Types

  1. Aneurysmal (aSAH)
  2. Traumatic SAH

Background

Risk Factors

Prevention of aSAH

  1. Control hypertension
  2. Reduce tobacco and alcohol use
  3. Healthy diet
  4. consider noninvasive screening to patients with familial aSAH or history of aSAH to evaluate for de novo aneurysms
  5. After any aneurysm repair, immediate cerebrovascular imaging is generally recommended to identify remnants or recurrence of the aneurysm that may require treatment

Natural History of aSAH

Clinical Manifestations and Diagnosis of aSAH

Diagnosis

  1. Non-con CT head is the cornerstone of diagnosis
    1. ~100% sensitivity in the first 3 days
    2. sensitivity decreases sharply after 5-7 days, and lumbar puncture is often then required to show xanthochromia
  2. CT angiography can miss aneurysms <3 mm in size
  3. If CT is non-diagnostic, consider MRI or DSA (if planning NSX)

Acute Management

Rebleeding Prevention

Rebleeding is associated with very high mortality and a poor neurological prognosis. The risk is maximal in the first 2-12 hours, and up to 13% in the first 24 hours. More than 1/3 of rebleeds occur in the first 3 hours from symptom onset. 1. Blood pressure management 1. The optimal BP target is not known. For most patients, the goal should be SBP < 160 mmHg or MAP < 110 mmHg (Class IIa) 3. Antifibrinolysis: patients with an unavoidable delay in obliteration of aneurysm, a significant risk of rebleeding, and no compelling medical contraindications, short-term (<72 hours) therapy with tranexamic acid or aminocaproic acid is reasonable to reduce the risk of early aneurysm rebleeding (Class IIa)

Surgical/Endovascular Treatment

Cerebral Vasospasm and Delayed Cerebral Ischemia (DCI)

Narrowing (vasospasm) of the angiographically visible cerebral arteries after aSAH is common, occurring most frequently 7 to 10 days after aneurysm rupture and resolving spontaneously after 21 days. Radiographic vasospasm does NOT correlate well with symptomatic cerebral ischemia. DCI remains a large cause of death and disability after aSAH as well.

Management: 1. Nimodipine should be given to ALL patients with aSAH (this improves neurological outcomes but not cerebral vasospasm). Whether other CCBs are useful is unknown 2. Maintain euvolemia and normal circulating blood volume 3. For patients with DCI, consider induced hypertension if tolerable 4. For symptomatic vasospasm, consider cerebral angioplasty and/or selective intra-arterial vasodilatory therapy. 5. For monitoring and diagnosis, consider TCD, perfusion imaging with CT or MR

Hydrocephalus secondary to aSAH

  1. CSF diversion --> EVD or lumbar drainage

Seizures secondary to aSAH

  1. consider prophylactic AEDs in the immediate post-hemorrhagic poeriod
  2. Routine long-term use of AEDs is not recommended, but can be considereed for patients with known risk factors for delayed epilepsy (prior seizure, hematoma, intractable hypertension, infarction, MCA aneurysm)

Medical complications of aSAH

  1. Sodium disorders
    1. Cerebral salt wasting/SIADH
  2. Fever --> target normothermia
  3. Dysglycemia -- target normal levels, avoid hypoglycemia

Long-Term Management

References

  1. AHA/American Stroke Association aSAH 2012 Guidelines: Guidelines for the Management of Aneurysmal Subarachnoid Hemorrhage | Stroke
  2. Treatment of Spontaneous Subarachnoid Hemorrhage | Stroke
  3. Aneurysmal subarachnoid hemorrhage: Treatment and prognosis - UpToDate
  4. https://emcrit.org/ibcc/tbi/