MD Notes

creation date: 2026-02-19 16:35
tags: Pathologies

Intracerebral Hemorrhage

Background

Definitions

Intracerebral hemorrhage (ICH) is a type of hemorrhagic stroke.

Hemorrhagic strokes account for 20% of all strokes, the other 80% being ischemic stroke, and is further subtyped into subarachnoid hemorrhage (10% of strokes) and intracerebral hemorrhage (10% of strokes).

Etiology

ICH is classified as either traumatic or spontaneous. Traumatic brain injury is discussed separately.

There are several underlying conditions but the most common are hypertension, amyloid angiopathy, and ruptured vascular malformation.

Hypertension
Penetrator arteries that branch off of major intracerebral arteries (often at 90 degrees) are especially susceptible due to the exposure to the pressure of the parent vessel without any gradual decrease in vessel caliber.

Typically these vessels affect the pons and midbrain, thalamus, putamen, caudate, and globus pallidus, and cerebellar nuclei.

In patients with chronic hypertension, intimal hyperplasia and hyalinosis of the vessel wall can result in focal necrosis and subsequent vessel wall injury (pseudoaneurysms). While small amounts of blood can leak into the extravascular space, massive hemorrhage occurs only when the clotting system is unable to compensate for the degree of damage.

Cerebral amyloid angiopathy
Deposition of amyloid proteins in small to medium-sized vessels of the brain and leptomeninges can weaken the structure of the vessel walls. This makes them prone to bleeding, especially in the lobar region.

Vascular malformations
Arteriovenous malformations (AVMs) and cavernous malformation (CMs) can rupture causing bleed.

AVMs may rupture due to the high-pressure arterial flow forming an aneurysm or weakening the vessel at the connection to the slow-flow venous system. These typically occur in lobar, intraventricular, or subarachnoid regions.

CMs are less common due to their slow-flow nature of thin-walled capillary. These occur in the brainstem, juxtacortical regions, or intraventricular space.

Other uncommon causes
Cerebral venous thrombosis

  • Increased venous pressure from obstruction of veins or sinuses
  • Causes venous or capillary rupture
    Hemorrhagic infarction
  • Breakdown of vascular structure during ischemic infarct

Other conditions include those affecting vasculature and blood.

Pathogenesis

There are two primary mechanism for brain injury in intracerebral hemorrhage.

Primary mechanical injury occurs during hematoma expansion and perilesional edema. The increasing volume contribute to the mass effect and increased intracranial pressure which reduce cerebral perfusion and thus ischemic injury. In extreme cases, cerebral herniation can occur.

Hematoma expansion occurs in the first few hours after onset and associated with neurological deterioration and generally worse outcomes. Perihematomal edema is associated with local neuronal ischemia and present in roughly half of patients.

Secondary brain injury occurs from the breakdown of the blood-brain barrier following initial hemorrhage. There are both excitotoxic and inflammatory processes involved but exact mechanisms are unclear.

Location of bleed
The manifestations depend on location of the hemorrhage. The INTERACT2 trial found the commonly affected brain structures from ICH are (in order of frequency):

  • Putamen/globus pallidus
  • Posterior limb of the internal capsule
  • Thalamus
  • External capsule
  • Lobar
  • Cerebellum or brainstem
  • Anterior limb of internal capsule
  • Caudate head

Clinical Presentation

Signs & Symptoms

Neurologic signs and symptoms depends on the location of the hemorrhage:

Putaminal hemorrhage

  • Hemiplegia
  • Hemisensory loss
  • Homonymous hemianopsia (loss of visual field on same side of both eyes)
  • Gaze palsy
  • Stupor/coma (if hemorrhage is large)

Internal capsule hemorrhage

  • Mild dysarthria
  • Contralateral hemiparesis
  • Sensory deficit

Thalamic hemorrhage

  • Hemiparesis
  • Hemisensory loss
  • Transient homonymous hemianopsia
  • Pupil changes or non-reactivity
  • Aphasia

Lobar hemorrhage

  • Dependent on lobe (eg. visual changes with occipital, plegia/paresis in frontopareital)
  • Associated with seizures

Cerebellar hemorrhage

  • Inability to walk due to imblanace
  • Vomiting
  • Occipital headache
  • Referred pain to the neck or shoulder
  • Gaze palsy
  • Facial weakness
  • Not associated with hemiparesis

Brainstem/pontine hemorrhage

  • Deep coma
  • Bilateral paralysis
  • Pinpoint pupils

Onset typically occurs during routine activity but hypertensive hemorrhage may occur with exertion/intense emotion.

Symptoms may be progressive over minutes or few hours (compared to cardioembolic or subarachnoid hemorrhagic stroke which are maximal at onset).

Other findings include:

  • Seizures (15% of patients)
  • Cardiac abnormalities (prolonged QT, ST-T wave changes)

History & Physical Exam

A rapid history should be taken eliciting the symptom, onset, progression of symptoms and neurologic deficits.

A rapid neurological exam should be performed.

Risk Factors

The major risk factors are:

  • Advancing age
  • Hypertension (most common etiology)
  • Antirhombotic medications (warfarin (highest risk), DOACs, heparins, thrombolytic agents)

Other risk factors include:

  • Obesity and inactivity
  • High alcohol intake
  • Race and ethnicity
  • Lower cholesterol and LDL (effect of statins unclear)
  • Genetics
  • Small vessel vascular disease
  • Tobacco or stimulant drug use
  • Infections (HIV, Hep C, varicella-zoster)

Diagnosis

Criteria

Diagnosis of ICH can be made using noncontrast head CT or brain MRI.

Nonconstrast head CT findings include:

  • Hyperdense hyperacute blood
  • Isodense with ring-enhancement subacute blood

CT angiography may be performed along noncontrast head CT to identify underlying vascular cause.

