Subarachnoid hemorrhage

Etiology

 - Elderly individuals experience age-related cerebral atrophy. This brain shrinkage puts increased tension on the bridging veins, making them highly susceptible to tearing from shearing forces, even with relatively minor head trauma (like a fall).

• 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. c
      • 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)

Charcot-Bouchard aneurysms vs Saccular (berry) aneurysms

Feature	Charcot-Bouchard	Saccular (Berry)
Etiology	Chronic HTN	Congenital weakness + Hemodynamics
Pathology	Lipohyalinosis of microvessels	Lacking Internal Elastic Lamina & Media
Location	Deep Brain (Basal Ganglia, Thalamus)	Circle of Willis Bifurcations (ACom > PCom)
Vessels	Lenticulostriate arteries	Medium-sized arteries
Rupture	Intraparenchymal Hemorrhage	Subarachnoid Hemorrhage
Symptoms	Focal deficits (Hemiparesis)	“Thunderclap” Headache, Meningismus
Associations	Lacunar strokes	ADPKD, Ehlers-Danlos, Marfan

• Saccular: This term means “resembling a sac.” Saccular aneurysms are outpouchings or bulges on one side of a blood vessel wall.
• Berry: The “berry” description refers to the characteristic round shape of these aneurysms. They look like a berry connected to the main artery.

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Clinical Features

• History:
  • “Worst headache of my life” / “Thunderclap” headache (hyperacute onset, reaching maximal intensity within seconds to minutes).
  • Transient LOC, nausea, vomiting, syncope, photophobia.
  • Sentinel headache: Warning leak occurring days-to-weeks prior in ~10-40% of cases.
• Physical Examination:
  • Meningismus (nuchal rigidity, (+) Kernig, (+) Brudzinski signs; can take 6-12 hrs to develop).
  • CN III palsy with pupillary involvement (fixed, dilated pupil + “down and out” eye) suggests PCom aneurysm compression.
  • Subhyaloid/preretinal hemorrhages (Terson syndrome).
  • Focal neurological deficits or depressed GCS (indicates elevated ICP or intraparenchymal extension).

Diagnosis

• Initial / Screening Imaging:
  • Non-Contrast Head CT (NCCT): c2
    • Sensitivity >95–98% within first 6–12 hrs (drops significantly after 24–48 hrs because CSF dilutes blood).
    • Hyperattenuation/blood seen in basal cisterns, sulci, and Sylvian fissures.
• Next Step if NCCT is Negative / Equivocal & Suspicion High:
  • Lumbar Puncture (LP): c
    • Xanthochromia (yellow supernatant from RBC lysis/bilirubin; peaks 6–12 hrs, gold standard LP marker; centrifuge CSF to assess).
    • Elevated RBC count that persists from tube 1 to tube 4 (differentiates SAH from traumatic tap).
    • Elevated opening pressure (>200 mm H₂O).
• Confirmatory / Vascular Mapping:
  • CT Angiography (CTA): Rapid, non-invasive initial vascular imaging for aneurysm localization.
  • Digital Subtraction Angiography (DSA): Gold standard for identifying aneurysm anatomy, source of bleeding, and planning intervention.
• Key Labs:
  • Baseline CBC, PT/INR, PTT, Type and Screen.
  • BMP (serial monitoring for hyponatremia).
  • Cardiac enzymes and ECG (rule out neurogenic stunned myocardium/arrhythmias).

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
• Prevention & Treatment
  • Nimodipine (Calcium Channel Blocker): t
    • Standard of Care: Started on admission (Day 1) for all SAH patients.
    • Mechanism: It blocks this calcium influx into the neurons, preventing cellular death. Prevents ischemic neurological deficits and improves mortality (neuroprotection).
    • Note: It does not necessarily prevent the angiographic vasospasm itself, but prevents the cellular injury associated with it.
  • Hemodynamic Augmentation (formerly “Triple H”):
    • Current Goal: Maintain Euvolemia and Induced Hypertension (using vasopressors like phenylephrine or norepinephrine).
    • Rationale: ↑ MAP pushes blood through the narrowed vessels to maintain Cerebral Perfusion Pressure (CPP).
  • Refractory Cases:
    • Intra-arterial vasodilators (e.g., verapamil, nicardipine).
    • Balloon angioplasty (mechanical dilation).