Hemorrhagic stroke is a neurological emergency requiring immediate stabilization, rapid identification of the hemorrhage subtype, prevention of continued bleeding, management of intracranial pressure and hydrocephalus, and timely treatment of the underlying vascular lesion. Patients with clinically significant intracerebral hemorrhage (ICH) or aneurysmal subarachnoid hemorrhage (aSAH) should receive coordinated care involving stroke neurology, neurocritical care, neurosurgery, and neurointerventional specialists.[1][2]
Immediate stabilization and triage
Stabilize the airway, oxygenation, ventilation, and circulation. Consider definitive airway management when consciousness is declining or airway protection is impaired.
Perform frequent neurological examinations, including the Glasgow Coma Scale, pupillary findings, focal deficits, and comparison with the initial examination.
Review emergency neuroimaging for hemorrhage location, volume, intraventricular extension, hydrocephalus, mass effect, herniation, and an underlying aneurysm or other vascular lesion.
Determine the time of symptom onset or last known well.
Identify recent exposure to anticoagulants, antiplatelet agents, heparin, thrombolytic drugs, or other medications affecting hemostasis.
Obtain urgent laboratory studies, including complete blood count, glucose, electrolytes, renal and hepatic function, prothrombin time/INR, activated partial thromboplastin time, and drug-specific anticoagulant testing when available.
Obtain urgent stroke, neurocritical care, neurosurgical, and neurointerventional consultation when indicated.
Admit patients with clinically significant ICH or aSAH to a specialized stroke unit or neurological intensive care unit whenever available.
Repeat neuroimaging promptly after neurological deterioration and according to institutional protocols for hemorrhage stability or procedural planning.[1][2]
Management of spontaneous intracerebral hemorrhage
Acute blood pressure management
Use titratable intravenous medication to achieve early, smooth, and sustained blood pressure control while avoiding abrupt reductions, hypotension, and excessive blood pressure variability.[1]
Venous vasodilators such as sodium nitroprusside should generally be avoided because of potential adverse effects on hemostasis and intracranial pressure. A meta-analysis of 50 studies found that calcium channel blockers and alpha/beta-adrenoceptor blockers were associated with favorable outcomes compared with renin-angiotensin system blockers, nitrates, and magnesium.[3]
Commonly used titratable intravenous agents include nicardipine, clevidipine, and labetalol. Intravenous nicardipine was the protocolized agent in ATACH-2, while a range of intravenous and oral agents were used in INTERACT-2 and INTERACT3.[3]
For adults with acute spontaneous ICH presenting with systolic blood pressure between 150 and 220 mmHg, the 2025 AHA/ACC hypertension guideline recommends immediately lowering systolic blood pressure to 130 to less than 140 mmHg and maintaining this range for at least 7 days, while stopping or reducing antihypertensive therapy if systolic blood pressure falls below 130 mmHg (Class 2a, Level A).[3]
The preceding 2022 ICH guideline recommended lowering systolic blood pressure to a target range of 130 to 140 mmHg in patients with mild-to-moderate ICH presenting with systolic blood pressure of 150 to 220 mmHg (Class 2b, Level B-R).[1]
Lowering systolic blood pressure below 130 mmHg is potentially harmful (Class 3: Harm, Level B-NR per the 2025 AHA/ACC hypertension guideline).[3]
Treatment should be initiated as soon as possible. The INTERACT3 protocol sought to achieve its blood pressure target within 1 hour after treatment initiation.
Secondary and post hoc analyses suggest that reduction within approximately 2 hours of symptom onset may reduce hematoma expansion and improve outcome; this timing should be interpreted as trial-derived evidence rather than a universal prerequisite for treatment.
Continuous, smooth, and sustained control that minimizes peaks and large variability can be beneficial.
