STROKE & CEREBROVASCULAR ACCIDENTMOHD HANAFI RAMLEE

Definition

• Transient Ischaemic Attack (TIA) – an acute focal neurological deficit resulting from cerebrovascular disease with resolution of signs and symptoms within 24 hours.

• Reversible Ischaemic Neurological Deficit (RIND) – attack lasting longer than 24 hours but with complete clearance of signs and symptoms within 7 days.

• Completed Stroke – neurological deficit lasts longer than 7 days.

HOW YOU GIVE THE DIAGNOSIS?• The diagnosis should provide answers to the following

questions:• 1. What is the neurological deficit?• 2. Where is the lesion?• 3. What is the lesion?• 4. Why has the lesion occurred?• 5. What are the potential complications and prognosis?

What Artery Involved?• Aphasia (dominant hemisphere)• Hemiparesis / plegia• Hemisensory loss/disturbance• Homonymous hemianopia• Parietal lobe dysfunction, e.g. astereognosis, agraphaesthesia,

impaired two-point discrimination, sensory and visual inattention, left-right dissociation and acalculia

What Artery Involved?• Weakness of lower limb more than upper limb

What Artery Involved?• Homonymous hemianopia• Cortical blindness• Ataxia• Dizziness or vertigo• Dysarthria• Diplopia• Dysphagia• Horner’s syndrome• Hemiparesis or hemisensory loss contralateral to the cranial

nerves palsy• Cerebellar signs

SO… BASIC IS IMPORTANT!!!!!!!!

Brain Blood Supply Features:• High oxygen requirement.

• Brain 2% of body weight - 15% of cardiac output • 20% of total body oxygen.

• Continuous oxygen requirement• Few minutes of ischemia - irreversible injury.

• Neurons - Predominantly aerobic.• Sensitive areas:

• Adults -Hippocampus, 3,5th & 6th layer of cortex, Purkinje cells. Border zone (watershed areas)

• Brain stem nuclei in infants.

Anatomy – Stroke.

Brodman’s Cortical Map:

Frontal[f*ck – motor] Lobe Functions:

• High level cognitive functions. i.e reasoning, abstraction, concentration

• Storage of information – memory• Control of voluntary eye movement• Motor control of speech in the dominant hemisphere.• Motor Cortex – Motor control of the contralateral side of

the body• Urinary continence• Emotion and personality

Parietal[p-sx – sensory] Lobe Functions:

• Sensory cortex – sensory input is interpreted to define size, weight, texture and consistency (contralateral)

• Sensation is localised, and modalities of touch, pressure and position are identified.

• Awareness of the parts of body• Non-dominant – processes visuospatial information and• controls spatial orientation• Dominant is involved in ideomotor praxis (ability to

perform learned motor tasks

Temporal[t-telinga] Lobe Functions:

• Primary auditory receptive areas• In dominant ability to comprehend speech

(wernicke’s) – reception• Interpretive area – area at the junction of the

temporal, parietal and occipital lobes.• Plays an important role in visual, auditory and

olfactory perception• Important role in learning; memory and

emotional affect.

Occipital[O-optic] Lobe Functions:

• Primary visual cortex• Visual association areas• Visual perception• Some visual reflexes (i.e. visual

fixation)• Involuntary smooth eye movement

Diencephalon Functions:

• Brain Stem:• Midbrain, Pons & Medulla• 10 of the 12 ranial nerves arise from the brainstem

(ipsilateral signs)• Cortical pathway decussation contralateral signs.• Some major functions: eye movement, swallowing,

breathing, blood pressure, heat beat, consciousness• Cerebellum:

• movement – Balance & coordination

Motor & Sensory Cortex:

Diencephalon & Brain stem:

Cranial Nerves:

Stroke Types:• Clinical

• Transient Ischemic Attack –TIA resolve <24h• Evolving stroke – increasing >24h. – Thromb.

• Recurrent / multiple stroke – sec. factors.

• Completed stroke – no change… embolic.• Pathological

• Focal / Global• Ischemic & hemorrhagic (chronic/acute)• Venous infarcts. (young, infections)

Common Types and Incidence:• Infarction: Incidence 80% - mortality 20%

• 50% - Thrombotic – atherosclerosis • Large-vessel 30% (carotid, middle cerebral)• Small vessel 20% (lacunar stroke)

• 30% Embolic (heart dis / atherosclerosis) • Young, rapid, extensive.

• Venous thromboembolism (rare)

• Hemorrhage: Incidence 20% - mortality 80% • Berry aneurysm, Microaneurysm, Atheroma.• Intracerebral or subarachnoid.

