After reading this note you will be able to describe the clinical approach to a patient with stroke, list the locally relevant aetiologies, interpret the key investigations and outline immediate and definitive management – remembering to verify doses and local protocols against the Kenya MoH guideline and your hospital formulary.
Definition
- Ischaemic stroke – sudden neurological deficit lasting >24 h (or until death) caused by an acute interruption of cerebral blood flow due to arterial occlusion.
- Haemorrhagic stroke – sudden neurological deficit caused by intracerebral bleeding (parenchymal haemorrhage) or subarachnoid haemorrhage (SAH) from rupture of a vessel.
Anatomy and physiology you need
| Structure | Relevance to stroke |
|---|---|
| Middle cerebral artery (MCA) | Most common site of large‑vessel ischaemia; produces contralateral face‑arm‑leg weakness and aphasia (dominant side). |
| Internal carotid artery (ICA) | Proximal source of emboli; carotid stenosis is a major preventable cause. |
| Basilar artery | Posterior circulation strokes give brain‑stem signs, cranial nerve palsies, and “locked‑in” syndrome. |
| Lenticulostriate arteries | Small‑penetrating vessels; occlusion → lacunar infarcts with pure motor or sensory deficits. |
| Cerebral autoregulation | Maintains perfusion between MAP 50‑150 mmHg; failure predisposes to both ischaemia and haemorrhage. |
| Blood‑brain barrier | Disruption after ischaemia leads to oedema; rupture leads to haemorrhage. |
Causes and risk factors
| Category | Ischaemic | Haemorrhagic |
|---|---|---|
| Atherosclerotic disease | ICA/MCA stenosis, plaque rupture | Small‑vessel lipohyalinosis → deep intracerebral bleed |
| Cardio‑embolism | Atrial fibrillation, rheumatic mitral stenosis, ventricular thrombus | Rare, but can cause lobar bleed after embolic infarct conversion |
| Small‑vessel disease | Hypertension, diabetes, smoking | Chronic hypertension → Charcot‑Bouchard micro‑aneurysms |
| Infectious / tropical | HIV‑associated vasculitis, TB meningitis vasculopathy, malaria cerebral sequestration | TB meningitis → basal SAH, HIV‑related vasculitis → bleed |
| Haematological | Sickle cell disease (vaso‑occlusion) | Sickle cell crisis → intracerebral bleed, especially in children |
| Coagulopathy | Anticoagulant use, liver disease | Warfarin/DOAC excess, severe thrombocytopenia, vitamin K deficiency |
| Lifestyle | Obesity, physical inactivity, alcohol excess | Alcohol binge → hypertension spikes, aneurysm rupture |
| Age / sex | >55 yr, male predominance | Similar age, slight female preponderance for SAH |
Pathophysiology
Ischaemic stroke
Atherosclerotic plaque → thrombus formation → arterial occlusion → ↓ cerebral perfusion → neuronal energy failure → excitotoxic glutamate release → calcium influx → cell death → infarct core + penumbra (ischemic but salvageable).
Haemorrhagic stroke
Chronic hypertension → lipohyalinosis → micro‑aneurysm formation → rupture → extravasation of blood → mass effect + toxic blood products → peri‑haematomal oedema → increased intracranial pressure → herniation if untreated.
Subarachnoid haemorrhage
Berry aneurysm wall weakness → rupture → blood in subarachnoid space → meningeal irritation → vasospasm (days 3‑14) → delayed cerebral ischemia.
The above arrows illustrate the cascade from risk factor to clinical event.
