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Hospital Based Practice – Stroke.

• Result from ischemic infarction or bleeding into the brain.


• Manifest as.
○ Focal CNS signs and symptoms.
○ Onset over minutes.
• Major neurological disease of the 21st century.
○ 1.5/1000/year
○ 10/1000/year by age 75.
• Causes.
○ Thrombosis.
 In situ
 |Emboolising from heart.
• > 30% of strokes
• AF
○ Overall risk of 4.5% per year.
○ Often results in more severe forms of ischemic stroke
○ Warfarin reduces risk by 68%.
 Target INR of 2.5 – 3.5
○ Aspirin monotherapy is sufficient when there are no additional risk
factors.
 Advancing age
 Previous strokes/ TIA
 Hypertension
○ No benefit in giving aspirin with warfarin.
• Endocarditis
○ Prosthetic metal valves are major emboli risk.
○ Require INR of 3.5 – 4.5
• MI.
○ Changes to left ventricular mobility on echocardiogram
predisposed to left ventricular thrombus.
○ Emboli arise in 10% of these patients within 6 – 12 months.
○ Warfarin therapy reduces risk by two – thirds.
• Cardioversion.
○ Similar risk if external or pharmacological.
○ Complicated by emboli in 1 – 3%
• Anatomical abnormalities.
○ Causes paradoxical systemic emboli.
○ May cause reccurence if not repaired.
○ Patent foramen ovale
○ Atrial or ventricular septal defects.
• Cardiac surgery.
○ All heart surgery causes risk of stroke.
○ CABG has a particular risk.
 0.9 – 5.2%
○ Atherothromboembolism.
 Eg. From carotids.
○ Failure of cerebral autoregulation of blood flow.
 May explain association with
• Morning arousal
• Stress/ Activity
• Winter
• Rarer causes include.
○ Sudden drop in BP of > 40 mmHg
○ Vasculitis
○ Venous sinus thrombosis
○ In younger patients suspect.
 Thrombophilia
 Vasculitis
 Subarachnoid haemorrhage
 Venous – sinus thrombus
 Carotid artery dissection.
• Spontaneous
• Neck trauma
• Fibromuscular dysplasia.

• Risk factors.
○ Hypertension
○ Smoking
○ Diabetes
○ Heart disease.
 IHD
 Valvular disease
 AF
○ Peripheral vascular disease
○ Previous TIA
○ Raised packed cell volume
○ Caroid bruit
○ COCP
○ Raised lipids
○ Alcoholism
○ Increased clotting
 Raised plasma fibrinogen
 Lowered antithrombin III levels.

• Signs.
○ Sudden onset, or stepwise progression over days.
 Rarely can progress over days.
○ In theory, focal signs relate to distribution of affected artery.
 Can be complicated by collateral supply .

○ Cerebral hemisphere infarcts.


 50% of cases.
 Contralateral hemiplegia
 Initially flaccid, but progresses to spasticity.
 Contralateral sensory loss
 Homonymous hemianopia.
 Dysphagia
 Visuo – spatial defects.
○ Depends on site.
○ Brainstem infarcts.
 25% of cases.
 Wide range of affects.
• Quadriplegia
• Disturbed gaze and vision
• Locked – in syndrome.
○ Awareness, but unable to respond.
○ Lacunar infarcts.
 25% of cases.
 Small infarcts around
• Basal ganglia
• Internal capsule
• Thalamus
• Pons
 May cause symptoms that are.
• Pure motor
• Pure sensory
• Mixed motor and sensory.
• Ataxia
 Consciousness and cognition remains intact.

• Arterial territories.

