Subarachnoid hemorrhage (SAH) refers to bleeding into the subarachnoid space. While SAH is often caused by trauma, 5–10% of cases are nontraumatic or spontaneous, in which case they are often due to the rupture of an aneurysm involving the circle of Willis (aneurysmal SAH). Nontraumatic SAH typically manifests with sudden and severe headache, which may be accompanied by nausea, vomiting, signs of meningism, and/or acute loss of consciousness. The best initial diagnostic test is a head CT without contrast, in which acute subarachnoid bleeding can be seen as hyperdensities in the subarachnoid space. If a head CT is negative for SAH, this diagnosis can be ruled out in many patients. However, if clinical suspicion remains high, it may be necessary to perform a lumbar puncture or CT angiography. Once SAH is confirmed, angiography is always necessary in order to identify the source of bleeding (e.g., aneurysms or other vascular abnormalities) and plan definitive treatment. The management of traumatic and nontraumatic SAH consists mostly of neuroprotective measures (e.g., control of blood pressure) to prevent secondary brain injuries. In aneurysmal SAH, microsurgical clipping or endovascular coiling of the aneurysm is indicated to prevent potentially fatal rebleeding. Aneurysmal SAH has a high mortality rate as a result of complications such as rebleeding and delayed cerebral ischemia.
- Subarachnoid hemorrhage: bleeding into the subarachnoid space that may be traumatic or spontaneous
- Intracerebral hemorrhage: bleeding within the brain parenchyma
- Intracranial hemorrhage: a broad term used to describe any bleeding within the skull (including intracerebral hemorrhage, subarachnoid hemorrhage, or subdural hemorrhage)
- Hemorrhagic stroke: cerebral infarction due to hemorrhage
- Intraventricular hemorrhage: bleeding within the ventricles
- Head trauma is the most common cause of SAH.
- 40–60% of patients with have subarachnoid bleeding. 
Epidemiological data refers to the US, unless otherwise specified.
- Traumatic SAH: 
Nontraumatic (spontaneous) SAH
- Ruptured intracranial aneurysms
- Ruptured arteriovenous malformations (AVM)
- Others: cortical thrombosis, angioma, neoplasm, infection
- Triggers: most cases unknown, may be triggered by an acute rise in blood pressure; (e.g., caffeine consumption, fits of anger, physical exertion) 
- Risk factors 
There is no universally accepted grading scale for SAH, but the scales presented here are among the most commonly used and have some value in predicting the neurological outcome (probability of death and expected level of disability). They have been created for the assessment of aneurysmal SAH and are usually not validated for use in traumatic SAH. 
Clinical severity should be graded at the time of presentation.
|Hunt-Hess classification of aneurysmal SAH |
|Grade||Symptoms and level of consciousness||Neurological exam|
|I|| || |
Do not use the Hunt-Hess scale to predict the likelihood of a diagnosis of SAH, but rather to estimate the prognosis of patients with confirmed SAH. 
|World Federation of Neurological Surgeons (WFNS) grading scale for SAH |
|May be present|
|May be present|
In addition to scales for clinical severity, the radiological appearance of SAH can also be graded. The most reliable tool is the modified Fisher scale, which is used to predict the incidence of delayed cerebral ischemia. 
|Modified Fisher scale |
|Grade||Subarachnoid hemorrhage||Intraventricular hemorrhage|
- Thunderclap headache
- Meningeal signs:
- Nonspecific signs
- Signs due to mass effect
- Prodromal symptoms due to sentinel leak (a "warning leak")
Maintain a high index of suspicion for SAH in patients with isolated headache or cranial nerve palsy, as they are more often misdiagnosed, resulting in poor outcomes due to delayed diagnosis and interventions. 
The following information applies to the diagnostic workup of suspected SAH in patients without a history of trauma. See “” for the treatment of patients with SAH due to head trauma.
Since a missed diagnosis of SAH can have devastating consequences, clinicians should maintain a high index of suspicion when deciding whether to pursue testing.
- Common indications for testing
Best initial test: immediate head CT without contrast 
- Confirmation of SAH: Obtain angiography to confirm source of bleeding and plan treatment.
- Nondiagnostic head CT but persisting suspicion: Perform second-line diagnostic tests.
