Cerebrovascular Accident (Stroke)
Definition
A Cerebrovascular Accident (CVA), or stroke, is a clinical syndrome characterized by the sudden onset of focal or global neurological deficits, which lasts for more than 24 hours or leads to death, with no apparent cause other than a vascular origin (1). The crucial distinction is between an ischaemic stroke, caused by the occlusion of a cerebral blood vessel, and a haemorrhagic stroke, resulting from the rupture of a blood vessel (2, 3). A Transient Ischaemic Attack (TIA) is now defined as a brief episode of neurological dysfunction caused by focal ischaemia without evidence of acute infarction on imaging, representing a critical warning sign for a major stroke (4).
Epidemiology
In Malaysia, stroke is the third leading cause of death and a major cause of significant disability (5). The mean age of stroke onset in Malaysia is approximately 63 years, which is notably younger than in many Western countries (5). There has been an alarming rise in stroke incidence among Malaysians under 65, with the most significant increase observed in the 35-39 year age group, highlighting the urgent need for aggressive primary prevention in younger adults (6). Ischaemic strokes account for the majority of cases in Malaysia (5).
Globally, stroke is the second leading cause of death and the third leading cause of disability-adjusted life-years (DALYs) (7). It is estimated that one in four adults over the age of 25 will have a stroke in their lifetime (7). There are significant regional differences, with Asian populations having a higher proportion of haemorrhagic strokes and a greater incidence of ischaemic strokes due to intracranial atherosclerosis compared to Western populations (8).
Pathophysiology
Ischaemic Stroke
The core of an ischaemic stroke is the cessation of blood flow, which starves brain tissue of oxygen and glucose, initiating the ischaemic cascade. The affected area is divided into the ischaemic core, where blood flow is severely reduced leading to rapid and irreversible cell death (necrosis), and the surrounding ischaemic penumbra. The penumbra is dysfunctional but still viable tissue, and it is the primary target of acute reperfusion therapies (9). The cascade involves:
Energy Failure: Depletion of ATP.
Ion Pump Failure: Leading to cytotoxic oedema (cell swelling).
Excitotoxicity: Massive release of the neurotransmitter glutamate, which causes a toxic influx of calcium into neurons.
Calcium Overload & Cell Death: Activation of destructive enzymes and production of reactive oxygen species, culminating in apoptosis and necrosis.
Neuroinflammation: An inflammatory response that can cause further secondary damage to the blood-brain barrier and the penumbra (9, 10).
Haemorrhagic Stroke
In haemorrhagic stroke, the initial injury is mechanical. An expanding haematoma compresses and destroys brain tissue, leading to a dangerous rise in intracranial pressure (ICP) (3). This mass effect can reduce cerebral perfusion pressure, causing secondary ischaemia, and may lead to fatal brain herniation (3). The secondary injury is driven by the inflammatory response to the blood in the brain parenchyma and the direct neurotoxicity of blood components like iron and thrombin, which are released as the clot breaks down, causing vasogenic oedema and oxidative stress in the surrounding tissue (10, 11).
Clinical Presentation
The hallmark of a stroke is the sudden onset of neurological symptoms. The BE-FAST acronym (Balance, Eyes, Face, Arm, Speech, Time) is a useful tool for rapid recognition (12). Clinical syndromes typically correspond to the affected vascular territory.
Anterior Circulation Syndromes (Internal Carotid Artery System)
Middle Cerebral Artery (MCA) Infarction: This is the most common type of ischaemic stroke.
Diagnostic Clues: Contralateral hemiparesis and sensory loss affecting the face and arm more than the leg. Contralateral homonymous hemianopia and a gaze preference towards the side of the lesion are also common (13).
Dominant Hemisphere (usually left) Lesion: Results in aphasia (e.g., Broca's expressive aphasia, Wernicke's receptive aphasia, or global aphasia) (13).
Non-Dominant Hemisphere (usually right) Lesion: Leads to hemispatial neglect (inattention to the left side of space) and anosognosia (unawareness of the deficit) (13).
Anterior Cerebral Artery (ACA) Infarction: Less common.
Diagnostic Clues: Contralateral weakness and sensory loss affecting the leg more than the arm or face.
Common Symptoms: Abulia (profound apathy), impaired judgment, and urinary incontinence due to frontal lobe involvement (14).
Posterior Circulation Syndromes (Vertebrobasilar System)
Diagnostic Clues: The "5 Ds" are classic: Dizziness (vertigo), Diplopia (double vision), Dysarthria (slurred speech), Dysphagia (difficulty swallowing), and Dyssynergia/Ataxia (incoordination) (15). The presence of "crossed findings" (ipsilateral cranial nerve palsy with contralateral motor/sensory deficits) is pathognomonic for a brainstem lesion.
Posterior Cerebral Artery (PCA) Infarction:
Common Symptoms: Contralateral homonymous hemianopia is the hallmark sign, often with macular sparing (16).
Less Common Symptoms: Cortical blindness (with bilateral PCA infarcts), memory impairment, and pure sensory loss if the thalamus is involved (16).