Stroke location and incidence:

Cause %Clinical presentation

30day mort(%) Pathogenesis

Cerebral infarction

85 Slowly / sudden evolving signs and symptoms

15-45 Cerebral hypoperfusion Embolism Thrombosis

Intracerebral hemaemorrhage

10 Sudden onset of stroke with raised intracranial pressure

80 Rupture of micro-aneurysm or arteriole

Subarachnoid haemorrhage

5 Sudden headache with meningism

45 Rupture of saccular aneurysm on circle of Willis

Clinical Categories:

• Global Ischemia.• Hypoxemic encephalopathy• Hypotension, hypoxemia, anemia.

• Focal Ischemia.• Obstruction to blood supply to focal

area.• Thrombosis, embolism or hemorrhage.

GLOBAL ISCHAEMIA

Global Ischemia:• Etiology:

• Impaired blood supply - Lung & Heart disorders.• Impaired O2 carrying – Anemia/Blood dis.• Impaired O2 utilization – Cyanide poisoning.

• Morphology:• 3rd, 5th and 6th layers of the cortex, hippocampus and in the

Purkinje cells in the cerebellum • Laminar necrosis, Hippocampus, Purkinje cells.• Border zone infarcts – “Watershed”• Sickle shaped band of necrosis on cortex.

• Clinical Features:• Mild transient confusion state to• Severe irreversible brain death. Flat EEG, Vegetative state. Coma.

Morphology in Global Ischemia1. Watershed zone

(Acute - ACA-MCA)2. Laminar necrosis -

(chronic- short penetrating arteries)

3. Sommer sector of hippocampus.

4. Purkinje cells of cerebellum.

Watershed/Boundary zone infarcts:

Carotid thrombosis

Lamellar necrosis in global ischemia.

Chronic

Local infarction:

Cell death ~ 6mincentral infarct area or umbra, surrounded by a penumbra of ischemic tissue that may recover

Infarct Pathogenesis:• Reduced blood supply – hypoxia/anoxia.• Altered metabolism Na/K pump block. • Glutamate receptor act. calcium influx.• ischemic injury – Red neuron, vacuolation.• cell death, karyorrhexis.• Inflammation – edema.• Macrophages - > 5d.• Liquifaction cavity – >1wk• Glial proliferation – >1wk. (astrocytes)

Hours

1-day3-day

1 wk.

>4wk

Infarct Stages:• Immediate – <24 hours

• No Change gross, micro Na/K loss, Ca+ influx.• Acute stage – < 1week

• Oedema, loss of grey/white matter border.• Inflammation, Red neurons, necrosis, neutrophils

• Intermediate stage – 1- 4 weeks.• Clear demarcation, soft friable tissue, cysts• Macrophages, liquifactive necrosis

• Late stage – > 4 weeks.• Removal of tissue by macrophages• Fluid filled cysts with dark grey margin (gliosis)• Gliosis – proliferation of glia at periphery.

FOCAL ISCHAEMIA

Brain Stem Stroke: Common Pattern

• Pure Motor - Weakness of face and limbs on one side of the body without abnormalities of higher brain function, sensation, or vision (MCA/ACA)

• Pure Sensory - Decreased sensation of face and limbs on one side of the body without abnormalities of higher brain function, motor function, or vision (PCA).

MCA [most common] Features:• Paralysis of the contralateral

face, arm and leg• Sensory impairment over the

contralateral face, arm & leg• Homonymous hemi or

quadrantonopia• Paralysis of gaze to the

opposite side

• Aphasia (dominant) and dysarthria [broca/wernicke]

• Penetrating - contralateral hemiplegia/paresis, slurred speech.

• Impaired spatial perception

MCA stroke.

MCA stroke.

Wikipedia: GNU Free Documentation license

MCA stroke.

Wikipedia: GNU Free Documentation license

ACA stroke.• Paralysis of contralateral foot and

leg• Sensory loss over toes, foot and

leg• Impairment of gait and stance• Abulia (slowness and prolonged

delays to perform acts)• Flat affect, lack of spontaneity,

slowness, distractibility• Cognitive impairment, such as

perseveration and amnesia• Urinary incontinence

Wikipedia: GNU Free Documentation license

PCA stroke.Peripheral (cortical)• Homonymous hemianopia• Memory deficits• Perseveration• Several visual deficits (cortical blindness,

lack of depth perception, hallucinations)Central (penetrating)• Thalamus - contralateral sensory loss,

spontaneous pain, mild hemi• Cerebral peduncle - CN III palsy with

contralateral hemiplegia• Brain stem - CN palsies, nystagmus,

pupillary abnormalities

Wikipedia: GNU Free Documentation license

Posterior Cerebral Artery• Visual disturbances

• contralateral homonymous hemianopsia

• (central vision is often spared) • L. Hemi: lesions alexia

• (with or without agraphia) • Bilateral lesions: cortical

blindness • patients unaware they cannot see • (Anton's syndrome)

• Memory impairment if temporal lobe is affected ~

• Proximal occlusion• contralateral hemisensory

loss, • spontaneous pain and

dysesthesia if thalamus affected

• (thalamic pain syndrome) • contralateral severe proximal

chorea • (hemiballism) ~

Haemorrhagic - Arterial embolus

Embolic stroke: sudden, pin point hemorrhages over a triangular area.

