Hemorrhagic Stroke

Written By Danial Mirza

Definition

Hemorrhagic stroke is a neurological emergency defined by the rupture of a blood vessel, which causes bleeding into the brain parenchyma (intracerebral hemorrhage) or the surrounding subarachnoid space (subarachnoid hemorrhage) (4). This is distinct from ischemic stroke, which results from the blockage of a cerebral artery (1).

Epidemiology

In Malaysia, stroke is the third leading cause of death and a primary cause of long-term disability (13). While ischemic stroke is more common, hemorrhagic stroke accounts for a significant portion, representing about 18-20% of all stroke cases—a figure that is higher than in many Western nations (7). Some hospital-based reports in Malaysia suggest this proportion could be as high as one-third of all stroke admissions (7). This condition carries a high mortality rate; data from the Malaysian National Stroke Registry (2009-2013) showed a median survival of just 10.8 months for patients with intracerebral hemorrhage (ICH) and 1.7 months for those with subarachnoid hemorrhage (SAH), compared to 56.3 months for ischemic stroke (6).

Alarmingly, Malaysia is seeing a rise in strokes among younger individuals, particularly in the 35 to 39-year-old age group (17). Consequently, the average age of stroke onset in Malaysia is about a decade younger than in Western countries (18). The high prevalence of uncontrolled hypertension is the most critical risk factor driving this trend, creating a "perfect storm" for hypertensive intracerebral hemorrhages, even in patients in their 30s and 40s (22, 23).

Pathophysiology

The pathophysiology of hemorrhagic stroke differs based on its subtype:

  • Intracerebral Hemorrhage (ICH): This occurs when a weakened blood vessel ruptures directly within the brain tissue, forming a hematoma (5). The initial bleed causes mechanical damage, and the resulting mass effect increases intracranial pressure (ICP) (10). This is followed by a secondary injury cascade, including hematoma expansion, perihematomal edema (swelling around the hematoma), and cellular death, which worsens brain damage over hours to days (1). Chronic hypertension is the most common cause, leading to bleeds in deep brain structures like the basal ganglia, thalamus, pons, and cerebellum (5, 10). In older adults, Cerebral Amyloid Angiopathy (CAA) is a frequent cause of lobar hemorrhages (near the brain's surface) (1).

  • Subarachnoid Hemorrhage (SAH): This typically results from the rupture of a saccular "berry" aneurysm in the Circle of Willis (9, 12). The sudden bleed into the space containing cerebrospinal fluid (CSF) causes a global, instantaneous rise in ICP, leading to a severe "thunderclap" headache and potential loss of consciousness (9, 10). The blood irritates the meninges, causing chemical meningitis (12). A feared delayed complication is cerebral vasospasm (narrowing of cerebral arteries), which occurs 3-14 days later and can cause secondary ischemia and infarction (12). Other risks include acute hydrocephalus (blockage of CSF flow) and re-bleeding of the aneurysm (10, 12).

Clinical Presentation

The onset is typically sudden. While symptoms can overlap with ischemic stroke, certain features are more suggestive of a hemorrhagic event (35).

  • Diagnostic Clues: The classic presentation of SAH is a "thunderclap headache," described as the "worst headache of my life" that reaches maximum intensity within a minute (2).

  • Common Symptoms (>50%):

    • Headache: Abrupt, severe headache is much more common than in ischemic stroke (35, 36).

    • Impaired Consciousness: A decreased level of consciousness at onset (a lower Glasgow Coma Scale score) is frequent due to the rapid rise in ICP (10, 35).

    • Nausea and Vomiting: Often projectile, driven by raised ICP (4).

    • Focal neurological deficits (e.g., weakness on one side of the body) (10).

  • Less Common Symptoms (10-50%):

    • Seizures: Seizures at stroke onset are significantly more frequent in hemorrhagic cases (~17%) (36, 4).

  • ⚠️ Red Flag Signs & Symptoms:

    • Sudden, explosive "thunderclap" headache (2).

    • Rapid deterioration in consciousness (GCS score) (10).

