Intracerebral hemorrhage

Intracerebral hemorrhage (ICH) refers to bleeding within the brain parenchyma. The term should not be confused with intracranial hemorrhage, which is a broader term that encompasses bleeding within any part of the skull, i.e., extradural, subdural, subarachnoid, or intracerebral bleeding. The most significant risk factor for spontaneous ICH is arterial hypertension. Symptoms are often nonspecific (e.g., headache); however, depending on the affected vessel and cerebral region, focal neurological deficits (e.g., hemiparesis) may occur. Compared with ischemic stroke, patients with ICH are more likely to present with severe headache and have rapidly progressing symptoms. The initial imaging investigation of choice is CT head without contrast, which typically shows a hyperdense mass lesion. Treatment involves management of the underlying and associated conditions (e.g., controlling hypertension, reversing coagulopathy) in order to limit hematoma expansion and prevent secondary brain injury. In severe cases, neurosurgical intervention may be required. Approximately half of patients with spontaneous ICH die within 30 days of symptom onset. Traumatic ICH may result from traumatic brain injury (TBI) and is managed similarly to spontaneous ICH.

See also “Overview of intracranial hemorrhage” and “Overview of stroke” for more information.

• Intracerebral hemorrhage (ICH): bleeding within the brain parenchyma
• Intracranial hemorrhage: a broad term used to describe any bleeding within the skull (including intracerebral hemorrhage, subarachnoid hemorrhage, subdural hemorrhage, and epidural hemorrhage) due to traumatic brain injury or nontraumatic causes (e.g., hemorrhagic stroke, ruptured aneurysm, hypertensive vasculopathy)
• Hemorrhagic stroke
  • Rupture of a blood vessel within the brain or the cerebrospinal fluid
  • Subtypes
    • Intracerebral hemorrhage (intraparenchymal hemorrhage): bleeding within the brain parenchyma
    • Subarachnoid hemorrhage: bleeding into the subarachnoid space
    • Intraventricular hemorrhage: bleeding within the ventricles

• ICH is responsible for approx. 10% of all strokes. ^[1]
• Most commonly affects the deep structures of the brain ^[2]
• Intraventricular extension occurs in approx. 30% of patients with ICH.

Epidemiological data refers to the US, unless otherwise specified.

• Nontraumatic (spontaneous)
  • Hypertension: most common cause of spontaneous ICH
  • Cerebral amyloid angiopathy: most common cause of spontaneous ICH in individuals > 60 years of age
  • Arteriovenous malformations: most common cause of spontaneous intracerebral hemorrhage in children
  • Vasculitis (e.g., giant cell arteritis)
  • Neoplasms (e.g., meningioma)
  • Ischemic stroke (due to reperfusion injury)
  • CNS infections (e.g., HSV encephalitis)
  • Septic emboli
  • Coagulopathy (e.g., hemophilia, anticoagulant use)
  • Stimulant use (e.g., cocaine and amphetamines; possibly also caffeine)
• Traumatic: : see traumatic brain injury

References:^[3][4][5]

• 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
    • Putamen most commonly affected
    • 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
  • Structural abnormalities (e.g., vascular malformations) → exposure of parts of the abnormal vascular segment to excessive strain → rupture
  • Venous outflow obstruction and stimulant use (e.g., cocaine) → acute arterial hypertension
  • Coagulopathies: impaired hemostasis → vascular microtrauma
  • Inflammatory tissue necrosis → damage to vessels
• Traumatic: blunt or penetrating injury → damage to vessels

• Headache
  • Absent in small hemorrhages
  • Most common in cerebellar and lobar hemorrhages ^[2][6]
• Focal neurologic signs and symptoms may occur, depending on the location and size of the hemorrhage (see “Stroke symptoms by affected vessel” and “Stroke symptoms by affected region”) ^[2]
  • 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
• 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

For the approach to patients with suspected traumatic ICH, see “Management of traumatic ICH.”