Clinical features
History – what to ask
| Domain | Key questions | Rationale |
|---|---|---|
| Onset | “When did the symptoms start? Sudden or progressive?” | Sudden maximal deficit → arterial occlusion; step‑wise or delayed onset → hemorrhage or evolving infarct. |
| Time course | “Did the symptoms reach a peak within 1 hour? Any fluctuation?” | Determines eligibility for reperfusion therapy and helps differentiate transient ischemic attack from completed stroke. |
| Symptom type | “Weakness, numbness, speech difficulty, visual loss, facial droop, gait imbalance, headache, vomiting, loss of consciousness?” | Focal cortical signs → ischemic infarct; severe headache, vomiting, decreased consciousness → intracerebral bleed or subarachnoid bleed. |
| Laterality | “Which side of the body is affected? Any facial involvement?” | Contralateral motor/sensory signs point to supratentorial lesion; brain‑stem lesions give ipsilateral cranial nerve findings. |
| Speech & cognition | “Any trouble speaking, understanding, reading, writing?” | Dysphasia (dominant‑hemisphere cortical stroke) vs. dysarthria (brain‑stem or basal ganglia). |
| Visual field | “Any loss of vision in one or both eyes?” | Homonymous hemianopia → occipital or optic radiations infarct; cortical blindness → posterior circulation. |
| Pre‑stroke functional status | “What was your usual activity level? Any recent falls?” | Baseline helps gauge severity and plan rehabilitation. |
| Vascular risk profile | “History of hypertension, diabetes, dyslipidaemia, smoking, atrial fibrillation, prior stroke/TIA, coronary disease?” | Identifies modifiable risk factors; atrial fibrillation strongly suggests cardio‑embolic ischemia. |
| Infectious / tropical exposures | “HIV status, TB treatment, recent malaria, sickle‑cell disease, rheumatic fever?” | HIV‑associated vasculitis, TB meningitis with vasculopathy, malaria‑related cerebral sequestration, sickle‑cell vaso‑occlusion, rheumatic heart disease with embolic risk are relevant in Kenya. |
| Medications & substances | “Current drugs (anticoagulants, antiplatelets, antiretrovirals), alcohol, illicit drugs?” | Anticoagulant use influences hemorrhagic risk; certain antiretrovirals may affect lipid profile. |
| Recent procedures / trauma | “Any recent surgery, dental work, or head injury?” | Post‑procedural emboli or trauma‑related bleed. |
| Family history | “Stroke or early cardiovascular disease in relatives?” | Genetic predisposition to small‑vessel disease or hypercoagulable states. |
Examination – what to look for and why
| System | Findings | Pathophysiologic explanation |
|---|---|---|
| General | Level of consciousness (GCS), pupil size/reactivity, blood pressure, cardiac rhythm | Depressed consciousness suggests large hemispheric infarct, brain‑stem involvement, or raised intracranial pressure (ICP). Hypertension is common in acute stroke, especially hemorrhagic. |
| Cranial nerves | Facial droop (upper vs lower), tongue deviation, dysphagia, dysarthria, gaze palsy, visual field cuts | Upper‑face sparing indicates central lesion; gaze palsy points to brain‑stem or frontal eye field involvement; visual field defects map to occipital cortex or optic radiations. |
| Motor | Muscle strength (Medical Research Council scale), pronator drift, hemiparesis, hemiplegia, limb ataxia | Contralateral weakness reflects corticospinal tract interruption; ataxia suggests cerebellar or proprioceptive pathway involvement. |
| Sensory | Pinprick, temperature, vibration, proprioception, cortical sensory loss (stereognosis) | Cortical sensory loss is typical of parietal lobe infarct; diffuse loss suggests thalamic or brain‑stem lesion. |
| Coordination | Finger‑nose, heel‑shin, dysmetria, dysdiadochokinesia | Cerebellar infarcts or hemorrhage produce ipsilateral limb ataxia and gait instability. |
| Reflexes | Deep tendon reflexes, Babinski sign, clonus | Upper motor neuron signs (hyperreflexia, extensor plantar) confirm supratentorial corticospinal involvement. |
| Gait & balance | Ability to sit, stand, walk, Romberg test | Posterior circulation strokes often impair gait and balance; cerebellar lesions cause truncal ataxia. |
| Cardiovascular | Irregular pulse, murmurs (e.g., mitral stenosis), peripheral pulses | Irregular pulse → atrial fibrillation; murmurs suggest rheumatic valve disease as embolic source. |