• Carotid artery.
○ Internal carotid occlusion can cause total and fatal infarction of anterior two – thirds of:
 Ipsilateral hemisphere.
 Basal ganglia
○ Most commonly, picture is similar to that of middle cerebral infarction.
• Cerebral artery anatomy.
○ 3 pairs of arteries leave the circle of Willis.
○ Anterior and Middle cerebral arteries are branches of the carotid arteries.
○ Basilar artery splits to form the two posterior cerebral arteries.
○ Ischemia due to occlusion of arteries may be prevented or reduced by retrograde supply by
meningeal arteries.
• Anterior cerebral artery.
○ Supplies forntal and medial parts of cerebrum.
○ Occlusion may cause.
 Weak, numb contralateral leg
 Milder weak, numb contralateral arm.
 Facial sparing
 Bilateral infarction can cause a kinetic mutism.
• Due to damage to cingulated gyri
• Can also, rarely, cause paraplegia.
• Middle cerebral artery.
○ Supplies lateral (external) parts of the cerebral hemisphere
○ Occlusion may cause.
 Contralateral hemiplegia.
 Hemisensory loss.
• Mainly face and arm.
 Contralateral homonymos hemianopia
• Due to involvement of optic radiation.
 Cognitive change.
• Dysphagia if dominant hemisphere affected.
• Visuo – spatial disturbances if non – dominant hemisphere affected.
○ Inability to dress
○ Getting lost.
• Posterior cerebral artery.
○ Supplies occipital lobe.
○ Occlusion causes contralateral homonymous hemianopia.
 Often with macula sparing.
• Vertebrobasilar circulation.
○ Supplies.
 Cerebellum
 Brainstem
 Occipital lobes
○ Occlusion causes.
 Hemianopia
 Cortical blindness
 Diplopia
 Vertigo
 Nystagmus
 Hemi – or quadriplegia
 Unilateral or bilateral sensory symptoms.
 Hiccups
 Dysarthria
 Dysphagia
 Coma
○ Infarctions of the brainstem can produce various syndromes.
 Eg. Lateral medullary syndrome
• Occlusion of one vertebral artery or the posterior inferior cerebral artery.
• Due to infarction of lateral medulla and inferior cerebellar surface.
• Results in.
○ Vertigo with vomiting
○ Dysphagia
○ Nystagmus
○ Ipsilateral ataxia
○ Soft palate paralysis
○ Ipsilateral Horner’s syndrome
○ Crossed – pattern sensory loss.
 Analgesia to pin prick on ipsilateral face and contralateral
trunk and limbs.
• Subclavian steal.
○ If there is subclavian stenosis proximal to origin of vertebral artery, use of the arm may lead to
retrograde flow away from the brain into the arm, causing brainstem ischemia.
○ Suspect if BP in arms differs by > 20 mmHg.
• Arterial dissection
○ Disection of carotid or vertebral artery causes an acute ischemic stroke.
○ Usually occurs in younger patients.
○ May have preceding neck trauma
○ Need MRI or MR angiography.
○ Treat with antiplatelets and anticoagulants
○ Most patients will be part of a RCT.
• Cerebral Venous Thrombosis
○ Rare
○ More common in.
 Pregnancy.
 Local infection
 Dehydration
 Widespread malignancy.
○ Headaches and seizures are common.
○ Require
 MRI
 CT
 MR venography.
○ Management.
 Anticoagulation
• Heparin
• Warfarin.

• Oxford/ Bamford Classification of Strokes..


TACS Total Anterior Deficits in all three of: 25% Most likely to cause
Circulation death.
syndrome • Higher cortical function
• Homonymous hemianopia
• Motor/ sensory deficit in 2
of Face, Arm or Leg.
PACS Partial Anterior Deficits in all three of: 24% High chance of
Circulation recurrence.
syndrome • Higher cortical function
• Homonymous hemianopia
• Motor/ sensory deficit in 2
of Face, Arm or Leg.

• Isolated deficits in Higher


Function.
• Pure motor/sensory loss that
is less severe than in LACS
LACS Lacunar syndrome • Pure motor/ sensory deficit 34% Hypertension and
in at least 2 of Face, Arm or Diabetes are big
Leg. risk factors.
POCS Posterior • Isolated hemianopia/ cortical 17% High chance of
Circulation blindness. recurrence.
syndrome
• Cerebellar dysfunction.
• Ipsilateral cranial nerve
palsy
• Bilateral sensory/motor loss
• Disorders of conjugate eye
movements.