The safety and effectiveness of intensive lowering are less certain in patients with large or severe ICH, markedly elevated intracranial pressure, compromised cerebral perfusion, or an immediate indication for surgical decompression.[1][4]
For patients presenting with systolic blood pressure above 220 mmHg, the 2025 AHA/ACC guideline states that systolic blood pressure should not be lowered below 130 mmHg (Class 3: Harm, Level B-NR). Cautious, modest lowering to the range of 160 to 180 mmHg might be reasonable, although evidence for this population remains limited.[3]
Protocolized bundle of care
A coordinated bundle addressing blood pressure, anticoagulation reversal, glucose, temperature, and neurological surveillance is preferred to isolated interventions. The INTERACT3 trial demonstrated improved functional outcomes after implementation of an early goal-directed care bundle. The primary outcome favored bundle care, with a common odds ratio of 0.86 (95% confidence interval 0.76 to 0.97; P=0.015). Serious adverse events occurred in 16.0% of patients receiving bundle care compared with 20.1% receiving usual care.[5]
Mediation analysis identified blood pressure control and glucose management as the components contributing most to the bundle's observed benefit.[6]
Principal INTERACT3 care-bundle targets
Component
Protocol target
Blood pressure
Reduce systolic blood pressure to less than 140 mmHg.
Glucose in patients without diabetes
Maintain glucose between 6.1 and 7.8 mmol/L (110–140 mg/dL).
Glucose in patients with diabetes
Maintain glucose between 7.8 and 10.0 mmol/L (140–180 mg/dL).
Temperature
Treat fever and maintain temperature below 37.5°C.
Vitamin K antagonist reversal
Reverse anticoagulation and achieve an INR below 1.5.
These were trial protocol targets, generally pursued within 1 hour after treatment initiation or identification of the relevant abnormality. They should be implemented through local protocols while accounting for individual contraindications and clinical circumstances.[5]
Anticoagulant reversal
Discontinue anticoagulant therapy immediately and initiate reversal as soon as possible after diagnosis of clinically significant anticoagulant-associated ICH. Reversal should not be delayed while awaiting specialized coagulation testing when recent clinically relevant exposure is strongly suspected.[1]
The 2024 AHA/ASA performance measure uses a hospital arrival-to-reversal target of 90 minutes. A future target of 60 minutes is encouraged as systems of care improve.[7]
Acute reversal of anticoagulant-associated intracerebral hemorrhage
Administer four-factor prothrombin complex concentrate together with intravenous vitamin K.
Four-factor prothrombin complex concentrate is preferred to fresh frozen plasma for rapid INR correction. Recheck the INR because rebound anticoagulation may occur.
Administer idarucizumab when clinically relevant dabigatran activity is suspected.
Consider the time of the last dose, renal function, and diluted thrombin time or ecarin-based testing when available.
Factor Xa inhibitor in the United States
Administer four-factor prothrombin complex concentrate or activated prothrombin complex concentrate according to the institutional protocol.
Andexanet alfa is no longer manufactured or commercially available in the United States.
Factor Xa inhibitor where andexanet alfa remains authorized and available
Consider andexanet alfa or a prothrombin complex concentrate according to regional approval, drug exposure, thrombotic risk, and the institutional protocol.
European authorization applies to reversal of apixaban or rivaroxaban in adults with life-threatening or uncontrolled bleeding.
Estimate residual heparin exposure from the administered dose and time since administration.
Low-molecular-weight heparin
Consider protamine according to the specific drug, dose, and time since administration.
Reversal may be incomplete.
Recombinant activated factor VII should not be used as the sole agent for vitamin K antagonist reversal because it does not replace all deficient clotting factors and may not restore in vivo hemostasis despite lowering the INR (Class 3: Harm, Level C in the 2015 AHA/ASA guideline; retained in the 2022 guideline).[1]
Andexanet alfa evidence and regulatory status
ANNEXA-I found greater hemostatic efficacy with andexanet alfa than usual care (67.0% versus 53.1%). However, thrombotic events were more frequent with andexanet alfa (10.3% versus 5.6%), including ischemic stroke in 6.5% versus 1.5%, and the trial did not demonstrate improvement in 30-day functional outcome or mortality.[8]
The U.S. Food and Drug Administration subsequently determined that the serious risks, including increased thromboembolic events, outweighed the benefits. The manufacturer ended U.S. commercial sales on December 22, 2025, discontinued manufacture for the U.S. market, and requested voluntary withdrawal of the biologics license.[9]
Andexanet alfa, marketed as Ondexxya, retains conditional authorization in the European Union for adults treated with apixaban or rivaroxaban when reversal is required because of life-threatening or uncontrolled bleeding. It remains subject to additional monitoring and regional availability.[10]
Antiplatelet-associated hemorrhage
Platelet transfusion should not be administered routinely to patients with aspirin-associated spontaneous ICH who are not undergoing emergency neurosurgery because it is potentially harmful (Class 3: Harm, Level B-R).
