Subarachnoid haemorrhage

The Case

To follow – in time we hope to populate a case file database with real cases, real results and real reflections in order to facilitate your learning and link the theory to EM in the real world.

The Deep Dive

EPIDEMIOLOGY

• 1/10 000 of population
• 1/1000 of headache presentations to ED
• Up to 10% of thunderclap headache presentations
• 10-15% die at time of bleed
• 50% die with re-bleed
• Of those remaining, 50% go back to normal function

AETIOLOGY

• 85% ruptured aneurysms
• 10% non-aneurysmal perimesencephalic haemorrhage
• 5% other – AV malformations, inflammatory, cocaine
• DDx
  • AV malformation
  • Cerebal venous thrombosis
  • Dissection of carotid/vertebrobasilar arteries
  • Sinusitis
  • Benign intracranial hypertension
  • Migraine
  • ICH

PRESENTATION

• 50% describe instantaneous thunderclap headache
• Followed by period of depressed consciousness for <1 hour in 50% of patients and focal neurology in 30% of patients
• 20% of patients recall similar headaches (sentinel bleeds)
• 5-10% of ED patients with suspected SAH will be proven correct

ANEURYSMS

• 1/40 people
• Arise at sites of arterial branching
  • Anterior circulation 90%
    • ACA/ACoA (30-40%)
    • ICA and ICA/PCoA (30%)
    • MCA bi/trifurcation (20-30%)
  • Posterior circulation 10%
• Multiple in 30%
• 90% saccular ‘berry aneurysms
• 10% fusiform: Usually vertebrobasilar presenting with compressive symptoms
• Risk factors
  • Familial (first-degree 5x risk)
  • Smoking, HTN, heavy drinking, female

PERIMESENCEPHALIC HAEMORRHAGE

• Haemorrhage restricted to cisterns about brainstem and suprasellar cistern AND negative cerebral angiogram
• Much better prognosis
• Presumed venous origin but some suggest repeat angiogram

TRADITIONAL APPROACH

• In the neurologically normal patient
  • Non-contrast CT
  • Lumbar puncture for xanthochromia

CAN CT WITHIN 6 HOURS RULE OUT SAH?

• Perry et al. 2011
  • 3000 patients. Prospective. 
  • Normal CT at <6 hours: No patients died, 13 lost to follow-up
  • Alive at 6 months used as gold standard. Doesn’t exclude aneurysm but does make it far less likely
  • Not all patients had a lumbar puncture performed
  • 95% confidence interval 97-100%

• Backes et al. 2012
  • Retrospective study
  • 69 patients with negative CT at 6 hours, 1 patient had positive LP for cervical AV malformation
  • Sensitivity 92.1-100%
• Blok et al. 2015
  • Retrospective study
  • NPV of 99.9%
  • Staff radiologist vs. neuroradiologist
  • No re-admissions within 2 years
  • 8 found aneurysms, 3 already clipped and the rest thought to be incidental (despite positive CSF xanthochromia) but didn’t get re-admitted so probably correct
• Dubosh et al. Meta-analysis 2016
  • <1.5 in 1000 patients would have missed SAH if just CT within 6 hours for patients with normal neurological examination, isolated thunderclap headache and experienced radiologist
• UpToDate caveats
  • Patient factors: Clear time of onset, CT within 6 hours, isolated severe rapid-onset headache (i.e. no primary neck pain/syncope/seizure), no meningismus and normal neurological examination
  • Radiologic factors: Modern scanner and experienced radiologist
  • Communication factors: Communicated concern to reporting radiologist of SAH and communicated to patient 1-2/1000 missed

CT

• Factors that reduce sensitivity
  • Few clinical signs
  • Small aneurysm
  • Hb <10
  • Inexperienced radiologist

