Management of Intracerebral Hemorrhage
Intracerebral hemorrhage is a medical emergency requiring immediate CT imaging, rapid blood pressure reduction to systolic <140 mmHg (if presenting between 150-220 mmHg), urgent reversal of any coagulopathy, and admission to a neuroscience intensive care unit or stroke unit. 1
Prehospital and Emergency Response
- Activate emergency medical services (9-1-1) immediately upon recognition of stroke symptoms to minimize time to diagnosis and treatment 1
- EMS personnel should use stroke recognition tools to identify potential ICH and provide advance notification to the receiving hospital, which significantly shortens time to CT scanning 1
- Primary objectives include airway management, cardiovascular support, and transport to the closest facility with neurology, neuroradiology, neurosurgery, and critical care capabilities 1
- Obtain focused history regarding symptom onset timing, medications (especially anticoagulants and antiplatelets), vascular risk factors, recent trauma, and drug use 1
Immediate Diagnostic Evaluation
Rapid neuroimaging with non-contrast CT is mandatory and considered the gold standard for distinguishing ICH from ischemic stroke—MRI with gradient echo sequences is equally sensitive but often impractical 1, 2
Essential Initial Workup
- Perform baseline severity score (Glasgow Coma Scale or ICH Score) as part of initial evaluation to streamline assessment and communication between providers 1
- Complete blood count, electrolytes, renal function, glucose, cardiac troponin 1
- Prothrombin time with INR and activated partial thromboplastin time to identify coagulopathy 1
- Toxicology screen for cocaine and sympathomimetic drugs 1
- ECG and continuous cardiopulmonary monitoring including automated blood pressure, telemetry, and pulse oximetry 2
- Consider CT angiography to identify patients at high risk for hematoma expansion (contrast extravasation within hematoma predicts expansion) 1, 2
Acute Blood Pressure Management
For patients presenting with systolic BP 150-220 mmHg without contraindications, immediately lower systolic BP to <140 mmHg—this is safe and improves functional outcomes. 1, 2
- Begin blood pressure control measures immediately after ICH onset, ideally within 6 hours 1, 2
- Avoid excessive BP reductions ≥60 mmHg within 1 hour, as this may worsen outcomes 3
- Maintain sustained control with minimal variability during the first 24 hours 3
- The mechanism of benefit appears independent of reducing hematoma growth 4
Reversal of Coagulopathy
Vitamin K Antagonists (Warfarin)
Patients with elevated INR from warfarin must have immediate reversal: 1, 2
- Withhold warfarin immediately 1
- Administer prothrombin complex concentrate (PCC)—preferred over fresh frozen plasma for rapid INR correction 2, 5, 3
- Give intravenous vitamin K 1, 2
Direct Oral Anticoagulants
- Dabigatran: administer idarucizumab for reversal 6, 3
- Factor Xa inhibitors (rivaroxaban, apixaban): administer andexanet alfa where available, or PCC 6, 3
- Rapid reversal reduces hematoma expansion risk and may improve outcomes 3
Thrombocytopenia and Coagulation Factor Deficiency
- Patients with severe thrombocytopenia should receive platelet transfusion 1
- Patients with severe coagulation factor deficiency should receive appropriate factor replacement 1
Critical Care Management
All patients must be admitted to a neuroscience intensive care unit or dedicated stroke unit with specialized nursing and physician expertise—this reduces mortality 1, 2
Intracranial Pressure Management
- ICP monitoring should be considered in patients with Glasgow Coma Scale ≤8, hydrocephalus, or clinical evidence of transtentorial herniation 6, 2
- Use osmotic agents (mannitol or hypertonic saline) to produce hyperosmolality and euvolemia in patients with elevated ICP 6, 7
- Mannitol dosing for adults: 0.25 to 2 g/kg as 15-25% solution over 30-60 minutes 7
- Maintain cerebral perfusion pressure 50-70 mmHg depending on autoregulation status 2
- Place external ventricular drain for CSF drainage in patients with decreased consciousness due to hydrocephalus 6, 2
Fluid Management
