Continuing Education Activity

Cerebrovascular accident, commonly known as stroke, ranks as the second leading cause of death globally and a major contributor to long-term disability. Stroke may be ischemic, caused by interruption of blood flow to the brain, or hemorrhagic, which involves bleeding into brain tissue or the subarachnoid space. Hemorrhagic strokes, though less common, carry the highest mortality and often result from hypertension, anticoagulation, cerebral amyloid angiopathy, or vascular malformations. This course reviews the rapid recognition, imaging, and intervention of hemorrhagic stroke that are critical to prevent neurological deterioration. Management of this condition, including blood pressure control, reversal of coagulopathy, seizure management, intracranial pressure monitoring, and, in selected cases, surgical intervention, as well as advances in minimally invasive hematoma evacuation, neurocritical care, and interprofessional rehabilitation, are also discussed. 

This activity outlines the recognition, diagnosis, and integration of evidence-based strategies for the acute management of hemorrhagic stroke, the prevention of complications, and the mitigation of secondary injury while tailoring care to patient-specific risk factors for hemorrhagic stroke. Participants gain updated knowledge on imaging modalities, acute and surgical interventions, blood pressure and intracranial pressure management, coagulopathy reversal, seizure control, and rehabilitation strategies. This activity for healthcare professionals is designed to enhance the learner's competence in identifying hemorrhagic stroke, performing the recommended evaluation, and implementing an appropriate interprofessional approach to manage this condition, thereby optimizing patient outcomes.

Objectives:

• Identify the clinical manifestations associated with hemorrhagic stroke to support timely recognition.
• Apply current evidence-based management recommendations for hemorrhagic stroke. 
• Interpret imaging features that differentiate primary hemorrhagic stroke from secondary causes to guide further evaluation.
• Coordinate interprofessional management strategies to coordinate care and improve patient outcomes in those with hemorrhagic stroke.

Introduction

Cerebrovascular accident, otherwise called a stroke, is the second leading cause of death worldwide and one of the major causes of long-term disability. Stroke can be either ischemic or hemorrhagic. An ischemic stroke is due to the loss of blood supply to an area of the brain and is the most common type of stroke. Hemorrhagic stroke comprises approximately 10% to 15% of all strokes globally but carries the highest mortality.

Hemorrhagic stroke results from bleeding into brain tissue or the subarachnoid space, most commonly due to vascular rupture or anticoagulation-related coagulopathy. Hemorrhagic stroke may be further subdivided into intracerebral hemorrhage (ICH) and subarachnoid hemorrhage (SAH); ICH is bleeding into the brain parenchyma, and SAH is bleeding into the subarachnoid space. Hemorrhagic stroke is associated with severe morbidity and high mortality.[1] The progression of hemorrhagic stroke is associated with worse outcomes. Thirty-day mortality remains around 30% to 40%, and half of all deaths occur within the first 48 hours.[2][3][4] Early diagnosis and treatment are essential, given the usual rapid expansion of hemorrhage, causing sudden deterioration of consciousness and neurological dysfunction.

Etiology

Hypertension

Hypertension is the leading cause of hemorrhagic stroke.[5][6][7] Chronic high arterial pressure pushes plasma proteins into the arteriolar wall, leading to hyaline arteriosclerosis. Over time, hypertension causes degeneration of the media, rupture of the elastic lamina, and fragmentation of the arteries' smooth muscles. Observations in the arterioles include lipohyalinosis, fibrinoid necrosis of the subendothelium, microaneurysms, and focal dilatations; the microaneurysms are known as Charcot-Bouchard aneurysms. Common sites for hypertension-related intracerebral hemorrhage are small penetrating arteries originating from the basilar, anterior, middle, or posterior cerebral arteries. These small artery branches, measuring 50 to 700 μm in diameter, often have multiple rupture points associated with layers of platelet and fibrin clots. Hypertensive changes typically lead to nonlobar intracerebral hemorrhage. Additionally, eclampsia can cause ICH due to the loss of cerebrovascular autoregulation; it more commonly results in Posterior Reversible Encephalopathy Syndrome (PRES) and vasogenic edema, but intracerebral hemorrhage may also occur.