- Nondiagnostic CT in the first 6 hours in a neurologically intact patient: SAH unlikely; consider other differential diagnoses. 
Second-line tests: lumbar puncture (LP) or CT angiography (CTA) ; 
- Lumbar puncture
- CTA (alternative)
- Additional studies: Obtain CBC, BMP, coagulation panel, and type and screen.
If patients are unstable or have , diagnostics should not delay stabilizing and .
The Ottawa SAH clinical decision rule 
- Inclusion criteria (all of the following need to be fulfilled):
- Risk features
- Presence of 0 risk features: SAH ruled out
- Presence of ≥ 1 risk feature: SAH cannot be ruled out
CT head without contrast 
- Indication: all patients with suspected acute SAH
- Timing: as early as possible (when performed within 6 hours of onset, sensitivity is close to 100%) 
- Defining feature: blood in subarachnoid space (hyperdense) with variable extension and location ; 
- Additional findings: bleeding in other compartments (see “Differential diagnosis of intracranial hemorrhage”)
If there is a high index of suspicion for SAH, a negative CT head does not exclude the diagnosis and second-line tests are necessary. 
Lumbar puncture (LP) 
- Indication: history and/or examination that is concerning for SAH, but negative CT head 
- Opening pressure: normal or elevated
- The following may be evaluated to identify cerebrospinal fluid (CSF) features suggestive of SAH:
- CSF color
- Cell count (normal RBC:WBC ratio)
- Glucose: normal
- Protein: elevated
Neurovascular imaging 
CT angiography (CTA)
- Indications 
- Findings 
- Visualization of aneurysms (accumulation of contrast)
- May detect extravasation of contrast in the case of active bleeding
- May detect vascular abnormalities (e.g., AVM)
- Digital subtraction angiography (DSA): gold standard for cerebral vessel imaging ; 
MRI and/or MR angiography 
- Used to rule out
- Consider if other studies are nondiagnostic.
- May show bleeding not detected by CT scans, especially several days after the incident
The initial management of all patients with spontaneous SAH is similar, but further management depends on the underlying etiology. While aneurysmal hemorrhage can be treated with endovascular coiling or microsurgical clipping, there are few specific definite treatment options for nonaneurysmal SAH.
Initial management 
Primary measures should be initiated urgently in the ED. The goal is to stabilize the patient and prevent early rebleeding and secondary brain injury.
Prevention of rebleeding
Management of blood pressure and cerebral perfusion pressure ; (CPP; ): See “Blood pressure control in brain injury” for a general approach. .
- Start IV antihypertensive agents if blood pressure is elevated.
- Target SBP < 160 mm Hg (reasonable for patients with aneurysmal SAH) 
- Suspected increased ICP: Consider permissible hypertension (e.g., MAP > 90 mm Hg) to maintain and prevent cerebral hypoperfusion. 
- Consider placing an arterial line for continuous .
- Control symptoms that can increase ICP: Administer and as needed. 
- Antifibrinolytic therapy: not routinely recommended; potentially useful for patients with an expected delay in aneurysm repair 
- Other 
Consults and disposition
- Consult neurosurgery and interventional radiology.
- Admit to neurological critical care or, if possible, transfer to a high-volume center. 
Rebleeding is a life-threatening complication that most commonly occurs in the first 6 hours after SAH. Start measures to prevent rebleeding immediately. 
Treatment of aneurysmal SAH 
All aneurysmal SAHs require definitive endovascular or microsurgical aneurysm repair as early as possible. Patients should be admitted to critical care for further management to prevent and treat secondary brain injury and systemic complications.
|Intracranial aneurysm repair |
|Endovascular coiling||Microsurgical clipping|
|Characteristics|| || |
Further management 
Prevention of vasospasm and delayed cerebral ischemia
Administer oral nimodipine in all patients, preferably within 96 hours of symptom onset.
- Ensure appropriate neurological monitoring: 
- Transfusion of packed RBCs: Consider transfusions to keep the hemoglobin concentration > 8–10 g/dL. 
- Administer oral nimodipine in all patients, preferably within 96 hours of symptom onset.