Initial evaluation ^[7][8][9]

Consider the sudden onset of focal neurological deficits a vascular event until proven otherwise and evaluate patients as promptly as possible (preferably within the so-called “golden hour”). ^[10][11][12]

• Perform an ABCDE survey.
• Initiate neuroprotective measures: These take precedence over diagnostics if they cannot be performed in parallel.
• Take a focused history, perform a neurological examination, and measure the GCS score.
• Order immediate diagnostic studies.
  • Neuroimaging: CT head without contrast or MRI head
  • Laboratory studies: coagulation panel, platelets, and POC glucose
• Admit or urgently transfer the patient to a neurocritical care unit.
• Urgent consultations
  • Neurosurgery: to evaluate if urgent operative intervention is indicated
  • Neurology
  • Hematology: if the patient is taking antiplatelet agents or anticoagulants

Patients with signs of brain herniation should be evaluated immediately for neurosurgical intervention!

Monitoring

• All patients should receive:
  • Continuous cardiac telemetry
  • Blood pressure (BP) monitoring
  • Continuous pulse oximetry
  • Hourly POC glucose monitoring
• Consider:
  • An arterial line
  • ICP monitoring (see “Acute stabilization” for indications)
  • Continuous EEG monitoring

Acute stabilization should begin immediately after symptom onset, in parallel with diagnostic measures, with the goal of reducing hematoma expansion and limiting secondary brain injury. ^[7]

• Airway management
  • Immediately initiate basic airway maneuvers for airway compromise, e.g., signs of partial airway obstruction.
  • Intubate if airway protective reflexes are lost.
  • Intubation of patients with high ICP can be very risky and requires a specialized approach.
• Standard neuroprotective measures
  • Provide supplemental O₂ as needed to maintain target SpO₂ > 94%.
  • If mechanical ventilation is required: maintain long-term normocapnia (PaCO₂ 35–45 mm Hg). ^[13]
  • Maintain normoglycemia (see also “Treatment of hypoglycemia” and “Management of hyperglycemia in critically ill patients”). ^[7][13]
  • Maintain normothermia: e.g., prevent neurogenic fever.
• Blood pressure management in ICH: The optimal approach is unclear. ^{[7][14][15][16][17]};
  • If systolic BP is > 220 mm Hg, promptly lower to 140–180 mm Hg; , e.g., using nicardipine AND/OR labetalol
  • If systolic BP is 150–220 mm Hg and no contraindications to antihypertensive agents: Consider BP lowering on an individual basis in consultation with a specialist.
  • Alternative antihypertensive agents include: ^[9][18]
    • ACE inhibitors, e.g., enalapril or ARBs
    • Furosemide
    • Hydralazine
  • Avoid systemic hypotension (e.g., MAP < 65 mm Hg).
• Anticoagulation reversal
  • Stop all anticoagulants and antiplatelet agents.
  • Administer reversal agents as soon as possible to patients with an INR > 1.4 to reduce the risk of hematoma expansion.
• Platelet transfusion in intracranial bleeding: only for severe thrombocytopenia ^[7]
• ICP management
  • Considering invasive ICP monitoring if:
    • The patient's GCS score is ≤ 8
    • Significant intraventricular hemorrhage or hydrocephalus is present
    • There is evidence of transtentorial herniation
  • Consider measures to maintain ICP < 20 mm Hg and a cerebral perfusion pressure of 60–70 mm Hg: e.g., head elevation to 30°, hyperosmolar therapies for ICP management (mannitol, hypertonic saline), placement of an external ventricular drain or VP shunt for hydrocephalus ^[8]
  • Avoid corticosteroids. ^[19]

Remember to stop all anticoagulants and antiplatelet medication, including aspirin, in patients with ICH.

Platelet transfusion is not routinely indicated in patients with normal platelet counts taking antiplatelet agents (e.g., aspirin, clopidogrel). ^[7][20][21]

Characteristic neuroimaging findings ^[24]

• Hematoma within the cerebral parenchyma (i.e., intraaxial lesion)
  • Typical locations
    • Supratentorial: lobar, or within the thalamus or basal ganglia
    • Infratentorial: in the cerebellum or brainstem
  • The density of the hematoma varies depending on the imaging modality used and age of the hematoma.

