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 neurologic 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 the 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|| || |
|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")
The following information applies to the diagnostic workup of suspected SAH in patients without a history of trauma. See “Traumatic SAH” for information specific to trauma patients.
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 CT in the first 6 hours in a neurologically intact patient: SAH is not likely; consider other differential diagnoses. 
- Nondiagnostic head CT but persisting suspicion: Perform second-line diagnostic tests.
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
Head CT without contrast 
- 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 head CT does not exclude the diagnosis and second-line tests are necessary. 
Lumbar puncture (LP) 
- Opening pressure: normal or elevated
- Cerebrospinal fluid (CSF) color
- Cell count (normal RBC/WBC ratio)
- Glucose: normal
- Protein: elevated
CT angiography (CTA) 
- Widely available and minimally invasive
- High sensitivity and specificity for aneurysms larger than 3–4 mm.
- Can provide enough information to plan aneurysm repair. 
- Findings 
Additional studies 
- Digital subtraction angiography (DSA): gold standard for cerebral vessel imaging 
MRI and/or MR angiography
- Useful for detecting other differential diagnoses of headache
- Consider if other studies are nondiagnostic.
- May show bleeding not detected by CT, 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.
- Stabilization of the patient: Perform ABCDE survey, secure airway, and provide hemodynamic support as needed.
Prevention of rebleeding
- Management of blood pressure and cerebral perfusion pressure
- Symptom control: antiemetics as needed  and
- Antifibrinolytic therapy: not routinely recommended, potentially useful for patients with an expected delay in aneurysm repair 
Additional measures 
- Start ICP management (e.g., elevate head 30°, IV mannitol, short-term controlled hyperventilation)
- Maintain euvolemia, normoglycemia, and start targeted temperature management.
- Identify and treat hyponatremia.
- Consider seizure prophylaxis.
- See “Secondary brain injury and neuroprotective measures” for detailed recommendations.
Consults and disposition
- Consult neurosurgery and interventional radiology.
- Admit to neurologic critical care or, if possible, transfer to a high-volume center.
Rebleeding is a life-threatening complication that occurs most commonly in the first 6 hours after SAH. Start measures to prevent rebleeding immediately. 
Do not use nitrates for blood pressure management, since they may raise ICP. 
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. 
- Ensure appropriate neurologic monitoring: 
- Transfusion of packed RBCs: Consider transfusions to keep the hemoglobin concentration > 8–10 g/dL. 
- 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)
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 neurologic deficits or Ottawa SAH criteria fulfilled: Obtain immediate head CT without contrast.
- Negative CT but persisting suspicion: Consider lumbar puncture or CTA.
- Positive CT or suspicious lumbar puncture: 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, glucose, coagulation, 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.
Typically, patients present with a clear history of trauma, and the diagnosis of SAH is then made based on imaging. For the initial TBI), see also the respective articles.and the (
- Assess severity of traumatic brain injury (TBI) based on GCS.
- Head CT without contrast
- For further information, 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
- 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 
We list the most important complications. The selection is not exhaustive.
- Approx. 30% mortality rate in the U.S. within the first 30 days 
- Survivors: increased rates of neurologic impairment (e.g., cognitive, mood changes, functional, epilepsy) and increased risk of recurrent SAH