Work-up

Initial evaluation
Neuroimaging is performed as soon as possible for diagnosis and to excluse ischemic stroke and stroke mimics.

Following imaging (or without delaying imaging), the following testing are done:

  • CBC
  • Electrolytes, BUN, creatinine
  • Glucose
  • Coagulation studies
  • HS Troponin
  • Toxic screen (cocaine and other sympathomimetic drugs)
  • Urinalysis
  • Pregnancy test

An ECG may also be obtained for baseline and investigation of coexisting cardiac concerns.

Further investigation
In patients with seizures or encephalopathy unexplained by the ICH location or size, an electroencephalogram may be indicated.

Follow up imaging (CT or MR head) may be indicated to determine:

  • Underlying cause
  • Evaluate for expansion or rebleeding

Differential

The diagnoses to consider is ischemic stroke as that alters management.

Other conditions that may present like stroke include:

  • Reversible cerebral vasoconstriction syndromes
  • Cerebral infections
  • Cerebral venous thrombosis
  • Cervical artery dissection
  • Acute hypertensive crisis
  • Spontaneous intracranial hypotension
  • Hypo/hyperglycemia
  • Seizure
  • Syncope

Red Flags / Complications

The 30 day mortality rate from ICH is around 40% with half of the deaths occuring within the first two days.

Complications include:

  • DVT and PE
  • Aspiration pneumonia
  • Seizures
  • Fever

Management

Stroke management occurs in the ICU or stroke unit. Admission should be done promptly.

Prognostication and care limits are typically delayed until following the first 1-2 days and aggressive care performed unless the patient has a preexisting DNR.

Treatment of Acute Bleed

Reversing anticoagulation and antiplatelet drugs
Any anticoagulant and antiplatelet drug should be discontinued promptly. Medications are used to reverse the effects of anticoagulants:

  • Warfarin: 4-factor prothrombin complex concentrate (4F PCC); if not available, three-factor prothrombin with recombinant VIIa or fresh frozen plasma
  • DOACs: 4F PCC or andexenet alfa
  • Dabigatran: idarucizumab or activated PCC (aPCC)
  • Heparin and LMWH: protamine sulfate

Blood Pressure Management

Elevated BP and BP variability are risk factors for hemorrhagic expansion and poorer outcomes.

Blood pressure targets
For patients presenting with SBP 150-220, targets are SBP 140 within 1 hour of presentation once stable.

For patients presenting with SBP >220, targets are to lower SBP <220 rapidly, then gradually reduced to target of 140-160 over period of hours.

Antihypertensive agents
Selection depends on:

  • Rapidity and extent of blood pressure reduction
  • Method of delivery (bolus vs. infusion)
  • Patient comorbidities
  • Potential adverse effects

Generally:

  • If SBP ≥160: nicardipine
  • If SBP <160: labetalol

Note, nitroprusside and nitroglycerin are typically avoided due to risk of increasing intracranial pressure.

Treatment of Intracranial Pressure

Space-occupying lesions such as ICH can result in progressive neurologic impairment due to compression.

In patients with concerning features for elevated ICP-related rapid neurological impairment, surgery may be indicated. Features include:

  • Cerebellar hemorrhage ≥3 cm in diameter associated with compression or neurological deterioration, or hydrocephalus due to ventricular obstruction
  • Intraventricular hemorrhage with ventricular enlargement with deterioration
  • Supratentorial hemorrhage associated with deterioration or hydrocephalus

In all other patients:

  • Elevated head to bed to 30 degrees
  • Mild sedation for agitated patients
  • Antipyretic medication if fever >38 degrees C
  • Avoid positioning that reduce cerebral venous outflow (eg. neck rotation, internal jugular central line placement, tight device securement)
  • Isotonic solutions (not hypotonic) for fluids
  • Maintain serum sodium >135 mEq/L

Monitoring
ICP should be monitored using clinical exams and CT head if ICP elevation is suspected.

Clinical exam findings include:

  • Pupillary changes (eg. impaired reactivity to light)
  • Abducen nerve palsy (medial eye movement) and/or horizontal diplopia
  • Progressive drowsiness
  • Crushing triad (bradycardia, respiratory depression, hypertension)
  • Focal symptom related to herniation syndromes

Measures for severe signs of elevated ICP or mild ICP elevation non-responsive to initial measures
Initial measures consist of osmotic therapy. Options include:

  • Severe including those awaiting surgery:
    • Hypertonic saline 15-30 mL q6h via a central IV line
    • Mannitol 1 g/kg IV bolus via central IV line
  • Milder signs:
    • 3% saline continuous infusion via peripheral or central IV line titrated to sodium target of 145-155 mEq/L
    • Mannitol 0.25-0.5 g/kg q6h

Glucocorticoids are not indicated due to the lack of benefit and risk of infection and hyperglycemia.

Surgical options
Patients undergoing surgical management may undergo:

  • CSF drainage via ventriculostomy satheter
  • Decompression via craniectomy and hematoma evacuation

Complication Management

Seizures
Patients who have a seizure with acute ICH, IV antiseizure medication is administered.

If patients with seizure <14 days from ICH onset, medication is continued for several days and then weaned once stable if seizures do not recur.

If patients had the seizure >14 day after onset, medication is typically continued long term.

Aspiration
For patients who require endotracheal intubation, a single dose of ceftriaxone 2g IV is administered to reduce the risk of ventilator-associated pneumonia.

Venous thromboembolism
Hospitalization increases risk of VTE. Prophylaxis includes:

  • Intermittent pneumatic compression
  • LMWH 4 days following ICH onset once bleeding has stopped (note risk of hematoma expansion)

References

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