Infarct with Punctate hemorrhage

Cerebral Infarction - Late

Cerebral Infarction - Late

Hypertensive CVD

• Intraerebral/Subarachnoid Hemorrhage• Microaneurysm hemorrhages – Basal ganglia.

Putamen(60%), thalamus, ventricles.• Berry aneurysm hemorrhages – subarachnoid.

• Chronic Hypertension: (dementia) • Slit hemorrhages. Microhemorrhages heal as slit with

pigment.• Lacunar infarcts: Brain stem - pale infarcts. A.sclerosis

• Hypertensive encephalopathy-Malignant.• Headache, confusion, vomiting – Raised ICP.

Central Pontine Hemorrhage - Herniation

Subarachnoid Hemorrhage:

Ruptured Berry Aneurism

Fusiform atherosclerotic aneurysm

Saccular(berry) Aneurysm:

Intracerebral Hemorrhage:

Lacunar Infarct in pons

Left (Dominant) Hemisphere Stroke: Clinical

• Aphasia • Right hemiparesis • Right-sided sensory loss • Right visual field defect • Poor right conjugate gaze • Dysarthria • Difficulty reading, writing, or

calculating

Diagnosis: Recent cerebral infarction in left MCA distribution.Left cerebral hemisphere shows swelling with compression of the lateral ventricle mainly in the frontal area, due to recent infarct in the Middle Cerebral Artery (MCA) distribution. The brain in the MCA area shows discoloration of the cortex and also blurring between the cortex and white matter.

L affect R

Right (Non-dominant) - Hemisphere Stroke:• Defect of left visual field • Extinction of left-sided

stimuli • Left hemiparesis • Left-sided sensory loss • Left visual field defect • Poor left conjugate gaze • Dysarthria • Spatial disorientation

R affect L

CNS AV Malformations:• Many types:

• AV Malformation *• Cavernous angioma• Telangiectasia• Venous angioma

• Cause of Seizure disorders & hemorrhage.

• Most common congenital vascular malformation.

• Typically located in the outer cerebral cortex underlying white matter.

Pathological Review:• Stroke: Ischemic / Thrombotic / Hemorrhagic

• Acute neurological deficit - Clinical• Cerebro Vascular Accident – Pathology.

• Etiology: Thrombosis, Embolism, Hemorrhage.• Risk factors: AS, Hypertension, Smoking.• Global – Systemic Hypoxia – Watershed & lamellar infarct• Focal – Basal ganglia, Putamen, Int. capsule (MCA) • Pathogenesis: Infarction Liquifaction necrosis Cyst formation

with peripheral gliosis. (loss of neural function)• Hypertension & CVA:

• Atherosclerosis - Thrombosis• Haemorrhage (Intra/subarachnoid), • chronic benign: Lacunar infarcts & slit hemorrhages. • Hypertensive Encephalopathy,

Stroke – Risk Factors• Modifiable

• Hypertension• Tobacco use• Excess Alcohol• Hx of TIA’s• Heart Disease• Diabetes Mellitus• Hypercoagulopathy

• Pregnancy, cancer, etc.• Sickle Cell and increased

RBC• Hx of carotid Bruit

• Unmodifiable• Age• Gender• Race• Previous CVA• Heredity

Stroke – Signs and Symptoms• Ischemic

• Carotid Circulation• Unilateral paralysis (opposite side)• Numbness (opposite side)• Language disturbance

• Aphasia – difficult comprehension, nonsense, difficult reading/writing• Dysarthria – slurred speech, abnormal pronunciation.

