Subarachnoid Hemorrhage (SAH)

Subarachnoid hemorrhage (SAH) is a type of cerebrovascular accident (stroke) resulting from intracranial hemorrhage into the subarachnoid space between the arachnoid and the pia mater layers of the meninges surrounding the brain. Most SAHs originate from a saccular aneurysm in the circle of Willis but may also occur as a result of trauma, uncontrolled hypertension, vasculitis, anticoagulant use, or stimulant use. The most classic symptom is a sudden-onset (thunderclap) headache along with neck stiffness, vomiting, a decreased level of consciousness, and seizure. As with any stroke, focal neurologic deficits are commonly present, and rapid neurologic deterioration may ensue without prompt diagnosis and intervention. An SAH should be suspected in any person presenting with thunderclap headache and neurologic symptoms, and the diagnosis can be confirmed with neuroimaging or lumbar puncture (LP). Treatment consists of reversal of anticoagulation, control of blood pressure, and neurosurgical intervention to contain the bleed and/or relieve elevated intracranial pressure (ICP). Even with prompt neurosurgical intervention, SAH carries a high mortality rate.

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Definition and Epidemiology


  • SAH is a type of cerebrovascular accident (stroke) resulting from intracranial hemorrhage into the subarachnoid space. 
  • Subarachnoid space: area between the arachnoid mater and the pia mater layers of the meninges surrounding the brain
Subarachnoid hemorrhage

Meninges and meningeal spaces:
The image depicts the 3 layers (dura mater, arachnoid mater, pia mater) surrounding the brain and spinal cord. The meninges serve as mechanical protection of the CNS. They also support the cerebral and spinal blood vessels and allow for passage of the CSF. The subarachnoid space is filled with CSF.

Image by Lecturio.


  • Hemorrhagic strokes:
    • Account for 15%–20% of cerebrovascular accidents 
    • 50% of hemorrhagic strokes are due to SAH.
  • Saccular aneurysms:
    • Ruptured saccular aneurysms are the most common cause of SAH.
    • Approximately 3%–5% of the population has radiographic evidence of unruptured saccular aneurysm.
  • 15%–20% percent of SAH cases are non-aneurysmal.
  • Incidence:
    • Global incidence of SAH: 6–10 cases/100,000 person-years
    • Blacks > whites
    • Women > men (slightly)
  • Manifests most commonly at 40–60 years of age


Risk factors

  • Genetics, increased incidence seen in:
    • Autosomal dominant polycystic kidney disease (ADPKD)
    • Ehlers-Danlos syndrome (EDS)
    • Primary aldosteronism (glucocorticoid-remediable aldosteronism (GRA))
  • Family history:
    • Up to fivefold increased risk in 1-degree relatives
    • Familial cerebral aneurysms rupture more frequently than nonfamilial aneurysms
  • Hypertension
  • Stimulant use:
    • Cocaine
    • Amphetamine/methamphetamine
    • Sympathomimetics:
      • Cold remedies
      • Appetite suppressants
  • Coagulopathy:
    • Genetic or acquired bleeding diathesis
    • Therapeutic or supratherapeutic anticoagulation
  • Cigarette smoking
    • Dose dependent
    • Risk decreases after cessation.
  • Alcohol abuse
  • Estrogen deficiency (increased incidence observed in women > 50 years of age)
  • Increased incidence observed in multiparous females


  • Trauma
  • Ruptured aneurysms
    • Saccular aneurysms (“berry aneurysms,” round shape) are the most common cause of SAH.
    • Fusiform aneurysms (dilatation of the entire vessel wall for a short distance) and mycotic aneurysms (bacterial, fungal, or viral infection of the vessel wall) are also possible.
  • Arteriovenous malformations (AVMs)
  • Arterial dissections
  • Vasculitis
  • Vascular amyloid deposition
  • Illicit stimulant use


Given that saccular aneurysm is the most common etiology of SAH, this section will focus on the pathogenesis of saccular aneurysm rupture. Events downstream of the rupture itself are common to other etiologies of SAH. 

