Cerebral Stroke Clinical Overview
I. The "On-Call" Snapshot
Clinical Significance in Malaysia: Stroke is a principal cause of mortality and the leading cause of adult disability in Malaysia. You will see it frequently in the Emergency Department and on the wards.
High-Yield Definition: An acute episode of focal neurological dysfunction resulting from cerebral infarction or hemorrhage, with symptoms lasting more than 24 hours or leading to an earlier death.
Clinical One-Liner: This is a "brain attack." A blood vessel is either blocked (ischemic) or has burst (hemorrhagic), causing brain tissue to die.
II. Etiology & Risk Factors
Etiology:
Ischemic Stroke (~85%): Caused by occlusion of a cerebral artery.
Thrombotic: A clot forms locally on an atherosclerotic plaque.
Embolic: A clot travels from a distant source (e.g., heart in Atrial Fibrillation, carotid artery).
Lacunar: Occlusion of small, deep perforating arteries.
Hemorrhagic Stroke (~15%): Caused by rupture of a blood vessel.
Intracerebral Hemorrhage (ICH): Bleeding within the brain parenchyma, most commonly due to hypertension.
Subarachnoid Hemorrhage (SAH): Bleeding into the subarachnoid space, often from a ruptured aneurysm.
Risk Factors (Malaysian Context):
Non-Modifiable:
Age (>60 years)
Male gender
Family history of stroke
Modifiable:
Hypertension (Most important)
Diabetes Mellitus
Dyslipidemia
Smoking
Atrial Fibrillation
Obesity & Sedentary lifestyle
III. Quick Pathophysiology
Ischemic: Vessel occlusion stops blood flow. The core brain tissue dies within minutes (infarct). Surrounding this is the ischemic penumbra—tissue that is dysfunctional but still viable. Our goal in hyperacute management is to restore blood flow to save the penumbra.
Hemorrhagic: Leaking blood causes direct tissue damage and increases intracranial pressure (ICP), leading to reduced cerebral perfusion and secondary ischemic injury.
IV. Clinical Assessment
Red Flags & Immediate Actions:
Reduced GCS (<9) or Poor Airway Patency: Alert senior/anaesthetist, prepare for intubation.
Signs of Raised ICP/Herniation (Cushing's triad, unilateral dilated pupil): Alert Neurosurgery, elevate head of bed to 30°, consider IV Mannitol after discussion.
Systolic BP >185 mmHg or Diastolic BP >110 mmHg in a potential thrombolysis candidate: Alert senior, start IV Labetalol or GTN infusion to cautiously lower BP.
History:
CRUCIAL: Exact time of onset or last seen well. This determines eligibility for thrombolysis.
Common symptoms: Unilateral weakness (hemiparesis), facial droop, slurred speech (dysarthria), inability to speak or understand (dysphasia/aphasia).
Less Common symptoms: Vertigo, ataxia (coordination issues), visual field defects (hemianopia).
Pertinent Negatives: Ask about recent head trauma, fever (to rule out meningitis/encephalitis), history of seizures, and palpitations.
Physical Examination:
NIHSS (National Institutes of Health Stroke Scale): Perform this immediately. It is the standard tool to quantify the deficit.
General: Check for neck stiffness (SAH), signs of endocarditis, or carotid bruit.
Neurological:
GCS and conscious level.
Cranial nerves (especially facial asymmetry, gaze palsy, visual fields).
Motor system (power, tone, reflexes - look for unilateral signs).
Sensation.
Cerebellar signs (dysdiadochokinesia, finger-nose test).
Cardiovascular: Check for an irregularly irregular pulse (Atrial Fibrillation), murmurs.
Clinical Pearl: Always, always check the capillary blood glucose (CBG). Hypoglycemia is the great stroke mimic and is easily reversible.
V. Diagnostic Workflow
Differential Diagnosis:
Hypoglycemia:
Points For: Focal neurological deficit, altered mental status.
Points Against: Sweating, tremors may be present.
How to Differentiate: CBG.
Seizure (Todd's Paresis):
Points For: Post-event focal weakness.
Points Against: History of tonic-clonic movements, tongue biting, incontinence.
How to Differentiate: History from witness; weakness typically resolves within 48 hours.
Brain Tumour:
Points For: Focal neurological deficit.
Points Against: Symptoms are usually gradual and progressive over weeks to months.
How to Differentiate: CT/MRI Brain.
Investigations Plan:
Bedside / Initial (First 15 Mins):
CBG: To rule out hypoglycemia.
ECG: To look for Atrial Fibrillation, or evidence of recent MI.
Vital Signs: BP, HR, SpO2, Temperature.
First-Line Labs & Imaging:
URGENT Non-Contrast CT Brain (NCCT): The single most important initial investigation. The purpose is to rule out hemorrhage, not to confirm ischemia (acute infarcts may not be visible initially).
Bloods: FBC, Renal Profile, Coagulation Screen (PT/APTT/INR), Group & Screen.
Confirmatory / Gold Standard:
CT Angiogram (CTA) / MR Angiogram (MRA): To identify large vessel occlusion (LVO) for potential mechanical thrombectomy.
MRI Brain with Diffusion-Weighted Imaging (DWI): Gold standard for diagnosing an acute ischemic infarct, but slower and less available in the hyperacute setting.
VI. Staging & Severity Assessment
NIHSS Score: Used to quantify stroke severity and guide treatment.
0: No stroke symptoms.