| Skin | Rashes, petechiae, stigmata of HIV (oral thrush, Kaposi lesions) | May point to underlying infection or coagulopathy. |
Differential diagnosis
| Condition | Points toward it | Distinguishing features |
|---|---|---|
| Ischaemic stroke (large‑artery, cardio‑embolic, small‑vessel) | Sudden focal deficit, risk factors (HTN, AF, diabetes) | No severe headache, CT early may be normal, diffusion‑weighted MRI shows restricted diffusion. |
| Intracerebral haemorrhage | Sudden headache, vomiting, decreased consciousness, hypertension, anticoagulant use | CT shows hyperdense bleed, mass effect, rapid neurological decline. |
| Subarachnoid haemorrhage | Thunderclap headache, neck stiffness, photophobia | CT shows sulcal blood; lumbar puncture shows xanthochromia if CT negative. |
| Cerebral venous sinus thrombosis | Headache, seizures, papilledema, pro‑thrombotic states (HIV, pregnancy) | MR venography shows venous occlusion; often normal CT. |
| Brain tumour (acute presentation) | Progressive symptoms, seizures, constitutional signs | Imaging shows mass lesion with contrast enhancement; slower onset. |
| Infective encephalitis (e.g., cerebral malaria, TB meningitis) | Fever, altered mental status, focal deficits, exposure history | CSF pleocytosis, MRI may show meningeal enhancement; malaria smear positive. |
| Hypoglycaemia / metabolic encephalopathy | Altered consciousness, seizures, no focal deficit | Rapid reversal with glucose; labs abnormal. |
| Migraine with aura | Recurrent visual/sensory aura, headache, younger age | Symptoms develop gradually, resolve, no permanent deficit. |
Investigations
| Test | What it answers | Interpretation |
|---|---|---|
| Non‑contrast CT head (within 24 h) | Hemorrhage vs. early ischaemia, mass effect | Hyperdense area = bleed; hypodensity may indicate established infarct; normal CT does not exclude early ischemia. |
| MRI brain with diffusion‑weighted imaging | Tissue viability, infarct age | Restricted diffusion = acute infarct (minutes‑hours); FLAIR helps age lesion. |
| CT/MR angiography (head & neck) | Large‑vessel occlusion, stenosis, dissection | Absence of flow in MCA → occlusion; vertebral dissection shows intimal flap. |
| Carotid duplex ultrasound | Extracranial atherosclerotic disease | >70 % stenosis suggests surgical/endovascular intervention. |
| Echocardiography (transthoracic ± transesophageal) | Cardio‑embolic source (thrombus, valvular disease) | Left atrial thrombus, prosthetic valve vegetation, rheumatic mitral stenosis. |
| ECG & continuous cardiac monitoring | Atrial fibrillation, arrhythmias | Irregularly irregular rhythm confirms AF; paroxysmal episodes may need prolonged monitoring. |
| Full blood count, coagulation profile, electrolytes, renal & liver function | Baseline for therapy, identify anemia, coagulopathy, infection | INR >1.7 contraindicates thrombolysis; thrombocytopenia raises bleed risk. |
| Lipid profile, HbA1c | Chronic risk factor assessment | Dyslipidaemia or uncontrolled diabetes guide secondary prevention. |
| HIV test, CD4 count, viral load (if status unknown) | HIV‑related vasculopathy or opportunistic infection | Low CD4 may predispose to TB meningitis or cryptococcal disease. |
| Malaria rapid test / peripheral smear (if febrile) | Cerebral malaria | Parasitaemia >2 % supports malaria as a contributor. |
| Sickle‑cell screen (Hb electrophoresis) | Sickle‑cell disease | Positive result explains vaso‑occlusive stroke in young patients. |
| Lumbar puncture (if infection or SAH suspected) | CSF cell count, glucose, protein, cultures | Xanthochromia = SAH; lymphocytic pleocytosis = TB meningitis. |
Diagnosis and severity
- Establish stroke type – combine clinical timing, CT/MRI appearance, and laboratory data.
Ischaemic if no bleed on CT and diffusion restriction on MRI; haemorrhagic if hyperdense collection on CT or MRI susceptibility artefact.
- Classify ischaemic mechanism (TOAST criteria adapted):
- Large‑artery atherosclerosis (≥50 % stenosis on imaging)
- Cardio‑embolic (AF, cardiac thrombus, valvular disease)
- Small‑vessel (lacunar syndrome, normal angiography)
- Other determined (dissection, vasculitis, sickle‑cell)
- Undetermined (multiple possible causes).
- Assess severity – use bedside scales:
- NIH Stroke Scale (NIHSS) – quantifies neurological deficit; higher scores predict poorer outcome and guide reperfusion eligibility.
