Intracranial hemorrhage

Feature	Epidural Hematoma (EDH)	Subdural Hematoma (SDH)	Subarachnoid Hemorrhage (SAH)	Intracerebral Hemorrhage (ICH)
Location	Potential space between dura and skull.	Between dura and arachnoid mater.	Between arachnoid and pia mater (in CSF space).	Within the brain parenchyma itself.
Vessel	Middle Meningeal Artery (arterial bleed).	Bridging Veins (venous bleed).	Cerebral Arteries (often from ruptured saccular/berry aneurysm).	Lenticulostriate arteries, Charcot-Bouchard microaneurysms.
Cause	Trauma (esp. temporal bone fracture at the pterion).	Trauma (acceleration-deceleration). Can be acute or chronic.	Ruptured aneurysm (most common non-traumatic), trauma.	Hypertension (most common), amyloid angiopathy, AVM, tumor, trauma.
Patient	Young adult, head trauma (e.g., MVC, baseball injury).	Elderly, alcoholics, shaken babies (due to brain atrophy stretching veins).	Aneurysm rupture often in 40s-60s. Associated w/ PKD, Ehlers-Danlos.	Older patients with chronic HTN.
Presentation	”Lucid interval” followed by rapid decline, signs of ↑ ICP (headache, N/V, CN III palsy).	Varies widely. Acute: ↓ consciousness. Chronic: gradual cognitive decline, focal deficits, headache.	”Worst headache of my life” (thunderclap headache, sudden blood leakage into CSF irritates meninges), nuchal rigidity, photophobia, no focal deficits initially.	Abrupt onset of focal neurological deficits (e.g., hemiparesis, aphasia), headache, seizure, N/V.
Head CT	Biconvex (lens-shaped) hyperdensity. Does NOT cross suture lines.	Crescent-shaped hyperdensity. CAN cross suture lines.	Hyperdensity in sulci, cisterns, and fissures.	Hyperdense mass within the brain tissue. Common in basal ganglia, thalamus, pons, cerebellum.
Management	Emergent neurosurgical evacuation (craniotomy).	Surgical evacuation if large or symptomatic.	Supportive care, nimodipine (prevents vasospasm), coiling/clipping of aneurysm.	BP control (aggressive reduction), reverse anticoagulation, manage ICP; surgery in select cases.
Key Buzzword	Lucid interval, lentiform.	Crescent-shaped, bridging veins.	Worst headache of my life, thunderclap, berry aneurysm.	Hypertensive bleed, Charcot-Bouchard.

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)

Charcot-Bouchard aneurysms vs Saccular (berry) aneurysms

Feature	Charcot-Bouchard Microaneurysms	Saccular (Berry) Aneurysms
Associated Conditions	Hypertension	ADPKD, Ehlers-Danlos syndrome, hypertension
Location	Basal ganglia Cerebellum Thalamus Pons	Circle of Willis
Size	<1 mm	Variable, 2-25 mm
Result of Rupture	Intracerebral hemorrhage	Subarachnoid hemorrhage
Symptoms of Rupture	Progressive neurologic deficits Headache may follow	Sudden severe headache Focal neurologic deficits uncommon

• 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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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