Platelet transfusion may be considered in selected aspirin-treated patients requiring emergency neurosurgery (Class 2b, Level C-LD).
A single dose of desmopressin 0.4 micrograms/kg intravenously may be considered in selected patients with antiplatelet-associated ICH, although its effectiveness for preventing hematoma expansion remains uncertain (Class 2b, Level C-LD). Some retrospective studies have used 0.3 micrograms/kg.[1][11]
Nonspecific hemostatic therapy
In patients with spontaneous ICH, recombinant activated factor VII has not demonstrated improvement in functional outcome despite reducing hematoma expansion. The FASTEST trial, the largest phase 3 randomized controlled trial of recombinant activated factor VII (80 µg/kg) in ICH, was stopped for futility after treatment administered within 2 hours of onset failed to improve functional outcome at 180 days (adjusted common odds ratio 1.09, 95% confidence interval 0.79 to 1.51; P=0.61) despite reducing ICH growth by 3.7 mL. Life-threatening thromboembolic events were significantly more frequent with recombinant activated factor VII (risk ratio 3.41, 95% confidence interval 1.14 to 10.15; P=0.020). A more selected subgroup, defined by a spot sign or treatment within 90 minutes, is being tested in the ongoing FASTEST-2 trial.[12] The effectiveness of tranexamic acid for improving functional outcome is also not well established (Class 2b, Level B-R per the 2022 AHA/ASA guideline). These therapies should not replace rapid anticoagulant reversal, blood pressure management, and definitive treatment of an underlying lesion.[1][13]
Intracranial pressure, edema, and hydrocephalus
Elevate the head and optimize oxygenation, ventilation, analgesia, sedation, temperature, and cerebral venous drainage when intracranial pressure is suspected to be elevated.
Perform ventricular drainage when ICH or intraventricular hemorrhage causes hydrocephalus contributing to reduced consciousness (Class 1, Level B-NR).
Intracranial pressure monitoring and treatment may be considered in selected patients with moderate-to-severe ICH or intraventricular hemorrhage and reduced consciousness (Class 2b, Level B-NR).
The effectiveness of early prophylactic hyperosmolar therapy for improving outcome is not established (Class 2b, Level B-NR).
Bolus hyperosmolar therapy may be considered for transient reduction of elevated intracranial pressure (Class 2b, Level C-LD).
Corticosteroids should not be administered for ICH-related intracranial pressure elevation or cerebral edema (Class 3: No Benefit, Level B-NR). Multiple randomized trials have shown increased complications with lack of benefit.[1][7]
Medical treatment of intracranial pressure should not delay definitive surgical decompression when a surgically treatable lesion is present.[1]
Seizure management
Administer antiseizure medication to patients with impaired consciousness and confirmed electrographic seizures to reduce morbidity (Class 1, Level C-LD).
Treat clinical seizures with an appropriate antiseizure medication to improve outcome and prevent brain injury from prolonged or recurrent seizures (Class 1, Level C-EO).
Obtain continuous electroencephalography for at least 24 hours when mental status is unexplained or fluctuating or when nonconvulsive seizures are suspected (Class 2a, Level C-LD).
Do not administer routine prophylactic antiseizure medication in the absence of clinical or electrographic seizures (Class 3: No Benefit, Level B-NR).[1]
Temperature, glucose, swallowing, and systemic care
Monitor serum glucose to identify and prevent clinically important hypoglycemia and hyperglycemia.
Treat hypoglycemia promptly.