    • Nuchal rigidity (neck stiffness) and photophobia (light sensitivity), which are classic signs of meningism from SAH (12).

    • A unilaterally dilated and fixed ("blown") pupil, an ominous sign of uncal herniation and a neurosurgical emergency (10).

    • Markedly elevated blood pressure (e.g., SBP >220 mmHg) (10).

Complications

Patients are vulnerable to numerous complications, which are a significant cause of readmission and mortality in Malaysia (62, 63).

  • Neurological:

    • Hematoma expansion (1).

    • Perihematomal edema and raised ICP (1).

    • Hydrocephalus, especially with SAH or ICH with intraventricular extension (10).

    • Delayed cerebral ischemia from vasospasm (after SAH) (12).

    • Re-bleeding (12, 62).

    • Seizures (45).

  • Medical:

    • Infections: Pneumonia (often from aspiration due to dysphagia) and Urinary Tract Infections (UTIs) are very common and are predictors of poor outcomes (20, 63). Sepsis is a leading cause for 28-day readmission after stroke in Malaysia (62).

    • Venous Thromboembolism (VTE): Deep vein thrombosis (DVT) and pulmonary embolism (PE) due to immobility (45).

    • Cardiac Complications: Myocardial infarction, cardiac arrhythmias (such as new-onset atrial fibrillation), and stress-induced cardiomyopathy (Takotsubo cardiomyopathy) can be precipitated by the intracranial event (45).

    • Gastrointestinal (GI) Bleeding: Stress ulceration is a significant complication associated with mortality (63).

Prognosis

Hemorrhagic stroke has a grim prognosis, with mortality rates significantly higher than for ischemic stroke (6). The Intracerebral Hemorrhage (ICH) Score is a widely used and validated tool in Malaysia to provide an objective measure of severity and predict 30-day mortality (40, 60, 67). It is calculated based on GCS score, age, ICH volume, presence of intraventricular hemorrhage, and infratentorial location (40). A higher score correlates with higher mortality (40). However, it is crucial that this score is not used as the sole justification for withdrawing aggressive medical care, as this can lead to a self-fulfilling prophecy (40). For SAH, prognosis is most powerfully predicted by clinical grade at presentation using the Hunt and Hess or WFNS scales (12).

Differential Diagnosis

It is impossible to reliably differentiate hemorrhagic from ischemic stroke clinically; emergency neuroimaging is mandatory (35). However, when considering the cause of an acute neurological deficit, key differentials include:

  • Ischemic Stroke: This is the most common type of stroke and a critical differential (1). It is caused by a vessel blockage (1). The absence of a severe headache, vomiting, or early impaired consciousness makes an ischemic event more likely, but these signs are not definitive (35). An emergency non-contrast CT brain will reliably distinguish between ischemia and hemorrhage (35).

  • Seizure with Post-ictal State (Todd's Paralysis): A focal seizure can be followed by a period of temporary focal neurological deficit, mimicking a stroke. However, seizures are more common at the onset of a hemorrhagic stroke itself (36). A history of epilepsy might be present. Neuroimaging is still required to rule out an underlying structural cause like a bleed.

  • Hypoglycemia: Low blood sugar can present with focal neurological signs and altered consciousness, perfectly mimicking a stroke. This is why a bedside blood glucose check is a mandatory and immediate first step in the assessment of any patient with suspected stroke (28). The symptoms will rapidly reverse with glucose administration.

Investigations

The diagnostic workflow is a time-critical emergency pathway focused on rapid imaging (42).

Immediate & Bedside Tests

  • Bedside Blood Glucose: This is a mandatory first step to immediately rule out hypoglycemia as a stroke mimic (the action), as this is a common and easily reversible cause of focal neurological deficits (the rationale) (28).

  • Bedside ECG: This is essential to detect any concurrent cardiac issues like arrhythmias or myocardial infarction (the action), which can be either a cause or a complication of the acute intracranial event (the rationale) (28).

