What is the management and treatment of a hemorrhagic stroke?

Comprehensive Management of Hemorrhagic Stroke

Emergency Recognition and Initial Stabilization

Hemorrhagic stroke must be treated as a medical emergency requiring immediate evaluation by physicians with expertise in hyperacute stroke management, as early deterioration occurs in over 20% of patients within the first few hours. 1, 2

Immediate Assessment (First 15 Minutes)

• Perform rapid ABC assessment (airway, breathing, circulation) immediately upon patient arrival to identify life-threatening conditions 1, 2
• Conduct neurological examination using the National Institutes of Health Stroke Scale (NIHSS) for awake or drowsy patients to quantify stroke severity and focal deficits 1, 3
• Assess Glasgow Coma Scale at baseline, as a decrease of 2 or more points indicates early deterioration and predicts poor outcomes 2, 3
• Obtain vital signs including pulse, blood pressure, temperature, oxygen saturation, and glucose—repeat blood pressure assessment every 15 minutes until stabilized 1, 3

Critical Diagnostic Workup

Obtain immediate non-contrast CT scan to confirm diagnosis, location, and extent of hemorrhage—this is mandatory and should not be delayed. 1, 2

• Complete urgent blood work including complete blood count, coagulation status (INR, aPTT), and blood glucose within 20 minutes of blood sampling 3
• Obtain detailed medication history with particular attention to anticoagulant therapy (warfarin, DOACs, antiplatelet agents) 1, 3
• Perform vascular imaging (CT angiography, MR angiography, or catheter angiography) in confirmed acute ICH to exclude underlying lesions such as aneurysms or arteriovenous malformations 1, 3
• Look for the "spot sign" on CT angiography, which indicates contrast extravasation and predicts hematoma expansion in 30-40% of patients 2, 3

Blood Pressure Management

For patients with systolic blood pressure between 150-220 mmHg without contraindications, acutely lower systolic BP to 140 mmHg—this is safe and improves functional outcomes. 1, 2, 3

Specific BP Targets and Agents

• Maintain mean arterial pressure below 130 mmHg in ICH patients with a history of hypertension 3
• Use nicardipine as first-line agent over labetalol, as it achieves and maintains goal blood pressure faster with fewer treatment failures 1
• Avoid sodium nitroprusside and other cerebral vasodilators in patients with markedly elevated intracranial pressure, as these worsen cerebral edema 1, 2
• Monitor blood pressure every 15 minutes until stabilized, then hourly for the first 24 hours 1, 2

Reversal of Coagulopathy

Patients on warfarin with elevated INR must receive prothrombin complex concentrate plus intravenous vitamin K immediately—rapid reversal while limiting fluid volumes is critical. 1, 2

Specific Reversal Protocols

• For warfarin-associated ICH: Withhold warfarin, administer prothrombin complex concentrate to replace vitamin K-dependent factors, correct INR, and give intravenous vitamin K 1, 3
• For severe thrombocytopenia: Administer platelet transfusion to achieve adequate platelet count 1, 3
• For severe coagulation factor deficiency: Provide appropriate factor replacement therapy based on specific deficiency 1, 3

Fluid and Osmotic Management

Use isotonic fluids to maintain hydration while preventing volume overload—avoid hypo-osmolar fluids such as 5% dextrose in water as they worsen cerebral edema. 4, 1, 2

Specific Fluid Strategies

• Implement mild fluid restriction to help manage brain edema without causing dehydration 1
• Avoid all hypo-osmolar solutions including 5% dextrose in water, which exacerbate cerebral edema 4, 1

Management of Increased Intracranial Pressure

Elevate the head of the bed by 20-30 degrees to facilitate venous drainage and treat all factors that exacerbate raised intracranial pressure (hypoxia, hypercarbia, hyperthermia). 4, 1, 2

Osmotherapy and Medical Management

• Administer mannitol 0.25-0.5 g/kg IV over 20 minutes, every 6 hours (maximum 2 g/kg) for patients deteriorating due to increased intracranial pressure 1, 2
• Use hyperventilation as a temporizing measure for patients with herniation syndromes, though this is only temporary 1
• Do NOT use corticosteroids for management of cerebral edema and increased intracranial pressure following hemorrhagic stroke, as they are ineffective 4, 1
• Consider surgical drainage of cerebrospinal fluid to treat increased intracranial pressure secondary to hydrocephalus 4, 1

