Hospital Based Practice – Stroke.

Result from ischemic infarction or bleeding into the brain. Manifest as.

o Focal CNS signs and symptoms.

o Onset over minutes.

Major neurological disease of the 21st century.o 1.5/1000/year

o 10/1000/year by age 75.

Causes.o Thrombosis.

In situ |Emboolising from heart.

> 30% of strokes AF

o Overall risk of 4.5% per year.

o Often results in more severe forms of ischemic stroke

o Warfarin reduces risk by 68%.

Target INR of 2.5 – 3.5o Aspirin monotherapy is sufficient when there are no additional risk

factors. Advancing age Previous strokes/ TIA Hypertension

o No benefit in giving aspirin with warfarin.

Endocarditiso Prosthetic metal valves are major emboli risk.

o Require INR of 3.5 – 4.5

MI.o Changes to left ventricular mobility on echocardiogram

predisposed to left ventricular thrombus.o Emboli arise in 10% of these patients within 6 – 12 months.

o Warfarin therapy reduces risk by two – thirds.

Cardioversion.o Similar risk if external or pharmacological.

o Complicated by emboli in 1 – 3%

Anatomical abnormalities.o Causes paradoxical systemic emboli.

o May cause reccurence if not repaired.

o Patent foramen ovale

o Atrial or ventricular septal defects.

Cardiac surgery.o All heart surgery causes risk of stroke.

o CABG has a particular risk.

0.9 – 5.2%o Atherothromboembolism.

Eg. From carotids.o Failure of cerebral autoregulation of blood flow.

May explain association with Morning arousal Stress/ Activity

Winter Rarer causes include.

o Sudden drop in BP of > 40 mmHg

o Vasculitis

o Venous sinus thrombosis

o In younger patients suspect.

Thrombophilia Vasculitis Subarachnoid haemorrhage Venous – sinus thrombus Carotid artery dissection.

Spontaneous Neck trauma Fibromuscular dysplasia.

Risk factors.o Hypertension

o Smoking

o Diabetes

o Heart disease.

IHD Valvular disease AF

o Peripheral vascular disease

o Previous TIA

o Raised packed cell volume

o Caroid bruit

o COCP

o Raised lipids

o Alcoholism

o Increased clotting

Raised plasma fibrinogen Lowered antithrombin III levels.

Signs.o Sudden onset, or stepwise progression over days.

Rarely can progress over days.o In theory, focal signs relate to distribution of affected artery.

Can be complicated by collateral supply .

o Cerebral hemisphere infarcts.

50% of cases. Contralateral hemiplegia Initially flaccid, but progresses to spasticity. Contralateral sensory loss Homonymous hemianopia. Dysphagia Visuo – spatial defects.

o Depends on site.

o Brainstem infarcts.

25% of cases. Wide range of affects.

Quadriplegia Disturbed gaze and vision Locked – in syndrome.

o Awareness, but unable to respond.

o 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.o Internal carotid occlusion can cause total and fatal infarction of anterior two – thirds of:

Ipsilateral hemisphere.

Basal gangliao Most commonly, picture is similar to that of middle cerebral infarction.

Cerebral artery anatomy.o 3 pairs of arteries leave the circle of Willis.

o Anterior and Middle cerebral arteries are branches of the carotid arteries.

o Basilar artery splits to form the two posterior cerebral arteries.

o Ischemia due to occlusion of arteries may be prevented or reduced by retrograde supply by

meningeal arteries. Anterior cerebral artery.

o Supplies forntal and medial parts of cerebrum.

o 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.o Supplies lateral (external) parts of the cerebral hemisphere

o 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.

o Inability to dress

o Getting lost.

Posterior cerebral artery.o Supplies occipital lobe.

o Occlusion causes contralateral homonymous hemianopia.

Often with macula sparing.

Vertebrobasilar circulation.o Supplies.

Cerebellum Brainstem Occipital lobes

o Occlusion causes.

Hemianopia Cortical blindness Diplopia Vertigo Nystagmus Hemi – or quadriplegia Unilateral or bilateral sensory symptoms. Hiccups Dysarthria Dysphagia Coma

o 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.

o Vertigo with vomiting

o Dysphagia

o Nystagmus

o Ipsilateral ataxia

o Soft palate paralysis

o Ipsilateral Horner’s syndrome

o Crossed – pattern sensory loss.

Analgesia to pin prick on ipsilateral face and contralateral trunk and limbs.

Subclavian steal.o 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.o Suspect if BP in arms differs by > 20 mmHg.

Arterial dissectiono Disection of carotid or vertebral artery causes an acute ischemic stroke.

o Usually occurs in younger patients.

o May have preceding neck trauma

o Need MRI or MR angiography.

o Treat with antiplatelets and anticoagulants

o Most patients will be part of a RCT.

Cerebral Venous Thrombosiso Rare

o More common in.

Pregnancy. Local infection Dehydration Widespread malignancy.

o Headaches and seizures are common.

o Require

MRI CT MR venography.

o Management.

Anticoagulation Heparin Warfarin.

Oxford/ Bamford Classification of Strokes..TACS Total Anterior

Circulation syndrome

Deficits in all three of: Higher cortical function Homonymous hemianopia Motor/ sensory deficit in 2

of Face, Arm or Leg.