Saccular aneurysm

  • Acquired lesions rather than congenital
  • Most commonly located in the circle of Willis
    • Located in the anterior circulation > posterior circulation
    • Sites of bifurcation are the most vulnerable.
  • Develop over a short time in response to abnormal vascular shear forces:
    • Time period thought to be short (hours to days)
    • May rupture or harden after initial dilation
  • Not all saccular aneurysms rupture:
    • Stabilization may occur if for capacity collagen deposition > limits of elasticity
    • Stable saccular aneurysms are relatively common.

Pathologic features of ruptured saccular aneurysms

  • Abnormalities in smooth muscle organization
  • Hypocellularity
  • Intimal hyperplasia
  • Infiltration with T cells and macrophages
  • Thin layer of thrombosis
  • Presence of odontogenic bacterial DNA (possible role of dental/periodontal infection)

Risk factors for rupture

  • Aneurysm size (diameter) > 7 mm:
    • Larger aneurysms are more likely to grow than smaller aneurysms.
    • The rate of rupture risk is proportional to the diameter of the aneurysm.
  • Aneurysm growth: 
    • Aneurysmal growth increases the diameter of the lesion.
    • Rapid growth outpaces the ability for collagen-mediated stabilization.
  • Aneurysm site:
    • The risk of rupture varies based on the parent vessel giving rise to the aneurysm.
    • Posterior circulation > anterior circulation > cavernous carotid artery

Factors that may trigger rupture

  • Trauma
  • Physical exertion within 2 hours of rupture
  • Valsalva maneuver (prolonged or repetitive)
  • Uncontrolled hypertension

Clinical sequelae of rupture

  • Leakage of blood into the CSF:
    • Leads to increased intracranial pressure (ICP)
    • Initial bleeding (sentinel bleed) may last only seconds but with a high incidence of rebleeding.
  • Hydrocephalus/increased ICP:
    • Blockage of CSF flow and/or reabsorption caused by buildup of blood products and or/adhesions 
    • Continued leakage of blood into the subarachnoid space compounds the problem.
    • Endothelial dysfunction from the site of rupture causes local hyperemia and inflammation.
  • Cerebral vasospasm:
    • Release of inflammatory mediators from injured vessels may cause local vasoconstriction.
    • Vasospasm causes local hypoperfusion, worsening the ischemic insult.

Clinical Presentation


The classic presenting symptom of SAH is a thunderclap headache. There are other presenting symptoms as well.

  • Thunderclap headache
    • Sudden onset (seconds to minutes)
    • “Worst headache of my life”
    • Often (10%–40%) preceded by less severe prodromal headaches (“sentinel headaches”)
    • Headache location/description is inconsistent among SAH sufferers.
  • Neck stiffness/pain
    • Correlates with spread of blood into the CSF causing meningeal irritation
    • Often presents hours after the onset of headache
  • Altered level of consciousness
    • Brief loss of consciousness 
    • Altered mental status/confusion/agitation 
    • Coma is uncommon.
    • Sudden death occurs in > 20% of affected individuals before presenting to medical attention. 
  • Seizure
    • In approximately 10% of SAH cases
    • Generally occur in the first 24 hours
    • Associated with poor outcome 
  • Nausea/vomiting

Physical examination

  • Elevated blood pressure
    • Often in the severe range
    • May be a precipitating event for aneurysmal rupture
    • May be a reactive phenomenon to intracerebral events
  • Meningismus
    • Correlates with spread of blood into the CSF causing meningeal irritation
    • Kernig and Brudzinski signs may be present
  • Preretinal hemorrhage
    • Associated with increased ICP as opposed to true retinal involvement
    • Associated with poor outcome
  • Oculomotor nerve (CN III) palsy
    • Often presents as a unilateral pupillary defect
    • Due to CN III compression from aneurysm of the posterior communicating artery or superior cerebellar artery (located near CN III exit site from the brainstem)
  • Focal neurologic deficit
    • SAH can manifest with a wide variety of neurologic findings.
    • Findings depend on the size and location of the hemorrhage.


Any thunderclap headache presenting with or without neurologic symptoms/signs or altered mental status should be emergently evaluated with neuroimaging. Noncontrast CT is readily available at most acute care hospitals and is the initial test of choice. 