Cerebral Amyloid Angiopathy 

Cerebral amyloid angiopathy (CAA) is a leading cause of primary lobar intracerebral hemorrhage in older adults.[8][9] This process involves the accumulation of amyloid-β peptide in the capillaries, arterioles, and small to medium-sized arteries within the cerebral cortex, leptomeninges, and cerebellum. This buildup can lead to intracerebral hemorrhages in older individuals and is often associated with variations in the gene encoding apolipoprotein E. A familial form may occur in young individuals, typically associated with mutations in the gene encoding the amyloid precursor protein. The prevalence of CAA increases with age, affecting nearly 50% of those older than 80, with recurrent hemorrhages being a possible outcome. The Boston Criteria 2.0, established in 2022, are now the standard for the noninvasive diagnosis of CAA, based on MRI findings such as lobar microbleeds and cortical superficial siderosis.

Other Important Risk Factors

These tisk factors include: 

• Cigarette smoking, moderate or heavy alcohol use, and chronic alcoholism are significant risk factors.
• Chronic liver disease also raises the risk of ICH due to coagulopathy and thrombocytopenia.
• Very low levels of low-density lipoproteins have been reported as a potential risk factor in some observational studies, but the evidence remains inconsistent.
• Dual antiplatelet therapy carries a higher risk of ICH compared to monotherapy.
• Sympathomimetics such as cocaine, heroin, amphetamine, ephedrine, and phenylpropanolamine increase the risk of cerebral hemorrhage.
• Cerebral microbleeds associated with hypertension, diabetes mellitus, and cigarette smoking augment the risk of ICH.
• Older age and male sex are also risk factors—the incidence of ICH increases with age (especially in those older than 55), with a relative risk of 7 after age 70. Tumors more prone to bleeding include glioblastoma, lymphoma, metastasis, meningioma, pituitary adenoma, and hemangioblastoma. 

The usual causes of spontaneous SAH are ruptured aneurysm, arteriovenous malformation, vasculitis, cerebral artery dissection, dural sinus thrombosis, and pituitary apoplexy. The risk factors are hypertension, oral contraceptive pills, substance abuse, and pregnancy. Perimesencephalic nonaneurysmal SAH accounts for 10% to 20% of cases and has a distinctly better prognosis. Intracranial hemorrhage of pregnancy (ICHOP-intracerebral or subarachnoid hemorrhage) occurs with eclampsia and is due to the loss of cerebrovascular autoregulation.

Epidemiology

Hemorrhagic stroke accounts for approximately 10% to 15% of all strokes; incidence is highest in Asian and low- or middle-income populations.[1][2][7][10][11][10][7][12] The percentage of hemorrhage in stroke is 8% to 15% in the United States, the United Kingdom, and Australia, and 18% to 24% in Japan and Korea. The incidence is approximately 12% to 15% per 1,000,000 population per year. The incidence is high in low- and middle-income countries, including those in Asia. The incidence is more common in men and increases with age.

The global incidence is increasing, predominantly in African and Asian countries. Japanese data have shown that control of hypertension reduces the incidence of ICH. The case-fatality rate is 25% to 30% in high-income countries and 30% to 48% in low- to middle-income countries. The ICH fatality rate depends on the efficacy of critical care. The ICH score is widely used to predict mortality and to guide care escalation. Computed tomogram (CT) predictors of hematoma expansion, such as the ‘spot sign’, blend sign, and black hole sign, are now incorporated into early management strategies.

Pathophysiology

Common sites of bleeding include the basal ganglia (40%-50%), the thalamus (20%-25%), the cerebral lobes (15%-20%), the cerebellum (10%-15%), and the pons and brainstem (5%-10%) (see Image. Lobar Hemorrhage, Computed Tomography [CT]; and see Image. Pontine Hemorrhage, Computed Tomography [CT]).[1][7] The hematoma disrupts the neurons and glia. This results in oligemia, neurotransmitter release, mitochondrial dysfunction, and cellular swelling. Thrombin activates microglia, causing inflammation and edema.[11][13] The primary injury is due to the compression of brain tissue by the hematoma and an increase in the ICP.[14]