• Visual disturbance (opposite side)• Monocular blindness (same side)

Stroke – Signs and Symptoms• Ischemic

• Vertebrobasilar Circulation• Vertigo• Visual disturbance

• Both eyes simultaneously• Diplopia

• Ocular palsy – inability to move to one side• Dysconjugate gaze – asynchronous movement

• Paralysis• Numbness• Dysarthria• Ataxia

Stroke – Signs and Symptoms• Hemorrhagic

• Subarachnoid hemorrhage• Sudden severe HA• Transient LOC• Nausea/Vomiting• Neck pain• Intolerance of noise/light• AMS

• Intracerebral hemorrhage• Focal sx w/ LOC, N/V

History• Detailed history from relative or friend or patient if he is able

to speak.• Rapidity of onset – sudden onset of a focal neurological

deficit.• Time course of symptoms – maximum deficit over seconds or

minutes before starting to improve.• Headache, coma at onset and vomiting at onset are more

common in haemorrhage but also occur with infarction.• Sudden onset of severe generalised headache associated with

neck stiffness – subarachnoid haemorrhage.• Specific record should be made about the presence of vascular

risk factors.

ExaminationGeneral Examination• BP – should be taken in both arms.• Stroke may cause an acute rise in BP and therefore

hypertension should not be diagnosed in the first few days after a stroke unless left ventricular hypertrophy of fundal changes are present.

• Pulse – for arrhythmias particularly atrial fibrillation.• Peripheral pulses.• Auscultation for a carotid bruit.• Heart – for valvular heart disease especially mitral stenosis.• Neck stiffness – subarachnoid haemorrhage or meningitis.• Identify the anatomical localization of the lesion and record

the degree of disability.

OXFORDSHIRE COMMUNITY STROKE PROJECT CLASSIFICATION

OCSP

Causes of ischaemic stroke

Causes of ischaemic stroke 2

Causes of ischaemic stroke 3

Causes of intracranial haemorrhage

Subarachnoid haemorrhage• Initial headache or coma – sudden rise in intracranial pressure.• Focal symptoms if aneurysm ruptures into underlying brain.• Cerebral vasospasm causes delayed cerebral infarction 4-14

days after onset in 30% of patients.• Recurrent haemorrhage and hydrocephalus are other

complications.

Intracerebral Haemorrhage• Sudden rupture of microaneurysms caused by hypertensive

vascular disease.• Characteristically occurs in the basal ganglia, pons and

cerebellum.• Elderly patients – cerebral amyloid angiopathy, a degenerative

disorder affecting the walls of the artey – subcortical haematomas.

• Cryptic av malformations are suspect especially in younger patients < 40 yrs and when the haemotoma is Lobar (frontal, temporal, parieto-occipital).

Investigations

Confirm the diagnosis

CT Scan To establish the site, size and pathological diagnosis by

showing infarction or haemorrhage. To exclude other conditions that may mimic stroke like

subdural haematoma, intracranial tumour.

(a) There is doubt about the diagnosis.(b) Symptoms progress or fluctuate.(c) Conscious level is depressed or patient is in coma.(d) If thrombolytic therapy or anticoagulant treatment is

considered.(e) Neck stiffness is present.(f) Has severe headache.(g) Deteriorates unexpectedly.(h) Haemorrhage can be seen within a few minutes as an area of

increased attenuation.(i) Infarction as a low density lesion which conforms to a

vascular territory usually wedge shaped.(j) It is not immediately visible on CT but in most patients

becomes apparent in 4-7 days.

Y CT Scan?

MRI Scan• Posterior circulation strokes are more readily identified than

by CT.

General Investigations• identify conditions which may predispose towards premature

cerebrovasculardisease.• Full blood count – polycythemia, thrombocytopoenia.• Blood glucose – diabetes mellitus.• Serum lipids – hypercholesterolemia.• Blood cultures – SBE.

General Investigations II• HIV screen – AIDS.• Syphilis serology – VDRL.• Clotting Screen.• Thrombophilia Screen – Protein C, Protein S, Antithrombin III.• Anticardolipin antibodies – SLE.• Lumbar Puncture – subarachnoid haemorrhage.

DD Stroke• Differential Diagnosis of Stroke

• Head/Cervical trauma• Meningitis/encephalitis• Hypertensive encephalopathy• Intracranial mass

• Tumor• Sub/epi dural hematoma

• Todd’s paralysis• Migraine w/ neuro sx• Metabolic

• Hyper/hypo glycemia• Post arrest ischemia• Drug OD

Differential Diagnosis• Space occupying lesion• 5% of people with stroke like symptoms have a subdural

haematoma, tumour or cerebral abscess. • Distinction is readily made on CT or MRI. • If there is any doubt repeat the scan after 6 weeks.

Differential Diagnosis II• Multiple sclerosis• May present with hemiparesis, sensory impairment or

brainstem symptoms that mimic stroke. • Symptoms occur gradually over a few days.• Hypoglycaemia• May cause hemiparesis.• Migraine

Complications I

• Cerebral oedema• Should be suspected in a patient

with a large infarct or haemorrhage experiences a lucid interval of 24-48 hours and then shows a decline in consciousness.

