Epidural hematoma

Subarachnoid hemorrhage

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Etiology

• Traumatic SAH: traumatic brain injury
• Nontraumatic (spontaneous) SAH
  • Ruptured intracranial aneurysms
    • Most commonly occur in the circle of Willis
    • Berry aneurysms account for approx. 80% of cases of nontraumatic SAH.
      • Also known as Saccular aneurysm because of the shape
      • Round, saccular shape
      • Most common type of cerebral aneurysm
      • Typically occur at vessel junctions in the circle of Willis, most commonly between the anterior communicating artery and anterior cerebral artery
      • Account for ∼ 80% of cases of nontraumatic subarachnoid hemorrhage
  • Ruptured arteriovenous malformations (AVM)

Diagnosis

CT head without contrast

• Defining feature: blood in subarachnoid space (hyperdense) with variable extension and location

Treatment

Initial management

• Prevention of rebleeding
  • Anticoagulant reversal
  • Management of blood pressure and cerebral perfusion pressure
    • Target SBP < 160 mm Hg
• Other neuroprotective measures
  • Start ICP management (e.g., elevate head 30°, IV mannitol, short-term controlled hyperventilation).

Treatment of aneurysmal SAH

• Intracranial aneurysm repair
  • Endovascular coiling
  • Microsurgical clipping
• Prevention of vasospasm and delayed cerebral ischemia
  • Administer oral nimodipine
    • 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 hydrocephalus: may include an external ventricular drain (EVD), lumbar drainage, or permanent ventriculoperitoneal shunt

Warning

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

Complications

Vasospasm

• Occurs in approx. 30% of patients with SAH
• 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
• Oral nimodipine should be given after subarachnoid hemorrhage to prevent vasospasm