Secondary injury is mediated by inflammation, disruption of the blood-brain barrier, edema, overproduction of free radicals, including reactive oxygen species, glutamate-induced excitotoxicity, and the release of hemoglobin and iron from the clot (see Image. Hemorrhagic Stroke Process). Thrombin, iron, and complement activation are central drivers of perihematomal injury; complement blockade and iron chelation are being evaluated as potential therapeutic targets. Most hematoma expansion occurs within 3 to 12 hours; approximately one-third expand within the first 3 hours. Perihematomal edema increases within 24 hours, peaks around 5 to 6 days, and persists for up to 14 days. There is hypoperfusion surrounding the hematoma. Factors contributing to ICH deterioration include hematoma expansion, intraventricular hemorrhage, perihematomal edema, and inflammation.[1] A cerebellar hematoma can cause hydrocephalus by compressing the fourth ventricle in the early stage.

Nonaneurysmal spontaneous SAH may be either perimesencephalic or nonperimesencephalic SAH. In perimesencephalic SAH, bleeding is mainly in the interpeduncular cistern. Physical exertion, such as the Valsalva maneuver, which increases intrathoracic pressure and elevates intracranial venous pressure, is a common trigger factor for perimesencephalic nonaneurysmal SAH.[15] There is diffuse blood distribution in nonperimesencephalic SAH.[16]

Histopathology

The histopathological features of chronic hypertension in the small arteries and arterioles are degeneration of smooth muscle cells, concentric hyaline wall thickening, loss of smooth muscle cells, and fibrinoid necrosis.[7] The hyaline arteriosclerosis, fibrosis, atrophy of the outer muscular layer, and weakening of the arteriolar wall result in the formation of Charcot–Bouchard microaneurysms (true microaneurysms of penetrating arterioles). Breach of the arteriolar wall with fibrinoid necrosis and rupture of microaneurysms are the major mechanisms of hypertensive ICH.

History and Physical

The common presentations of stroke are headache, aphasia, hemiparesis, and facial palsy.[17] The presentation of hemorrhagic stroke is usually acute and progressive. Acute onset headache, vomiting, neck stiffness, increased blood pressure, and rapidly developing neurological signs are the common clinical manifestations of hemorrhagic stroke.[11] Symptoms can indicate the extent and location of hemorrhage. Other symptoms include the following:

• A headache is more common in a large hematoma.
• Vomiting indicates raised intracranial pressure (ICP) and is common with cerebellar hematoma.
• Coma results from involvement of the reticular activating system in the brainstem. 
• Seizure, aphasia, and hemianopia are seen in a lobar hemorrhage. A prodrome consisting of numbness, tingling, and weakness may also occur in a lobar bleed.
• Contralateral sensorimotor deficits are characteristic of hemorrhage in the basal ganglia and thalamus.
• Loss of all sensory modalities is the main feature of thalamic hemorrhage.
• Extension of the thalamic hematoma into the midbrain can cause vertical gaze palsy, ptosis, and an unreactive pupil.
• Cranial nerve dysfunction with contralateral weakness indicates a brainstem hematoma.[11]
• Usually, a large pontine hematoma produces coma and quadriparesis.[18]

Cerebellar hemorrhage produces symptoms of raised ICP, eg, lethargy, vomiting, and bradycardia. Progressive neurological deterioration indicates hematoma enlargement or increased edema. The clinical features of subarachnoid hemorrhage are severe headache described as a thunderclap, vomiting, syncope, photophobia, nuchal rigidity, seizures, and decreased level of consciousness.[15][16] Signs of meningismus, eg, the Kernig sign (pain on straightening the knee when the thigh is flexed to 90 degrees) and the Brudzinski sign (involuntary hip flexion on neck flexion), may be positive.

Evaluation

CT is usually the initial investigation.[19] The hemorrhage increases in attenuation from 30 to 60 Hounsfield units (HU) in the hyperacute phase to 80 to 100 HU over hours.[20] Attenuation may be reduced in anemia and coagulopathy. Vasogenic edema around the hematoma may increase for up to 2 weeks. Noncontrast CT is the first-line imaging modality for suspected ICH. However, gradient-echo and T2* susceptibility-weighted MRI have the same sensitivity as CT for detecting acute hemorrhage. These sequences are more sensitive than CT for detecting prior hemorrhage. However, these sequences are inferior to CT for detecting hyperacute (<6-hour) ICH due to their lower speed and accessibility.

