Subarachnoid hemorrhage

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.

See also “Overview of stroke” and “Traumatic brain injury” for more information.

• 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

• Traumatic
  • Head trauma is the most common cause of SAH.
  • 40–60% of patients with traumatic brain injury have subarachnoid bleeding. ^[1]
• Nontraumatic
  • Ruptured cerebral aneurysm is the most common cause of nontraumatic SAH.
  • Peak incidence: approx. 50 years of age
  • ♀ > ♂ (3:2)
  • Nontraumatic SAH is responsible for 5–10% of all strokes. ^[2][3]

References:^[2][4]

Epidemiological data refers to the US, unless otherwise specified.

• Traumatic SAH: traumatic brain injury ^[5]
• Nontraumatic (spontaneous) SAH
  • Causes
    • Ruptured intracranial aneurysms
      • Most commonly occur in the circle of Willis ^[6]
      • Berry aneurysms account for approx. 80% of cases of nontraumatic SAH. ^[7]
      • See “Cerebral aneurysm” in the article on aneurysms for more information.
    • 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) ^[7]
  • Risk factors ^[7][8][9]
    • Smoking
    • Hypertension
    • High alcohol consumption
    • Family history of SAH
    • Methamphetamine and cocaine use
    • Large aneurysms ^[9]
    • Aneurysm location ^[9]

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. ^[10][11][12]

Clinical classification

Clinical severity should be graded at the time of presentation.

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. ^[14]

Radiological classification

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. ^[11]

• Thunderclap headache
  • Sudden, severely painful headache (often described by patients as the worst headache they have ever experienced)
  • Holocephalic
  • Radiates to the neck and back
  • May present with opisthotonus
• Meningeal signs:
  • Neck stiffness
  • Photophobia
  • Nausea and vomiting
  • Kernig sign
  • Brudzinski sign
• Nonspecific signs
  • Impaired consciousness (somnolent to comatose)
  • Fever
  • Sweating, hemodynamic instability
• Signs due to mass effect
  • Cranial nerve disorders
  • Altered mental status (e.g., delirium)
  • Focal neurological deficits: See stroke symptoms by affected vessel and stroke symptoms by affected region.
  • Seizures
• Prodromal symptoms due to sentinel leak (a "warning leak")
  • 30–50% of patients with SAH report prodromal symptoms days-to-weeks prior to SAH. ^[17]
    • Sudden, severe headache
    • Transient diplopia
  • Likely due to low-grade leak of blood into the subarachnoid space → thrombus formation → fibrinolysis → hemorrhage

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. ^[14]

References:^[2][4][11]

The following information applies to the diagnostic workup of suspected SAH in patients without a history of trauma. See “Management of traumatic SAH” for the treatment of patients with SAH due to head trauma.

Approach ^{[10][18][19][20]}

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
  • Headache with impaired consciousness or abnormal findings on neurological examination (see also “Red flags for headache”)
  • Clinical suspicion for SAH in patients fulfilling criteria of the Ottawa SAH clinical decision rule
• Best initial test: immediate head CT without contrast ^[19][21]
  • 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. ^[21]
• Second-line tests: lumbar puncture (LP) or CT angiography (CTA) ; ^[18][21]
  • Lumbar puncture
    • LP positive: Identify the source of bleeding with angiography (e.g., CTA, DSA) and plan intervention.
    • LP negative; : SAH can be ruled out in most cases. If suspicion remains high, obtain CTA.
  • CTA (alternative)
    • CTA positive: Consider if additional angiographic imaging is necessary (e.g., DSA, MRA) and plan intervention.
    • CTA negative: SAH can be ruled out; consider other diagnoses. If suspicion remains high (which is rare), consider additional imaging (e.g., DSA, MRA).
• Additional studies: Obtain CBC, BMP, coagulation panel, and type and screen.

If patients are unstable or have signs of increased ICP, diagnostics should not delay stabilizing and neuroprotective measures.

The Ottawa SAH clinical decision rule ^[21][22]

The Ottawa SAH clinical decision rule can be used as a tool to exclude SAH in selected patients presenting to the emergency department with acute headache.

• Inclusion criteria (all of the following need to be fulfilled):
  • Age > 15 years
  • Neurologically intact and alert (GCS 15)
  • New, nontraumatic, severe headache, reaching maximum intensity in < 1 hour
• Risk features
  • Age ≥ 40 years
  • Reported neck pain or stiffness
  • Witnessed loss of consciousness
  • Headache triggered by physical exertion
  • Thunderclap headache (peak intensity at onset)
  • Neck rigidity on physical examination
• Interpretation ^[22]
  • Presence of 0 risk features: SAH ruled out
  • Presence of ≥ 1 risk feature: SAH cannot be ruled out

CT head without contrast ^[11][18][23]