- Use 0.9% normal saline as the crystalloid of choice to prevent worsening cerebral edema 6
- Avoid medications that cause cerebral vasodilation or increase cerebral blood volume, as these worsen intracranial compliance and can precipitate herniation 6
Prevention of Secondary Complications
- Begin intermittent pneumatic compression on day of admission for venous thromboembolism prophylaxis 1, 2
- Do NOT use graduated compression stockings—they provide no benefit and may cause harm 2
- Perform formal dysphagia screening before initiating oral intake to reduce pneumonia risk 1
- Monitor and manage glucose levels, avoiding both hyperglycemia and hypoglycemia 2
- Provide continuous cardiopulmonary monitoring 2
Seizure Management
- Treat clinical seizures with antiseizure medications 1
- Patients with electrographic seizures on EEG and altered mental status should receive antiseizure drugs 1
- Do NOT use prophylactic antiseizure drugs routinely—they are associated with increased death and disability 2
Surgical Management
Cerebellar Hemorrhage
Patients with cerebellar hemorrhage >3 cm who are deteriorating neurologically or have brainstem compression and/or hydrocephalus must undergo surgical removal as soon as possible—do not delay with ventricular catheter alone 1, 2
Supratentorial ICH
- Consider early surgery for patients with Glasgow Coma Scale 9-12 2
- Superficial lobar hemorrhages within 1 cm of cortical surface may benefit from evacuation 2
- Meta-analyses suggest surgery increases likelihood of good functional outcome and lowers death risk, though no single large phase III trial has shown overall benefit 3
Hydrocephalus
- External ventricular drainage is recommended for patients with hydrocephalus or ventricular obstruction 6
Interventions to AVOID
Never administer corticosteroids (dexamethasone or other glucocorticoids) for ICH—they provide no benefit and may cause harm 6, 2, 8
Avoid hemostatic therapy (recombinant factor VIIa) for acute ICH not associated with anticoagulant use—it reduces hematoma expansion but does not improve outcomes and increases thromboembolic complications 2, 5
Do NOT use acetazolamide in ICH management 6
Avoid concomitant nephrotoxic drugs or other diuretics with mannitol, as this increases risk of renal failure 7
Monitoring and Prognostication
- Discontinue mannitol if renal, cardiac, or pulmonary status worsens, or CNS toxicity develops 7
- More than 20% of patients experience GCS decrease ≥2 points between prehospital assessment and ED arrival 1
- Another 15-23% demonstrate continued deterioration within first hours after hospital arrival 1
- Early do-not-resuscitate orders or withdrawal of active care should be used judiciously in the first 24-48 hours—early prognostication is difficult 3
Rehabilitation and Long-Term Management
All ICH patients should have access to multidisciplinary rehabilitation beginning as early as possible, with coordinated transition to community-based programs 1, 2
Secondary Prevention
- Control blood pressure long-term in all ICH survivors—this is the single most important modifiable risk factor for recurrence 2
- Treated hypertension reduces ICH risk (OR 1.4) compared to untreated hypertension (OR 3.5) 2
- Strongly discourage smoking, heavy alcohol use, and cocaine use 2
Common Pitfalls
- Delaying neuroimaging can miss opportunities for intervention, as hematoma expansion commonly occurs within first few hours 2
- Failing to correct coagulopathy rapidly in anticoagulated patients leads to continued hematoma expansion and worse outcomes 2
- Overlooking secondary causes (vascular malformations, tumors, cerebral venous thrombosis) in patients with atypical presentations or hemorrhage locations 2
- Prolonged ED stays lead to worse outcomes—initiate urgent treatment of time-sensitive issues (BP lowering, coagulopathy reversal) in the ED rather than waiting for ICU transfer 1
- Mannitol may increase cerebral blood flow and risk of postoperative bleeding in neurosurgical patients, and may worsen intracranial hypertension in children with generalized cerebral hyperemia during first 24-48 hours post-injury 6