Diagnostic Workup

  • First-Line & Gold Standard for Initial Diagnosis: Non-Contrast CT (NCCT) Brain: This is the absolute cornerstone of diagnosis and must be performed immediately (30, 35). It is highly sensitive for detecting acute blood, which appears as a hyperdense (bright white) area (the rationale), allowing for the crucial and immediate differentiation of hemorrhagic from ischemic stroke (the action) (35).

  • Advanced Vascular Imaging (CTA/MRA/DSA):

    • CT Angiography (CTA): This is a fast, non-invasive scan performed after the initial NCCT to visualize cerebral blood vessels (45). It is highly effective for identifying an underlying cause like an aneurysm or arteriovenous malformation (AVM) (the rationale), which is critical for planning definitive treatment (the action) (45).

    • Digital Subtraction Angiography (DSA): This remains the gold standard for detailed vascular evaluation (12). It is an invasive procedure that provides the most detailed images of aneurysms and AVMs (the rationale), essential for planning endovascular coiling or surgical clipping (the action) (12).

Monitoring & Staging

  • The Intracerebral Hemorrhage (ICH) Score: This clinical grading scale is used at presentation to objectively stage the severity of the bleed (the action), as it combines key clinical and radiological factors (GCS, age, volume, IVH, location) to provide a validated prediction of 30-day mortality and facilitate communication among the clinical team (the rationale) (40).

Management

Management is a medical emergency focused on preventing further injury by controlling bleeding and intracranial pressure (45). Notably, Malaysia does not have a dedicated national CPG for hemorrhagic stroke; the existing MOH guidelines focus on ischemic stroke (28, 30). Therefore, management is adapted from international guidelines.

Management Principles

The management of hemorrhagic stroke focuses on immediate hemodynamic stabilization, urgent reversal of any coagulopathy, strict blood pressure control, and management of intracranial pressure to prevent secondary brain injury (45).

Acute Stabilisation (The First Hour)

  • Airway/Breathing: Administer supplemental oxygen to maintain SpO2 >95% to prevent tissue hypoxia (49). Patients with a GCS ≤8 or who cannot protect their airway require immediate endotracheal intubation and ventilation (the action) to secure the airway and control ventilation, preventing aspiration and managing CO2 levels (the rationale) (45).

  • Circulation: Secure two large-bore IV cannulas and administer isotonic fluids like Normal Saline (45). Avoid hypotonic fluids (e.g., dextrose solutions) as they can worsen cerebral edema (45).

  • Disability (Neurological): Keep the patient nil by mouth (NBM) until a dysphagia screen is performed to prevent aspiration pneumonia (28, 45). Treat fever >38°C aggressively with paracetamol to prevent secondary brain injury (28).

Definitive Therapy

  • Blood Pressure Control:

    • For ICH: In patients with an SBP between 150-220 mmHg, acutely lower the SBP to a target of <140 mmHg within the first hour (the action), as this is proven to be safe and may reduce hematoma expansion and improve outcomes (the rationale) (45, 51). Titratable IV agents like Labetalol (e.g., 10-20 mg IV bolus) are first-line (28).

    • For SAH: Before an aneurysm is secured, carefully lower SBP to a target of <160 mmHg using a titratable IV agent (the action) to reduce the high risk of a fatal re-bleed while maintaining cerebral perfusion (the rationale) (12).

  • Reversal of Anticoagulation (A Time-Critical Emergency):

    • Warfarin-Associated ICH: Immediately administer IV Vitamin K 10mg AND Prothrombin Complex Concentrate (PCC) (the action). PCC (e.g., Prothrombinex-VF® in Malaysia) provides rapid reversal of coagulopathy, which is critical to stop ongoing bleeding and is superior to FFP (the rationale) (45, 54).

    • DOAC-Associated ICH: Use specific antidotes if available. For Dabigatran, use Idarucizumab (Praxbind®); for Factor Xa inhibitors (Rivaroxaban, Apixaban), use Andexanet alfa (45, 46, 56). If unavailable, consider PCC in consultation with a senior (45).

    • Antiplatelet-Associated ICH: DO NOT give platelet transfusions. This is a critical contraindication. The PATCH trial showed that platelet transfusion is harmful and increases death and dependency (45).

