The key issue in stroke management is to reverse the ischaemia of tissue in the ‘mismatch penumbra’.
Stroke is defined as a rapid onset, focal neurological deficit due to a vascular lesion lasting >24 hours. (Cause: 80% Ischaemic + 20% Haemorrhagic). 90% of strokes can be explained by modifiable risk factors – HTN (#1), A.Fib, Dyslipidaemia, Diabetes, Smoking, Alcohol Use, Poor Diet, Obesity and Inactivity.
Recognizing the type of stroke
Clinically the type of stroke is defined based on the clinical localisation of the infarct. The OXFORD/BAMFORD classification is used for this purpose.
S = Syndrome (Prior to Imaging), I = Infarct (After imaging when infarct confirmed)
1. TACI (Total Anterior Circulation Infarct) – MCA/ACA – 60% mortality
All three symptoms of hemiparesis/sensory deficit + homonymous hemianopia + higher cortical dysfunction (dysphasia/hemineglect)
2. PACI (Partial Anterior Circulation Infarct) – MCA/ACA – 20% mortality
Two of three symptoms incl. hemiparesis/sensory deficit + homonymous hemianopia + higher cortical dysfunction (dysphasia/hemineglect) – usually less severe
3. POCI (Posterior Circulation Infarct) – Vertebrobasilar Territory
Any of the following 3:
- a) Cerebellar Syndrome
- b) Brainstem syndrome
- c) Contralateral homonymous hemianopia
4. LACI (Lacunar Infarct) – Small infarcts around internal capsule, thalamus, pons and BG
- Pure motor – Posterior Int. Capsule
- Pure sensory – VPL of Post. Thalamus
- Mixed sensorimotor – Int. Capsule
- Dysarthria/Clumsy Hand syndrome – Ant. Int Capsule
- Ataxic Hemiparesis – Ant. Int Capsule
As with our management of previous conditions, inital assessment of the patient should involve your ABC MOVE approach. Time is brain is the prevailing motto in stroke care – with a ‘door to needle’ target of 60 minutes ideally for best outcomes.
1. Airway, Breathing, Circulation, Monitoring, Oxygen, Venous access, Examine/ECG
2. Check blood pressure, glucose, neuro observations and take a focused history and clinical examination
3. Focused History + Brief CNS Exam (Speech, Facial weakness, Limb Motor function, Limb Sensory function, UL/LL Tone, UL/LL Power, Reflexes) + Contact Stroke Team
- Time of symptom onset/Time last well?
- Contraindications to tPA?
- Was this a ‘Wake Up Stroke‘? (there is lack of a high-level evidence to support acute treatment in the setting of patients who wake up with neurological symptoms after going to sleep asymptomatic)
- Assess Stroke differentials – Head injury/Fall, Hypoglycaemia, Opiate OD, Infections, Post-SeizureSignificant medical history
- NIH Stroke Scale (ask nurses to print it out while assessing the patient)
4. Bloods: FBC/ U+E/Coag/Glucose(POC)/Group+Hold/Troponin
5. Order an urgent non-contrast CT brain – Remember, the CT brain is to rule out a bleed, not to assess for an ischaemic stroke – as no imaging changes may be apparant in the early stages.
6. Rule out anti-tPA (tissue Plasminogen Activator) contraindications (Calculator)
- >4.5 hours from onset
- HTN > 185/110
- Seizure at stroke onset
- Hx of haemorrhage/AVM/recent stroke
- Haemorrhage on CTB
- Recent neurosurgery/head trauma
- Known bleeding diathesis (if patient not on Warfarin/LMWH etc there is no need to wait for platelet levels/INR)
- Very low/Very high blood glucose
- Relative contraindications include: Minor stroke/Rapidly improving stroke/Pregnancy/Recent major surgery/Recent LP
- Extra criteria if time 3 – 4.5 hours from stroke onset:>80yrs, Diabetes, Warfarin, NIHSS >25
7. Mix IV tPA (Alteplase 0.9mg/kg – mixed 1:1 with normal saline) – in an ideal situation the tPA should be brought to the patients bedside immediately post CT Brain and administered there and then following radiological assessment of haemorrhage.
8. Monitor the patient for decreased GCS/Angioedema/Haemorrhagic transformation – early transferral to a stroke unit should be advised.
At this stage the acute phase has been appropriately managed and secondary prevention begins.
Secondary (Post tPA) Management
- Transfer to Stroke Unit/Stepdown Unit
- Nil per mouth until swallow assessed
- IV fluids
- Regular Blood pressure + Neurological Observations – Every 15 mins x 2 hrs, then 30 mins x 6 hrs, then 60 mins x 16 hours.
- Treat hyperglycaemia if present (assoc. w/ poor outcomes) – Target <12mmol/L – do no drop glucose too low in first 2-3 days post stroke
- Treat BP aggressively if >180/110 – other wise do not drop BP too early, blood pressure will run relatively high for 5-7 days post stroke. (PRoFESS trial – BP < 120/80 post stroke is assoc w/ poorer outcomes)
- Repeat CT Brain at 24 hours
- Ultrasound of carotids (Stenosis) after 24 – 48 hours & Transthoracic U.S (LVH)
- Begin anti-platelet therapy w/ Aspirin 300mg & Clopidogrel 300mg (CHANCE trial)
- Alter modifiable risk factors (Statin, Glucose control, Smoking cessation etc.)
- Treat Atrial Fibrillation if present
- Perform emergent CT brain if any acute decrease in GCS, Acute HTN episode or sudden onset nausea/vomiting – in order to rule out haemorrhagic transformation
- DVT prophylaxis when appropriate
- MDT assessment approach + Neurorehabilition
Remember: 80% of stroke recurrence can be prevented with optimal medical managment – of which hypertension is by far #1
Note: This post focuses on ischaemic stroke and the authors wish to acknowledge that many other novel treatments for acute stroke exists – including intra-arterial administration of thrombolytics, radiological removal of large emboli/thrombi, coiling of bleeding aneurysms and emergent neurosurgical hemicraniectomy for some forms of large MCA infarctions. Furthermore, there is much debate currently regarding the benefit of thrombolysis and on the justification of extending tPA use to >4.5 hours. However, this post is designed to give a good management skeleton for the most common type of stroke.
Last Updated (August 2016)