Intracranial hemorrhage

Type	Vessel / Cause	Key Associations	CT Appearance
Epidural	Middle Meningeal Artery	Pterion fracture, Lucid interval	Lens-shaped (Biconvex) Stops at sutures
Subdural	Bridging Veins	Elderly, Alcoholics, Shaken Baby	Crescent-shaped Crosses sutures
Subarachnoid	Berry Aneurysm / AVM	”Thunderclap” headache, Meningeal signs	Blood in Sulci LP: Xanthochromia
Intraparenchymal	Charcot-Bouchard (HTN)	HTN, Amyloid angiopathy, Basal Ganglia	Focal hyperdensity within brain
Intraventricular	Germinal Matrix	Premature infants (<32 wks)	Blood inside Ventricles

Epidural hematoma

Subarachnoid hemorrhage

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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.
      • 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

• Gradual/Insidious Onset: Neurologic decline over hours to days.
• Sx: Headache, somnolence, confusion, light-headedness, focal neurologic deficits (e.g., focal weakness).
• Chronic SDH (weeks to months old): Can present with subtle cognitive impairment, dementia-like symptoms, and gait disturbances, particularly in the elderly.

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
• 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).