Ottawa SAH rule

  • Clinical decision tool used to evaluate suspected SAH with emergent noncontrast CT of the head
  • Evaluated in neurologically intact patients presenting with thunderclap headache
  • Sensitivity: 100%, specificity: 15% 
  • The presence of any of the following features is an indication for emergent CT:
    • Neck pain or stiffness
    • Limited neck flexion on examination
    • Witnessed loss of consciousness
    • Onset during exertion
    • Thunderclap headache (instantly peaking pain)
    • Age ≥ 40 years

Noncontrast head CT

  • Cornerstone of SAH diagnosis
  • Sensitivity of up to 100%:
    • If performed within 6 hours of presentation
    • If reviewed by qualified neuroradiologist
  • Should include cuts through the base of the brain
  • Locations of blood in SAH:
    • Basal cistern(s): most common
    • Sylvian fissure(s)
    • Interhemispheric fissure
    • Interpeduncular fossa
Subarachnoid hemorrhage on CT

Subarachnoid hemorrhage (SAH):
CT scan showing intracranial bleeding

Image: “CT of subarachnoid hemorrhage” by Shazia Mirza and Sankalp Gokhale. License: CC BY 4.0

Lumbar puncture (LP)

An LP should be performed promptly (despite negative CT if clinical suspicion of SAH is high). Studies should include:

  • Opening pressure
  • Cell counts:
    • RBCs
    • WBCs
    • Visual inspection for xanthochromia (yellowish appearance due to presence of bilirubin)
  • Classic LP findings:
    • Elevated opening pressure
    • Elevated RBC count 
  • False-positive LP findings:
    • A ”traumatic tap” may reveal a falsely elevated RBC count.
    • Differential of RBC counts between successive sample tubes can help differentiate false positives from true positives.
    • The RBC count should decrease or clear with successive tubes.

Identification of the bleeding source

  • After SAH is established, angiographic studies should be performed to identify the hemorrhagic source:
    • Digital subtraction angiography (DSA): preferred method, allows for intervention to be performed simultaneously with identification of the source
    • CTA and MRA: noninvasive alternatives
  • Once the bleeding source is identified, clinical decisions about appropriateness of intervention are undertaken.

Diagnostic criteria

Several scales are utilized clinically in the diagnosis and grading of severity in SAH. The Hunt and Hess grading system is among the most commonly used in clinical medicine.

Table: Hunt and Hess score with associated mortality rate
GradeNeurologic findingsMortality rate (5)
1 Asymptomatic or mild headache and slight nuchal rigidity 1
2 Severe headache, stiff neck, no neurologic deficit except cranial nerve (CN) palsy 5
3 Drowsy or confused, mild focal neurologic deficit 19
4 Stuporous, moderate or severe hemiparesis 42
5 Coma, decerebrate posturing 77


Stabilize life-threatening conditions

  • Secure airway by intubation for:
    • Comatose state
    • Hemodynamically instability
    • Heavy sedation 
    • Paralysis
    • Hypoxemia
    • Hypoventilation
    • Elevated ICP
  • Address any trauma-related conditions:
    • Address blood loss anemia
    • Address internal organ damage
  • Normalizing cardiovascular abnormalities:
    • Check cardiac troponins on admission
    • Address arrhythmia
    • Stabilize blood pressure
  • Treat seizures 
  • Discontinue anticoagulants:
    • Reversal of anticoagulation:
      • Vitamin K if on Warfarin
      • Specific reversal agents available for Factor X inhibitors
      • FFP if specific agents are unavailable or delayed
  • Consider transfer to an appropriate facility:
    • Neurologic ICU
    • Availability of specialists:
      • Neurosurgeons
      • Endovascular specialists

Neurosurgical and endovascular intervention

Consult neurosurgery and/or endovascular interventionist! The goal is to stop belling, prevent rebleeding, manage ICP to prevent secondary ischemia. Possible interventions include:

  • Surgical aneurysm clipping
  • Endovascular coiling
  • Ventriculostomy placement
  • Decompressive hemicraniectomy: 
    • May be indicated to relieve ICP in case of intracerebral hemorrhage
    • May be indicated to relieve ICP in case of severe cerebral edema


Monitoring should be performed in an ICU by specially trained staff equipped to continuously and simultaneously address the following:

