Subarachnoid Hemorrhage (SAH)
Subarachnoid hemorrhage (SAH) is bleeding into the subarachnoid space between the arachnoid mater and pia mater where cerebrospinal fluid (CSF) circulates.
It is one of the most devastating neurological emergencies with:
- Mortality: 25–50%
- Significant disability among survivors
- Peak incidence: 40–60 years
Approximately 80–85% of spontaneous SAH results from rupture of an intracranial aneurysm.
Relevant Anatomy
The subarachnoid space contains:
- Cerebral arteries
- Cerebral veins
- Cranial nerves
- CSF
Blood entering this space spreads rapidly throughout basal cisterns and ventricular system causing:
- Raised ICP
- Cerebral ischemia
- Hydrocephalus
- Vasospasm
Etiology
Aneurysmal SAH (Most Common)-80–85%
Common aneurysm locations:
Anterior circulation (85%)
- Anterior communicating artery (ACom) (most common)
- Posterior communicating artery (PCom)
- Middle cerebral artery (MCA)
Posterior circulation
- Basilar tip
- Vertebral artery
- PICA
Non-Aneurysmal SAH
Perimesencephalic SAH
- Venous bleeding
- Better prognosis
- Rare rebleeding
Others
- AVM rupture
- Dural AV fistula
- Vasculitis
- Cerebral venous thrombosis
- Moyamoya disease
- Coagulopathy
- Cocaine abuse
- Trauma
Risk Factors
|
Nonmodifiable Risk Factors |
Modifiable Risk Factors |
|
Female sex |
Hypertension – Most important risk factor |
|
Age >40 years |
Smoking – Strongest modifiable risk factor |
|
Family history |
Alcohol – Heavy consumption increases risk |
|
Connective tissue disorders |
Cocaine use – Markedly increases aneurysm rupture risk |
|
• Ehlers-Danlos syndrome |
|
|
• Marfan syndrome |
|
|
• Autosomal Dominant Polycystic Kidney Disease (ADPKD) |
|
Pathophysiology
Step 1: Aneurysm Rupture
Arterial blood suddenly enters subarachnoid space.
Step 2: Sudden ICP Rise
ICP may transiently approach MAP.
Consequences:↓ Cerebral perfusion pressure
CPP=MAP−ICP
This produces:
- Global cerebral ischemia
- Loss of consciousness
- Cardiac instability
Step 3: Blood Breakdown Products
Hemoglobin degradation releases:
- Oxyhemoglobin
- Free radicals
- Endothelin
Leading to:
- Endothelial injury
- Vasoconstriction
- Inflammation
Step 4: Delayed Cerebral Ischemia
Occurs days later.
Major cause of morbidity.
Step 5: Hydrocephalus
Blood blocks:
- Arachnoid granulations
- CSF pathways
Result:Acute obstructive hydrocephalus.
Clinical Presentation
Classic Symptom
Thunderclap Headache
Patient often says:”Worst headache of my life”
Characteristics:
- Abrupt
- Seconds to minutes
- Explosive onset
Occurs in >90%.
Associated Symptoms
Meningeal Irritation
- Neck stiffness
- Photophobia
- Vomiting
Neurological Symptoms
- Altered sensorium
- Seizures
- Focal deficits
- Coma
Cranial Nerve Palsies
CN III palsy-Suggests PCom aneurysm.
Features:
- Ptosis
- Dilated pupil
- Ophthalmoplegia
Sentinel Headache
- Occurs days to weeks before rupture.
- Represents minor aneurysm leak.
- Seen in 10–40%.
Physical Examination
Vital Signs
May show:
- Severe hypertension
- Bradycardia
- Cushing response
Neurological Findings
- Meningismus
- Reduced GCS
- Focal deficits
- Coma
Diagnosis
Non-Contrast CT Head-First-line investigation.
|
Time |
Sensitivity |
|
<6 h |
>95–99% |
|
6–24 h |
90–95% |
|
>3 days |
Falls significantly |
Typical findings:
- Basal cistern blood
- Sylvian fissure blood
- Intraventricular hemorrhage
- Hydrocephalus
Lumbar Puncture
Indication:High suspicion despite negative CT.
Look for:Xanthochromia
Best detected:12 hours–2 weeks
Findings:
- Bilirubin in CSF
- Persistent RBCs
CT Angiography (CTA)
Current standard vascular imaging.