Complication II• Haemorrhagic transformation

• Can occur as a result of thrombolysis.• Pneumonia

• In patients with swallowing difficulties as a result of aspiration.• Pressure sores

• Develop rapidly and may be exacerbated because of incontinence.

• Oedema of Weak Limbs• Is common and has a partially autonomic basis.

Complication III

• Anxiety and Depression• Common reactions to stroke but

depression may have an organic basis related to damage of the frontal and limbic systems.

• Emotional Lability• Precipitated by minor emotional stimuli.

Management I

• Has the following aims• Confirmation of the diagnosis,

anatomical site of the lesion, pathology and aetiology.

• Acute care.• Rehabilitation of persistent disability

and handicap.• Prevention of recurrence.

Management IIAcute CareTreatment aims• Prevent progression of present event.• Prevent immediate complication.• Prevent the development of subsequent events.• To rehabilitate the patient.

Management IIIGeneral Measures• Around the edge of the infarct, ischaemic tissue is at risk, but is

potentially recoverable. • This must be protected by ensuring a good supply of glucose

and oxygen.• Maintain hydration, oxygenation and blood pressure.

Specific MeasuresMedical TreatmentAnticoagulation• Patient with high risk of developing deep vein

thrombosis.• Thromboembolic stroke - started as soon as

possible, except in large infarcts where it may be wise to delay anticoagulation for 2 weeks.

• Stroke in a patient with myocardial infarct - due to mural thrombus.

• Stroke in evolution.Exclude a haemorrhage by doing a CT scan first.

Medical Treatment IIAntiplatelet Agents

• Especially in TIA.Thrombolysis• I/V thrombolysis espcially recombinant tissue plasminogen

activator rTPA to be given only within the first 3 hours after onset to those patients who have not developed CT abnormalities especially in patients with basilar artery occlusion.

• Risk – haemorrhage.

Hypertension

• Treated cautiously in acute stroke.• A reduction in blood pressure may lower cerebral blood flow in

the regions surrounding the infarct below a critical level at which further ischaemic brain damage will occur.

• Mild to moderate elevations in BP – no treatment unless they are maintained for several days after admission.

• If stroke associated with hypertensive encephalopathy or if diastolic BP is persistently above 120 mm Hg.

• The BP should be lowered cautiously using oral agents. • Sudden precipitious fall in BP should be avoided.

Hypertension II

Medical TreatmentCalcium Antagonist

• Nimodipine prevents ischaemic brain damage and reduces the number of patients remaining disabled after subarachnoid haemorrhage.

• Prescribed as soon as diagnosis is made (within 12 hours).

Neurosurgery• Should be considered in subaracnoid and intracerebral

haemorrhage.• Evacuation of cerebellar haematoma.• Evacuation of supratentorial haematomas should only be

considered in younger patients with superficial cortical haematomas causing mass effect with a deteriorating level of conciousness.

Nursing Care and Rehabilitation• Physiotherapy, proper positioning and early mobilization –

prevent pressure sores.• Support stockings – prevent deep vein thrombosis and

pulmonary embolism.• Swallowing difficulties.• Lead to silent aspiration – aspiration pneuomonia.

• Nasogastric tube feeding.• Percutanious endoscopic gastrostomy.

Rehabilitation• Physiotherapy, occupational therapy, speech therapy and

psychology input – multidisciplinary stroke rehabilitation team.

• Home visit by occupational therapist to plan adaptations to home before discharge.

Secondary Preventation

• Control hypertension and diabetes mellitus.• Correct lipid abnormality.• Stop cigarette smoking.• Stop thrombogenic drugs e.g. oral contraceptives.

• Give platlet antiaggregation drugs to reduce the rate of reinfarction.

• Low dose aspirin (75 mg – 150 mg), if patient allergic or has gastrointestinal side effects give ticlopidine. Regular blood tests because of a small risk of neutropoenia.• Remove or treat embolic source (long term anticoagulation in

atrial fibrillation).• Treat inflammatory or vascular inflammatory diseases.

Secondary Preventation II

• Carotid Endarterectomy – preventing stroke in symptomatic patients with recent TIA and stroke and severe stenosis of the internal carotid artery (at least 70%).

Secondary Preventation III

Chain of Survival Stroke• Stroke Chain of Survival

• Detection• Early sx recognition

• Dispatch• Prompt EMS response

• Delivery• Transport, approp, prehospital care, prearrival notification

• Door• ER Triage

• Data• ER evaluation incl, CT, etc.