In the subacute phase, the hematoma may be isodense to brain tissue, and MRI may be necessary. The volume of the hematoma can be calculated using the formula A × B × C/2, where A and B are the largest diameter and the diameter perpendicular to it.[21] C is the vertical height of the hematoma. ICH with a volume greater than 60 mL is associated with high mortality.[22] The other poor prognostic factors are hematoma expansion, intraventricular hemorrhage, infratentorial location, and contrast extravasation on CT scan (spot sign).[11] The paramagnetic properties of deoxyhemoglobin allow early detection of hemorrhage in MRI.[23] Gradient-echo imaging is as good as CT for detecting acute bleeding. MRI can distinguish between the hemorrhagic transformation of an infarct and primary hemorrhage. MRI can detect underlying causes of secondary hemorrhages, such as vascular malformations, including cavernomas, tumors, and cerebral vein thrombosis.

Extravasation of contrast in a CT angiogram (CTA) (eg, spot sign) indicates ongoing bleeding associated with fatality.[24] Multidetector CTA helps rule out the causes of secondary hemorrhagic stroke, eg, arteriovenous malformation, ruptured aneurysm, dural venous sinus (or cerebral vein) thrombosis, vasculitis, and Moyamoya disease (see Image. Cerebellar Hemorrhage, Computed Tomography [CT]).[25] 

Certain imaging characteristics aid in differentiating the underlying disease:

• Multiple hemorrhages of different ages in the parieto-occipital lobes are seen in cerebral amyloid angiopathy.
• Hemorrhage in an arterial territory indicates hemorrhagic infarction.
• Multiple stages of bleeding in the same hematoma with a fluid level are seen in anticoagulation-induced hemorrhages.
• A combination of small ischemic and hemorrhagic lesions indicates vasculitis.
• Hemorrhage in the presence of arterial occlusion is a feature of Moyamoya disease.[26]

Four-vessel digital subtraction angiography (DSA) is necessary in the case of SAH. A repeat study is needed to confirm if the DSA is negative for an aneurysm. If initial DSA is negative after nonperimesencephalic SAH, repeat DSA is typically performed at 1 to 2 weeks; routine 6-week follow-up is no longer universally recommended.

Vascular abnormalities need to be suspected if the following findings are present on a plain CT scan:

• Subarachnoid hemorrhage
• Enlarged vessels or calcifications along the margins of the ICH
• Hyperattenuation within a dural venous sinus
• A cortical vein along the presumed venous drainage path
• Unusual hematoma shape
• Presence of edema out of proportion to the time of presumed ICH
• An unusual hemorrhage location
• Presence of other abnormal structures in the brain (like a mass) [27][28]

An additional MRI scan will be beneficial in the following circumstances to identify the secondary causes for ICH:

• Lobar hemorrhage location
• Age <55 years
• No history of hypertension

Magnetic resonance venography or CT venography is indicated based on the following conditions that suggest cerebral venous thrombosis:

• Hemorrhage location
• Relative edema volume
• Abnormal signal in the cerebral sinuses

Blood investigations, eg, clotting time, platelet count, peripheral smear, prothrombin time, and activated partial thromboplastin time, will detect abnormalities in bleeding or coagulation and any hematological disorders that can cause hemorrhage. Liver and renal function tests are also needed to exclude hepatic or renal dysfunction as a cause. Investigations to rule out vasculitis include quantitative evaluation of immunoglobulins, thyroid antibodies, rheumatoid factor, antineutrophil cytoplasmic antibodies, antiendothelial antibodies, and quantitative assessment of antineutrophil cytoplasmic antibodies, complement, and anti-Ro (Sjögren syndrome–related antigen A) and anti-La (Sjögren syndrome–related antigen B) antibodies; and cytoplasmic and perinuclear staining.[29] For direct oral anticoagulant-related ICH, add anti–factor Xa activity level (for apixaban/rivaroxaban) and thrombin time (for dabigatran) where available.