Treat moderate-to-severe hyperglycemia while avoiding overly intensive glucose lowering.
Identify and treat fever while investigating infection and other causes.
Perform formal swallowing assessment before oral intake when consciousness or bulbar function is impaired.
Prevent aspiration and provide appropriate nutritional support.
Evaluate and treat hypoxia, infection, electrolyte disturbances, cardiac complications, and other reversible contributors to neurological deterioration.
Use standardized protocols or order sets to reduce disability and mortality.[1]
Venous thromboembolism prevention
Begin intermittent pneumatic compression on the day of diagnosis in nonambulatory patients (Class 1, Level B-R).
Low-dose unfractionated heparin or low-molecular-weight heparin can be useful for reducing pulmonary embolism risk (Class 2a, Level C-LD).
After documentation of cessation of bleeding, low-dose subcutaneous unfractionated heparin or low-molecular-weight heparin may be considered for VTE prevention. A meta-analysis of 4 studies supports initiation at 48 to 96 hours after onset without significant increase in hematoma enlargement. If prophylaxis is started earlier, in the 24- to 48-hour window after ICH onset, documentation of hematoma stability on repeat imaging is reasonable. The guideline recommends a general timeframe of 1 to 4 days from onset (Class 2b).[1]
Graduated knee-high or thigh-high compression stockings alone are not beneficial for venous thromboembolism prevention (Class 3: No Benefit, Level B-R).[1]
Surgical and procedural escalation
Urgent neurosurgical evaluation is required for cerebellar hemorrhage, obstructive hydrocephalus, progressive mass effect, neurological deterioration, herniation, or a potentially treatable structural lesion. Immediate surgical evacuation, with or without ventricular drainage, is recommended for cerebellar ICH accompanied by neurological deterioration, brainstem compression, obstructive hydrocephalus, or a hemorrhage volume of 15 mL or greater. [1]
Medical management of aneurysmal subarachnoid hemorrhage
Initial management before aneurysm repair
Transfer the patient to a center with neurocritical care, cerebrovascular neurosurgery, and endovascular capability when feasible.
Use frequent blood pressure monitoring and short-acting titratable medication to avoid severe hypertension, hypotension, and excessive blood pressure variability.
Before aneurysm securement, severe hypertension, particularly systolic blood pressure above 180 to 200 mmHg, should be reduced gradually while avoiding abrupt reductions and hypotension.
Observational evidence suggests that systolic blood pressure above 160 mmHg is associated with increased rebleeding risk. Previous guidance has used targets below 160 or 180 mmHg, but the 2023 AHA/ASA aSAH guideline concludes that available evidence is insufficient to recommend a single universal blood pressure target.
Preserve adequate cerebral perfusion and avoid a mean arterial pressure below approximately 65 mmHg.
Treat acute symptomatic hydrocephalus with cerebrospinal fluid diversion when indicated.
Minimize delays to definitive aneurysm treatment.[2][14]
Nimodipine
Administer nimodipine enterally at 60 mg every 4 hours for 21 consecutive days, beginning as early as feasible, unless contraindicated or not tolerated. Nimodipine improves neurological outcome after aSAH and should not be withheld solely because angiographic vasospasm is absent.[2][15]
In patients with hepatic cirrhosis, reduce the enteral dose to 30 mg every 4 hours and monitor blood pressure and pulse closely because nimodipine exposure and the risk of adverse effects are increased.[15]
Clinically significant hypotension may require correction of reversible causes, adjustment of other antihypertensive medication, or individualized modification of the nimodipine regimen. Whenever possible, maintain consistent nimodipine administration rather than routinely withholding doses.
Definitive aneurysm repair
Secure the ruptured aneurysm as early as feasible, preferably within 24 hours of presentation, to reduce rebleeding risk. Selection between endovascular and microsurgical treatment should be made by a multidisciplinary cerebrovascular team based on aneurysm morphology and location, associated hematoma, patient condition, procedural risk, durability, and local expertise. Detailed clipping, coiling, flow-diversion, and adjunctive-device considerations are addressed in the dedicated SAH chapter.[2]
Delayed cerebral ischemia and vasospasm
Continue nimodipine when tolerated.
