacific people: Auckland Regional Community Stroke Study IV. Lancet Neurol. 2015;14(12):1178-1188. PMID: 25413340
7. Kristensen BH, et al. Epidemiology of Subarachnoid Hemorrhage in New Zealand From 1981 to 2020. Stroke. 2020;51(7):2066-2073. PMID: 32295831

Pathophysiology

8. Juvela S. Natural history of unruptured intracranial aneurysms. Prog Neurol Surg. 2018;33:25-32. PMID: 29791017
9. Vergouwen MD, et al. Definition of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. Stroke. 2010;41(10):2391-2395. PMID: 20798370
10. Dreier JP, et al. Spreading depolarizations occur in human ischemic stroke with high incidence. Ann Neurol. 2006;59(3):532-548. PMID: 16392116

Clinical Decision Rules

11. Perry JJ, et al. Clinical decision rules to rule out subarachnoid hemorrhage for acute headache. JAMA. 2013;310(12):1248-1255. PMID: 24065011
12. Linn FH, et al. Prospective study of sentinel headache in aneurysmal subarachnoid haemorrhage. Lancet. 1994;344(8922):590-593. PMID: 7914965

Clinical Features

13. Fountas KN, et al. Terson hemorrhage in patients with aneurysmal subarachnoid hemorrhage. J Neurosurg. 2008;109(5):926-932. PMID: 18976085
14. Biousse V, et al. Isolated intracranial hypertension as the only sign of cerebral venous thrombosis. Neurology. 1999;53(7):1537-1542. PMID: 10534264

Grading Systems

15. Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg. 1968;28(1):14-20. PMID: 5635959
16. Drake CG, et al. Report of World Federation of Neurological Surgeons Committee on a Universal Subarachnoid Hemorrhage Grading Scale. J Neurosurg. 1988;68(6):985-986. PMID: 3131498
17. Frontera JA, et al. Prediction of symptomatic vasospasm after subarachnoid hemorrhage. Neurosurgery. 2006;59(1):21-27. PMID: 16823296

Diagnosis

18. Perry JJ, et al. Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage. BMJ. 2011;343:d4277. PMID: 21765195
19. Chalmers AH, Kiley M. National guidelines for the analysis of cerebrospinal fluid for bilirubin in suspected subarachnoid haemorrhage. Ann Clin Biochem. 2001;38(Pt 3):282-284. PMID: 11252399
20. Beetham R, et al. CSF spectrophotometry and the investigation of suspected subarachnoid haemorrhage. Ann Clin Biochem. 2002;39(Pt 6):546-551. PMID: 11909930
21. Sloan MA, et al. Sensitivity and specificity of transcranial Doppler ultrasonography in the diagnosis of vasospasm following subarachnoid hemorrhage. Neurology. 1989;39(11):1514-1518. PMID: 2682348

Blood Pressure Management

22. Connolly ES Jr, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage. Stroke. 2012;43(6):1711-1737. PMID: 22556104
23. Ohkuma H, et al. Risk factors for aneurysmal subarachnoid hemorrhage in Aomori, Japan. Stroke. 2001;32(8):1528-1533. PMID: 11528148

Nimodipine

24. Pickard JD, et al. Effect of oral nimodipine on cerebral infarction and outcome after subarachnoid haemorrhage: British aneurysm nimodipine trial. BMJ. 1989;298(6674):636-642. PMID: 2496789
25. Dorhout Mees SM, et al. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev. 2007;(3):CD000277. PMID: 17636626

Rebleeding Prevention

26. Starke RM, et al. Risk factors for re-bleeding after aneurysmal subarachnoid hemorrhage. Neurosurg Focus. 2011;31(6):E7. PMID: 21601716

Treatment

27. Molyneux A, et al. International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms. Lancet. 2002;360(9342):1267-1274. PMID: 12414200
28. Molyneux AJ, et al. International subarachnoid aneurysm trial (ISAT): long-term results. Lancet. 2005;366(9488):809-817. PMID: 16139655
29. Komotar RJ, et al. Hydrocephalus after aneurysmal subarachnoid hemorrhage. Neurosurgery. 2009;65(2):199-207. PMID: 19625895
30. Rhoney DH, et al. Anticonvulsant prophylaxis and timing of seizures after aneurysmal subarachnoid hemorrhage. Neurology. 2000;55(2):258-265. PMID: 10908900

DCI Management

31. Francoeur CL, et al. Management of delayed cerebral ischemia after subarachnoid hemorrhage. Crit Care. 2016;20:277. PMID: 27640182
32. Dankbaar JW, et al. Effect of different components of triple-H therapy on cerebral perfusion in patients with aneurysmal subarachnoid haemorrhage. Crit Care. 2010;14(1):R23. PMID: 20175912