⚠️ Red Flag Signs & Symptoms:
Sudden "thunderclap" headache (worst headache of my life)
Rapid deterioration in level of consciousness
Seizures at onset
Neck stiffness or meningism
These signs are highly suggestive of a haemorrhagic stroke, particularly a subarachnoid haemorrhage (SAH) (3, 17).
Complications
Neurological: Cerebral oedema, haemorrhagic transformation of an ischaemic stroke, seizures, hydrocephalus, and vasospasm (following SAH).
Systemic: Aspiration pneumonia, deep vein thrombosis (DVT), pulmonary embolism, urinary tract infections, pressure sores, and cardiac complications (e.g., myocardial infarction, arrhythmias).
Prognosis
Prognosis is highly dependent on stroke type, severity, location, and the patient's age and comorbidities. Haemorrhagic strokes have a significantly higher mortality rate (around 40-50%) than ischaemic strokes (around 10-20%) (3, 18). For ischaemic stroke, timely reperfusion therapy is the single most important factor for a good functional outcome. Long-term disability is common, with many survivors requiring ongoing rehabilitation.
Differential Diagnosis
Hypoglycaemia/Hyperglycaemia: This is a critical stroke mimic that must be excluded immediately with a bedside blood glucose test, as it is easily reversible.
Seizures with Todd's Paresis: A post-ictal focal neurological deficit can mimic a stroke. The deficit is transient, and a history of seizure activity is a key distinguishing feature.
Migraine with Aura: Complicated migraines can present with focal neurological symptoms, including weakness and sensory changes. The headache typically follows the neurological aura, and patients often have a prior history of similar episodes.
Brain Tumour or Abscess: These conditions typically have a more subacute or gradual onset of symptoms compared to the hyperacute presentation of a stroke, although they can sometimes present acutely due to bleeding into the tumour or a seizure.
Conversion Disorder: A psychological condition where neurological symptoms appear without an underlying neurological cause. The examination may reveal inconsistent or non-anatomical findings.
Investigations
The approach is phased to facilitate rapid, life-saving decisions. The guiding principle is "Time is Brain."
Immediate & Bedside Tests
Finger-stick Blood Glucose: This is mandatory for every suspected stroke patient to immediately rule out hypoglycaemia, a key stroke mimic, which would alter the entire management pathway (1).
Bedside ECG: This is crucial to identify atrial fibrillation as a potential cause for a cardioembolic stroke or to detect concurrent myocardial ischaemia, which can influence treatment decisions (1).
Diagnostic Workup
First-Line Imaging: An urgent Non-Contrast CT (NCCT) of the brain is the cornerstone of hyperacute stroke imaging. Its primary role is to reliably and quickly exclude haemorrhage (which appears as bright hyperdensity), the most critical step in determining eligibility for thrombolysis (1). In the very early hours of an ischaemic stroke, the NCCT may appear normal, though subtle signs like the "hyperdense MCA sign" can sometimes be seen (1).
Gold Standard (for Ischaemia): A Diffusion-Weighted MRI (DWI) is the most sensitive imaging modality for detecting acute ischaemic injury. It can confirm an infarct within minutes of onset and is the gold standard for diagnosing ischaemia, particularly when the NCCT is negative (19).
Further Vascular Imaging: CT Angiography (CTA) of the head and neck is essential for identifying a large vessel occlusion (LVO) in the arteries of the neck and brain. This is performed immediately after the NCCT in potential candidates for mechanical thrombectomy to confirm the blockage and guide the intervention (1).
Monitoring & Staging
Baseline Bloods: A Full Blood Count is required to check for thrombocytopenia or polycythaemia; Coagulation Profile (PT/INR, aPTT) is essential before thrombolysis; Renal profile is needed as contrast may be used for CTA (1). Treatment must not be delayed waiting for these results, except for glucose.
Cardiac Monitoring: Continuous cardiac telemetry is performed to detect paroxysmal atrial fibrillation, a common cause of stroke that requires anticoagulation for secondary prevention (1).
Advanced Imaging (Perfusion Scans): CT or MR perfusion imaging is used in patients presenting in an extended time window (up to 24 hours) to differentiate the salvageable penumbra from the irreversibly damaged ischaemic core, thereby selecting appropriate candidates for late-window thrombectomy (1).
Management
Management begins with the ABCDE approach and diverges based on the distinction between ischaemic and haemorrhagic stroke. All stroke patients should be managed in a dedicated Stroke Unit.
Management Principles
The overarching goals are to restore cerebral perfusion in ischaemic stroke, control bleeding and intracranial pressure in haemorrhagic stroke, prevent complications, and initiate secondary prevention and rehabilitation.
Acute Stabilisation (The First Hour)
Airway/Breathing: "Administer supplemental oxygen via nasal prongs or face mask only if SpO2 is <95% to prevent unnecessary hyperoxia, which could be harmful" (1). Secure the airway with intubation if the GCS is ≤8 or airway reflexes are compromised.