Maintain euvolemia and avoid preventable volume depletion.
Do not use prophylactic hypervolemia or routine prophylactic hemodynamic augmentation.
Perform frequent neurological examinations and use adjunctive monitoring when the examination is unreliable.
Evaluate new focal deficits or reduced consciousness for delayed cerebral ischemia, rebleeding, hydrocephalus, seizures, infection, metabolic disturbance, and medication effects.
Induced hypertension may be reasonable for symptomatic delayed cerebral ischemia after the aneurysm has been secured and when no contraindication exists.
In patients with severe symptomatic vasospasm that does not respond adequately to medical treatment, intra-arterial vasodilator therapy or cerebral angioplasty may be considered in an experienced center.[2][16]
Hydrocephalus and cerebrospinal fluid diversion
Acute symptomatic hydrocephalus generally requires urgent external ventricular drainage. Persistent communicating hydrocephalus may require a ventriculoperitoneal shunt after the acute phase. The drainage strategy should account for aneurysm securement, intracranial pressure, rebleeding risk, infection risk, and anticipated duration of cerebrospinal fluid diversion.[2]
Fluid, sodium, fever, and glucose management
Maintain euvolemia using isotonic fluids appropriate to the clinical context.
Avoid routine fluid restriction that produces hypovolemia in a patient at risk for delayed cerebral ischemia.
Evaluate hyponatremia for cerebral salt wasting, inappropriate antidiuretic hormone activity, medication effects, adrenal dysfunction, and other causes.
Treat clinically significant sodium disturbances while avoiding overly rapid correction.
Identify and treat fever.
Avoid clinically significant hypoglycemia and severe hyperglycemia.[2]
Seizure management in aneurysmal subarachnoid hemorrhage
Treat clinical and electrographic seizures.
Continuous electroencephalographic monitoring is reasonable when consciousness is depressed or fluctuating and the clinical examination is unreliable.
Routine prophylactic antiseizure medication is not recommended in patients without high-risk features.
Short-term prophylaxis may be considered when high-risk features are present, including high-grade aSAH, associated ICH, hydrocephalus, cortical infarction, or a ruptured middle cerebral artery aneurysm.
Avoid routine phenytoin prophylaxis because it is associated with excess morbidity, including poorer cognitive outcomes and potential metabolic competition with nimodipine. The 2023 AHA/ASA aSAH guideline states that phenytoin use is potentially harmful and should not be used for seizure prophylaxis.[2]
Goals of care and prognostic decision-making
Severity scores may support communication and risk stratification but should not be used alone to predict an individual patient's outcome or limit life-sustaining treatment. Avoid irreversible early treatment limitations based solely on age, initial neurological score, hemorrhage volume, or a single prognostic scale.[1][2]
When prognosis remains uncertain:
Use multidisciplinary reassessment and time-limited trials of treatment.
Distinguish expected survival from the probability of favorable neurological recovery.
Discuss possible long-term cognitive, functional, communication, and behavioral disability.
Incorporate the patient's previously expressed values and acceptable quality of life.
Reassess prognosis after physiological stabilization rather than relying only on the initial presentation.