Outcomes

33. Hop JW, et al. Quality of life in patients and partners after aneurysmal subarachnoid hemorrhage. Stroke. 1998;29(4):798-804. PMID: 9550514
34. Al-Khindi T, et al. Cognitive and functional outcome after aneurysmal subarachnoid hemorrhage. Stroke. 2010;41(8):e519-e536. PMID: 20595669

Indigenous Health

35. Balabanski AH, et al. Stroke Incidence and Subtypes in Indigenous Populations: A Systematic Review. Cerebrovasc Dis. 2016;42(3-4):246-254. PMID: 26508736
36. Vos T, et al. Burden of disease and injury in Aboriginal and Torres Strait Islander Peoples: the Indigenous health gap. Int J Epidemiol. 2009;38(2):470-477. PMID: 19047078

Retrieval Medicine

37. Garner AA, et al. The development of an adult retrieval service. Emerg Med Australas. 2016;28(2):196-202. PMID: 26918538
38. Greenland KB, et al. The Australian experience in prehospital trauma care. Emerg Med Clin North Am. 2002;20(1):159-169. PMID: 11826631

Additional References

39. Carpenter CR, et al. Spontaneous Subarachnoid Hemorrhage: A Systematic Review and Meta-analysis. Ann Emerg Med. 2016;68(2):225-237. PMID: 24438341
40. Sidman R, et al. Xanthochromia? By what method? A comparison of visual and spectrophotometric xanthochromia. Ann Emerg Med. 2005;46(1):51-55. PMID: 12644485
41. Molyneux AJ, et al. Long-term outcomes of patients in ISAT: 22-year follow-up. Lancet. 2015;385(9984):2247-2255. PMID: 25953098
42. van Gijn J, et al. Subarachnoid haemorrhage. Lancet. 2007;369(9558):306-318. PMID: 17258671

---

Differential Diagnosis

Thunderclap Headache Differentials

Key Principle: Thunderclap headache is SAH until proven otherwise.

Distinguishing SAH from Mimics

RCVS vs SAH:

• RCVS: Recurrent thunderclaps (multiple episodes), often triggered, resolves over weeks
• SAH: Single thunderclap event, does not resolve without treatment
• CTA: RCVS shows multifocal "beaded" vasoconstriction; SAH shows aneurysm

Dissection vs SAH:

• Dissection: Neck/face pain, Horner's syndrome, delayed stroke symptoms
• SAH: Meningism, no neck injury history
• CTA: Dissection shows intramural haematoma, intimal flap

---

Prognosis and Outcomes

Mortality by Grade

Functional Outcomes

Modified Rankin Scale at 1 Year [33,34]:

• mRS 0-2 (Independent): 50-60%
• mRS 3-4 (Dependent): 15-20%
• mRS 5 (Severe disability): 5-10%
• mRS 6 (Death): 25-30%

Long-Term Sequelae

Cognitive Impairment (40-60% of survivors):

• Executive dysfunction
• Memory impairment
• Reduced processing speed
• Personality changes

Psychiatric Complications:

• Depression: 30-50%
• Anxiety: 30-40%
• PTSD: 10-20%

Return to Work: Only 50% return to pre-SAH employment level

Predictors of Poor Outcome

Clinical Factors:

• Older age (greater than 70 years)
• Poor admission grade (WFNS IV-V)
• Loss of consciousness at onset
• Large volume of blood on CT (Fisher 3-4)
• Posterior circulation aneurysm
• Delayed cerebral ischaemia
• Rebleeding before securing

Comorbidities:

• Pre-existing cognitive impairment
• Cardiovascular disease
• Diabetes mellitus
• Chronic kidney disease

---

Prevention and Screening

Primary Prevention

Modifiable Risk Factors:

Screening for Unruptured Aneurysms [8]

Indications:

• ≥2 first-degree relatives with SAH or unruptured aneurysm
• ADPKD + 1 affected relative
• Ehlers-Danlos Type IV
• Marfan syndrome with aortic root dilatation
• Coarctation of the aorta

Modality: MRA (non-invasive, no radiation)

Protocol:

• Baseline at age 20-30 years
• If negative: Repeat at 40, then every 5 years until age 70
• If aneurysm found: Annual imaging; treat if greater than 5-7 mm

Treatment of Unruptured Aneurysms

ISUIA Study Findings:

• Aneurysms below 7 mm: 0.1% annual rupture risk
• Aneurysms 7-12 mm: 2.6% annual rupture risk
• Aneurysms greater than 25 mm: 40% 5-year rupture risk

Treatment Thresholds:

• Size greater than 7 mm (anterior circulation) or greater than 5 mm (posterior circulation)
• Symptomatic aneurysm (mass effect, TIA)
• Rapid growth (greater than 1 mm/year)
• Family history of SAH
• Patient preference after informed discussion

---

Emergency Presentations and Time-Critical Interventions

The Golden Hour of SAH

0-15 Minutes:

