creation date: 2026-02-09 18:43
tags: Pathologies
Subarachnoid Hemorrhage
Background
Definitions
Subarachnoid hemorrhage (SAH) is a type of hemorrhagic stroke.
Hemorrhagic strokes account for 20% of all strokes, the other 80% being ischemic stroke, and is further subtyped into subarachnoid hemorrhage (10% of strokes) and intracerebral hemorrhage (10% of strokes).
The subarachnoid space refers to the space between the arachnoid membrane and the pia mater.
Etiology and Risk Factors
SAH is found in up to 60% of moderate-to-severe traumatic brain injuries.
In non-traumatic cases, 85% are secondary to aneurysmal rupture. Risk factors include:
- Hypertension
- Smoking
- Family history
- Alcohol use
- Sympathomimetic drugs
- Estrogen deficiency
- Older age
In cases of nonaneurysmal subarachnoid hemorrhage (NASAH), etiologies include:
- Perimesencephalic NASAH (specific pattern of blood but with normal cerebral angiography)
- Occult aneurysm (undetected aneurysm that is later found on repeat studies)
- Vascular malformations (eg. arteriovenous malformations or dural arteriovenous fistulae)
- Intracranial arterial dissection
Other causes of SAH include:
- Cocaine abuse
- Cerebral amyloid angiopathy
- Cerebral venous thrombosis
- Sickle cell disorders
- Cerebral vasculitis
- Moyamoya disease
Pathogenesis
The subarachnoid space consist of cerebrospinal fluid and blood vessels that supply the brain with blood. The exact pathogenesis varies by etiology but results in the accumulation of blood in this space.
In cases of aneurysmal SAH, hemodynamic stress results in the enlargement of vessels. This itself can cause neurological signs due to compression.
Rupture of aneurysm or other causes of vessel rupture (eg. trauma) results in reduced blood flow, vasospasm, and thus cerebral ischemia.
Clinical Presentation
Signs & Symptoms
The classic presentation is a headache that is:
- Sudden in onset
- Maximal at onset
- Severe (“worst headache of life”)
It should be noted that onset may not always be instantaneous. The headache may also be localized or generalized. Prodromal headaches may occur days to weeks prior.
Associated symptoms include:
- Brief loss of consciousness
- Vomiting
- Neck pain or stiffness
- Meningismus and lower back pain (may develop several hours later)
Findings on physical exam include:
- Hypertension
- Meningismus
- Neurological signs (which ones will depend on location of hemorrhage and the characteristics of the stroke)
History & Physical Exam
A compliant of headache characteristic of SAH should be sufficient for immeduate evaluation, even in those who are alert and able to provide a history.
In a neurologically intact patient with an acute nontraumatic headache that reached maximum intensity within one hours, the Ottawa Subarachnoid Hemorrhage Rule can be used to rule out SAH (100% sensitivity) if none of the following is present:
- Age ≥40
- Neck pain or stiffness
- Limited neck flexion on examination
- Witnessed loss of consciousness
- Onset during exertion
- Thunderclap headache (maximal at onset)
A neurological exam may be conducted but should not delay CT evaluation.
Diagnosis
Criteria
Diagnosis can be made with noncontrast head CT or lumbar puncture
Noncontrast head CT
Cornerstone of diagnosis. Blood appears as hyperdense fluid. COmmon locations include:
- Basal cisterns
- Sylvian fissures
- Interhemispheric fissure
- Interpeduncular fossa
- Suprasellar, ambient, and quadrigeminal cisterns
CT is most sensitive in the first 6 hours after SAH but declined over time due to lysing of RBC and clearance from CSF.
Lumbar puncture
In most patients with a normal head CT, a lumbar puncture is required to rule out SAH (exception: isolated headache, normal examination, negative CT within 6 hours).
Findings include:
- Elevated opening pressure
- Elevated RBC count that does not diminish from CSF tube 1 to tube 4 (would diminish in traumatic tap)
- Xanthochromia
Work-up
Initial diagnostic approach
Immediate head CT is indicated. Lumbar puncture should be performed if head CT is negative in most cases.
Additional investigations (should not delay CT) include:
- Finger stick blood glucose
- Oxygen saturation
- ECG and troponin
- CBC
- PT and INR
Identifying source of bleeding
Digital subtraction angiography (DSA) can be performed immediately while patient is still in the scanner should SAH be diagnosed. Identifying the source of bleed aids management.