• Decision• Appropriate therapies

• Drug/Therapy

Detect & Dispatch• Detection: Early Recognition

• Public education of Stroke sx• Early access to medical care

• Dispatch: Early EMS and PDI’s• Caller triage

• EMD recognition of Stroke sx

How to detect?

• Delivery: • Pre-hospital Transport and

Management

How we scale the pre-hospital management of the

patient?

CINCINNATI STROKE SCALE

CINCINNATI STROKE SCALE

• Identifies patients with strokes.• It evaluates three major physical

findings.• Facial droop• Motor arm weakness• Speech abnormalities

CSS - Facial Droop

• Have the patient show their teeth or smile.

• Normal – both sides of the face move equally well

• Abnormal – one side of the face does not move as well as the other side

Arm Drift

• Have the patient close his/her eyes and hold both arms out.

• Normal – both arms move the same way, or both arms do not move at all.

• Abnormal – one arm does not move or one arm drifts down compared to the other arm.Other findings such as pronator grip, may

be helpful

Speech

• Have the patient say “You can’t teach an old dog new tricks.” – “Perlambagaan Malaysia”

• Normal – patient uses correct words with no slurring.

• Abnormal – patient slurs words, uses inappropriate words, or is unable to speak

“You can’t teach an old dog new tricks.”

Cincinnati Prehospital Stroke Scale• Patients with 1 of these 3 findings -as a

new event - have a 72% probability of an ischemic stroke.

• If all 3 findings are present the probability of an acute stroke is more than 85%

• Immediately contact medical control and the destination ED and provide prearrival notification.

Stroke – Management In Review:

Prehospital Critical Actions• Assess and support cardiorespiratory function• Assess and support blood glucose• Assess and support oxygenation and ventilation• Assess neurologic function• Determine precise time of symptom onset • Determine essential medical information• Provide rapid emergent transport to ED• Notify ED that a possible stroke patient is en route

Stroke - Management• Door: ER Triage

• Stroke evaluation targets for stroke patients who are thrombolytic candidates

Door-to–doctor first sees patient …….………… 10 min Door-to–CT completed …….………………….. 25 min Door-to–CT read ...…………..………………… 45 min Door-to–fibrinolytic therapy starts …………….. 60 min Neurologic expertise available* …..…………… 15 min Neurosurgical expertise available* …………… 2

hours Admitted to monitored bed ..……...…………… 3

hours *By phone or in person

Stroke - Management• Data: ER Evaluation and Management

• Assessment Goal: in first 10 minutes• Assess ABCs, vital signs• Provide oxygen by nasal cannula• Obtain IV access; obtain blood samples (CBC, ’lytes, coagulation

studies)• Obtain 12-lead ECG, check rhythm, place on monitor• Check blood sugar; treat if indicated• Alert Stroke Team: neurologist, radiologist, CT technician• Perform general neurologic screening assessment

Stroke - ManagementAssessment Goal: in first 25 minutes• Review patient history• Establish symptom onset (<6 hours required for fibrinolytics)• Perform physical examination

• Perform neurologic exam• Determine level of consciousness (Glasgow Coma Scale) • Determine level of stroke severity (NIHSS or Hunt and Hess Scale)

• Order urgent non-contrast CT scan/angiogram if non-hemorrhage (door-to–CT scan performed: goal <25 min from arrival)

• Read CT scan (door-to–CT read: goal <45 min from arrival)• Perform lateral cervical spine x-ray (if patient comatose/trauma

history)

Stroke - Management

• ER Diagnostic Studies• CT scan – done w/in 25 mins, read w/in 45 mins

• r/o hemorrhage• Often normal early in ischemic stroke

• Lumbar puncture• EKG

• Changes may be caused by or cause of stroke

• MRA (Magnetic Resonance Angiography)• Cerebral Angiography

Hypodense area:

• Ischemic area with edema, swelling

• Indicates >3 hours old

• No fibrinolytics!

(White areas indicate hyperdensity = blood)

Large left frontal intracerebral

hemorrhage.

Intraventricular bleeding

is also present

No fibrinolytics!

Acute subarachnoid hemorrhage

Diffuse areas of white (hyperdense) images

Blood visible in ventricles

and multiple areas on surface of brain

Stroke - Management• Decision: Specific Therapies

• General Care• ABC’s, O2

• IV w/ BSS• Treat hypotension• Avoid over-hydration• Monitor input/output

• Normalize BGL• Manage Elevated BP?

Stroke - Management• Indications for Antihypertensive therapyIn general:• Consider: absolute level of BP?