LUMBAR PUNCTURE

• Should be performed at 12 hours as 100% sensitive if xanthochromia study performed
• No validated way to be certain of traumatic tap vs. SAH
  • Normal CSF pressure
  • Marked decrease between tubes 1-3
  • RBC:WBC 500-1000:1
  • Clot formation
  • Absence of xanthochromia
• 0.4% positive rate after negative plain CT
• 1/2000 if new gen CT within 6 hours though

LP

• So who actually needs one after negative CT within 6 hours?
  • Very high risk patients
    • Previous SAH
    • Polycystic kidney disease
    • Multiple relatives with SAH
  • UpToDate caveats above
  • If alternative diagnoses suspected

CTA

• Mathematical model showed negative CT brain and negative CTA had post-test probability of excluding SAH of 99.43% [9]
• Issues
  • Aneurysms missed if small
  • Exposure to ionising radiation/contrast
  • Aneurysm may be in spasm and not appear
  • Aneurysm may not have bled
  • May assist in other diagnoses e.g. AV malformation/dissection
• Should be performed if CT or LP positive for SAH to visualise aneurysm location/size

CTA

• May detect incidental aneurysms that then undergo unnecessary testing with inherent risk (e.g. DSA) (3% population risk)
• 15% of SAH are due to perimesencephalic haemorrhage so may be missed if CTA vs. LP
• Less cost-effective than LP

MRA

• Probably about equal to non-contrast CT in acute phase
• FLAIR and T2 high sensitivity at 4-14 days delayed presentation
• Limited access
• No real benefit
• UpToDate still advises LP after negative MRI

RECOMMENDED APPROACH

• Non-contrast CT
  • If <6 hours: Shared decision making re: LP
  • If >6 hours: Strongly recommend LP due to lower sensitivity
• LP at 12 hours
  • Opening pressure
  • Xanthochromia study
• If patient declines LP, or another vascular cause considered, offer CTA
• If refuses LP and CTA, book for MRI

MANAGEMENT

• BP control – Systolic 90-140mmhg
  • Labetalol IV preferred
  • Sodium nitroprusside
• Normothermia
• Prophylactic antiemetics
• DVT prophylaxis (pharmacological witheld)
• Prophylactic laxatives and good oral fluid intake if swallow okay
• Consider haematoma evacuation

MANAGEMENT

• Coiling better than clipping
  • Survival benefit at 1 and 7 years with higher risk of late rebleeding in coiling
  • Those with wide necks, multiple filling vessels or giant aneurysms are not amenable to coiling
• Early surgery (<3 days) vs. delayed (10-12 days)
  • Early reduces risk of vasospasm/rebleed but friable tissues
  • Delayed easier but risks vasospasm/rebleed
  • No clear benefit of one over the other
• Nimodipine 60mg q4h for 3 weeks (NNT = 20)
  • Reduces risk of ischaemic stroke by 34%
• Seizure prophylaxis (controversial)

WFNS GRADE

• I – GCS 15 – Absent motor deficit 
  • 70% survival
• II – GCS 13-14 – Absent motor deficit
  • 60% survival
• III – GCS 13-14 – Motor deficit
  • 50% survival
• IV – GCS 7-12 – May have motor deficit
  • 20% survival
• V – GCS <7 – May have motor deficit
  • 10% survival

FISHER SCALE

• I – No visible bleed – 0-21% risk of vasospasm
• II – <1mm thick – 0-25% risk of vasospasm
• III – Localised clot and/or vertical layer >1mm thick – 23-96% risk of spasm (HIGHEST)
• IV – ICH or IVH – 0-35% risk of spasm

HUNT & HESS

• Older one
• I – Asymptomatic or minimal headache and slight nuchal rigidity
• II – Moderate to severe headache, CN palsy, nuchal rigidity but no other neuro deficit
• III – Drowsy, confused or mild focal deficits
• IV – Stupor, moderate-severe hemiparesis, early decerebrate rigidity and vegetative
• V – Coma, decerebrate, moribund