Post-acute transition
Begin rehabilitation assessment after physiological and neurological stabilization. Evaluate mobility, swallowing, communication, cognition, mood, continence, self-care, caregiver needs, and the discharge environment. Detailed rehabilitation, long-term blood pressure control, recurrence prevention, antithrombotic resumption, and aneurysm surveillance are addressed in the secondary-prevention and rehabilitation micro-chapters respectively.[1][2]
"1. For adult patients with acute spontaneous ICH who present with SBP between 150 and 220 mmHg, it can be beneficial to immediately lower SBP to 130 to 140 mmHg (Level of Evidence: A)"
Adults with acute spontaneous ICH requiring acute BP lowering
"1. In adults with acute spontaneous ICH requiring acute BP lowering, careful titration to ensure smooth, nonlabile, and sustained control of BP, avoiding peaks and large variability in SBP, can be beneficial for improving functional outcomes (Level of Evidence: B-NR)"
Adult patients with acute spontaneous ICH presenting with SBP greater than 220 mmHg
"1. For adult patients with acute spontaneous ICH who present with SBP greater than 220 mmHg, SBP should not be lowered below 130 mmHg to reduce adverse events (Level of Evidence: B-NR)"
2022 AHA/ASA Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage[18]
"1. Regional systems should provide initial ICH care and the capacity for rapid transfer to facilities with neurocritical care and neurosurgical capabilities"
"1. Initial monitoring and management of ICH patients should take place in an intensive care unit or dedicated stroke unit with physician and nursing neuroscience acute care expertise (Level of Evidence: B-NR)"
Acute Blood Pressure Lowering: Recommendations
Patients with mild-to-moderate ICH presenting with SBP between 150 and 220 mmHg
"1. Lowering SBP to a target range of 130 to 140 mmHg is safe and may be reasonable for improving functional outcome in patients with mild-to-moderate ICH presenting with SBP between 150 and 220 mmHg (Level of Evidence: B-R)"
Timing and method of BP lowering
Recommendation
1. Acute BP treatment should be initiated as soon as possible.
2. BP should be carefully titrated to provide continuous, smooth, and sustained control.
"1. Four-factor PCC is preferred over plasma for rapid replacement of vitamin K-dependent coagulation factors in VKA-associated ICH and should be given with intravenous vitamin K, 5 to 10 mg"
"1. rFVIIa is not recommended for unselected noncoagulopathic ICH because it can increase thromboembolic risk without clear clinical benefit (Level of Evidence: A)"
Venous Thromboembolism Prophylaxis and Treatment: Recommendations
"1. Patients with ICH should have intermittent pneumatic compression for VTE prevention beginning on the day of hospital admission (Level of Evidence: B-R)"
"1. After documentation that bleeding has ceased, low-dose subcutaneous LMWH or unfractionated heparin may be considered for VTE prevention in patients with limited mobility 1 to 4 days after onset"
"1. Patients with impaired consciousness and confirmed electrographic seizures on EEG should be treated with antiseizure drugs to reduce morbidity (Level of Evidence: C-LD)"
"1. Continuous EEG monitoring for at least 24 hours is probably indicated in ICH patients with depressed mental status that is out of proportion to the degree of brain injury (Level of Evidence: C-LD)"
"1. Ventricular drainage should be performed in patients with ICH or IVH when hydrocephalus contributes to a decreased level of consciousness (Level of Evidence: B-NR)"
"1. In patients with ICH and a GCS score of 8 or less, ICP monitoring and treatment might be considered to reduce mortality and improve outcomes (Level of Evidence: B-NR)"
"2. ICP monitoring and treatment might also be considered in patients with clinical evidence of transtentorial herniation, significant IVH, or hydrocephalus"
"3. A CPP of 50 to 70 mmHg may be reasonable depending on cerebral autoregulation"
"1. Urgent surgical evacuation with or without external ventricular drainage is recommended for cerebellar ICH with neurological deterioration, brainstem compression, hydrocephalus, or hematoma volume of 15 mL or greater"
"1. Minimally invasive surgery may improve functional outcomes"
Craniotomy for stable supratentorial ICH
Recommendation
1. Routine craniotomy for stable supratentorial ICH has not shown an overall functional benefit.
Goals of Care: Recommendations
Recommendation
1. DNAR status should be treated as distinct from decisions to limit other medical and surgical interventions.
2. Baseline severity scales should not be used as the sole basis for limiting life-sustaining treatment.
Rehabilitation and Recovery: Recommendations
Recommendation
1. Coordinated multidisciplinary inpatient team care should include early discharge planning and a goal of early supported discharge for patients with mild-to-moderate ICH.
2. Rehabilitation activities, including stretching and functional task training, may be considered 24 to 48 hours after moderate ICH.
3. Early aggressive mobilization within the first 24 hours should be avoided because it appears to worsen 14-day mortality.