Treatment / Management

Opinions differ on the optimal treatment of hemorrhagic stroke. However, results from recent trials have refined the evidence base for blood pressure control, minimally invasive surgery, and anticoagulant reversal. There are many trials on the optimal management of hemorrhagic stroke: Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH), Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT), Factor VIIa for Acute Hemorrhagic Stroke Treatment (FAST), and Surgical Trial in Intracerebral Haemorrhage (STICH), and more recent major trials include INTERACT-2, ATACH-2, MISTIE III, and ENRICH (2023–2024), which have significantly impacted practice guidelines.[30] The role of surgery in hemorrhagic stroke is a controversial topic.

Blood Pressure Management

The American Stroke Association (ASA) recommends that, for patients presenting with systolic blood pressure between 150 and 220 mm Hg, acute lowering of systolic blood pressure to 140 mm Hg is safe and may improve functional outcomes. For patients presenting with systolic blood pressure greater than 220 mm Hg, an aggressive reduction of blood pressure with a continuous intravenous infusion is needed. Beta-blockers (eg, labetalol, esmolol), angiotensin-converting enzyme inhibitors (eg, enalapril), calcium channel blockers (eg, nicardipine), or hydralazine may be used for this purpose.[10] Blood pressure should be checked every 10 to 15 minutes. The ATACH study observed a nonsignificant relationship between the magnitude of systolic blood pressure reduction and hematoma expansion and the 3-month outcome.[31] But the INTERACT study showed that early intensive blood pressure-lowering treatment attenuated hematoma growth over 72 hours.[32] Evidence has shown that high systolic blood pressure is associated with neurological deterioration and death.[27] 

Management of Raised Intracranial Pressure

The initial treatment for elevated ICP is elevating the head of the bed to 30 degrees and administering osmotic agents (eg, mannitol, hypertonic saline). Mannitol 20% is given at a dose of 1.0 to 1.5 g/kg.[10] Short-term hyperventilation after intubation and ventilation to a partial pressure of arterial carbon dioxide of 30 to 35 mm Hg may be used only as a brief temporizing measure in the setting of impending herniation. ASA recommends monitoring ICP with a parenchymal or ventricular catheter in all patients with a Glasgow Coma Scale score less than 8, or with evidence of transtentorial herniation or hydrocephalus.[27] The ventricular catheter has the advantage of allowing cerebrospinal fluid drainage in cases of hydrocephalus. The aim is to keep cerebral perfusion pressure between 50 and 70 mm Hg.

Hemostatic Therapy

Hemostatic therapy is administered to reduce hematoma progression.[10] This is especially important for reversing coagulopathy in patients taking anticoagulants. Vitamin K, prothrombin complex concentrates (PCCs), recombinant activated factor VII (rFVIIa), and fresh frozen plasma (FFP) are used.[10][27] ASA recommends that patients with thrombocytopenia receive platelet concentrate.[27] Patients with elevated prothrombin time and/or international normalized ratio should receive intravenous vitamin K and FFP or PCCs. FFP has the risk of allergic transfusion reactions. PCCs are plasma-derived factor concentrates containing factors II, VII, IX, and X. PCCs can be reconstituted and administered rapidly. Results from the FAST trial showed that rFVIIa reduced hematoma growth but did not improve survival or functional outcomes.[33] rFVIIa is not recommended for unselected individuals, as it does not replace all clotting factors.[27] Idarucizumab is the first-line reversal agent for dabigatran. Tranexamic acid is safe but does not improve functional outcomes, and its role remains adjunctive in selected cases of hyperacute ICH. Results from the Tranexamic Acid for Hyperacute Primary IntraCerebral Haemorrhage trial concluded that tranexamic acid did not affect functional status at day 90. However, potential benefits were observed in reductions in hematoma expansion, early death, and serious adverse events [12].

