Intracerebral hemorrhage is the sudden burst of blood into the brain tissue itself.
It causes sudden onset of focal neurological deficit.
The focal neurologic findings are related to the anatomic location, size and speed of development of intracerebral hemorrhage.
Neurological deficit usually progresses over a minute to an hour.
Rapid recognition and diagnosis of intracerebral hemorrhage are essential because of its frequently rapid progression.

Emergency Measures

  • Ensure the status of the patient’s airway, breathing and circulation
    • Intubate if insufficient ventilation (pO2 <60 mmHg/7.9 kPa or pCO2 >50 mmHg/6.3 kPa), cyanosis, impending respiratory failure, obvious aspiration risk, or depressed level of consciousness
  • Detection of focal neurological deficits
  • Detection of signs of external trauma
  • Admit in an intensive care unit (ICU) or acute stroke unit for at least the 1st 24-72 hours

Elevated Intracranial Pressure (ICP) Management

  • Elevated intracranial pressure (ICP): ICP >20 mmHg for >5 minutes
  • Goal ICP <20 mmHg and cerebral perfusion pressure (CPP) 50-70 mmHg
  • Monitor intracranial pressure using ventricular catheter
  • Intracranial pressure monitoring and treatment may be considered in the following patients: Glasgow Coma Scale (GCS) score of ≤8, clinical evidence of transtentorial herniation, significant intraventricular hemorrhage, and hydrocephalus
  • Treatment should include a balanced and graded approach beginning with simple measures to more aggressive therapies
  • Recommended step-by-step approach for ICP >20-25 mmHg:
    • Cerebrospinal fluid (CSF) drainage
    • Mannitol or hypertonic saline bolus
    • Sedation
    • Neuromuscular blockade
    • Consider mild hyperventilation
    • Hypothermia, hemicraniectomy, barbiturate coma
  • Consider repeat computed tomography (CT) scan if intracranial pressure is still >20-25 mmHg
  • Withdraw intracranial pressure therapies once ICP <20 mmHg

Cerebrospinal Fluid (CSF) Drainage

  • Effective especially in the setting of hydrocephalus
  • Used when an intraventricular catheter is in place to monitor intracranial pressure

Osmotic Therapy

  • Target serum osmolality: 300-320 mOsm/kg
  • Should only be used in patients with type B intracranial pressure waves, progressively increasing intracranial pressure waves or clinical deterioration associated with mass effect
  • Mannitol is the most commonly used intravenous (IV) osmotic agent
    • Produces lowering of intracranial pressure within 20 minutes of administering an IV bolus
  • Furosemide may be administered simultaneously to maintain osmotic gradient
  • Hypertonic saline solutions have been shown to reduce intracranial pressure, even in cases refractory to hyperventilation and Mannitol

Analgesia and Sedation

  • Titrate to minimize pain and increase in intracranial pressure while allowing evaluation of clinical status
    • Can be achieved with IV Propofol, Etomidate, or Midazolam for sedation and Morphine or Alfentanil for analgesia

Neuromuscular Blockade

  • Used with sedation and/or analgesia to prevent elevated intracranial pressure due to increased intrathoracic pressure & obstruction in cerebral venous outflow
  • Nondepolarizing agents: Eg Vecuronium or Pancuronium


  • One of the most effective methods to rapidly reduce intracranial pressure
    • Reserved for use as a temporizing measure while awaiting more definitive treatments
  • Reduction of pCO2 to 30–35 mmHg lowers intracranial pressure by 25-30% in most patients
  • Intracranial pressure reduction may take up to 30 minutes to occur after pCO2 is changed
  • Failure of intracranial pressure to respond to hyperventilation indicates a poor prognosis

Head-of-Bed Elevation

  • Keep head-of-bed elevated at 30o with patient’s neck in neutral position to maximize venous outflow, lowering intracranial pressure

Barbiturate Coma

  • Depresses cerebral metabolic activity, reducing cerebral blood flow and intracranial pressure
  • Barbiturates effectively reduce brain swelling
    • Eg Pentobarbital, Thiopental
    • Safe limit ≈10 mg/kg/day