- Treatment of hydrocephalus: may include an (EVD), lumbar drainage, or permanent 
- Detection of cardiopulmonary complications 
- DVT prophylaxis: mechanical from the beginning, and pharmacological 24 hours after aneurysm repair (preferably with unfractionated heparin)
Treatment of nonaneurysmal SAH
Depending on the etiology, some specific measures may help improve the outcome.
Arteriovenous malformations 
- Admit to neurocritical care unit and start neuroprotective measures.
- Emergency surgery may be necessary for hemorrhage control and evacuation of larger hematomas.
- Endovascular embolization may be performed preoperatively or as definitive treatment.
- Complete obliteration of the AVM is achieved via planned microsurgery or stereotactic radiosurgery.
SAH without associated vascular abnormalities (rare): Consider repeating DSA to look for aneurysms that were overlooked before. 
- Perimesencephalic hemorrhage: Provide supportive measures.
- Other nonaneurysmal hemorrhages: Treatment is mainly supportive and management depends on local/institutional protocols.
- Perform ABCDE survey, secure airway, and provide hemodynamic support as needed.
- Perform rapid focused neurological examination.
- Presence of neurological deficits or Ottawa SAH criteria fulfilled: Obtain immediate head CT without contrast.
- Negative CT but persisting suspicion: Consider LP or CTA.
- Positive CT or suspicious LP: Obtain angiography to plan intervention.
- Consult neurosurgery and interventional radiology for early definitive treatment (e.g., endovascular repair, surgical clipping).
- Transfer patient to neurocritical care or to a specialized center.
- Obtain laboratory studies: BMP, POC glucose, coagulation panel, CBC, type and screen.
- Start rebleeding prophylaxis: anticoagulant reversal and blood pressure control as needed.
- Consider antifibrinolytic therapy in consultation with experts.
- If aneurysmal bleeding: Start oral nimodipine.
- Administer analgesia and antiemetics as needed.
- Monitor closely with neurological examination, GCS, continuous monitoring of vitals, pulse oximetry, and capnography.
- Start additional neuroprotective measures.
- Consider additional diagnostic studies (e.g., ECG, echocardiography) to identify potential complications.
- Start DVT prophylaxis.
- Perform an , including a .
- Assess severity of TBI based on score.
- Once the patient is stable, proceed with diagnostic studies and further management.
- CT head without contrast
- See also “Diagnostics in traumatic brain injury.”
There is no specific surgical or interventional treatment for traumatic SAH. Management is mostly supportive, with the goal of preventing secondary brain injury. If there are associated lesions, surgical intervention may be required.
- Mild TBI with isolated SAH 
- Moderate or severe TBI with SAH 
- SAH with other pathologic radiographic findings 
- Occurs in approx. 30% of patients with SAH 
- Transcranial doppler ultrasound study can help identify vasospasm.
- Can lead to ischemic stroke
- Most common in patients with nontraumatic SAH due to a ruptured aneurysm
- Usually occurs between 3–10 days after SAH
- Increases the risk of developing communicating and/or obstructive hydrocephalus
- Occurs in 4–14% of patients with SAH in the first 24 hours 
- Risk of rebleeding is highest in the first 2–12 hours after SAH
- The cumulative risk of recurrent bleeding within the first six months is about 50%.
Other complications 
Delayed cerebral ischemia
- A complication of aneurysmal subarachnoid hemorrhage (SAH) defined as a worsening neurological status that cannot be attributed to other causes (e.g., hypoxemia or seizures)
- Typically occurs 3 days to 2 weeks after SAH
- While it is associated with cerebral vasospasm, the exact pathophysiology is not known
- Elevated ICP: hypertension, bradycardia, and irregular breathing (see )
Cerebral salt wasting (rare)
- Causes hypovolemic, hypotonic hyponatremia, although the mechanism is poorly understood.
- Classically, its onset occurs within 10 days of an inciting event within the central nervous system (particularly subarachnoid hemorrhage) or neurosurgical procedure.
- Severe symptoms are treated with hypertonic saline and fludrocortisone.
- Cardiac dysfunction (e.g., arrhythmias, acute MI)
- Terson syndrome (20% of cases): preretinal hemorrhage due to SAH
- Delayed cerebral ischemia
We list the most important complications. The selection is not exhaustive.