• Indication: all patients with suspected acute SAH
• Timing: as early as possible (when performed within 6 hours of onset, sensitivity is close to 100%) ^[19][21]
• Defining feature: blood in subarachnoid space (hyperdense) with variable extension and location ; ^[11][23]
  • Aneurysmal SAH: typically located in the basal cisterns
  • Nonaneurysmal SAH (uncommon)
    • Ruptured AVM: Bleeding is often seen adjacent to the dural venous sinuses. ^[24][25]
    • Perimesencephalic SAH: bleeding around perimesencephalic cisterns, with no extension into the ventricles or parenchyma ^[11][26]
• 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. ^[18]

Lumbar puncture (LP) ^[21][27][28]

• Indication: history and/or examination that is concerning for SAH, but negative CT head ^[29]
• Opening pressure: normal or elevated
• The following may be evaluated to identify cerebrospinal fluid (CSF) features suggestive of SAH:
  • CSF color
    • Early findings: pink to red blood-tinged discoloration ^[30][31]
    • Late findings: xanthochromia; , which is the presence of bilirubin in the CSF secondary to the breakdown of RBCs, resulting in yellow discoloration ^[20]
  • Cell count (normal RBC:WBC ratio)
    • RBC count: elevated (no specific threshold) ^{[30] [19][32]}
    • WBC count: may be mildly elevated
  • Glucose: normal
  • Protein: elevated

Concerns for elevated ICP (e.g., on physical examination or CT scan) or coagulopathy are relative contraindications for LP.

Neurovascular imaging ^{[10][18][19][33]}

• CT angiography (CTA)
  • Indications ^[33][34][35]
    • Patients with SAH identified on CT head without contrast
    • First-line imaging in patients with suspected SAH and ≥ 2 first-degree relatives with known aneurysmal SAH
    • Patients with a negative CT head who decline or have contraindications to LP
  • Benefits
    • Widely available and minimally invasive
    • High sensitivity and specificity for aneurysms larger than 3–4 mm
    • Can typically provide enough information to plan aneurysm repair ^[11][36]
  • Findings ^[37]
    • Visualization of aneurysms (accumulation of contrast)
    • May detect extravasation of contrast in the case of active bleeding
      • No blood visualized or a perimesencephalic SAH blood pattern: No further imaging is required. ^[38]
      • Diffuse or peripheral SAH blood pattern: Proceed to catheter-directed angiography with DSA. ^[18][33][39]
    • May detect vascular abnormalities (e.g., AVM)
• Digital subtraction angiography (DSA): gold standard for cerebral vessel imaging ; ^[11]
  • Indications
    • Detection of small aneurysms in selected patients with a negative CT
    • To plan interventions (when CTA is insufficient)
  • Invasive imaging modality
  • Findings: similar to CTA
• MRI and/or MR angiography ^{[11][18][36][40]}
  • Used to rule out differential diagnoses of headache
  • Consider if other studies are nondiagnostic.
  • May show bleeding not detected by CT scans, especially several days after the incident

CTA has poor sensitivity for detecting aneurysms < 3 mm in size and aneurysms that overlie bone (e.g., at the skull base). ^[18][33][39]

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 ^[11][18][20]

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
  • Perform an ABCDE survey.
  • Secure the airway if indicated; If patients are unconscious or have a declining GCS score, manage the airway while considering precautions for intubating patients with increased ICP.
  • Provide hemodynamic support as needed.
• Prevention of rebleeding
  • Anticoagulant reversal
  • 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) ^[18]
    • Suspected increased ICP: Consider permissible hypertension (e.g., MAP > 90 mm Hg) to maintain cerebral perfusion pressure and prevent cerebral hypoperfusion. ^[41][42]
    • Consider placing an arterial line for continuous invasive blood pressure monitoring.
  • Control symptoms that can increase ICP: Administer pain management and antiemetics as needed. ^[20]
  • Antifibrinolytic therapy: not routinely recommended; potentially useful for patients with an expected delay in aneurysm repair ^[18][43]
• Other neuroprotective measures ^[11]
  • Start ICP management (e.g., elevate head 30°, IV mannitol, short-term controlled hyperventilation).
  • Treatment goals
    • Euvolemia
    • Euglycemia (See “Glycemic management in secondary brain injury.”)
    • Normothermia (see “Targeted temperature management.”)
    • Eunatremia: Patients are at risk for cerebral salt wasting and SIADH.
  • Consider neuroprotective seizure prophylaxis following an intracranial event.
• Consults and disposition
  • Consult neurosurgery and interventional radiology.
  • Admit to neurological critical care or, if possible, transfer to a high-volume center. ^[43]

Rebleeding is a life-threatening complication that most commonly occurs in the first 6 hours after SAH. Start measures to prevent rebleeding immediately. ^[11][18]

Generally avoid nitrates for blood pressure control in brain injury, as they may elevate ICP. Consider alternative agents (e.g., titratable nicardipine or labetalol). ^[18]

Treatment of aneurysmal SAH ^[18][43]