• If BP: >185/>110 mm Hg = fibrinolytic therapy contraindicated• Consider: other than BP, is patient candidate for fibrinolytics?

• If patient is candidate for fibrinolytics: treat initial BP >185/>110 mm Hg

• Consider: response to initial efforts to lower BP in ED? • If treatment brings BP down to <185/110 mm Hg: give fibrinolytics

• Consider: ischemic vs hemorrhagic stroke?• Treat BP in the 180-230/110-140 mm Hg range the same• The obvious: no fibrinolytics for hemorrhagic stroke

Stroke - Management• Decision: Specific Therapies (cont.)

• Management of Seizures• Benzodiazepines• Long-acting anticonvulsants

• Management of Increased ICP• Maintain PaCO2 30mm Hg• Mannitol/Diuretics• Barbiturates• Neurosurgical decompression

Stroke - Management• Drugs: Thrombolytic Therapy

• Fibrinolytic Therapy Checklist Ischemic Stroke

Candidates for Neurointerventional Therapy Age 18 years or older Acute signs and symptoms of CVA <6 hours onset. No contraindications.

Stroke - ManagementContraindications for Interventional TherapyAbsolute

Evidence of intracranial hemorrhage on non-contrast head CT Patient with early infarct signs on CT scan.

Relative Recent (w/in 2 mo’s) cranial or spinal surgery, trauma, or injury Known bleeding disorder and/or risk of bleeding including:

- Current anticoagulant therapy, prothrombin time >15 sec.

- Heparin within 48 hrs of admission, PTT elevated- Platelet count <100,000/mm

Active internal bleeding w/in the previous 10 days Known or suspected pregnancy History of stroke w/in past 6 weeks

Stroke - ManagementContraindications for Interventional Therapy (cont.) Relative Patient comatose >85 years old Diabetic hemorrhagic retinopathy or other opthalmic

hemorrhagic disorder Advanced liver or kidney disease Other pathology with a propensity for bleeding

Infectiouse endocarditis Severe EKG disturbance, uncontrolled angina or acute MI

Stroke - Management• Thrombolytic Agents

• TPA• NINDS trial

• Streptokinase• VEGGIE trial

• Anticoagulant Therapy• Heparin• ASA/Warfarin/Ticlodipine

Stroke - Management• Management of Hemorrhagic Stroke

• Subarachnoid• Neurosurgical intervention• Nimodipine

• Intracerebral• Management of ICP• Neurosurgical decompression

• Cerebellar• Surgical evacuation

• Often associated with good outcome

• Lobar• Surgical evacuation

141

THE END

If they come to you with stroke, what investigation what you like to do?

QUIZ ON STROKEMOHD HANAFI RAMLEE

ANSWER GILIR2 TAU

QUESTION 1

On the history of a patient with suspected or known stroke, what should you ask about?

ANSWER 1

Ask about the presenting symptoms of stroke initially, for example

1. Unilateral weakness or clumsiness2. Difficulty understanding or expressing spoken

language3. Altered sensation unilaterally4. Partial or complete loss of vision in one eye

ANSWER 1 Questions to focus on the causes of stroke1. Atherosclerosis, e.g. enquire about vascular risk factors (smoking,

DM, hyperlipids, PVDs, etc…)2. History of heart disease, e.g. recent myocardial infarction, history

of AF requiring anticoagulation, palpitations3. History of hypertension (lacunar infarcts due to arteriosclerosis of

small penetrating arteries of the brain)4. Migraine5. Manipulation of neck (precipitating cause for dissection of carotid

artery or vertebral artery)6. Any recent cessation of anticoagulation 7. Family history of stroke8. History of connective tissue disease (e.g. SLE, vasculitis, etc…)

ANSWER 1

1. History of connective tissue disease (e.g. SLE, vasculitis, etc…) Medication history, esp. those that increase risk of stroke include

oral contraceptives, some antihypertensives Ask about alcohol consumption and recent falls (may have caused

an intracranial haemorrhage) Enquire about premorbid as well as the current level of

independence and mobility If patient is incapacitated, ask about social support available at

home Don’t forget to screen for depression

QUESTION 2

On examination, what features should you be looking for?

ANSWER 2A complete examination of the neurological and cardiovascular systems is essential Check the fundi for evidence of emboli, hypertensive changes, diabetic changes and

ischaemic neuropathy Test the visual fields for homonymous hemianopia Listen for bruit over the carotids and orbits (commonly heard in the side opposite

the carotid occlusion, due to increased contralateral flow) Decide whether patient is in AF Assess BP and test for postural drop Listen for murmurs (e.g. AS, infective endocarditis, rheumatic heart disease or

prosthetic valve) Note presence of electronic pace maker and assess whether it’s working Perform peripheral vascular examination Look for complications, e.g. pressure sores, limb contractures and disuse atrophy of

the paralysed limbs See if patient has a percutaneous gastrostomy (PEG) feeding tube inserted and, if

present, inspect for cellulitis or pus around the insertion site

QUESTION 3

What clinical features are suggestive of a carotid arterial stroke?