Treatment of Other Medical Conditions

Elevated Glucose

  • High blood glucose on admission predicts an increased fatality rate in both non-diabetic and diabetic patients with intracerebral hemorrhage (ICH)
  • Monitoring of glucose level is important; normoglycemia should be maintained
  • Hypoglycemia and hyperglycemia should be avoided


  • The majority of seizures occur within the 1st 24 hours of intracerebral hemorrhage onset
  • Clinical (or proven subclinical) seizures or patients with a change in mental status with electrographic seizures on electroencephalography (EEG) should be treated with antiepileptic drugs
  • Continuous electroencephalography monitoring may be indicated in patients with depressed mental status that is disproportionate to the degree of brain injury
  • Anticonvulsant can usually be discontinued after 1 month in patients who do not suffer from further seizures
    • Long-term treatment with anticonvulsant may be necessary if patients experience seizures >2 weeks after intracerebral hemorrhage
  • Prophylactic treatment is not recommended

Body Temperature

  • Fever (temperature >38.5°C) is a common occurrence in patients with intracerebral hemorrhage and increased fever duration is associated with poor outcomes
  • Fever should be aggressively treated even as appropriate testing for systemic infection is being undertaken
    • May use cooling blankets and Paracetamol [intravenous (IV)/per orem (PO)/rectal]

Other General Measures

  • Fluid management, nutrition, and prevention of aspiration pneumonia and bed sores are the same as for patients with ischemic stroke
  • Prophylactic administration of H2 blockers or drugs that can protect the mucosa decreases the incidence of gastric hemorrhage
  • It is suggested that careful consideration of aggressive full care early after intracerebral hemorrhage onset and postponement of new do-not-resuscitate (DNR) orders until at least the 2nd full day of hospitalization

Special Aspects of Management of Intracerebral Hemorrhage

  • Decision to restart antithrombotic therapy after intracerebral hemorrhage (ICH) related to antithrombotic therapy depends on the risk of subsequent arterial or venous thromboembolism, the risk of recurrent intracerebral hemorrhage, and the overall state of the patient
  • Prothrombin complex concentrate, factor IX complex concentrate, fresh frozen plasma (FFP) and recombinant activated factor VII (rFVIIa) normalize the laboratory elevation of the international normalized ratio (INR) very rapidly
  • Treat patients with severe coagulation factor deficiency with appropriate factor replacement
  • Patients with thrombocytopenia should receive platelets
  • It is recommended that patients with elevated INR, due to intake of oral anticoagulants, should stop warfarin, replace vitamin K-dependent factors, correct INR, & start IV vitamin K

Recombinant Activated Factor VII (rFVIIa)

  • Can rapidly normalize INR in oral anticoagulant (OAC)- associated hemorrhages but does not replace all clotting factors
  • Treatment option for patients ≤ 70 years of age with baseline ICH volume <60 mL, intraventricular hemorrhage volume <5 mL and time from onset-to-treatment ≤ 2.5 hours
  • Not recommended as routine treatment for Warfarin reversal

Vitamin K

  • Adjunct therapy to OAC-associated hemorrhages

Fresh Frozen Plasma (FFP)

  • Limited by risk of allergy, infection, processing time and volume required for correction

Prothrombin Complex Concentrates (PCC)

  • Recommended for Warfarin reversal
  • Considered as an alternative to fresh frozen plasma
  • Advantages: rapid reconstitution and administration, high concentration of coagulation factors (eg II, VII, IX &X) in small volume, and less infections

Heparin-associated Intracerebral Hemorrhage

  • Protamine sulfate may be used to reduce bleeding tendency, with the dose depending on the time from cessation of Heparin

Warfarin-associated Intracerebral Hemorrhage

  • Should be treated w/ intravenous vitamin K (IV vitamin K)
  • Treatment should also aim to replace clotting factors with fresh frozen plasma

Deep Vein Thrombosis (DVT) Prophylaxis

  • Use of intermittent pneumatic compression with elastic stockings is advised to prevent deep vein thrombosis (DVT)
  • After confirming bleeding cessation, low-dose subcutaneous unfractionated Heparin or low-molecular-weight Heparin may be started after 1-4 days of onset to prevent deep vein thrombosis in immobile patients
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