4. Fluoxetine does not improve functional recovery after ICH. It reduced depression but increased fractures.
2015 AHA/ASA Guidelines for the Management of Spontaneous Intracerebral Hemorrhage[19]
Hemostasis and Coagulopathy, Antiplatelet Agents, and DVT Prophylaxis: Recommendations
Patients with a severe coagulation factor deficiency or severe thrombocytopenia
"1.Patients with ICH whose INR is elevated because of VKA should have their VKA withheld, receive therapy to replace vitamin K–dependent factors and correct the INR, and receive intravenous vitamin K (Level of Evidence: C)"
"1.rFVIIa does not replace all clotting factors, and although the INR may be lowered, clotting may not be restored in vivo; therefore, rFVIIa is not recommended for VKA reversal in ICH (Level of Evidence: C)"
"1.For patients with ICH who are taking dabigatran, rivaroxaban, or apixaban, treatment with FEIBA, other PCCs, or rFVIIa might be considered on an individual basis. Activated charcoal might be used if the most recent dose of dabigatran, apixaban, or riva- roxaban was taken <2 hours earlier. Hemodialysis might be considered for dabigatran (Level of Evidence: C)"
"1. Although rFVIIa can limit the extent of hematoma expansion in noncoagulopathic ICH patients, there is an increase in thromboembolic risk with rFVIIa and no clear clinical benefit in unselected patients. Thus, rFVIIa is not recommended (Level of Evidence: A)"
"1.Patients with ICH should have intermittent pneu- matic compression for prevention of venous throm- boembolism beginning the day of hospital admission (Level of Evidence: A)"
"1.After documentation of cessation of bleeding, low- dose subcutaneous low-molecular-weight heparin or unfractionated heparin may be considered for pre- vention of venous thromboembolism in patients with lack of mobility after 1 to 4 days from onset (Level of Evidence: B)"
"1.Systemic anticoagulation or IVC filter placement is probably indicated in ICH patients with symptom- atic DVT or PE (Level of Evidence: C)"
"2. The decision between these 2 options should take into account several factors, including time from hem- orrhage onset, hematoma stability, cause of hemor- rhage, and overall patient condition (Level of Evidence: C)"
BP-Lowering: Recommendations
ICH patients presenting with SBP between 150 and 220 mmHg
"1.For ICH patients presenting with SBP between 150 and 220 mmHg and without contraindication to acute BP treatment, acute lowering of SBP to 140 mm Hg is safe (Level of Evidence: A)"
"1.For ICH patients presenting with SBP between 150 and 220 mmHg and without contraindication to acute BP treatment, acute lowering of SBP to 140 mm Hg ) can be effective for improving functional outcome (Level of Evidence: C)"
"1. For ICH patients presenting with SBP >220 mm Hg, it may be reasonable to consider aggressive reduction of BP with a continuous intravenous infusion and frequent BP monitoring (Level of Evidence: C)"
General Monitoring and Nursing Care: Recommendation
"1.Initial monitoring and management of ICH patients should take place in an intensive care unit or dedicated stroke unit with physician and nursing neuroscience acute care expertis (Level of Evidence: B)"
"1.Clinical seizures should be treated with antiseizure drugs (Level of Evidence: A)"
"2.Patients with a change in mental status who are found to have electrographic seizures on EEG should be treated with antiseizure drugs (Level of Evidence: C)"
"1.Continuous EEG monitoring is probably indicated in ICH patients with depressed mental status that is out of proportion to the degree of brain injury (Level of Evidence: C)"
Management of Medical Complications: Recommendations
"1.A formal screening procedure for dysphagia should be performed in all patients before the initiation of oral intake to reduce the risk of pneumonia(Level of Evidence: B)"
"1.Ventricular drainage as treatment for hydrocephalus is reasonable, especially in patients with decreased level of consciousness (Level of Evidence: B)"