• Additional possible features
  • Midline shift and/or mass effect; (if significant, this should raise suspicion for impending herniation)
  • Intraventricular extension ^[9]

Angiography findings

Angiography may be performed to assess for signs of further bleeding and structural abnormalities in patients with suspected underlying pathology (e.g., patients aged < 55 years and those without risk factors for ICH). ^[7]

• CTA spot sign ^[27]
  • Definition: localized area of enhancement visible within an intracerebral hemorrhage only after administration of IV contrast
  • Implication: indicates active hemorrhage; is a predictor of hematoma expansion ^[7][27][28]
• Aneurysms or other vascular lesions

Approach

• Most patients are managed conservatively, with treatment focused on prevention of secondary brain injury.
• Patients should be screened for common complications.
• Select patients may benefit from neurosurgical intervention.

Detection and management of complications

Prophylactic anticonvulsants are not recommended in patients with ICH. ^[7]

Surgical management ^[7]

Neurosurgical consultation is advised for acute ICP management (see “Acute stabilization”) and definitive management. Evacuation of the hematoma may be appropriate depending on the size, location, and associated clinical features of the ICH.

Hematoma evacuation

• Can be performed using standard craniotomy or minimally invasive surgical techniques ^[7][36]
• Hematoma evacuation is recommended in patients with infratentorial hemorrhage who have any of the following: ^[7]
  • Large hematoma (> 3 cm)
  • Declining neurological status
  • Hydrocephalus
  • Signs of brain herniation (e.g., Cushing triad)
• Consider in patients with supratentorial hemorrhage and a declining GCS score or an initial GCS score of 10–13. ^[37]

Decompressive craniotomy

• Decompressive craniotomy may be performed alone or in combination with hematoma evacuation.
• Consider in patients with supratentorial hemorrhage and any of the following: ^[7]
  • Refractory elevated ICP
  • Large hematoma with a significant midline shift
  • GCS score ≤ 8

• Perform an ACBDE assessment and secure the airway, if needed.
• Start continuous monitoring of heart rate, BP, and SpO₂.
• Initiate acute stabilization and neuroprotective measures, e.g., BP control, anticoagulant reversal, ICP management.
• Order CT head without contrast, coagulation studies, CBC, and POC glucose test.
• Urgently consult with neurosurgery and neurology.
• Admit to a neurocritical care unit.
• Consider further imaging (e.g., CTA or magnetic resonance angiography) to determine underlying causes and monitor hematoma progression.
• Screen for and manage potential complications, e.g., mechanical VTE prophylaxis, clinical swallow assessment, electrolyte monitoring.

The management of traumatic ICH is similar to the management of spontaneous ICH, with some modifications.

• Diagnostics ^[38]
  • Follow the management approach for TBI and exclude concurrent injuries.
  • TBI diagnostics include CT head without contrast and additional imaging as needed.
• Management ^[8][10][38]
  • Focuses on the prevention of complications in brain injuries
  • Early surgical intervention can improve outcomes; consult neurosurgery as soon as possible. ^[39]
  • Recommendations for neuroprotective measures include seizure prophylaxis for severe TBI.
  • Follow-up neuroimaging is usually indicated; timing depends on injury severity.
  • For details, see “Management of moderate and severe TBI.”

See “Differential diagnoses of stroke.”

The differential diagnoses listed here are not exhaustive.

• Elevated ICP and brain herniation
• Intraventricular hemorrhage → hydrocephalus
• Recurrent hemorrhage
• Vasospasm and cerebral ischemia
• Dysphagia; : can lead to aspiration of food and pneumonia
• Seizures
• Hydrocephalus
• SIADH
• Deep vein thrombosis
• See “Complications of stroke.”

We list the most important complications. The selection is not exhaustive.

• 30-day mortality ranges from 25% to 50%. ^[41][42]
• Patients aged > 65 years and those with large hematomas and low GCS scores (≤ 11) typically have poor outcomes. ^[41][42]
• The ICH score is used to assess the severity of bleeds, and, in conjunction with other features, to estimate the patient's prognosis. ^[7]

The ICH score was designed to assess ICH severity and aid clinical communication; it should not be used in isolation to determine prognosis!