- Glasgow Coma Scale (GCS) – especially for haemorrhagic strokes; GCS ≤ 8 signals need for airway protection and possible neurosurgical intervention.
- Modified Rankin Scale (mRS) – baseline functional status for prognostication.
- Risk stratification for complications – large infarct volume, early neurological deterioration, uncontrolled hypertension, coagulopathy, or infection increase risk of cerebral oedema, hemorrhagic transformation, and pneumonia.
The clinician should document stroke type, presumed aetiology, NIHSS score, and any contraindications to acute therapies (thrombolysis, thrombectomy) before proceeding to definitive management.
Management
| Phase | Key actions | Rationale / safety notes |
|---|---|---|
| Immediate stabilisation | • Airway, breathing, oxygen (target SpO₂ ≥ 94 %); • Blood pressure control – lower SBP < 185 mmHg & DBP < 110 mmHg for thrombolysis, otherwise keep MAP ≥ 70 mmHg; • Rapid glucose check – treat hypoglycaemia < 3 mmol/L; • Position head 30°; • IV access, cardiac monitoring, urine output catheter. | Prevent hypoxia, hypotension and hyperglycaemia which worsen penumbra; avoid over‑rapid BP drop that can precipitate cerebral hypoperfusion. |
| Definitive treatment – Ischaemic stroke | • Assess eligibility for IV thrombolysis (within 4.5 h) – give recombinant tissue plasminogen activator; • If large‑vessel occlusion and within 6–24 h, arrange endovascular thrombectomy; • Initiate antiplatelet (aspirin) after imaging rules out haemorrhage; • Statin therapy (high‑intensity) for secondary prevention; • Manage atrial fibrillation – start oral anticoagulant after haemorrhage excluded. | Thrombolysis restores flow; thrombectomy for proximal MCA, ICA or basilar occlusions; antiplatelet reduces early recurrence; statins stabilise plaque; anticoagulation for cardio‑embolic sources. |
| Definitive treatment – Haemorrhagic stroke | • Reverse anticoagulation (vitamin K antagonists → vitamin K + PCC; DOACs → specific antidote if available); • Control BP aggressively to SBP < 140 mmHg (unless contraindicated); • Neurosurgical referral for lobar bleed > 30 mL, cerebellar bleed with brainstem compression, or hydrocephalus; • Osmotherapy (mannitol or hypertonic saline) for raised ICP; • Seizure prophylaxis only if seizures occur or high risk (e.g., cortical bleed). | Rapid reversal limits expansion; BP lowering reduces re‑bleeding; surgery evacuates mass effect; osmotherapy buys time; routine prophylaxis not recommended. |
| Monitoring | • Neurological checks (NIHSS or GCS) every 15 min for first hour, then hourly for 24 h; • Continuous cardiac rhythm; • Strict input‑output chart; • Repeat CT at 24 h or if deterioration; • Screen for dysphagia before oral intake. | Detect early neurological decline, arrhythmias, fluid overload, re‑bleed; dysphagia screening prevents aspiration pneumonia. |
| Safety & contraindications | • Thrombolysis contraindicated: intracranial haemorrhage, recent major surgery, uncontrolled hypertension, active bleeding, platelet < 100 × 10⁹/L; • Anticoagulation contraindicated in large haemorrhagic stroke, recent intracranial surgery; • Mannitol contraindicated in severe hypovolaemia or renal failure. | Avoid iatrogenic worsening. |
| Secondary prevention | • Lifestyle: smoking cessation, diet, exercise; • Blood pressure target < 130/80 mmHg; • Diabetes control (HbA1c < 7 %); • Lipid target LDL < 1.8 mmol/L; • Antiplatelet long‑term (aspirin) or anticoagulant for AF; • Vaccination (influenza, pneumococcal). | Reduces recurrent stroke risk. |
Complications and prognosis
- Early (first 48 h) – cerebral oedema, herniation, re‑bleeding (haemorrhagic), early seizures, aspiration pneumonia, deep‑vein thrombosis, cardiac arrhythmias.
- Late – post‑stroke epilepsy, spasticity, chronic pain, dysphagia with malnutrition, urinary incontinence, depression, cognitive impairment.
- Prognostic indicators – NIHSS score on admission, age, level of consciousness, lesion size/location, early recanalisation, presence of atrial fibrillation, uncontrolled hypertension.
