Intracerebral 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 c	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

Epidemiology

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Etiology

• Chronic HTN (most common overall): Causes Charcot-Bouchard microaneurysms in deep penetrating lenticulostriate arteries (basal ganglia, thalamus, pons).
• Cerebral Amyloid Angiopathy (CAA): Most common cause of spontaneous lobar/cortical ICH in the elderly; associated with Alzheimer disease. c
• Anticoagulant or thrombolytic therapy.
• Sympathomimetic illicit drugs (e.g., cocaine, amphetamines). c
• Vascular malformations (AVMs, cavernous hemangiomas) in younger pts.
• Common locations: Putamen/Internal capsule (most common, ~50%), Thalamus, Pons, Cerebellum, Subcortical white matter (Lobar).

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Pathophysiology

• Nontraumatic mechanisms of hemorrhage
  • Chronic arterial hypertension → lipohyalinosis of lenticulostriate vessels (which supply the basal ganglia) and/or formation and rupture of Charcot-Bouchard microaneurysms → lacunar strokes (ischemia) of the basal ganglia. See also Ischemic stroke > Lacunar infarction
    • Putamen most commonly affected, which is supplied by lenticulostriate arteries

    • 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.

      Link to original

    • Other locations: thalamus (second most common) and infratentorial parts of the brain (e.g., pons, cerebellum)
  • Cerebral amyloid angiopathy: deposition of β-amyloid peptides in vessel walls → focal damage with formation of microaneurysms → rupture → recurrent lobar intracerebral hemorrhage
• Traumatic: blunt or penetrating injury → damage to vessels

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Clinical features

• Headache
• Focal neurologic signs and symptoms
  • Putaminal hemorrhage: contralateral hemiparesis or hemiplegia with less severe contralateral hemisensory loss; eyes deviate toward the side of the hematoma
    • Thalamic hemorrhage: contralateral hemiparesis, contralateral hemisensory loss, decreased consciousness, wrong way eyes

Mnemonic

• The dorsal striatum is composed of both the caudate and the putamen.
• The caudate is involved in both motor activity as well as more cognitive functions, while the putamen is primarily involved in motor activity.
• The caudate nucleus is the most caugnitive part of the basal ganglia.
• When you see put-am-en on an exam, “put-an-em” for Motor.

• Course
  • Symptoms typically progress gradually over minutes to a few hours
  • Focal deficits worsen with expansion of the hematoma
  • Late: symptoms of increased ICP
    • Nausea and vomiting
    • Confusion and loss of consciousness
    • Bradycardia
    • Fixed pupils

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Diagnostics

• Initial & Best Step: Non-contrast Head CT
  • Identifies acute hyperdense (bright white) parenchymal collection with surrounding hypodense edema/mass effect.
• Key Labs:
  • Coagulation panel (PT/INR, PTT, Platelets): To identify coagulopathy.
  • Toxicology screen: Rule out sympathomimetic drug use. c
  • CBC, BMP, Type & Screen.
• Secondary/Confirmatory Vascular Imaging:
  • CTA or MRI/MRA brain: Performed once stable if suspecting secondary causes (AVM, aneurysm, venous sinus thrombosis, hemorrhagic tumor).

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Treatment

• 1. Airway/ABCs: Intubate if GCS ≤ 8; elevate HOB 30°.
• 2. BP Control (Immediate): Target SBP 130–140 mmHg with IV Nicardipine or Labetalol.
• 3. Reverse Anticoagulation (Stat):
  • Warfarin: 4F-PCC + IV Vitamin K.
  • Heparin: Protamine sulfate.
  • Dabigatran: Idarucizumab.
  • Factor Xa Inhibitors (Apixaban, Rivaroxaban): Andexanet alfa or 4F-PCC.
• 4. Manage ↑ ICP: IV Mannitol or 3% Hypertonic Saline.
• 5. Neurosurgery:
  • Cerebellar hematoma ≥ 3 cm or brainstem compression $\to$ Emergent surgical decompression.
  • EVD placement for acute obstructive hydrocephalus.