Investigations
• Should be done promptly to confirm diagnosis and avoid further strokes.
• Consider whether investigations will actually change management.

• Bloods
○ Glucose
○ Clotting
• CT scan.
○ Immediately if.
 Thrombolysis being considered
 Patient already anticoagulated
 Patient has known bleeding tendency
 GCS < 13
 Unexplained progressive/ fluctuating symptoms
 Papilloedema/ Neck stiffnes/ Fever
 Severe headache at onset of stroke symptoms.
○ Otherwise get one within 24 hours.

Thrombolysis
• Normally with Alteplase
• Has to be given within 3 – 4 hours of onset of symptoms.
• Only to be given by somebody experienced in thrombolysis in an appropriate stroke unit.
○ Telemetry
○ Stroke nurses
○ 24 hour access to CT & MRI
• Must exclude haemorrhagic stroke on CT before thrombolysis is given.
• Other contraindications.
○ Age < 18
○ Age >80
○ Convulsions accompanying stroke
○ Previous stroke within 3 months
○ Severe stroke
○ Recent haemorrhage, trauma or surgery.
• Intercranial bleeds are the most significant side effects.
• Dose calculated based on patient’s weight.
○ IV boluse followed by infusion over 1 hour.
○ Costs £480 for a dose for a 75 kg person.
Other management.
• High flow oxygen if Sats < 95%
• Maintain blood glucose between 4 – 11 mmol/L
○ Use glucose and insulin protocols for stroke if diabetic.
• Ensure good hydration.
• Aspirin
○ 300 mg within 24 hours
○ If history of dyspepsia, give PPI protection but still give aspirin.
○ If aspirin allergic give clopidogrel.
○ Continue for 2 weeks, then change to definitive anti – thrombotic therapy.

• Only give antihypertensives in hypertensive emergency.


• Anticoagulation should not be used in acute stroke.
○ Risk of haemorrhagic transformation.
• Don’t start statins within 24 hours of a stroke.
○ Can be started after that.

• Multidisciplinary management
○ Nursing.
 Monitoring bladder and bowels
 Monitor for pressure sores
 Co – ordinating social issues.
○ SALT & Dieticians.
 Swallow assessment on admission
 Nutritional assessment
 Modified diet
○ Physio/ occupational therapy.
 Early mobilisation & positioning
 Assessment of activities of daily living with Barthel Index.
 Provide.
• Mobility aids
• Exercises
• Passive stretching to prevent spasticity
• Strength training
• Task specific training.
Follow up.
• After initial management, investigate for modifiable risk factors for future stroke.
• CXR
○ Big heart suggests hypertension
○ Dilated left atrium can suggest AF.
• Echocardiogram
○ Dilated left atrium can suggest AF
○ Mural thrombus suggests previous MI
○ Endocarditis
• Carrotid artery Doppler.
○ Surgery for stenosis > 70% or rapidly progressing.
• ESR
○ Giant cell arteritis
• Syphilis screen
• FBC
○ Polycythemia.
• Clotting screen
• Sickling screen.

• Manage risk factors.


○ Stop smoking
○ Exercise
○ 5 portions of fruit or veg a day
○ 2 portions of oily fish per week.
○ Reduce saturated fat intake.
○ Lose weight if overweight
○ Reduce salt intake
○ Stick to recommended alcohol limit
○ Control BP.
 Target of 130/80
 Follow normal NICE guidelines.
○ Antiplatelets.
 Aspirin 50 – 300 mg/day
 Dipyridamole MR 200 mg BD
○ Statins.
○ Anticoagulation.
 For patients with AF.
• Aspirin for 2 weeks
• Then anticoagulate.
 For patients with prosthetic heart valves.
• Either continue anticoagulation throughout stroke period, or replace with
aspirin for first week.