Identifies:
- Aneurysm
- AVM
- Vasospasm
Sensitivity >95%.
Digital Subtraction Angiography (DSA)
Gold standard.
Used when:
- CTA negative
- High suspicion remains
- Endovascular planning
MRI
Useful later.
Sequences:
- FLAIR
- GRE
- SWI
Less useful in hyperacute setting.
Severity Grading
Hunt and Hess Scale
|
Grade |
Findings |
|
I |
Mild headache |
|
II |
Severe headache, nuchal rigidity |
|
III |
Drowsiness/confusion |
|
IV |
Stupor |
|
V |
Coma |
WFNS Grade-Based on GCS.
|
Grade |
GCS |
|
I |
15 |
|
II |
13–14 |
|
III |
13–14 + deficit |
|
IV |
7–12 |
|
V |
3–6 |
Fisher Scale-CT-based.
|
Grade |
Blood |
|
1 |
No blood |
|
2 |
Thin SAH |
|
3 |
Thick SAH |
|
4 |
IVH or ICH |
Modified Fisher Scale
Most used today.
|
Grade |
SAH |
IVH |
|
0 |
No SAH |
No |
|
1 |
Thin |
No |
|
2 |
Thin |
Yes |
|
3 |
Thick |
No |
|
4 |
Thick |
Yes |
Higher grade = higher vasospasm risk.
Emergency Stabilization
ABC Approach
Blood Pressure Management
- Before Aneurysm Securing Major goal:Prevent rebleeding.
- Current recommendations:SBP Target Usually:120–160 mmHg
Preferred Antihypertensives
|
Drug |
Comment |
|
Nicardipine infusion |
Most commonly used |
|
Clevidipine infusion |
Excellent titratable agent |
|
Labetalol bolus/infusion |
Commonly used |
|
Esmolol |
Occasionally used |
Avoid:
|
Drug |
Reason |
|
Nitroprusside |
May increase ICP |
|
Nitroglycerin |
May increase ICP |
|
Hydralazine |
Unpredictable effect |
Definitive Aneurysm Treatment
Should occur as early as possible (usually within 24 h).
Endovascular Coiling
Current preferred approach in many aneurysms.
Advantages:
- Less invasive
- Better short-term outcomes
Surgical Clipping
Preferred when:
- MCA aneurysm
- Large hematoma
- Complex anatomy
Rebleeding
Highest Risk Period-First 24 hours.
Prevention
- Early coiling/clipping
- BP control
- Avoid agitation
Tranexamic Acid
ULTRA trial showed that ultra-early (<24 h), short-course TXA reduces rebleeding tendency but does not improve 6-month functional outcome in aneurysmal SAH; therefore routine TXA use is not recommended.
Delayed Cerebral Ischemia (DCI)
Most important delayed complication.
Occurs:Day 4–14
Peak:Day 7–10
Mechanism
Not solely vasospasm.
Also:
- Microthrombosis
- Inflammation
- Cortical spreading depolarization
Clinical Features
New:
- Weakness
- Aphasia
- Reduced consciousness
Diagnosis
- TCD-Mean MCA velocity:
- 120 cm/s suggests vasospasm
- 200 cm/s severe vasospasm
- Lindegaard ratio >3–6.
- CTA-Useful screening tool.
- DSA-Gold standard.
Prevention of Vasospasm—Nimodipine
- Only therapy proven to improve neurological outcome.
- Dose-60 mg orally/NG every 4 h
- Duration:-21 days
- If hypotension:-30 mg every 2 h.
- Give to all aneurysmal SAH patients unless contraindicated.
Treatment of Symptomatic Vasospasm/DCI
Step 1
Optimize:Oxygenation/Hemoglobin/Volume status
Step 2
Induced Hypertension Recommended for sympt-omatic DCI after aneurysm securing.
Goal:
Increase cerebral blood flow through narrowed vessels.
Common Targets
|
Severity |
SBP Target |
|
Mild DCI |
160–180 mmHg |
|
Moderate DCI |
180–200 mmHg |
|
Severe DCI |
Up to 220 mmHg in selected patients |
or
|
Parameter |
Target |
|
MAP |
90–130 mmHg |
Targets are individualized.