  • Prevention of vasospasm:
    • Goal is prevention of delayed cerebral ischemia
    • Drug of choice is Nimodipine
    • Treatment is continued for 21 days
  • Blood pressure control
    • Goal systolic blood pressure <160 mm Hg 
    • Goal mean arterial pressure <110 mm Hg
    • Avoid rapid drops in blood pressure
    • Avoid hypotension
    • Drug of choice is Labetalol
  • Continuous monitoring for:
    • Hemodynamic instability:
      • May require central lines, arterial lines, ICP monitor
      • IV fluid infusions for maintenance of euvolemia
    • Neurologic deterioration
      • Focused neurologic exam every 2 hours by qualified ICU nurse
      • Emergent CT for any acute deterioration
    • Hypoxemia
    • Fever
    • Cardiac arrhythmia
    • ICP
    • Electrolyte imbalance:
      • Hyponatremia is especially common in this setting
      • IV fluid choice and drip rate may be adjusted to maintain eunatremia 
  • Ventriculostomy:
    • Intracranial line placed by neurosurgical staff
    • Used to monitor ICP
    • Allows for drainage of CSF to maintain to avoid ICP
  • DVT/PE prophylaxis:
    • Mechanical means are employed as anticoagulants are generally avoided until definitive repair has been undertaken
  • Seizure prophylaxis:
    • Levetiracetam is drug of choice
    • Phenytoin has been associated with poor outcomes
    • May be continued for months after initial insult


  • Rebleeding
  • Delayed cerebral ischemia secondary to cerebrovascular vasospasm
  • Neurologic deterioration
  • Hemodynamic instability
  • Elevated ICP
  • Hydrocephalus
  • Hyponatremia (mediated by hypothalamic injury)
  • Seizures
  • Anemia
  • Cardiopulmonary events
  • Arrhythmia
  • Fever (noninfectious)
  • Fever (infectious)/infection/sepsis


  • Early mortality rates as high as 10%–20%
  • 1-year mortality as high as 20%–25%
  • Survivors may have significant morbidity:
    • Increased incidence of cardiovascular events
    • Neurologic, cognitive, and memory deficits are common
    • Sleep disorders and mood disorders are common
    • Persistent seizure disorder is common
    • Anosmia is common


It is reasonable to offer screening (neuroimaging) to 1st-degree relatives of patients with SAH for saccular aneurysms.

Differential Diagnosis

  • Ischemic stroke: an ischemic infarct of the cerebral parenchyma caused by occlusion of a cerebral artery by atherosclerotic lesions or cardioembolic emboli. Ischemic stroke presents with neurologic deficits and/or altered mental status/level of consciousness that depends on the size and location of the infarct. Diagnosis is clinical and confirmed by neuroimaging. Management includes initial stabilization, possible cerebrovascular intervention, addressing identifiable underlying etiologies (severe hypertension, embolus), and management of cardiovascular risk factors. 
  • Other hemorrhagic cerebral conditions: carotid/cerebral artery dissection, epidural hemorrhage, intraparenchymal hemorrhage, and subdural hemorrhage are other hemorrhagic manifestations of the cerebral vasculature that can present with neurologic deficits and/or altered mental status/level of consciousness. Diagnosis is clinical and confirmed by neuroimaging. Management depends on the hemorrhagic etiology and includes initial stabilization, neurosurgical/endovascular consultation, management of ICP, and monitoring in a neurologic ICU. 
  • Hypertensive encephalopathy: neurologic deficit and/or altered mental status/level of consciousness that presents in the setting of severe hypertension. Diagnosis is based on the presence of elevated blood pressure and neurologic signs/symptoms. Neuroimaging is useful to rule out ischemic or hemorrhagic cerebrovascular accident. Management centers around careful acute lowering of the blood pressure and long-term blood pressure management.


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  5. Singer, R. (2021). Aneurysmal subarachnoid hemorrhage: Treatment and prognosis. UpToDate. Retrieved Sep 10, 2021, from
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  7. Singer, R. (2020). Unruptured intracranial aneurysms. UpToDate. Retrieved Sep 10, 2021, from
  8. Majeed, H, & Ahmad, F. (2021). Mycotic aneurysm. StatPearls. 
  9. Hacein-Bey, L, & Provenzale, JM. (2011). Current imaging assessment and treatment of intracranial aneurysms. AJR. American journal of roentgenology, 196(1), 32–44.

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