Management of Intracranial Bleeding
Admit all patients with intracranial hemorrhage immediately to a specialized neuroscience intensive care unit or acute stroke unit, as this single intervention provides the strongest evidence for reducing mortality and improving outcomes. 1
Immediate Assessment and Stabilization
Obtain emergent non-contrast CT scan to confirm diagnosis, establish baseline hematoma volume, and identify hemorrhage location (epidural, subdural, intraparenchymal, subarachnoid, or intraventricular). 1 This imaging combined with Glasgow Coma Scale (GCS) score represents the most powerful predictor of mortality. 1
Secure airway and provide ventilatory support in patients with GCS ≤8 or clinical deterioration, as over 20% of patients deteriorate within the first few hours. 1 Maintain adequate oxygenation and avoid hypercarbia, which exacerbates cerebral edema. 2
Establish cardiovascular monitoring with continuous blood pressure measurement, as acute management decisions depend heavily on hemodynamic parameters. 1
Blood Pressure Management
Target systolic blood pressure <140 mmHg within 6 hours of symptom onset using intensive blood pressure lowering to prevent hematoma expansion. 1 This aggressive approach reduces the risk of hemorrhage growth, which occurs in approximately 20% of cases and strongly correlates with worse outcomes. 3
However, avoid aggressive blood pressure reduction in patients with suspected elevated intracranial pressure (ICP), as this may compromise cerebral perfusion pressure (CPP). 1 In these cases, maintain CPP >60-70 mmHg. 1
Avoid sodium nitroprusside and other cerebral vasodilators, as these agents worsen cerebral edema and increase ICP. 2 Use short-acting IV agents like nicardipine or labetalol instead. 1
Maintain euvolemia throughout treatment using isotonic crystalloids (0.9% normal saline preferred). 1 Avoid hypo-osmolar fluids that exacerbate cerebral edema. 2
Reversal of Coagulopathy
For warfarin-associated intracranial hemorrhage, administer prothrombin complex concentrate (PCC) immediately rather than fresh frozen plasma, as PCC provides faster and more complete reversal. 3, 1 This is a strong recommendation given the life-threatening nature of anticoagulant-associated bleeding. 3
For dabigatran-associated hemorrhage, use idarucizumab as the specific reversal agent. 1
For factor Xa inhibitor-associated hemorrhage (rivaroxaban, apixaban, edoxaban), use andexanet alfa as the specific reversal agent. 1
Do NOT routinely transfuse platelets in patients taking aspirin or clopidogrel, as there is no evidence this improves outcomes and may cause harm. 4, 5 Platelet transfusion and desmopressin show very little hemostatic effect in the presence of newer antiplatelet agents like ticagrelor. 5
Maintain platelet count >50×10⁹/L in patients with thrombocytopenia and ongoing bleeding. 1
Intracranial Pressure Management
Initial Conservative Measures
Elevate head of bed to 30 degrees with head in midline position to improve jugular venous outflow and lower ICP. 2, 1 Ensure the patient is euvolemic before elevation, as this maneuver may decrease CPP in hypovolemic patients. 1
Correct factors that exacerbate cerebral edema immediately: hypoxemia, hypercarbia, hyperthermia, and hypo-osmolar states. 2
Provide adequate analgesia and sedation to reduce metabolic demand and prevent ICP spikes from agitation. 1
ICP Monitoring
Insert ICP monitoring device (fiberoptic monitor or ventricular catheter) in patients with GCS ≤8, hydrocephalus, or clinical evidence of transtentorial herniation. 2, 1 While no randomized trial has proven efficacy of ICP monitoring in intracerebral hemorrhage specifically, it provides crucial physiological information for guiding therapy. 2
Target ICP <20-25 mmHg and maintain CPP >60-70 mmHg (ideally >70 mmHg). 2
Osmotic Therapy for Elevated ICP
Administer mannitol 0.25-0.5 g/kg IV over 20 minutes, repeated every 6 hours as needed, as the primary osmotic agent for elevated ICP. 2, 6 This represents the FDA-approved standard treatment. 6
Alternatively, use hypertonic saline (3% or 23.4% NaCl), which may provide longer duration of ICP control compared to mannitol, though no randomized trials have demonstrated superiority for clinical outcomes in intracerebral hemorrhage specifically. 2
Monitor serum osmolarity, renal function, and electrolytes closely when using osmotic agents, as mannitol can cause renal failure, volume depletion, and rebound intracranial hypertension. 6 Discontinue if renal function deteriorates. 6
Advanced Interventions for Refractory Elevated ICP
Perform ventriculostomy with CSF drainage for refractory elevated ICP, particularly in patients with hydrocephalus. 3, 2 Removal of small CSF volumes can markedly reduce ICP. 3
Do NOT use hyperventilation, corticosteroids, furosemide, prophylactic hypothermia, or barbiturates in the management of elevated ICP in intracerebral hemorrhage, as these interventions lack evidence and may cause harm. 2
Surgical Intervention
Cerebellar Hemorrhage
Perform immediate surgical evacuation (decompressive suboccipital craniectomy) for cerebellar hemorrhage with any of the following: neurological deterioration, brainstem compression, hydrocephalus, or cerebellar ICH volume ≥15 mL. 2, 1 This is the clearest surgical indication with strong evidence for benefit.
Supratentorial Hemorrhage
For supratentorial ICH, surgical benefit remains uncertain for most patients. 1 Consider early surgery for patients with GCS 9-12 and accessible hemorrhages with mass effect. 1
Consider decompressive craniectomy for refractory intracranial hypertension in supratentorial hemorrhage, though this should be decided in multidisciplinary discussion weighing potential functional outcomes. 3, 2
Remove symptomatic extradural hematomas regardless of location. 3
Remove acute subdural hematomas with thickness >5 mm and midline shift >5 mm. 3
Prevention of Secondary Complications
Apply intermittent pneumatic compression immediately for venous thromboembolism prophylaxis in immobile patients. 1
Initiate pharmacological thromboprophylaxis within 24 hours after bleeding has stabilized (confirmed by repeat imaging showing no expansion). 1
Aggressively manage fever, as hyperthermia worsens secondary brain injury. 2, 1
Monitor for pneumonia, cardiac events, acute kidney injury, and seizures, which are common complications. 1
Critical Monitoring Parameters
Monitor fluid and electrolyte balance closely, particularly sodium and potassium, as imbalances lead to encephalopathy or cardiac complications. 1, 6 Electrolyte measurements are vital when infusing mannitol. 6
Perform repeat CT imaging to assess for hematoma expansion, particularly in the first 24 hours when expansion risk is highest. 3, 7 Larger bleeds and expansion are associated with substantially higher mortality. 7
Monitor cardiovascular status continuously, as sudden expansion of extracellular fluid from mannitol may precipitate congestive heart failure. 6
Common Pitfalls to Avoid
Do not add mannitol to whole blood for transfusion, and use a filter when infusing 25% mannitol. 6 Warm crystallized mannitol solutions before administration. 6
Do not give electrolyte-free mannitol conjointly with blood without adding at least 20 mEq sodium chloride per liter to avoid pseudoagglutination. 6
Do not use recombinant factor VIIa routinely, as it reduces hematoma expansion but does not improve outcomes and increases thromboembolic complications. 4
Recognize that mannitol may increase cerebral blood flow and worsen intracranial hypertension in children with generalized cerebral hyperemia during the first 24-48 hours post-injury. 6