Subarachnoid Haemorrhage
Intracranial haemorrhage into the subarachnoid space that occurs commonly with other forms of intracranial haemorrhage, and is secondary to:
Intracranial haemorrhage can be divided into:
- Intra-axial
Intracerebral haemorrhage. - Extra-axial
- EDH
- SDH
- SAH
- IVH
- Aneurysm rupture
85% of all cases. - Trauma
- Other
- AVM
- Pituitary apoplexy
- Cocaine
- Fistulae
- Reversible cerebral vasoconstriction syndrome
Grade | WFNS | Grade | Modified Fisher |
---|---|---|---|
1 | GCS 15 | 0 | No SAH or IVH |
2 | GCS 13-14, no motor deficit | 1 | Thin SAH, no IVH |
3 | GCS 13-14, motor deficit | 2 | Thin SAH, IVH present |
4 | GCS 7-12 | 3 | Thick SAH, no IVH |
5 | GCS 3-6 | 4 | Thick SAH, IVH present |
Notes: | Assists prognosis and determining post-operative destination. Graded from 1-5. | Radiological grading scale that predicts vasospasm risk. Graded from 0-4. |
The Hunt & Hess grading system is largely deprecated due to high inter-rater unreliability, but is included as a historical footnote.
Grade | Hunt & Hess |
---|---|
1 | Mild headache, no or minimal nuchal rigidity |
2 | Moderate to severe headache, nuchal rigidity, may have CN deficit |
3 | Confusion or lethargy, with or without mild focal deficit |
4 | Stuporous, severe focal deficit |
5 | Comatose, posturing or no motor response |
Epidemiology and Risk Factors
Aneurysmal SAH:
- Occurs in ~9/100,000
- Has a high mortality rate
- 15% prehospital
- 30% 30-day
- 40% make a good recovery
Prognostication:- Age
- Conscious state
- Blood volume
- Risk factors include:
- Patient
- Age
- Female
- Smoking
- Heavy ETOH use
- Sympathomimetic drug use
- Disease
- HTN
- PHx SAH
- FHx SAH
- Polycystic kidney disease
- Type IV Ehlers-Danlos syndrome
- Patient
Pathophysiology
Aetiology
Clinical Manifestations
Typical presentation of:
- Sudden, severe headache
- “Worst headache of life”
- Different from usual headaches
- 20% of patients may have had similar headache before
Potentially sentinel haemorrhage.
- Often associated with:
- Loss of consciousness
- Nausea
- Vomiting
- Photophobia
- Meningeal irritation
More reliable in patients iwth higher GCS.
Headache may occur without other symptoms, and patients may not seek medical attention or be misdiagnosed.
Diagnostic Approach and DDx
Investigations
Laboratory:
- LP
Recommended if negative or equivocal CT in the setting of high clinical suspicion. Important findings:- Opening pressure
- CSF collection in 4 consecutive tubes
RBC counts can be measured in each to exclude traumatic tap. - Xanthochromia
- By visual inspection
May take 12 hours to develop. - Spectrophotometry
Superior to visual inspection.
- By visual inspection
Imaging:
- Non-contrast CT head
- Sensitivity ↑ from 93% to 100% over 6 hours, and falls to 60% over the next 7 days.
- Repeat CT should occur at 24-48 hours to identify any new infarctions
Those not attributable to EVD or IPH should be considered to be due to delayed cerebral ischaemia.
- CTA
First-line vascular imaging to identify source, though may miss aneurysms ⩽4mm. - MRI
May be slightly superior to CT. - DSA
Gold-standard for vascular imaging, and facilitates treatment. - Transcranial Doppler
Used to monitor for vasospasm.- Suggested by a Lindegaard ratio >3
Mean velocity in the MCA/ velocity in ipsilateral ICA.
- Suggested by a Lindegaard ratio >3
Other:
- EEG
Consider continuous EEG monitoring in patients who- Have a poor grade of SAH
- Fail to improve
Management
Resuscitation:
- A
- Secure if required
- C
- Aggressive blood pressure control for the unsecured aneurysm
- Target SBP 100-160mmHg or MAP ≤110mmHg
Adjust target based on premorbid baseline BP. - Agents should preferably be given by infusion, and include:
- Labetalol 5-20mg/hr
- Short-acting opioids for analgesia
- Dexamethasone can be considered for meningeal irritation
- Avoid hypotension
- Target SBP 100-160mmHg or MAP ≤110mmHg
- Maintain euvolaemia
Avoid hypervolaemia.
- Aggressive blood pressure control for the unsecured aneurysm
- H
- Reverse anticoagulation
Specific therapy:
- Pharmacological
- Nimodipine
- 60mg Q4H PO
- Can adjust to 30mg Q2H PO if symptomatic hypotension
- Can adjust to continuous infusion (up to 0.5μg/kg/min) if enteral route unavailable
- Commonly requires vasopressors
- Administered to all SAH patients for 21 days
- Significantly improves outcome (↓ stroke by 34%) but does not appear to reduce radiological vasospasm
Neuroprotection probably by another mechanism.