Antiepileptic Therapy

Approximately 3% to 17% of patients experience seizures within the first 2 weeks, and 30% exhibit epileptiform activity on electroencephalogram (EEG) monitoring.[27] Those with clinical seizures or electrographic seizures should be treated with antiepileptic drugs. Lobar hematoma and the enlargement of the hematoma produce seizures associated with neurological worsening. Subclinical seizures and nonconvulsive status in those with epilepsy can also occur. Continuous EEG monitoring is indicated in patients with decreased consciousness. Otherwise, prophylactic anticonvulsant medication is not recommended per ASA guidelines.[34]

Surgery

The different types of surgical treatment for hemorrhagic stroke are craniotomy, decompressive craniectomy, stereotactic aspiration, endoscopic aspiration, catheter aspiration, and minimally invasive puncture surgery.[4][10] The mechanisms of surgical benefit are the prevention of brain herniation, reduction of ICP, and reduction of the toxic effects of hematomas on surrounding tissue.[4] The STICH trial showed no overall benefit from early surgery for supratentorial intracerebral hemorrhage compared with initial conservative treatment.[35] Current evidence supports early, minimally invasive evacuation for lobar ICH exceeding 30 mL when performed within 24 hours by experienced centers (eg, the ENRICH trial). Guidelines of the ASA state that craniotomy for hematoma evacuation might be considered as a lifesaving measure in patients who are deteriorating.[2] Emergency surgical evacuation is indicated in cerebellar hemorrhage with hydrocephalus or brainstem compression.[21] Patients with cerebellar hemorrhages of more than 3 cm in diameter will have better outcomes with surgery. Guidelines of ASA recommend urgent surgical hematoma evacuation with or without external ventricular drainage for patients having cerebellar ICH with volume 15 mL or greater, and or with brainstem compression, and/or with hydrocephalus.[2] Cerebellar hematoma is evacuated by suboccipital craniectomy. Evacuation of brainstem hemorrhages can be harmful and is not recommended. But successful evacuation of brainstem hematoma has been reported, both by suboccipital posterior fossa decompression and by stereotactic aspiration.[36][37]

A minimally invasive procedure, such as stereotactic aspiration, is also on trial. Results from a randomized study by Hattori et al reported that stereotactic evacuation is beneficial for patients with spontaneous putaminal hemorrhage who open their eyes in response to strong stimuli.[38] Minimally invasive evacuation of supratentorial ICHs and intraventricular hemorrhages‚ can reduce mortality.[2] Minimally Invasive Surgery plus recombinant tissue plasminogen activator (rt-PA) for Intracerebral Hemorrhage Evacuation (MISTIE) was a randomized, prospective trial that evaluated image-guided catheter-based removal of the blood clot.[39] This study's results showed a reduction in perihematomal edema with clot evacuation, but functional benefit was achieved only when 70% or more of the clot volume was evacuated. The ENRICH trial's results showed that minimally invasive hematoma evacuation was associated with better functional outcomes at 180 days, particularly for lobar hemorrhages [40]. The Clot Lysis: Evaluating Accelerated Resolution of IntraVentricular Hemorrhage (CLEAR IVH) trial's results demonstrated that low-dose rt-PA can be safely administered to stable intraventricular clots and increases lysis rates.[41]

Decompressive craniectomy and hematoma evacuation are now being done more frequently for hemorrhagic stroke. Moussa and Khedr showed the improvement in outcome gained by adding decompressive craniectomy with expansive duraplasty to the evacuation of large hypertensive hemispheric ICH in a randomized controlled trial.[42] Decompressive hemicraniectomy with hematoma evacuation is performed in patients with Glasgow Coma Scores of 8 or less and large hematomas with a volume greater than 60 mL (see Image. Intracerebral Hemorrhage, Computed Tomography Angiogram [CTA], Image. Spot Sign, Computed Tomography Angiogram [CTA], and Image. Left Basal Ganglia Hematoma Evacuation, Postoperative Computed Tomography [CT]).[43] Patient selection is crucial because the benefit is most substantial for younger patients, and dominant-hemisphere involvement carries a high risk of severe disability. This procedure reduces mortality and may improve functional outcomes. ASA guidelines state that decompressive craniectomy may be considered as a lifesaving procedure for large supratentorial ICH associated with clinical deterioration and elevated ICP that is refractory to medical management.[2]