Circulation: "Secure two large-bore IV cannulas and manage blood pressure according to the specific stroke subtype." For ischaemic stroke patients not receiving thrombolysis, permissive hypertension (up to 220/120 mmHg) is allowed to maximize perfusion to the penumbra. If thrombolysis is planned, BP must be carefully lowered to <185/110 mmHg and maintained below this level to reduce the risk of haemorrhagic transformation (1). For acute intracerebral haemorrhage, the goal is aggressive SBP reduction to a target of <140 mmHg using IV labetalol or nicardipine to limit haematoma expansion (20, 21).
Definitive Therapy
Acute Ischaemic Stroke (AIS)
First-Line Treatment (Medical): "Intravenous thrombolysis with a 'clot-busting' agent is the primary treatment for eligible patients. Alteplase (rt-PA) is administered at a dose of 0.9 mg/kg (maximum 90mg), with 10% given as a bolus over 1 minute and the remainder infused over 1 hour. It must be given within a 4.5-hour window from the last known well time" (1). Tenecteplase (TNK), given as a single bolus, is increasingly used as an alternative (1). Strict adherence to inclusion and exclusion criteria is mandatory.
First-Line Treatment (Surgical/Endovascular): "Mechanical thrombectomy is the standard of care for AIS caused by a Large Vessel Occlusion (LVO) in the anterior circulation. It is strongly recommended for eligible patients within 6 hours of onset. In selected patients with favourable imaging (a small core and large penumbra on perfusion scans), the window for thrombectomy can be extended up to 24 hours" (1).
Acute Haemorrhagic Stroke
Intracerebral Haemorrhage (ICH): The focus is on medical management.
Haemostatic Therapy: For patients on anticoagulants, immediate reversal is a medical emergency. Use Prothrombin Complex Concentrate (PCC) and Vitamin K for warfarin-associated ICH. For DOACs, specific reversal agents like Idarucizumab (for Dabigatran) or Andexanet Alfa (for Factor Xa inhibitors) should be used (21). Platelet transfusion is not recommended for patients on antiplatelet agents (21).
Surgical Intervention: Surgery is generally reserved for specific situations. Surgical evacuation is a life-saving intervention for patients with cerebellar haematomas >3cm causing brainstem compression or hydrocephalus (20). For most supratentorial (lobar or deep) haemorrhages, the benefit of routine surgery is not established (20).
Aneurysmal Subarachnoid Haemorrhage (SAH): The priority is to secure the ruptured aneurysm to prevent re-bleeding, preferably within 24 hours via endovascular coiling or neurosurgical clipping (22). All patients with aSAH should receive oral Nimodipine to prevent delayed cerebral ischaemia from vasospasm (22).
Supportive & Symptomatic Care
Maintain normoglycaemia (target range 6-10 mmol/L) with an insulin sliding scale if needed (1).
Maintain normothermia with antipyretics (e.g., Paracetamol 1g QID) as fever can worsen neurological injury.
Provide adequate analgesia for pain.
Initiate DVT prophylaxis with intermittent pneumatic compression devices. Pharmacological prophylaxis (e.g., heparin) should be delayed for at least 24 hours post-thrombolysis in AIS and is often contraindicated in acute ICH.
A formal swallow assessment is mandatory before any oral intake to prevent aspiration pneumonia. Keep the patient nil-by-mouth (NBM) until this is done (1).
Key Nursing & Monitoring Instructions
Admit to a dedicated Stroke Unit/HDU/ICU for close monitoring.
Strict hourly neurological observations (GCS, pupil size and reactivity, limb power) for the first 24 hours.
Continuous cardiac and haemodynamic monitoring.
Maintain a strict fluid balance chart, monitoring input and output.
Inform medical staff immediately if there is a drop in GCS by ≥2 points, development of new neurological signs, SBP >185 mmHg or <110 mmHg, or urine output <0.5mL/kg/hr.
Long-Term Plan & Patient Education
Initiate early multidisciplinary rehabilitation involving physiotherapy, occupational therapy, and speech and language therapy.
Aggressively manage all vascular risk factors for secondary prevention. This includes long-term antiplatelet therapy (e.g., Aspirin plus Clopidogrel for a limited duration post-stroke, then monotherapy) for most ischaemic strokes, or anticoagulation for those with atrial fibrillation. High-intensity statin therapy is essential (1, 23).
Educate the patient and family on the nature of the stroke, recognizing warning signs of recurrence, medication adherence, and necessary lifestyle modifications (diet, exercise, smoking cessation).
When to Escalate
Call Your Senior (MO/Specialist) if:
The patient's GCS drops by 2 or more points, or they develop a new fixed, dilated pupil.
Blood pressure remains uncontrolled despite initial measures.
The patient has a seizure.
You suspect haemorrhagic transformation in an ischaemic stroke patient (e.g., severe headache, neurological worsening). This requires an urgent repeat CT brain.
Referral Criteria:
Refer to the Neurosurgery team urgently for any patient with haemorrhagic stroke with a GCS <9, evidence of hydrocephalus, or a cerebellar haematoma >3cm.
Refer to the Interventional Neuroradiology/Neurosurgery team immediately for any patient with AIS who is a potential candidate for mechanical thrombectomy.
Refer to Palliative Care for patients with devastating strokes where the goals of care need to be discussed with the family to focus on comfort and dignity.
References
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