Makindo Medical Notes

Related Subjects: |Acute Stroke Assessment (ROSIER/NIHSS) |Atrial Fibrillation |Atrial Myxoma |Causes of Stroke |Ischaemic Stroke |Cancer and Stroke |Cardioembolic stroke |CT Basics for Stroke |Endocarditis and Stroke |Haemorrhagic Stroke |Stroke Thrombolysis |Hyperacute Stroke Care |Hypertension |Thrombophilia testing |Cerebral Venous Sinus thrombosis |Small Vessel Disease |CADASIL |CARASIL

About

• Sudden onset of focal neurological symptoms and signs
• Related to reduced blood flow supplying an area of the brain
• Focal brain ischaemia and infarction
• 80% of Strokes are Ischaemic

Definitions

• Stroke (WHO): A neurological deficit of presumed vascular origin that persists beyond 24 hours or is interrupted by death within 24 hours. It includes brain, retinal and spinal cord ischaemia.
• New imaging-based definitions are based on any CT or MRI/DWI signs of infarction.

Dense R MCA

Dense L MCA + ACA infarction with oedema

Trial of Org 10172 in Acute Stroke Treatment (TOAST)

• large-artery atherosclerosis
• cardioembolism
• small-vessel occlusion
• stroke of other determined aetiology
• stroke of undetermined aetiology

Anatomy of strokes

Vascular Territories

Aetiology

Causes

• Large Arterial Thrombosis - usually arterial in situ due to atherosclerosis. Cause large vessel syndromes MCA/ACA/PCA
  • Embolism (recurrent areas different territory) 30% of strokes
    • Aortic or mitral valve endocarditis
    • LV apex post STEMI
    • Atrial fibrillation from LA appendage
    • Mitral stenosis and rheumatic heart disease
    • Atrial myxoma (raised ESR)
    • Paradoxical calf/thigh/pelvic DVT via PFO)
    • Aortic arch plaque
    • Carotid/vertebral artery dissection
  • In situ thrombosis and occlusion of vessels (recurrent areas same territory)
    • Atherosclerosis within Internal carotid artery especially at its bifurcation. Into large intracranial vessels.
    • Same is seen in the vertebral artery and basilar artery.
    • Progressive increase in plaque size and obstruction, plaque rupture and thrombosis or even distal embolisation of thrombus and debris.
    • Progressive stenosis comes on gradually over time there is a chance of development of collaterals making subsequent occlusion much less severe.
• Small deep artery occlusion by lipohyalinosis causing lacunar strokes. 40%
  • Small ischaemic strokes affect the thalamus, internal capsule and basal ganglia and pons
  • Same aetiology and distribution as hypertensive bleeds
  • They are less than 15 mm in size
  • Obstruction of the lenticulostriate end arteries and other deep penetrating arteries
    • Pure motor (posterior limb of internal capsule)
    • Pure sensory (thalamus)
    • Sensorimotor (thalamus and posterior limb of internal capsule)
    • Ataxic (variable)
    • Dysarthria and Clumsy hand (pontine)
    • Eventual subcortical vascular encephalopathy.
• Venous thrombosis - thrombosis of cerebral veins/sinuses leads to venous infarction often with some secondary bleeding
• Low flow - hypotension, shock, perioperative usually gives a watershed type infarction between arterial territories
• Cryptogenic - in some cases no definitive cause can be found

List of General Causes

• Atherosclerosis - age, hypertension, diabetes, hyperlipidemia, smoking
• Dissection - hypertension, trauma, connective tissue disease, fibromuscular dysplasia
• Vasculitis - Temporal arteritis, Polyarteritis nodosa, Behcet's
• Arterial spasm - Migraine, Subarachnoid haemorrhage
• Embolic - AF, Endocarditis, Valve disease, atrial myxoma, PFO, ventricular dysfunction post-MI and mural thrombus
• Thrombophilia - Prothrombin, Factor V Leiden, Protein C and S def, Malignancy, Oestrogens, Antiphospholipid syndrome, Hyperviscosity

Clinical

• Middle cerebral artery: Contralateral Hemiplegia affecting face and arm with relative sparing of the leg. Contralateral Hemisensory loss and a homonymous hemianopia. Aphasia if dominant side affected. Dyspraxia if non dominant.
• Anterior cerebral artery: Hemiplegia affecting leg more than face and arm. Gait disturbance. Urinary Incontinence. Primitive reflexes.
• Vertebral and basilar: Ipsilateral cranial nerve palsies and contralateral hemiplegia and sensory deficits. Horner's syndrome.
• Lacunar strokes: Pure motor, pure sensory, dysarthria + clumsy hand, ataxic hemiplegia

Investigations (see Imaging topic)