HUNT & HESS

• I & II – 71% good outcome
• III – 14% good outcome
• IV and V – No good outcomes

COMPLICATIONS

• Acute hydrocephalus
  • Within first 24 hours often characterised by one-point drop in GCS, sluggish pupils and sunset eyes (bilateral downward deviation of gaze)
  • Needs EVD
• Rebleeds
  • Often within first few hours
  • 19% overall incidence in first 2 weeks with 1.5% per day after that for next 13 days

COMPLICATIONS

• Vasospasm
  • Seen in 70% of patients but not all symptomatic
  • Usually 4-14 days after bleed
  • Transcranial Doppler MCA velocity >120cm/s correlates with angiographic spasm
  • If depressed LOC in absence of rebleeding, hydrocephalus or metabolic disturbances, investigate spasm and treat
• Parenchymal haematoma
  • Up to 30% of aneurysm ruptures and has much worse outcome

COMPLICATIONS

• Medical
  • Arrhythmias (35%)
  • Liver dysfunction (24%)
  • Neurogenic pulmonary oedema (23%)
  • Pneumonia (22%)
  • ARDS (20%)
  • Renal dysfunction (5%)

COMPLICATIONS

• Cerebral salt-wasting syndrome
  • Excessive natriuresis of unclear cause
  • Usually within first week and resolves by 2-4 weeks
  • Urine sodium concentrations elevated in this and SIADH but urinary sodium excretion (urine sodium concentration x urine volume) is high in CSWS and normal in SIADH
  • Should respond to saline delivery (vs. SIADH that warrants fluid restriction  Although not in SAH where dehydration = bad)

ICP

• ICP monitors not clearly indicated
• EVD indicated in:
  • Obstructive hydrocephalus
  • WFNS >= 3

BP CONTROL

• 2012 American Stroke Guidelines
  • <160mmHg is reasonable until secured aneurysm
  • Labetalol preferred as does not vasodilate cerebral vessels
  • If conscious, can aim for <140mmHg as obviously have adequate CPP
  • If unconscious, avoid antihypertensives unless >180mmHg as may be due to inadequate CPP

SEIZURE PROPHYLAXIS

• Phenytoin avoided as associated with poorer outcomes
• Keppra if at all
• Avoid if possible given unclear benefit/risk ratio

WHAT IF PREVIOUSLY CLIPPED/COILED ANEURYSM?

• 3% risk of late rebleed SAH over 10 years
• May be from recurrence of treated aneurysm, rupture of pre-existing untreated aneurysm or de novo aneurysm formation
• Recurrence more likely in coiled aneurysms (9-30%) than clipped (<1%)
• Probably warrants usual protocol + CT-A to rule out recurrence (esp. if coiled) with lower threshold to LP

OTTAWA SAH RULE

• Inclusion criteria
  • >= 15 yo
  • Severe, atraumatic headache of peak intensity within 1 hour
  • No history of intracranial tumors
  • No history of chronic headache of similar type
  • No history of previous SAH or aneurysm
  • No new neurological deficits

OTTAWA SAH RULE

• Exclusion criteria
  • GCS <15
  • Head trauma in last 7 days
  • >14 days of headache
  • Chronic headaches of similar type
  • Papilloedema
  • New neuro deficits

OTTAWA SAH RULE

• Sensitivity of 100% and specificity of 13.6%
• May reduce investigation by 4.7% (89% to 84.3%)
• All validated in Canada in centres where rule designed

OTTAWA SAH RULE

• If meeting above inclusion criteria:
  • CT not required if all of the following:
    • Age <40
    • No neck pain or stiffness
    • No limited neck flexion
    • No witnessed LOC
    • No onset during exertion
    • No immediately peaking pain (thunderclap)