  • Neurosurgical Intervention:

    • ICH: Surgical evacuation is a neurosurgical emergency for a cerebellar hematoma >3 cm or one causing brainstem compression or hydrocephalus (10, 45). For supratentorial (lobar) bleeds, surgery may benefit patients with deteriorating neurology whose clot is close to the surface (45, 60).

    • SAH: The goal is to secure the ruptured aneurysm as early as possible to prevent re-bleeding (12). This is done via endovascular coiling (first-line for suitable aneurysms) or surgical clipping (4, 12).

Supportive & Symptomatic Care

  • ICP Management: Elevate the head of the bed to 30 degrees and keep the head midline to promote venous drainage (57). Provide adequate analgesia and sedation to prevent ICP spikes (57). For acute rises in ICP, use hyperosmolar therapy like IV Mannitol (0.25-1 g/kg) or Hypertonic Saline to draw fluid from the brain (28, 57).

  • Hydrocephalus Management: In patients with obstructive hydrocephalus from IVH or SAH, the insertion of an External Ventricular Drain (EVD) by neurosurgery is a life-saving intervention to drain CSF and control ICP (45, 48).

  • VTE Prophylaxis: Use mechanical prophylaxis with intermittent pneumatic compression (IPC) devices to prevent DVT/PE (45). Graduated compression stockings are ineffective (45).

Key Nursing & Monitoring Instructions

  • Strict hourly neurological observations (GCS, pupils) for at least the first 6-24 hours.

  • Continuous cardiac and BP monitoring, with BP checked every 5-15 minutes during IV antihypertensive titration.

  • Strict input/output chart monitoring, especially if mannitol is used.

  • Maintain head of bed elevation at 30 degrees.

  • Keep patient strictly NBM until a swallow assessment is cleared.

  • Inform the medical officer immediately if SBP targets are breached, GCS drops by >1 point, a pupil becomes dilated, or urine output is <0.5mL/kg/hr.

Long-Term Plan & Patient Education

The focus is on aggressive secondary prevention and rehabilitation.

  • Secondary Prevention:

    • Blood Pressure Control: This is the absolute cornerstone. The long-term target is consistently <130/80 mmHg (22, 52).

    • Lifestyle Modification: Counsel on a low-salt diet, regular physical activity, smoking cessation, and avoiding excessive alcohol (25).

  • Rehabilitation: Organized, multidisciplinary rehabilitation (physiotherapy, occupational therapy, speech therapy) should begin as soon as the patient is stable (70).

  • Patient Education: Given the fragmented rehabilitation services in Malaysia, discharge planning is critical (31, 32). Educate the patient and family on the importance of medication adherence and follow-up with their primary care doctor (Klinik Kesihatan). Inform them about available resources like caregiver support apps (e.g., MyStroke project) and integrated care pathways (iCaPPS®) that aim to improve community-based care (18, 32).

When to Escalate

  • Call Your Senior (MO/Specialist) if:

    • There is any acute drop in GCS, particularly a drop of 2 or more points.

    • The patient develops a new, fixed, and dilated pupil.

    • Blood pressure remains refractory to first-line IV medications.

    • The patient has a seizure.

    • There is any ambiguity or delay in securing an urgent CT scan.

    • You suspect anticoagulation-associated ICH, to activate the urgent reversal protocol.

  • Referral Criteria:

    • Immediate Neurosurgical Referral: Any patient with a confirmed hemorrhagic stroke on CT requires immediate discussion with the on-call neurosurgery team. This is especially urgent for patients with cerebellar hemorrhage, large clots with mass effect, hydrocephalus, or a suspected ruptured aneurysm (10, 12, 45). In district hospitals, this involves initiating urgent transfer to a tertiary center with neurosurgical capabilities (14).

    • Rehabilitation Medicine: Refer all stroke survivors for assessment by the rehabilitation team to create a comprehensive therapy plan (70).

    • Cardiology/Hematology: Consultation may be needed for complex decisions on restarting antithrombotic therapy post-ICH (69).

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Danial Mirza
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