Differential
SAH is the primary consideration with an abrupt onset headache. The differential diagnosis may be considered followed the ruling out of SAH:
- Reversible cerebral vasoconstriction syndromes
- Cerebral infections
- Cerebral venous thrombosis
- Cervical artery dissection
- Other forms of stroke
- Acute hypertensive crisis
- Spontaneous intracranial hypotension
Red Flags / Complications
Misdiagnosis or delayed diagnosis can lead to delays in treatment and poor outcomes.
SAH is associated with an early mortality of approximately 20% (decreasing from historical 50%).
Long term complications include neurocognitive dysfunction, epilepsy, and other focal neurologic deficits.
Management
Stroke management occurs in the ICU or stroke unit. Admission should be done promptly.
Prognostication and care limits are typically delayed until following the first 1-2 days and aggressive care performed unless the patient has a preexisting DNR.
Triage, Stabilization, and Grading
Initial care involves stabilization of life-threatening status, especially for comatose or trauma patients. This may involve
- Intubation
- Normalizing heart function
- Treatment of seizures
Grading of SAH can be made using a number of clinical tools. The most commonly used being the Hunt and Hess system:
| Grade | Neurologic status |
|---|---|
| 1 | Asymptomatic or mild headache and slight nuchal rigidity |
| 2 | Severe headache, stiff neck, no neurologic deficit except cranial nerve palsy |
| 3 | Drowsy or confused, mild focal neurologic deficit |
| 4 | Stuporous, moderate, or severe hemiparesis |
| 5 | Coma, decerebrate posturing |
| or the World Federation of Neurological Surgeons SAH scale: |
| Grade | GCS score | Motor deficit |
|---|---|---|
| 1 | 15 | Absent |
| 2 | 13-14 | Absent |
| 3 | 13-14 | Present |
| 4 | 7-12 | Present or absent |
| 5 | 3-6 | Present or absent |
| Ideally, treatment of SAH is done at tertiary centres with dedicated staff. Management should take place in an ICU. |
Initial Symptom Management
Prohemostatic treatment for antithrombotics
All antithrombotic agents and anticoagulation should be discontinued until aneurysm is definitively repaired.
Patients who have received antiplatelets are transfused with 1 unit of platelets prior to surgery.
Warfarin should be countered with 4-factor prothrombin complex concentrate (PCC) and intravenous vitamin K. PCC can be replaced by plasma product (eg. FFP) if not available.
DOACs should be reversed with their specific strategy (eg. idarucizumab for dibigatran).
Blood pressure control
A gradual reduction of systolic BP is recommended if elevated (SBP >180 or MAP >120). While the target should be individualized based on initial BP, a target of SBP <160 or MAP <110 is generally indicated.
Recommended options are IV:
- Labetalol
- Nicardipine
- Clevidipine
- Enalapril
Avoid vasodilators such as nitroprusside or nitroglycerin.
Euvolemia maintanance
Avoid hypovolemia due to ischemic complications. Maintain euvolemia with IV fluids and monitoring of fluid input and output.
Be aware of hyponatremia; monitor at least daily.
Neurologic monitoring
ICU care consist of constant hemodynamic, cardiac, and neurologic monitoring through:
- Transcranial doppler (monitoring for vasospasm)
- Brain and vascular imaging (CT angiography and CT perfusion) for delayed cerebral ischemia
- Continuous electroencephalography (subclinical seizures for nonconvulsive status epilepticus)
- Neurologic exam (q1-2h)
- Troponin and ECGs on admission
- Intracranial pressure monitoring via ventriculostomy (for those with enlarged ventricles or high grade SAH)
Vasospasm prevention
Nimodipine 60 mg PO (or by NG tube) q4h is administered within 48 hours of symptom onset or as soon as the patient is stabilized
Seizure prophylaxis
Seizure prophylaxis is controversial and benefits unclear. In most cases, antiseizure medication should be discontinued in absence of acute seizure until the aneurysm is secured.
General care
- Bed rest to limit hemodynamic fluctuation and risk of rebleeding
- Pain control (short acting opiates or acetaminophen 500mg q3h)
- DVT prophylaxis via intermittent pneumatic compression devices prior to aneurysm secured and unfractionated heparin or LMWH after
Aneurysm Treatment
For aneurysmal SAH, aneurysm repair consist of surgical clipping or endovascular coiling. This should be performed as early as feasible within 24 hours.
Management of Complications
Medical and neurologic complications can occur after SAH. Complications are treated as they occur:
- Rebleeding
- Vasospasm and delayed cerebral ischemia
- Elevated ICP
- Hyponatremia
- Seizures
- Anemia
- Cardiopulmonary complications
- Ventilator-associated pneumonia