- Outcome – Approximately one‑third die within the first month (higher in haemorrhagic). Survivors: 30 % achieve functional independence (mRS 0‑2) after ischaemic stroke; haemorrhagic stroke has lower independence rates. Early rehabilitation improves long‑term functional outcome.
High‑yield exam points
- Look‑alike conditions: hypoglycaemia, seizure with post‑ictal deficit, brain tumour, meningitis, conversion disorder.
- Commonest wrong first step: delaying neuro‑imaging; examiners expect CT head before any antithrombotic is given.
- Bedside examiner questions:
- “What is the target blood pressure for a patient you are considering for thrombolysis?”
- “Explain why you would give aspirin after a negative CT.”
- “How does a lobar haemorrhage differ from a deep basal ganglia bleed on CT?”
- “What are the contraindications to IV thrombolysis in this patient?”
- “Describe the steps you would take to assess dysphagia safely.”
Clinical case
Patient: 58‑year‑old man, known hypertensive and HIV‑positive (well‑controlled on ART), presents 2 h after sudden right‑sided weakness and aphasia. BP 190/110 mmHg, GCS 14, NIHSS 12. Non‑contrast CT shows left MCA territory hyper‑dense sign, no bleed.
Questions
- What is the immediate next step?
Answer: Assess eligibility and, if no contraindications, start IV thrombolysis with recombinant tissue plasminogen activator.
- How would you manage his blood pressure before thrombolysis?
Answer: Lower SBP to < 185 mmHg and DBP to < 110 mmHg using an IV antihypertensive (e.g., labetalol) while avoiding rapid drops that could compromise cerebral perfusion.
- What secondary prevention measures are indicated after acute management?
Answer: Initiate antiplatelet therapy (aspirin), start a high‑intensity statin, optimise blood pressure control, counsel on smoking cessation, and arrange cardiac monitoring for atrial fibrillation; continue ART and monitor for drug interactions.
Practice questions
Question 1
A 72‑year‑old woman is found unconscious with a left‑sided hemiplegia. CT shows a right basal ganglia haemorrhage measuring 35 mL with midline shift. What is the most appropriate next step?
A. Start IV thrombolysis
B. Give oral aspirin
C. Refer for emergent neurosurgical evacuation
D. Begin high‑dose steroids
Answer: C. emergent neurosurgical evacuation
Explanation: Large deep haemorrhage with mass effect warrants surgical decompression; thrombolysis and antiplatelets are contraindicated.
Question 2
A 45‑year‑old man with sickle cell disease presents with sudden left facial droop and weakness. CT is normal. Which investigation will most help to identify the cause?
A. Carotid Doppler ultrasound
B. Lumbar puncture
C. MRI brain with diffusion‑weighted imaging
D. Serum electrolytes
Answer: C. MRI brain with diffusion‑weighted imaging
Explanation: DWI MRI detects acute ischaemia when CT is negative, especially in young patients with atypical risk factors.
Question 3
A patient with acute ischaemic stroke is on warfarin with INR = 2.5. Which action is required before giving thrombolysis?
A. Give fresh frozen plasma
B. Administer vitamin K orally
C. Proceed – INR is acceptable
D. Reverse with prothrombin complex concentrate
Answer: D. reverse with prothrombin complex concentrate
Explanation: Therapeutic INR is a contraindication; rapid reversal with PCC (plus vitamin K) is needed before thrombolysis.
Question 4
Which of the following is a distinguishing feature of a posterior‑circulation stroke on examination?
A. Pure motor hemiparesis
B. Dysarthria‑clumsy hand syndrome
C. Vertigo, ataxia and diplopia
D. Aphasia
Answer: C. vertigo, ataxia and diplopia
Explanation: Brain‑stem/cerebellar signs point to posterior circulation involvement.
Question 5
A 60‑year‑old man with a recent ischaemic stroke develops a fever of 38.5 °C on day 3. Which complication should be high on the differential?
A. Deep‑vein thrombosis
B. Aspiration pneumonia
C. Post‑stroke seizure
D. Hemorrhagic transformation
Answer: B. aspiration pneumonia
Explanation: Dysphagia is common after stroke; early fever often signals aspiration pneumonia.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.