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 a 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 ICH die within 30 days of symptom onset.
- 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
- ICH is responsible for approx. 10% of all strokes. 
- Most commonly affects the deep structures of the brain 
- Intraventricular extension occurs in approx. 30% of patients with ICH. 
Epidemiological data refers to the US, unless otherwise specified.
- 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
Nontraumatic mechanisms of hemorrhage
- Chronic arterial hypertension → lipohyalinosis of lenticulostriate vessels, which supply the basal ganglia → formation and rupture of Charcot-Bouchard microaneurysms → lacunar strokes (ischemia) of the basal ganglia
- 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
- Absent in small hemorrhages
- Most common in cerebellar and lobar hemorrhages 
- Focal neurologic signs and symptoms may occur, depending on the location and size of the hemorrhage (see “ ” and “ ”) 
The following recommendations apply to spontaneous ICH and are consistent with the 2015 American Heart Association (AHA) ICH guidelines, the 2016 Brain Trauma Foundation guidelines, and the 2017 Neurocritical Care Society guidance on Emergency Neurological Life Support for ICH. Management of traumatic ICH is similar but not identical (see “Traumatic brain injury” for details). 
Initial evaluation 
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”). .
- Perform an , including , respiratory support, and either or as needed (see "Acute stabilization”).
- Initiate : 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.
- Admit or urgently transfer the patient to a neurocritical care unit.
- Urgent consultations
Patients with signs of brain herniation should be evaluated immediately for neurosurgical intervention!
- Provide supplemental O2 as needed to maintain > 94%.
- If mechanical ventilation is required: maintain long-term normocapnia (PaCO2 35–45 mm Hg). 
- Maintain normoglycemia (see also “Treatment of hypoglycemia” and “Management of hyperglycemia in critically ill patients”). 
- Maintain normothermia: e.g., prevent .
Blood pressure management in ICH: The optimal approach is unclear. 
- 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: 
- Avoid systemic hypotension (e.g., MAP < 65 mm Hg).
- 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.
- Considering invasive ICP monitoring if:
- Consider measures to maintain ICP < 20 mm Hg and a cerebral perfusion pressure of 60–70 mm Hg: e.g., head elevation to 30°, mannitol, hypertonic saline), placement of an external ventricular drain or VP shunt for hydrocephalus ( 
- Avoid corticosteroids. 
|Approach to ICH diagnostics |
|Time interval from initial presentation||Laboratory studies||Imaging|
|Within the first hour|| |
|Hours to days|
Characteristic neuroimaging findings 
- Hematoma within the cerebral parenchyma (i.e., intraaxial lesion)
|Variation in ICH density on imaging over time |
|Time since ICH||Hematoma density|
CT without contrast
|MRI (T2 weighted)|
|Hyperacute (< 24 hours)|
|Acute (1–3 days)|
|Early subacute (> 3 days to 1 week)|
|Late subacute (weeks to months)|
|Chronic (> months)|
- Additional possible features
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). 
- CTA spot sign 
- Aneurysms or other vascular lesions
- Most patients are managed conservatively, with treatment focused on limiting further damage.
- Patients should be screened for common complications.
- Select patients may benefit from neurosurgical intervention.
Detection and management of complications
See also “Prevention of complications in brain injuries” for the approach to traumatic ICH.
|Common complications following ICH |
|Complication||Screening and management|
Prophylactic anticonvulsants are not recommended in patients with ICH. 
Surgical management 
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.
- Can be performed using standard craniotomy or minimally invasive surgical techniques 
- Hematoma evacuation is recommended in patients with infratentorial hemorrhage who have any of the following: 
- Consider in patients with supratentorial hemorrhage and a declining GCS score or an initial GCS score of 10–13. 
- 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.
- 30-day mortality ranges from 25% to 50%. 
- Patients aged > 65 years and those with large hematomas and low GCS scores (≤ 11) typically have poor outcomes. 
- The ICH score is used to assess the severity of bleeds, and, in conjunction with other features, to estimate the patient's prognosis. 
|ICH score |
|ICH volume||≥ 30 cm3||1|
|< 30 cm3||0|
|ICH of infratentorial origin||Yes||1|
|Patient age||≥ 80 years||1|
|< 80 years||0|
Total ICH score: 0–6
Predicted 30-day mortality
The ICH score was designed to assess ICH severity and aid clinical communication; it should not be used in isolation to determine prognosis!