• FBC/ESR/U&E/LFT/Glucose/Lipids
• ESR and CRP: Raised usually suggest infection but also consider Vasculitis
• ECG - primarily to find AF or recent MI/LVH/Cardiomyopathy but should not delay thrombolysis
• CXR but should not delay thrombolysis
• Non-contrast CT head: must be done immediately. The main aim is to exclude a haemorrhagic stroke and any other haemorrhage (>99% sensitive). A normal CT is compatible with a very early acute ischaemic stroke. Classical very stroke signs include
  • Dense MCA or other artery that matches clinical syndrome
  • Loss of insular ribbon signs
  • loss of grey-white matter differentiation
  • Hypoattenuation of deep nuclei: lentiform nucleus changes are seen
  • Cortical hypodensity with associated parenchymal swelling with resultant gyral effacement.
• MRI scan is very useful and the Diffusion-weighted imaging will show up acute infarction very early. However, imaging slots are more limited and the scans can take longer than CT and more expensive however it gives a more accurate diagnosis and would often use if available and significant uncertainty especially when thrombolysis decisions.
• Day Two consider only after senior advice and not routine
  • Carotid Duplex: if mild and non-disabling stroke and fit candidate for surgery which would be an endarterectomy
  • 24 hr tape - done in most patients where PAF suspected e.g. cardioembolic strokes in different sides and both anterior and posterior circulations.
  • Echocardiogram to assess LV and LA and look for thrombus or source of emboli. Occasionally done early when endocarditis is a concern. Usually indicated age < 50 and cardioembolic source suspected,
  • Vasculitis/Thrombophilia screen should only be done when there are clear indications and this is a senior decision. Thrombophilia screen in those < 45 with h/o Venous/arterial thrombosis or Family history
  • MRI/MRA/MRV where diagnosis or location or extent of stroke in doubt or to look at vasculature for dissection or occlusion or vasculitic changes
  • Troponin - ACS or myocarditis suspected
  • Vasculitis screen
  • Sickle test if sickle cell suspected
  • LP - CSF pressure, protein, cells, lactate (MELAS)
  • Bubble echo +/- Trans oesophageal echo for PFO
  • Skin biopsy for CADASIL
  • Screen for Fabry's disease

Classical MRI appearances

Management

• Stroke Thrombolysis assesses that overall benefits likely exceed risks
  • Known onset and still within 3 hours (some treat up to 4.5 hrs if younger < 80)
  • GCS > 9 and functionally well and independent
  • Other pathology excluded by history and CT imaging
    • Hypoglycaemia
    • Post seizure
    • Migraine
    • Functional
    • SDH or SOL
    • Old stroke exacerbated by illness
  • NIHSS is between 4 and 25
  • Contraindications
    • BP > 185/110 mmHg ( lower with labetalol IV)
    • CT changes that suggest non stroke or late stroke
      • Hypodensity or sulcal effacement in >1/3 of MCA territory
      • Evidence of Haemorrhage, tumour , abscess or developed stroke
      • Evidence of Arteriovenous Malformation or Aneurysm
      • Major early infarct signs on a CT scan (substantial oedema, mass effect or midline shift)
• Stroke Unit: Admission to a stroke unit is fundamental and key for improving outcomes. Evidence-based to reduce mortality
• Hemicraniectomy: For those with Malignant MCA syndromes and under 60 years old. This is seen when cerebral oedema is at its maximal in the first 2-3 days post-infarct. The overlying skull can be removed and allows the brain to expand without causing large rises in ICP. This can be life-saving and may be considered in patients. Later the skull can be replaced or a titanium plate placed over the defect.
• Antiplatelet: Acutely Aspirin 300 mg stat (US ASA 325 mg) po/pr and x 2 weeks or load with Clopidogrel and then Clopidogrel 75 mg od (1st line therapy). Aspirin 75 mg and Dipyridamole 200 mg bd long term if unable to take Clopidogrel. Aspirin 75 mg alone if cannot take Dipyridamole. Dipyridamole 200 mg bd if unable to take Aspirin or Clopidogrel. There is no indication for Aspirin and Clopidogrel except in rare selected cases
• Hypertension: If hypertensive it is usual to start after 1 week unless severe HTN before then i.e BP > 200/100 mmHg and if so then Slow-release Nifedipine via NG or PO may be given. Long term commence thiazide + ACE inhibitor e.g. Bendroflumethiazide 2.5 mg od/ Ramipril 1.25 mg od
• Cholesterol management: Atorvastatin started after 48 hours if new else continue if already on statin
• Atrial Fibrillation: Consider Warfarin or a DOAC usually started anywhere from 3 days with a small stroke to 7-14 days for large volume strokes depending on the risk of haemorrhagic transformation
  • Transient ischaemic attack (TIA) after 1 day
  • Small, non-disabling infarct after 3 days
  • Moderate stroke after 6 days
  • Large infarcts involving large parts of the arterial territory will be treated not before 2 (or even 3) weeks.
• Blood glucose: Maintain Blood glucose between 4-11.0 mmol/l. Use a sliding scale and convert to regular Insulin asap. Avoid hypoglycaemia in comatose patients
• Supplemental oxygen therapy: Supplemental oxygen should only be given if oxygen saturation drops below 95%. The routine use of supplemental oxygen is not recommended in people with acute stroke who are not hypoxic. Pulmonary disease should be taken into account and a sensible target oxygen saturation should be documented. Consider starting at 2-4 L/min 28% oxygen by nasal cannula or mask and adjust according to O₂ saturations and blood gases if remains hypoxic
• Fluids/Nutrition: Bedside swallow assessment and if normal then allow normal intake. If nil orally starts IV fluids preferably N-Saline 2-3 L/day initially. If swallow remains poor then start NG feeding if indicated after assessment at 24-48 hrs. Do not place NG immediately unless vital oral meds are required e.g. Sinemet etc.
• VTE prophylaxis:
  • Intermittent calf compression is 1st line for 28 days in those who are immobile
  • VTE dose prophylactic dose LMWH may be considered after ischaemic stroke
• Carotid endarterectomy in patients with mild non disabling strokes and symptomatic carotid disease with > 70% stenosis
• Rehabilitation either inpatient or now more emphasis to early supported discharge can be very useful.