1-4: Minor stroke.
5-15: Moderate stroke.
16-20: Moderate to severe stroke.
21-42: Severe stroke.
Bamford (Oxford) Classification: Classifies stroke based on clinical signs to predict the location and extent of infarction.
TACS (Total Anterior Circulation Stroke): All 3 of: Unilateral weakness, homonymous hemianopia, and higher cortical dysfunction (e.g., dysphasia).
PACS (Partial Anterior Circulation Stroke): 2 of the 3 components of TACS.
LACS (Lacunar Stroke): Pure motor, pure sensory, or sensorimotor deficit with no cortical signs.
POCS (Posterior Circulation Stroke): Signs related to brainstem/cerebellar dysfunction (e.g., vertigo, ataxia, isolated hemianopia).
VII. Management Plan
Immediate Stabilisation (The ABCDE Plan):
Airway: Ensure patency. Nurse patient upright if conscious. Consider NGT if dysphagic.
Breathing: Administer oxygen only if SpO2 <95%.
Circulation: Secure IV access.
BP Management:
Ischemic Stroke (Thrombolysis Candidate): Cautiously lower BP to <185/110 mmHg using IV Labetalol.
Ischemic Stroke (Not for Thrombolysis): Permissive hypertension is allowed (do not treat unless BP >220/120 mmHg) to maintain cerebral perfusion.
Hemorrhagic Stroke: Aim for SBP <140 mmHg.
Disability: Monitor GCS, avoid hypoglycemia.
Exposure: Keep nil by mouth (NBM) until swallow assessment. Control fever (>37.5°C) with Paracetamol.
Definitive Treatment (The Ward Round Plan):
Ischemic Stroke:
IV Thrombolysis: If patient presents within 4.5 hours of onset, has no contraindications, and NCCT shows no hemorrhage.
IV Alteplase (Actilyse): 0.9 mg/kg (max 90mg). 10% as a bolus, the rest infused over 1 hour.
Mechanical Thrombectomy: For LVO in the anterior circulation. Can be done up to 24 hours from onset in selected patients. Only available in specialised stroke centres.
Antiplatelets: Start Aspirin 300mg OD stat (after 24 hours if thrombolysed, once bleed is excluded). Continue for 2 weeks, then switch to secondary prevention.
Hemorrhagic Stroke:
Mainly supportive.
Strict BP control.
Neurosurgical referral for consideration of hematoma evacuation.
Reverse any coagulopathy (e.g., Vitamin K for warfarin).
Long-Term & Discharge Plan:
Secondary Prevention:
Antiplatelet: Clopidogrel 75mg OD or Aspirin 100mg OD + Dipyridamole 200mg BD.
Statin: Atorvastatin 40-80mg ON, regardless of cholesterol level.
Anticoagulation (e.g., Warfarin, DOACs) if stroke is due to Atrial Fibrillation.
Aggressive management of risk factors (BP, glucose control).
Rehabilitation: Crucial. Refer to Physiotherapy, Occupational Therapy, and Speech Therapy.
VIII. Complications
Immediate (first 24-48 hours):
Hemorrhagic Transformation: Ischemic stroke converts to a bleed, especially post-thrombolysis. Management: Stop antiplatelets, urgent NCCT, neurosurgical consult.
Cerebral Edema: Can cause raised ICP and herniation. Management: IV Mannitol/hypertonic saline, neurosurgical consult.
Short-Term (days to weeks):
Aspiration Pneumonia: Due to dysphagia. Management: NBM, speech therapy review, antibiotics.
DVT/PE: Due to immobility. Management: Prophylactic LMWH (e.g., Clexane), TED stockings.
Long-Term (months to years):
Spasticity & Contractures. Management: Physiotherapy, Botulinum toxin in severe cases.
Post-stroke Depression. Management: Screening, psychological support, SSRIs.
Vascular Dementia.
IX. Prognosis
Prognosis is highly variable and depends on stroke severity, location, and patient age/comorbidities.
Mortality at 30 days is approximately 10-15% for ischemic stroke and 30-40% for intracerebral hemorrhage.
Top 3 Prognostic Factors:
Initial NIHSS score: The single best predictor of outcome.
Age.
Time to reperfusion therapy.
X. How to Present to Your Senior
"Dr., for review please. This is Mr. Lim in the Red Zone, a 65-year-old man with a background of hypertension and diabetes, who presented with right-sided weakness and slurred speech. His wife states the symptoms started at 8 AM this morning, about 2 hours ago. On examination, his GCS is 15, BP is 190/100, and he has a right facial droop with a power of 3/5 in the right arm and leg. His NIHSS is 9. My main differential is an acute ischemic stroke. I have sent off the stroke workup bloods, done an ECG which shows sinus rhythm, and the porter is on the way to send him for an urgent NCCT Brain. As he is within the thrombolysis window, I would like to ask about prepping for Alteplase pending the CT result."
XI. Summary & Further Reading
Top 3 Takeaways:
Time is Brain: Act with urgency. The clock starts from when the patient was last seen well.
First, Do No Harm: The immediate purpose of the NCCT is to exclude a bleed before giving any antiplatelets or thrombolytics.
Rule out Mimics: Always check a CBG.
Key Resources:
Malaysian CPG: Clinical Practice Guidelines on the Management of Ischaemic Stroke 2020 (3rd Edition)
Landmark Trial: The original NINDS rt-PA Stroke Study (foundational for thrombolysis).