The Summary

Introduction

• Subarachnoid haemorrhage is leakage of blood into the subarachnoid space, most often due to rupture of an intracranial aneurysm. 
• Classic presentation:
  • Sudden severe headache +/- ALOC +/- neurology 
• 1 – 4% of headache presentations to ED are due to SAH
• 10% of thunderclap headaches due to SAH

Rapid Review – SAH

•  Most (80 – 85%) SAH due to ruptured aneurysm. 10% due to perimesencephalic haemorrhage. 
• Ant communicating artery aneurysm most common. However posterior circulation aneurysms rupture at smaller size. 
• >10mm = 50% risk of rupture annually 
• >5mm = usually needs neurosurg intervention
• Grading Systems
  • World Federation of Neurosurgical Societies Scale
    • Grade 1 – GCS 15, no motor deficits
      • 70% survival
    • Grade 2 – GCS 13 – 14, no motor deficits (M6)
      • 60% survival
    • Grade 3 – GCS 13 – 14, with motor deficits (M < 6)
      • 50% survival 
    • Grade 4 – GCS 7 – 12, with or without motor deficits
      • 20% survival
    • Grade 5 – GCS 3 – 6, with or without motor deficits 
      • 10% survival
  • Modified Fischer Scale (Radiological) 
    • Grade 1 
      • No blood
    • Grade 2 
      • Thin (<1mm) SAH with no intraventricular extension 
    • Grade 3
      • Thin (<1mm) SAH with intraventricular extension 
    • Grade 4 
      • Thick (>1mm) SAH with no intraventricular extension
    • Grade 5 
      • Thick (>1mm) SAH with intraventricular extension 
• BP target —> 140 – 180mmHg (prevents rebleeding) 
• Imaging controversies 
  • CT brain < 6 hours symptoms onset —> Sn ~ 99%
  • CT brain + CTA —> Sn ~ 99.4% 
  • Absolute rule out 
    • CT brain as early as possible + LP at 12 hours post symptoms onset 
  • MRI no better then CT 
• Complications of SAH (Top 5 to think about, not full list) 
  • Rebleeding
  • Vasospasm
  • Obstructive Hydrocephalus 
  • Neurogenic Pulmonary Oedema 
  • Cerebral Salt Wasting Syndrome 

Clinical Features/Discriminating Features 

• History of presenting complaint in SAH:
  • Headache is principle presenting complaint for SAH ~ 95% patients present with headache
  • Sudden onset and severe (usually worst headache ever experienced by the patient)
  • About 1 in 4 patients with sudden onset severe headache will have SAH
  • 50% of patients will have a ‘warning leak’ with less severe headache that self-resolves in the preceding days
  • Upper neck pain is common with SAH
  • 1/3 of patients develop SAH during strenuous exercise
  • Nausea/vomiting present in 75% 
  • LOC either brief or permanent can occur with SAH
  • any headache with LOC needs a CT
  • Seizures occur in 15% of patients
• Physical Exam in SAH:
  • 2/3 of patients presenting to ED with SAH have impaired level of consciousness
  • 50% of these have coma
  • Acute confusion can occur
  • Neck stiffness common in SAH
  • Focal neurological signs present in 25%
  • 3rd nerve palsy, 6th nerve palsy
  • Bilateral lower limb weakness of anterior communicating artery aneurysm 
  • Fundoscopy may reveal haemorrhage or papiloedema 
  • ECG may demonstrate ST changes or characteristic deep t-wave inversions 

Diagnosis of SAH

• Diagnosis of SAH
  • Non-contrast CT Brain
    • Sensitivity of a non-contrast CT brain is highest closer to symptom onset
    • Sn=98% 6 – 12 hours following symptom onset
    • Sn = 91 – 93% at 24 hours following symptom onset 
    • Sn = 50% at 1 week following symptom onset 
  • CT angiography
    • Use of CTA following normal non-contrast CT brain should be used only if clinical suspicion of SAH is high
    • Normal CT brain + CTA has probability of ruling out SAH in 99.4% of cases 
  • Lumbar Puncture 
    • Most institutions recommend LP to rule out SAH in setting of normal CT brain
    • RBC count and Xanthochromia most useful CSF analysis tests for SAH
    • RBC count < 100 in tube 4 effectively rules out SAH
    • RBC count > 10,000 in tube 4 increases odds of SAH x 6 fold 
    • Absence of xanthochromia is a true negative finding and can rule out SAH 