"1. Patients with a GCS score of ≤8, those with clinical evidence of transtentorial herniation, or those with significant IVH or hydrocephalus might be considered for ICP monitoring and treatment. A CPP of 50 to 70 mm Hg may be reasonable to maintain depending on the status of cerebral autoregulation (Level of Evidence: C)"
"1.Although intraventricular administration of rtPA in IVH appears to have a fairly low complication rate, the efficacy and safety of this treatment are uncertain (Level of Evidence: B)"
"2.The efficacy of endoscopic treatment of IVH is uncertain (Level of Evidence: B)"
↑ 2.002.012.022.032.042.052.062.072.082.092.10Hoh BL, Ko NU, Amin-Hanjani S; et al. (2023). "2023 Guideline for the Management of Patients With Aneurysmal Subarachnoid Hemorrhage: A Guideline From the American Heart Association/American Stroke Association". Stroke. 54 (7): e314–e370. doi:10.1161/STR.0000000000000436.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑ 3.03.13.23.33.4Jones DW, Ferdinand KC, Taler SJ; et al. (2025). "2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults". Circulation. 152: e114–e218. doi:10.1161/CIR.0000000000001356.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Li Q, Lv X, Morotti A; et al. (2025). "Optimal Magnitude of Blood Pressure Reduction and Hematoma Growth and Functional Outcomes in Intracerebral Hemorrhage". Neurology. 104 (5): e213412. doi:10.1212/WNL.0000000000213412.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑ 5.05.1Ma L, Hu X, Song L; et al. (2023). "The Third Intensive Care Bundle With Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial (INTERACT3): An International, Stepped Wedge Cluster Randomised Controlled Trial". Lancet. 402 (10395): 27–40. doi:10.1016/S0140-6736(23)00806-1.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Ren et al. INTERACT3 mediation analysis. Neurology. 2025.
↑ 7.07.1Ruff IM, de Havenon A, Bergman DL; et al. (2024). "2024 AHA/ASA Performance and Quality Measures for Spontaneous Intracerebral Hemorrhage: A Report From the American Heart Association/American Stroke Association". Stroke. 55 (7): e199–e230. doi:10.1161/STR.0000000000000464.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Connolly SJ, Sharma M, Cohen AT; et al. (2024). "Andexanet for Factor Xa Inhibitor-Associated Acute Intracerebral Hemorrhage". The New England Journal of Medicine. 390 (19): 1745–1755. doi:10.1056/NEJMoa2313040.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Frontera JA, Lewin JJ, Rabinstein AA; et al. (2016). "Guideline for Reversal of Antithrombotics in Intracranial Hemorrhage: Executive Summary". Critical Care Medicine. 44 (12): 2251–2257. doi:10.1097/CCM.0000000000002057.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Broderick JP, Naidech AM, Elm JJ; et al. (2026). "Recombinant Factor VIIa Versus Placebo for Spontaneous Intracerebral Haemorrhage Within 2 H of Symptom Onset (FASTEST): A Multicentre, Double-Blind, Randomised, Placebo-Controlled, Phase 3 Trial". Lancet. 407 (10530): 773–783. doi:10.1016/S0140-6736(26)00097-8.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Eilertsen H, Menon CS, Law ZK; et al. (2023). "Haemostatic Therapies for Stroke Due to Acute, Spontaneous Intracerebral Haemorrhage". Cochrane Database of Systematic Reviews (10): CD005951. doi:10.1002/14651858.CD005951.pub5.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
↑Lawton MT, Vates GE (2017). "Subarachnoid Hemorrhage". The New England Journal of Medicine. 377 (3): 257–266. doi:10.1056/NEJMcp1605827.
↑Claassen J, Park S (2022). "Spontaneous Subarachnoid Haemorrhage". Lancet. 400 (10355): 846–862. doi:10.1016/S0140-6736(22)00938-2.
↑2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. Jones DW, Ferdinand KC, Taler SJ, et al. Journal of the American College of Cardiology. 2025;86(18):1567-1678. doi:10.1016/j.jacc.2025.05.007.
↑2022 Guideline for the Management of Patients With Spontaneous Intracerebral Hemorrhage. Greenberg SM, Ziai WC, Cordonnier C, et al. Stroke. 2022;53(7):e282-e361. doi:10.1161/STR.0000000000000407.