25% Most likely to cause death.

PACS Partial Anterior Circulation syndrome

Deficits in all three of: 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

24% High chance of recurrence.

LACS Lacunar syndrome Pure motor/ sensory deficit in at least 2 of Face, Arm or Leg.

34% Hypertension and Diabetes are big risk factors.

POCS Posterior Circulation syndrome

Isolated hemianopia/ cortical blindness.

Cerebellar dysfunction. Ipsilateral cranial nerve

palsy Bilateral sensory/motor loss Disorders of conjugate eye

movements.

17% High chance of recurrence.

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

Bloodso Glucose

o Clotting

CT scan.o 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.

o 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.

o Telemetry

o Stroke nurses

o 24 hour access to CT & MRI

Must exclude haemorrhagic stroke on CT before thrombolysis is given. Other contraindications.

o Age < 18

o Age >80

o Convulsions accompanying stroke

o Previous stroke within 3 months

o Severe stroke

o Recent haemorrhage, trauma or surgery.

Intercranial bleeds are the most significant side effects. Dose calculated based on patient’s weight.

o IV boluse followed by infusion over 1 hour.

o 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

o Use glucose and insulin protocols for stroke if diabetic.

Ensure good hydration. Aspirin

o 300 mg within 24 hours

o If history of dyspepsia, give PPI protection but still give aspirin.

o If aspirin allergic give clopidogrel.

o 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.

o Risk of haemorrhagic transformation.

Don’t start statins within 24 hours of a stroke.o Can be started after that.

Multidisciplinary managemento Nursing.

Monitoring bladder and bowels Monitor for pressure sores Co – ordinating social issues.

o SALT & Dieticians.

Swallow assessment on admission Nutritional assessment Modified diet

o 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

o Big heart suggests hypertension

o Dilated left atrium can suggest AF.

Echocardiogramo Dilated left atrium can suggest AF

o Mural thrombus suggests previous MI

o Endocarditis

Carrotid artery Doppler.o Surgery for stenosis > 70% or rapidly progressing.

ESRo Giant cell arteritis

Syphilis screen FBC

o Polycythemia.

Clotting screen Sickling screen.

Manage risk factors.o Stop smoking

o Exercise

o 5 portions of fruit or veg a day

o 2 portions of oily fish per week.

o Reduce saturated fat intake.

o Lose weight if overweight

o Reduce salt intake

o Stick to recommended alcohol limit

o Control BP.

Target of 130/80 Follow normal NICE guidelines.

o Antiplatelets.

Aspirin 50 – 300 mg/day Dipyridamole MR 200 mg BD

o Statins.

o 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.

o Botox

o Baclofen

o Gabapentine

o Tizanidine

Pain.o Neuropathic.

Antidepressants Anticonvulsants

o Muskuloskeletal.

Exercise Paracetamol NSAIDs Codeine.

Depression/ Emotionaluism.o Increase social interaction

o Exercise

o Set goals.

o Antidepressants

Anxiety.o Provide information and support.

o Desensitise

o CBT

Malignant Middle Cerebral Artery infarction.o Rare

o Life threatening

o Space occupying brain oedema.

Affects younger patients more often due to lack of brain atrophy meaning less space to expand.

o Presents within 2 – 5 days of stroke.

o 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.

o Prothrombin complex concentrate

o 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.

o Carotid bruit.

Absence doesn’t rule out carotid source of emboli. Tight stenoses often have no bruit.

o Hypertension

o Heart murmers

o AF.

Identify and treat.o Fundoscopy during TIA may show retinal emboli.

Differentials.o Hypoglycaemia

o Migraine aura

o Focal epilepsy

o Some conditions rarely mimic TIAs.

Malignant hypertension MS Space occupying lesions Phaeochromocytoma Somatization.

Investigations.o Aim to find cuase and identify vascular risk.

o FBC

o U&E

o ESR

o Glucose

o Lipids

o CXR

o ECG

o Carotid Doppler ± angiography

o CT/MRI ± cardiac echo.

Management.o Begin after first TIA.

o Control risk factors.

Cautiously treat hypertension. Aim for < 140/85 mmHg.

o Antiplatelets

Low – dose aspirin, if no history of peptic ulcer disease. Clopidogrel if aspirin intolerant.

Dipyridamoleo Warfarin

AF Mitral stenosis Recent big septal MI

o Carotid endarterectomy.

If origin of carotid has > 70% stenosis, and risk of stroke greater than that of surgery. Surgery risk increased by:

o Female

o Age > 75

o High SBP

o Contralateral carotid occlusion

o Stenosis of ipsilateral carotid siphon/ external carotid.

o 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.

o Avoid driving for at least 1 month.

o 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.o Combination risk of stroke and MI is 9% per year.

o Risk of stroke is 12% in first year after TIA

o Risk is > 10% in subsequent years if carotid stenosis is > 70%

o Mortality is 3 times that of the TIA – free population.

o In one study, 60% of patients are dead within 10 years of a TIA.

o 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 pointsSpeech disturbances without weakness 1 point

D = Duration of symptoms.≥ 60 minutes 2 points10 – 59 minutes 1 point

D = DiabetesIf present 1 point

If > 4 or crescendo TIAs.

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