Complications.
• Spasticity.
○ Botox
○ Baclofen
○ Gabapentine
○ Tizanidine
• Pain.
○ Neuropathic.
 Antidepressants
 Anticonvulsants
○ Muskuloskeletal.
 Exercise
 Paracetamol
 NSAIDs
 Codeine.
• Depression/ Emotionaluism.
○ Increase social interaction
○ Exercise
○ Set goals.
○ Antidepressants
• Anxiety.
○ Provide information and support.
○ Desensitise
○ CBT
• Malignant Middle Cerebral Artery infarction.
○ Rare
○ Life threatening
○ Space occupying brain oedema.
 Affects younger patients more often due to lack of brain atrophy meaning less space
to expand.
○ Presents within 2 – 5 days of stroke.
○ Treatment with Decompressive Hemicraniectomy if:
 Age > 60 years
 NIHSS score of > 15
 Decreased level of consciousness
 CT signs of infarct in > 50% of middle cerebral artery territory.
Management of Haemorrhagic stroke.
• Reverse any anticoagulation.
○ Prothrombin complex concentrate
○ IV Vitamin K
• Surgery if hydrocephalus develops

Transient Ischemic Attack.


• Clinical syndrome of rapidly developing clinical signs of disturbance of cerebral function lasting less
than 24 hours.
• Clinical picture similar to that of full blown stroke.
• Signs that suggest causes.
○ Carotid bruit.
 Absence doesn’t rule out carotid source of emboli.
 Tight stenoses often have no bruit.
○ Hypertension
○ Heart murmers
○ AF.
 Identify and treat.
○ Fundoscopy during TIA may show retinal emboli.
• Differentials.
○ Hypoglycaemia
○ Migraine aura
○ Focal epilepsy
○ Some conditions rarely mimic TIAs.
 Malignant hypertension
 MS
 Space occupying lesions
 Phaeochromocytoma
 Somatization.
• Investigations.
○ Aim to find cuase and identify vascular risk.
○ FBC
○ U&E
○ ESR
○ Glucose
○ Lipids
○ CXR
○ ECG
○ Carotid Doppler ± angiography
○ CT/MRI ± cardiac echo.
• Management.
○ Begin after first TIA.
○ Control risk factors.
 Cautiously treat hypertension.
• Aim for < 140/85 mmHg.
○ Antiplatelets
 Low – dose aspirin, if no history of peptic ulcer disease.
• Clopidogrel if aspirin intolerant.
 Dipyridamole
○ Warfarin
 AF
 Mitral stenosis
 Recent big septal MI

○ Carotid endarterectomy.
 If origin of carotid has > 70% stenosis, and risk of stroke greater than that of surgery.
• Surgery risk increased by:
○ Female
○ Age > 75
○ High SBP
○ Contralateral carotid occlusion
○ Stenosis of ipsilateral carotid siphon/ external carotid.
○ Wide territory TIA vs. Amaurosis fugax
 For benefit to outweight stroke risk, death rate from surgery must be < 3%
 Intra – operative Doppler can monitor middle cerebral artery flow.
 Using patches may reduce chances of restenosis.
 Don’t stop aspirin until after surgery.
 Do surgery within 2 weeks of TIA.
○ Avoid driving for at least 1 month.
○ MRI/CT if.
 Unclear which territory has been affected.
 Patient is on anticoagulant and a bleed is possible.
 If other diagnoses are suspected.
• Migraine
• Epilepsy
• Tumour.

• Prognosis.
○ Combination risk of stroke and MI is 9% per year.
○ Risk of stroke is 12% in first year after TIA
○ Risk is > 10% in subsequent years if carotid stenosis is > 70%
○ Mortality is 3 times that of the TIA – free population.
○ In one study, 60% of patients are dead within 10 years of a TIA.

○ Prognosis is calculated by the ABCD2 score.


 A = Age > 60 years 1 point
 B = BP at presentation ≥140/90 mmHg 1 point
 C = Clinical features.
Unilateral weakness 2 points
Speech disturbances without weakness 1 point
 D = Duration of symptoms.
≥ 60 minutes 2 points
10 – 59 minutes 1 point
 D = Diabetes
If present 1 point

 If > 4 or crescendo TIAs.


• Refer to stroke team for assessment within 24 hours.
 Carotid Doppler within 1 week

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