• Combinations used to rule out SAH:
  • Scenario 1 – Low Index of Clinical Suspicion of SAH, presentation within 6 hours
    • Normal CT brain within 6 hours of symptom onset = 99% sensitive for SAH 
    • No further testing required
  • Scenario 2 – High Index of Clinical Suspicion of SAH, presentation with 6 hours
    • Normal CT brain
    • Normal CT Angiogram (if positive CTA in high clinical suspicion, no LP just call neurosurg) 
    • < 0.5% risk of SAH but given the high clinical index of suspicion, use patient decision making, advocate for LP
    • LP performed at 12 hours, if negative xanthochromia —> NOT an SAH, need to consider other causes of severe headache 
  • Scenario 3 – Low index of clinical suspicion, presentation > 6 hours 
    • Normal CT Brain
    • Normal CT Angiogram
    • Sn of combination is 99.4% 
    • Discuss with patient, but likely advocate for no LP 
    • Scenario 4 – High index of clinical suspicion, presentation > 6 hours 
      • CT brain + CTA + likely needs LP (if CTB and CTA are normal) 

Management

• Resus = Supportive Management
  • Resuscitative measures is focused on general supportive measures and minimisation of early complications
  • Airway protection and neuroprotective ventilation strategies required if ALOC
  • Maintain oxygenation
  • Maintain normocapnia
  • Maintain BP – Sys BP 110 – 140mmHg
  • Reverse any anticoagulation or anti platelet effects 
  • Sit the patient up to 30 – 45 degrees
  • Treat seizures with benzodiazepines and load with leveciracetam 

• Definitive Management
  • Early neurosurgical intervention required 
  • Prevention of rebleeding
    • BP control
  • Early coiling of aneurysm

• Prevention of vasospasm 
  • Nimodipine 60mg PO/NG Q4H 

• Prevention of obstructive hydrocephalus
  • EVD should be placed if WFNS grade > 3 

• Patient Expectation
  • Explain the prognosis as per WFNS grade and in consultation with neurosurg
  • Explain the likely hospital management 

• Disposition 
  • Generally admitted to either neurosurgical HDU or ICU 

Key Decision Points/Consultant Level Thinking

• Earlier the CT the better the sensitivity. Therefore if you see a triage that looks suspicious, go review and organise the scan. It might save an LP or CTA on the patient. 
• Consider disposition early, any SAH patient likely to require neuro HDU, start planning for this. Also and EVD can be life saving, if you don’t have neurosurg at your facility start working on logistics of transfer as soon as the diagnosis is made 
• Create your own evidence based approach to diagnosis of SAH. Generally with presentations < 6 hours, 6 – 12 hours and > 12 hours. This will allow you to have an informed discussion with the patient (or NOK) about appropriate diagnostic strategies and ‘rule out’ plans. 

Critical Interventions for this Topic (what will actually make a difference to outcomes)

• Diagnostic certainty difficult in SAH. Must use clinical reasoning to assess pre-test probability and aid you to investigate appropriately 
• ED’s primary role in SAH is diagnosis and early instigation of preventative strategies to mitigate secondary complications
  • Neuroprotective intubation and ventilation if required
  • Monitor and control the BP
  • Reverse any reversible anticoagulants 
  • Administer Nimodipine 60mg 
  • Early referral to neurosurgical team 
• ED also has a key role in early (accurate) information for family, if possible this should be done in conjunction with the neurosurgical team to provide consistent information 

Last Updated on November 4, 2020 by Andrew Crofton