Vasopressors Used
|
Drug |
Preferred? |
|
Norepinephrine |
Yes |
|
Phenylephrine |
Yes |
|
Vasopressin |
Occasionally |
|
Dopamine |
Rarely |
Step 3
Endovascular Therapy
Balloon angioplasty
Best for proximal vessels.
Intra-arterial vasodilators
Examples:
- Verapamil
- Nicardipine
- Milrinone
Triple-H Therapy
Historical:
- Hypertension
- Hypervolemia
- Hemodilution
No longer recommended.
Current practice:Euvolemia + induced hypertension only.
Hydrocephalus
Occurs in 15–30%.
Features:
- Reduced consciousness
- Enlarged ventricles
- ICP elevation
Treatment—External Ventricular Drain (EVD)
Gold standard.
Provides:
- CSF diversion
- ICP monitoring
Current Practice
- Periprocedural antibiotic prophylaxis commonly used
- Prolonged antibiotics for entire EVD duration are not recommended
Typical example:
- Cefazolin before insertion
Extended prophylaxis has not shown benefit and increases resistant organisms.
ICP Management
Treat when:ICP >20–22 mmHg
Measures:
- Head elevation 30°
- Sedation
- Analgesia
- CSF drainage
- Hyperosmolar therapy
Hypertonic Saline
Preferred in many ICUs.
Mannitol
0.25–1 g/kg
Useful when:
- ICP crisis
- Hemodynamic stability
Seizures
Incidence:6–20%
Risk factors:
- Cortical hematoma
- MCA aneurysm
- Rebleeding
Antiepileptic Therapy
Not routinely given long-term.
Short-course prophylaxis may be used in:
- High-risk patients
- Early seizures
Common agents:
- Levetiracetam
- Valproate
Sodium Disorders
Very common.
- SIADH
- Cerebral Salt Wasting
Cardiac Complications
Due to catecholamine surge.
-ECG Changes
- QT prolongation
- ST changes
- T-wave inversion
-Arrhythmias—AF/VT/Bradycardia
-Stress Cardiomyopathy
Neurogenic stunned myocardium.
Can mimic MI.
Echo:
- Reduced EF
- Regional dysfunction
Pulmonary Complications
- Neurogenic pulmonary edema
- ARDS
- Aspiration pneumonia
ICU Monitoring
Daily assessment:
- Neurological examination
- GCS
- Pupils
- TCD
- Electrolytes
- Fluid balance
ICU Targets
|
Parameter |
Target |
|
SpO₂ |
>94% |
|
PaO₂ |
>80 mmHg |
|
Temperature |
Normothermia |
|
Glucose |
140–180 mg/dL |
|
Sodium |
Normal range |
|
CPP |
>60–70 mmHg |
|
ICP |
<20–22 mmHg |
Pharmacologic DVT Prophylaxis
Key Principle Balance: Rebleeding risk vs thrombosis risk
-Before Aneurysm Securing
Usually Avoid
UFH/LMWH generally withheld until aneurysm is secured.
Reason:Potential risk of catastrophic rebleeding.
=After Coiling or Clipping
Once:
- Aneurysm secured
- Repeat imaging stable
- Neurosurgical approval obtained
Then start:
Options
|
Drug |
Dose |
|
Enoxaparin |
40 mg SC daily |
|
UFH |
5000 U SC q8–12h |
Usually within 24–48 hours after securing aneurysm if no bleeding concern.
EVD Present?
Modern practice:Pharmacologic prophylaxis can still be used
After:
- Stable CT
- Neurosurgical agreement
Temporary withholding around EVD insertion/removal is common.
Clinical Perals
- ACom aneurysm = most common aneurysm causing SAH.
- Thunderclap headache = hallmark presentation.
- Non-contrast CT is first investigation.
- Negative CT + high suspicion → LP for xanthochromia.
- DSA = gold standard vascular study.
- Rebleeding risk highest during first 24 hours.
- Nimodipine is the only drug proven to improve neurological outcome.
- Vasospasm typically occurs day 3–14, peaks day 7.
- DCI is now considered more important than angiographic vasospasm alone.
- Triple-H therapy is obsolete.
- EVD is treatment of acute hydrocephalus.
- Induced hypertension is used for symptomatic DCI after aneurysm securing.
- Hyponatremia after SAH is commonly due to SIADH or cerebral salt wasting.
- Neurogenic stunned myocardium is a classic extracranial complication.
- Early aneurysm coiling/clipping is the single most important intervention to prevent rebleeding.