Cerebroprotection

The secondary injury of hemorrhagic stroke comprises inflammation, oxidative stress, and toxicity of erythrocyte lysates and thrombin. Strategies to reduce these are being implemented. Pioglitazone, misoprostol, and celecoxib have been tried to reduce inflammatory damage. Edaravone, flavonoid, and nicotinamide mononucleotide can reduce oxidative stress. The iron chelator deferoxamine is also in the experimental phase. The safety and neuroprotective efficacy of the cell membrane component citicoline (cytidine-5-diphosphocholine) have been demonstrated in several studies' results.[44] Rosuvastatin, a competitive inhibitor of the enzyme 3-hydroxy-3-methylglutaryl coenzyme A reductase, was associated with improved outcomes in a trial. Nimodipine reduces delayed cerebral ischemia in aneurysmal subarachnoid hemorrhage; the mechanism is vascular rather than neuroprotective.[45] To date, no neuroprotective agent has demonstrated improved functional outcome in phase 3 trials.

General Care

Quality medical and nursing care and rehabilitation are paramount.[27] Common adverse events include dysphagia, aspiration, cardiac arrhythmias, stress-induced cardiomyopathy, cardiac failure, acute kidney injury, gastrointestinal bleeding, and urinary tract infection. Percutaneous endoscopic gastrostomy (PEG) may be needed to prevent aspiration. PEG is usually deferred for 7 to 14 days to allow neurological recovery before long-term feeding decisions. Screening for myocardial ischemia with an electrocardiogram and cardiac enzyme testing is recommended in hemorrhagic stroke. Intermittent pneumatic compression reduces the occurrence of deep vein thrombosis, but the usefulness of elastic stockings is doubtful. Interprofessional rehabilitation is advised to reduce disability. Blood glucose should be monitored, and measures should be taken to prevent both hyperglycemia and hypoglycemia.[46]

Differential Diagnosis

The differential diagnoses of hemorrhagic stroke include:

• Acute hypertensive crisis
• Pituitary apoplexy
• Cerebral venous thrombosis
• Dural sinus thrombosis
• Cervical artery dissection
• Reversible cerebral vasoconstrictive syndrome 
• Hemorrhagic neoplasms
• Arteriovenous malformations
• Meningitis
• Acute subdural hematoma
• Hemorrhagic infarct

Imaging studies, such as CT and MRI, can exclude these entities.[47]

Prognosis

The poor prognostic factors are coma, large hematoma with volume greater than 30 mL, intraventricular hemorrhage, posterior fossa hemorrhage, age older than 80, hyperglycemia, and chronic kidney disease.[11] Early deterioration and mortality are significant problems associated with ICH. Coma, at the time of the presentation, indicates a grave prognosis. ASA recommends that the monitoring and management of patients with ICH should be in a dedicated stroke unit. At 6 months, only 20% of patients become independent. The survivors may enter into a persistent vegetative state or locked-in syndrome in case of extensive hemispherical damage or brainstem involvement, respectively.

The ICH score introduced by Hemphill et al predicts mortality.[48][49] The points are given as 2 points for GCS 3 to 4, 1 point for GCS 5 to 12, 0 points for GCS 13 to 15, 1 point for individuals older than 80, 0 points for individuals younger than 80, 1 point for infratentorial location, 0 points for supratentorial location, 1 point for ICH volume >30 mL, 0 points for volume of less than 30 mL, 1 point for intraventricular hemorrhage and 0 points for the absence of intraventricular hemorrhage. The 30-day mortality of each score is as follows: 0% for score 0, 13% for score 1, 26% for score 2, 72% for score 3, 97% for score 4, and 100% for scores 5 and 6. The Functional Outcome in Patients With Primary Intracerebral Hemorrhage score predicts the probability of functional independence after ICH and complements the ICH score.[50]

Complications

Complications of ICH include cerebral edema, increased ICP, hydrocephalus, seizures, venous thrombotic events, hyperglycemia, increased blood pressure, fever, and infections.[51] Intraventricular extension and hydrocephalus occur in 30% to 50% of patients with ICH.[2] Patients with ICH, especially women, have a risk of thromboembolic disease.[27] ASA recommends the use of intermittent pneumatic compression devices for mechanical prophylaxis of deep vein thrombosis.[2] 