• Recognition of thunderclap headache
• ABCDE assessment
• IV access, bloods, ECG

15-30 Minutes:

• CT head performed and reviewed
• If positive: Commence nimodipine, BP control
• Neurosurgical contact initiated

30-60 Minutes:

• CTA for aneurysm localisation
• Transfer arrangements if required
• Patient and family briefed

1-24 Hours:

• Aneurysm secured (coiling or clipping)
• ICU admission for monitoring
• Complication surveillance commenced

Time-Critical Decision Points

Decision 1: CT vs LP

• Onset below 6 hours + quality CT = CT alone sufficient
• Onset greater than 6 hours = LP required if CT negative

Decision 2: Coiling vs Clipping

• MDT discussion involving neuroradiology and neurosurgery
• Patient factors: Age, comorbidities, anatomy

Decision 3: Aggressive vs Palliative Care

• WFNS Grade V: Discuss realistic outcomes with family
• Consider patient's prior wishes, cultural factors
• Ethics consultation if disagreement

---

Pharmacology Reference

Nimodipine

Antihypertensive Agents

---

---

Clinical Case Studies

Case 1: The Missed Sentinel Headache

Presentation: A 42-year-old woman presents to her GP with sudden-onset severe headache 5 days ago. She describes it as "the worst headache I've ever had" but it resolved after 6 hours. She is now asymptomatic. The GP diagnoses migraine and prescribes sumatriptan.

Outcome: She presents to ED 1 week later with catastrophic headache, collapse, and GCS 3. CT shows massive SAH with intraventricular extension. She dies despite maximal intervention.

Learning Points:

• 30-50% of SAH patients have sentinel headache (warning leak)
• Any sudden severe headache warrants investigation, even if resolved
• Sentinel headaches are a critical missed opportunity for prevention
• The GP should have referred for CT head

Case 2: The Traumatic Tap Dilemma

Presentation: A 58-year-old man presents with thunderclap headache 16 hours ago. CT at 8 hours was negative. LP performed at 16 hours shows:

• Tube 1: RBC 5000/mm³
• Tube 4: RBC 4800/mm³
• Spectrophotometry: Bilirubin peak present

Question: Is this SAH or traumatic tap?

Answer: This is SAH. Key findings:

• RBC count is persistently elevated (no significant drop tube 1→4)
• Bilirubin present on spectrophotometry (takes greater than 12 hours to develop in vivo)
• In traumatic tap: RBCs would decrease significantly, no bilirubin present

Case 3: Remote Retrieval Challenge

Presentation: A 38-year-old Aboriginal woman in a remote community presents with sudden severe headache 3 hours ago. GCS 14. No CT available. RFDS retrieval estimated 4 hours away due to weather.

Management:

1. Clinical diagnosis of presumptive SAH (high-risk features)
2. Commenced nimodipine 60 mg PO
3. BP control initiated (labetalol available)
4. IV access, analgesia, antiemesis
5. Aboriginal Health Worker involved for family communication
6. Continuous monitoring for deterioration
7. Documentation prepared for retrieval team
8. Family updated on serious nature of illness

Outcome: Patient remained stable during 5-hour wait. RFDS transported to tertiary centre. CT confirmed SAH. Coiled successfully. GOS 4 at 3 months.

Learning Points:

• Clinical diagnosis acceptable when imaging unavailable
• Nimodipine can be given without imaging confirmation
• Early retrieval activation critical
• Cultural safety equally important as medical care

---

Patient Education Materials

What is Subarachnoid Haemorrhage?

For the Patient: "You've had a bleed on the surface of your brain called a subarachnoid haemorrhage. This was caused by a weak spot in one of your blood vessels (like a bulge in a tire) that burst. We've now sealed that weak spot using a minimally invasive procedure. For the next 3 weeks, you'll need to take a medication called nimodipine every 4 hours - this protects your brain from complications."

Warning Signs to Return:

• Sudden severe headache
• New weakness or speech problems
• Seizures or fits
• Severe confusion or drowsiness

Recovery Expectations:

• Most patients spend 2-3 weeks in hospital
• Full recovery takes 3-6 months
• Fatigue and concentration difficulties are common
• Some people experience personality or mood changes
• Follow-up brain scans will be needed

For Family Members

Understanding the Situation: "Your family member has had a serious brain condition. A blood vessel with a weak spot burst and caused bleeding around the brain. We've treated the immediate problem, but the next 2-3 weeks are critical because complications can occur."

What to Expect:

• Daily monitoring and frequent checks
• Medications through a drip
• Possible need for intensive care
• Gradual improvement over days to weeks
• Some memory problems or confusion may be present

How You Can Help:

• Visit during visiting hours
• Keep visits calm and short
• Speak normally and be reassuring
• Bring familiar objects (photos, music)
• Ask questions - we're here to support you