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 ^[18]

Further management ^[43]

• Prevention of vasospasm and delayed cerebral ischemia
  • Administer oral nimodipine in all patients, preferably within 96 hours of symptom onset.
    ^[18][20][29]
  • Ensure appropriate neurological monitoring: ^[11][43]
    • Neurological examination every 1–2 hours
    • Head CT 24–48 hours after aneurysm repair
    • Other measures to consider include daily transcranial Doppler scan, repeated angiography, monitoring of ICP and cerebral perfusion pressure, and continuous EEG.
  • Transfusion of packed RBCs: Consider transfusions to keep the hemoglobin concentration > 8–10 g/dL. ^[43]
• Treatment of hydrocephalus: may include an external ventricular drain (EVD), lumbar drainage, or permanent ventriculoperitoneal shunt ^[10][18]
• Detection of cardiopulmonary complications ^[11][44]
  • Chest x-ray: to exclude pulmonary complications (e.g., pulmonary edema)
  • Serum troponin: to detect myocardial ischemia ^[45]
  • ECG: to exclude myocardial ischemia and arrhythmias
  • Echocardiography: to assess contractility and ventricular function
• DVT prophylaxis: mechanical from the beginning, and pharmacological 24 hours after aneurysm repair (preferably with unfractionated heparin)

Only administer nimodipine orally or via enteral tube; Parenteral administration is associated with significant adverse effects (e.g., severe hypotension and cardiac arrest).

Treatment of nonaneurysmal SAH

Depending on the etiology, some specific measures may help improve the outcome.

• Arteriovenous malformations ^[25][46]
  • 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. ^[11][26]
  • 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.

Typically, patients present with a clear history of trauma, and the diagnosis of SAH is then made based on imaging. See also “Management of trauma patients” and “Initial management of traumatic brain injury” (TBI).

Approach

• Begin initial management of TBI.
  • Perform an ABCDE assessment, including a primary survey in TBI.
  • Assess severity of TBI based on GCS score.
• Once the patient is stable, proceed with diagnostic studies and further management.

Diagnostics

• CT head without contrast
  • Indicated in patients with mild TBI (mTBI) who meet the criteria for neuroimaging in mTBI, and all patients with moderate or severe TBI
  • Findings
    • Isolated SAH, visible as a hyperdensity in the subarachnoid space
    • Other intracranial hemorrhages, hematomas, cerebral edema, or skull fractures
• See also “Diagnostics in traumatic brain injury.”

Traumatic SAH is common in severe head injuries. CT head detects SAH in up to 33% of patients during the initial scan and in up to half of patients when subsequent imaging is included. ^[34]

Management

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 ^{[47][48][49][50]}
  • Typically, no surgical intervention is required and outcomes are good.
  • Consider neurosurgical and critical care consult if red flags for mTBI are present.
  • Repeat neuroimaging in the case of clinical deterioration or based on individual evaluation.
  • See the article on “Mild TBI” for additional information.
• Moderate or severe TBI with SAH ^[51]
  • SAH is associated with worse outcomes in patients with severe TBI.
  • The mainstays of treatment are monitoring and prevention of secondary brain injury.
  • See “Management of moderate and severe TBI” for more information.
• SAH with other pathologic radiographic findings ^[49]
  • Regardless of the initial GCS, these patients are at a higher risk of deterioration.
  • Admit the patient to a critical care unit.
  • Surgical intervention (e.g., hematoma evacuation) may be required.
  • See also “Treatment” in “SDH,” “EDH,” and “ICH.”

• Vasospasm
  • Occurs in approx. 30% of patients with SAH ^[18]
  • Transcranial doppler ultrasound study can help identify vasospasm.
  • Pathophysiology
    • Impaired CSF reabsorption from the arachnoid villi → nonobstructive (communicating) hydrocephalus → ↑ intracranial pressure → ↓ cerebral perfusion pressure → ischemia
    • Release of clotting factors and vasoactive substances → diffuse vasospasm of cerebral vessels → ischemia
  • 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
• Recurrent bleeding
  • Occurs in 4–14% of patients with SAH in the first 24 hours ^[18]
  • 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%.
• Hydrocephalus
  • Occurs in 20–30% of patients with SAH ^[52]
  • Acute obstructive hydrocephalus
    • Usually occurs within minutes to hours after SAH
    • Can lead to coma and death
  • Chronic communicating hydrocephalus
    • Usually occurs weeks or months after SAH
    • SAH impairs CSF resorption from the arachnoid villi.
• Other complications ^[18]
  • 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 Cushing triad)
  • Seizures
  • SIADH
  • 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

References:^[18]

We list the most important complications. The selection is not exhaustive.

• Approx. 30% mortality rate in the U.S. within the first 30 days ^[18]
• Survivors: increased rates of neurologic impairment (e.g., cognitive, mood changes, functional, epilepsy) and increased risk of recurrent SAH