Almost one-third of patients with ICH develop pulmonary complications, eg, pneumonia, aspiration, pulmonary edema, respiratory failure, and respiratory distress. About 4% of patients with ICH experience cardiac complications, eg, myocardial infarction, atrial fibrillation, ventricular fibrillation, ventricular tachycardia, stress-induced cardiomyopathy, and acute heart failure.[52] Vasospasm, ischemia, rebleeding, seizure, hyponatremia, and hydrocephalus are the complications of SAH. Neurogenic pulmonary edema, an increase in interstitial and alveolar fluid, commonly occurs in subarachnoid hemorrhage.[53]

Deterrence and Patient Education

ICH has a chance of recurrence. Hypertension and older age are risk factors. Blood pressure should be controlled. Disease-modifying therapy exists for CAA; the risk of recurrence remains high despite blood pressure control. Lifestyle modifications should be advised, including avoidance of alcohol, tobacco, and illicit drugs. Continued interprofessional rehabilitation should be performed.

The following are the possible risk factors for a recurrent ICH:

• Lobar location of the initial ICH
• Older age
• Presence and number of microbleeds on gradient-echo MRI
• Ongoing anticoagulation
• Presence of apolipoprotein E epsilon 2 or epsilon 4 alleles [27]

Pearls and Other Issues

Lifestyle modifications are part of primary and secondary prevention.[2] These include increased physical activity, cessation of smoking, avoidance of recreational drug use, reduced alcohol consumption, and a healthy diet that includes fish rich in long-chain omega-3 fatty acids, vegetables, fruits, and whole-grain products. The diet should consist of less red meat and a reduced intake of added sugar. The saturated fats should be replaced with polyunsaturated or monounsaturated fats. Achieving a strict blood pressure reduction to less than 130/80 mm Hg is the most effective intervention for secondary prevention.

Chronic small-vessel disease, characterized by pathological changes such as vessel lipohyalinosis, fibrinoid necrosis, and vessel rarefaction, can be detected on MRI by features including small subcortical infarcts, deep and periventricular white matter hyperintensities, haemosiderin-laden chronic haemorrhages, and cerebral microbleeds (CMBs).[6] Deep microbleeds are considered part of hypertensive changes, whereas lobar CMBs are characteristic of cerebral amyloid angiopathy (CAA).[9] Other MRI features of CAA include cortical superficial siderosis as a sequelae of convexity subarachnoid hemorrhage and white matter hyperintensity in posterior brain regions. The risk of ICH can be reduced in such patients by adequate blood pressure control.

Enhancing Healthcare Team Outcomes

Hemorrhagic stroke, a life-threatening cerebrovascular event, results from bleeding into the brain parenchyma or subarachnoid space and carries high morbidity and mortality. Rapid neurological deterioration often occurs due to hematoma expansion, elevated intracranial pressure, and complications such as seizures or hydrocephalus. Early recognition, appropriate imaging, and evidence-based interventions—including blood pressure reduction, intracranial pressure management, and timely reversal of coagulopathy—are essential to improving outcomes. Accurate differentiation between intracerebral and subarachnoid hemorrhage, along with identification of underlying causes such as hypertension, cerebral amyloid angiopathy, or vascular malformations, guides effective care planning.

Interprofessional management requires coordinated expertise across clinical disciplines. Physicians and advanced practitioners must rapidly interpret imaging, initiate acute therapies, and determine candidacy for surgical or minimally invasive evacuation. Nurses play a critical role in continuous neurological monitoring, blood pressure titration, and early detection of clinical deterioration. Pharmacists support safe and timely medication use, particularly anticoagulant reversal and blood pressure management. Rehabilitation specialists, therapists, and care coordinators contribute to recovery planning and long-term functional improvement. Effective communication among all team members enhances patient safety, reduces complications, and ensures a unified approach to patient-centered care.

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Disclosure: Ajaya Kumar Unnithan declares no relevant financial relationships with ineligible companies.

Disclosure: Joe Das declares no relevant financial relationships with ineligible companies.