- 60mg Q4H PO
- Nimodipine
- Procedural
- Aneurysm securing
- Transfer to high-volume aneurysm centre for securing of aneurysm
- Securing recommended within 48 hours of onset
- Decision for clipping or coiling depends on location aneurysm location and characteristics
- Clipping
Favoured for aneurysms:- From the MCA
- With a wide neck:body ratio
- With crucial arteries from aneurysm dome
- With a large parenchymal haematoma
- Coiling
- Higher 1-year survival in patients who are equally suitable for clipping or clipping
- ↑ Risk of rebleeding
- Risk of rupture without option for immediate surgical control
- Clipping
- EVD
Early if signs of hydrocephalus or IVH. Open at:- 10cmH2O for secured aneurysm
- 15cmH2O for unsecured aneurysm
- Aneurysm securing
Supportive care:
- C
- Defend CPP
- D
- Glucose control
Careful control with strict avoidance of hypoglycaemia.
- Glucose control
- E
- Temperature control
Treat >38°C targeting normothermia, with aggressiveness based on risk of delayed cerebral ischaemia.- Anti-pyretics
- Active cooling
- Temperature control
- F
- Hyponatraemia
Treat early with hydrocortisone and fludrocortisone.
- Hyponatraemia
- H
- Anaemia
Hb level should be maintained at 80-100g/L. - DVT prophylaxis
UFH should be considered:- 24 hours after coiling
- 48 hours after clipping
↑ Abstinence due ↑ bleeding risk of craniotomy.
- Anaemia
Disposition:
- ICU
- If intubated or airway concerns
- Often required for haemodynamic control prior to securing aneurysm
- May be required if EVD in situ, depending on ward skill
- Neurosurgical HDU
Anaesthetic Considerations
Marginal and Ineffective Therapies
- Prophylactic ‘triple-H’ therapy:
- Not recommended due to lack of efficacy and evidence of harm
- Consists of:
- Hypervolaemia
- Hypertension
- Haemodilution
Theorised to improve laminar flow and ↑ overall DO2.
- Prophylactic anticonvulsants
Routine use worsens outcomes. - Tranexamic acid
May ↑ risk of poor neurological outcome with no clear evidence of benefit.
Complications
DCI is covered in detail under Delayed Cerebral Ischaemia.
- C
- Myocardial injury
Catecholamine surge with risk of myocardial necrosis.- LV dysfunction in 10-30%
- Neurocardiogenic shock/Takotsubo cardiomyopathy may arise due to combination of ↑ preload and afterload (catecholamines), and ↓ inotropy (necrosis)
- Myocardial injury
- D
- Rebleeding
Major life-threatening complication- 20% of patients in first 24 hours
- Majority (50-90%) occur within 6 hours
- Uncommon after 72 hours
- 20-60% mortality
- DCI
Leading cause of neurological morbidity due to cerebral infarction. - Secondary hydrocephalus
- Occurs in 20% of patients
Within minutes to hours of onset. - Requires EVD
- Occurs in 20% of patients
- Seizures
- Occurs in 26% of patients
Correlated with blood volume and MCA aneurysms. - Levetiracetam is first line
- Occurs in 26% of patients
- Rebleeding
- F
- Hyponatraemia
30% of cases.- CSW
- Hypernatraemia
- Hyponatraemia
Delayed cerebral ischaemia is covered in detail under Delayed Cerebral Ischaemia.
Prognosis
Poor prognostic features:
- Age
- Medical comorbidities
- Delayed Cerebral Ischaemia
- Hyperglycaemia
- Anaemia
Good prognostic features:
- High-volume neurosurgical centre
Key Studies
Nimodipine:
- BRANT (1989)
- ~550 Britons with aneurysmal SAH
- Multicentre (4) RCT
- Nimodipine vs. placebo
- Nimodipine 60mg Q4H PO for 21 days
- ↓ Cerebral infarction with nimodipine (20% vs. 33%)
Clipping vs. coiling:
- ISAT (2002)
- ~2100 Britons with aneurysmal SAH with interventionalist equipoise for preferred therapy
- Multicentre RCT
- Coiling vs. clipping
- ↓ Dependency (mRS 3-6) or death at 1 year in coiling (24% vs. 36%)
- Slight ↑ risk of rebleeding with clipping (~1/600 patient-years)
TXA:
- ULTRA (2021)
- 955 non-pregnant Dutch adults with CT-confirmed, non-traumatic SAH and GCS <12 within <24 hours of onset
- Without DVT, PE, hypercoagulable state, or imminent risk of death
- Randomised, assessor-blinded, multicentre (24) RCT
- 950 patients provides 80% power of 8.1% difference in good (mRS 0-3) outcome
- TXA vs. placebo
- Balanced at baseline
- TXA group
- 1g bolus
- 1g infusion every 8 hours until aneurysm secured or 24 hours reached
- Median time from symptoms to TXA was ~3 hours
- No difference in good outcome at 6 months
- Secondary outcome: TXA group had ↓ (48% vs 56%, OR 0.74 CI 0.57-0.96) in excellent (mRS 0-2) outcome
- No difference in SAE, re-bleedings, or DCI
References
- Okazaki T, Kuroda Y. Aneurysmal subarachnoid hemorrhage: intensive care for improving neurological outcome. Journal of Intensive Care. 2018 May 8;6(1):28.
- Muehlschlegel S. Subarachnoid Hemorrhage. Continuum (Minneap Minn). 2018 Dec;24(6):1623–57.
- Bersten, A. D., & Handy, J. M. (2018). Oh’s Intensive Care Manual. Elsevier Gezondheidszorg.
- Post R, Germans MR, Tjerkstra MA, et al. Ultra-early tranexamic acid after subarachnoid haemorrhage (ULTRA): a randomised controlled trial. The Lancet. 2021;397(10269):112-118. doi:10.1016/S0140-6736(20)32518-6