Surgical Interventions

Patients with cerebellar hemorrhage who are deteriorating neurologically or have brainstem compression and/or hydrocephalus from ventricular obstruction must undergo surgical removal of the hemorrhage as soon as possible. 1, 2, 3

Specific Surgical Indications

• Perform immediate surgical evacuation for cerebellar hemisphere hematomas >3 cm diameter causing neurological deterioration 2, 3
• Consider ventriculostomy for patients with spontaneous ICH (with or without intraventricular hemorrhage) and symptomatic hydrocephalus 2
• For supratentorial hemorrhage: Routine surgery is not recommended, but consider stereotactic surgery for deep ICH or craniotomy when hematoma is superficial (<1 cm from surface) 3
• Obtain neurosurgical consultation promptly for all patients with significant hemorrhage to evaluate potential surgical interventions 1

Monitoring and Care Setting

Initial monitoring and management must take place in an intensive care unit or dedicated stroke unit with physician and nursing neuroscience acute care expertise. 1, 2

Specific Monitoring Parameters

• Maintain nurse-patient ratio of 1:2 for the first 24 hours, then 1:4 if patient condition is stable 2
• Repeat validated neurological scale at least hourly for the first 24 hours, depending on patient stability 1, 2
• Monitor for hematoma expansion, which occurs in 30-40% of patients and predicts poor outcome—risk factors include "spot sign" on CTA, early presentation (<3 hours), anticoagulant use, and initial hematoma volume 2, 3

Seizure Management

Treat new onset seizures occurring immediately before or within 24 hours of stroke onset with short-acting medications (e.g., lorazepam IV) if not self-limited. 1

Specific Seizure Protocols

• Do NOT use prophylactic anticonvulsants for patients who have had hemorrhagic stroke but not seizures, as this is not recommended 4, 1
• Treat recurrent seizures as with any other acute neurological condition using standard anticonvulsant protocols 4, 1
• Do NOT treat a single, self-limiting seizure occurring at onset or within 24 hours with long-term anticonvulsant medications 1

Prevention of Complications

Implement intermittent pneumatic compression for prevention of venous thromboembolism beginning the day of hospital admission—do NOT use graduated compression stockings as they are less effective. 1, 2

Specific Prophylaxis Strategies

• Consider starting pharmacological VTE prophylaxis with unfractionated heparin or low-molecular-weight heparin after documenting hemorrhage stability on CT, typically 24-48 hours after ICH onset 1
• Perform formal dysphagia screening before initiating oral intake to reduce the risk of aspiration pneumonia 1
• Provide oxygen supplementation to patients who are hypoxic to maintain adequate oxygenation 3
• Monitor and treat fever (temperature >38°C); investigate and treat sources of fever as hyperthermia exacerbates brain injury 2
• Monitor and manage hyperglycemia with appropriate glycemic therapy, as elevated glucose worsens outcomes 3

Critical Pitfalls to Avoid

Be vigilant for early deterioration—over 20% of patients experience a decrease in Glasgow Coma Scale of 2 or more points between prehospital assessment and initial ED evaluation. 1, 2, 3

Common Errors in Management

• Do not delay imaging or treatment decisions for diagnostic tests—CT scan must be obtained immediately 1
• Do not use cerebral vasodilators (sodium nitroprusside) in patients with elevated intracranial pressure, as this worsens cerebral edema 1, 2
• Do not miss cerebellar hemorrhage, which can be difficult to diagnose when chief complaints are dizziness, vertigo, and vomiting—carefully assess speech, gait, coordination, and eye movements, and do not miss truncal ataxia during bedside examination 4
• Do not assume initial CT is definitive for cerebellar stroke, as it can be normal in as many as 25% of patients initially 4
• Do not overlook hemorrhagic transformation in patients with ischemic stroke, as this complication involves damage to the blood-brain barrier and can cause sudden rapid decline due to new mass effect 4

Pathophysiology and Mechanisms of Injury

Hemorrhagic stroke involves complex interactions between hematoma expansion, perihaematomal edema, inflammation, and blood product toxicity 5, 6, 7. The mechanisms include:

• Acute progression (first 24-48 hours) caused by hematoma expansion, intraventricular hemorrhage, perihaematomal edema, and inflammation 5
• Subacute progression (days 3-14) caused by a specific "second peak" of perihaematomal edema and "tension haematoma" 5
• Matrix metalloproteinases (MMP-9), inflammatory mediators, reactive oxygen species, and iron-induced oxidative stress contribute to ongoing brain injury 4, 7