Subarachnoid hemorrhage

Last updated: January 9, 2022

Summarytoggle arrow icon

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.

References:[2][4]

Epidemiological data refers to the US, unless otherwise specified.

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.

Hunt-Hess classification of aneurysmal SAH [12][13]
Grade Symptoms and level of consciousness Neurological exam
I
II
III
IV
V

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]

World Federation of Neurological Surgeons (WFNS) grading scale for SAH [15]
Grade GCS Motor deficit
I

15

Absent
II

13–14

Absent
III

13–14

Present
IV

7–12

May be present
V

3–6

May be present

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]

Modified Fisher scale [11][16]
Grade Subarachnoid hemorrhage Intraventricular hemorrhage
0

None

None
1

Thin/minimal

None
2 Present
3

Thick

None
4 Present

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
  • 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
  • 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]

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.

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]

Intracranial aneurysm repair [10][18][29]
Endovascular coiling Microsurgical clipping
Characteristics
  • Minimally invasive
  • Higher risk of incomplete obliteration and recurrent bleeding
  • More invasive
  • Higher rate of complete aneurysm occlusion
  • Lower risk of recurrent bleeding
Indications
Procedure
  • Insertion of a catheter under fluoroscopic guidance
  • Placement of metal coils in the aneurysm lumen to interrupt blood flow and induce thrombotic occlusion

Further management [43]

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.

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

Diagnostics

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 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
  • Other complications [18]

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
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