ANSWER 3 Transient aphasia Ipsilateral amaurosis fugax Contralateral hemiplegia/monoplegia Contralateral hemi or monoparesis Carotid bruits (a/w >50% stenosis)

QUESTION 4

What clinical features are suggestive of vertebrobasilar insufficiency?

ANSWER 4

All the Ds Dizziness (vertigo and ataxia) Diplopia +/- blindness Dysphagia Dysarthria ‘Demi-anaesthesia’ – ipsilateral face, contralateral limb Quadraparesis – indicates basilar artery involvement

QUESTION 5

What clinical features are suggestive of a middle cerebral artery stroke?

ANSWER 5 Contralateral hemiplegia, hemiparesis, homonymous hemianopia UMN face, arm > leg, eyes deviated to side of lesion Aphasia (if dominant lobe)1. Expressive dysphasia, arm + leg involvement – anterior MCA2. Receptive dysphasia, visual fields defects – posterior MCA If non-dominant – speech + comprehension intact

QUESTION 6

What clinical features are suggestive of a posterior cerebral artery stroke?

ANSWER 6 Homonymous hemianopia (complete) Cortical blindness Hemisensory loss Ipsilateral III nerve palsy

QUESTION 7

What clinical features are suggestive of an anterior cerebral artery stroke?

ANSWER 7 Contralateral monoplegia (UMN) Confusion, behaviour disturbance Grasp reflex Urinary incontinence

QUESTION 8

What clinical features are suggestive of a lacunar syndrome?

ANSWER 8 Clumsy hand/dysarthria syndrome – lesion in mid pons Leg paresis + ataxia – pons or internal capsule Pure sensory stroke – usually thalamic Pure motor stroke (arm>leg) - pons or internal capsule

QUESTION 9

What investigations would you perform in a stroke patient? – MAINLY TO DIAGNOSE ANY STROKE….

ANSWER 9

CT or MRI of the head, looking for ischaemic infarcts, haemorrhage, or mass lesions

QUESTION 10

What investigations would you perform in a stroke patient? MAINLY TO FIND THE CAUSE OF STROKE

ANSWER 10 Doppler scan of the carotid arteries – if duplex scan suggest

significant carotid stenosis, esp. in patients <75, ask for results of carotid angiography, carotid digital substraction angiography or MR angiography

If patient is in AF, ask for results of transoesophageal echo, looking for thrombus or spontaneous atheromatous plaques in ascending aorta and arch of aorta that may have contributed to stroke

ECG for AMI and AF FBE, looking at Hb (to exclude polycythemia) and platelet count

(rarely, essential thrombocytopenia can contribute to stroke) ESR (to exclude an inflammatory arteritic/vasculitic process CXR (for cardiomegaly/neoplasm) Urea, creatinine and electrolytes

QUESTION 11

What investigations would you perform in a stroke patient?

MAINLY IN YOUNGER PATIENT?

QUESTION 11 Drug screen, looking for narcotic agents Vasculitic screen (if there are features of vasculitis) Blood cultures and cardiac imaging if endocarditis is suspected Cardiac event monitor looking for paroxysmal AF and Thrombophilic screen

WHAT 3 SPECIFIC STRATEGIES IN THE MANAGEMENT OF ACUTE STROKE THAT HAVE BEEN PROVEN TO IMPROVE OUTCOMES?

The 3 main strategies are Administration of iv tissue plasminogen activator (tPA) within 3hrs

of stroke onset Giving aspirin (100mg) within first 48hrs of ischaemic stroke Managing patient in a stroke unitNote that tPA and aspirin are never given before brain imaging to exclude intracranial haemorrhage

WHAT ARE THE STRATEGIES FOR SECONDARY PREVENTION OF STROKE?

There are now at least 4 early strategies for secondary prevention in improving long term outcomes after TIAs or stoke Antiplatelet therapy, e.g. aspirin, clopidogrel, aspirin with

dipyridamole Blood pressure lowering Warfarin (indicated for patients with AF) Carotid endarterectomy (indicated when stenosis >70%) Lipids lowering is the fifth strategy to consider

A PATIENT JUST HAD A STROKE, WHAT CRITERIA DO YOU LOOK FOR TO SELECT THIS PATIENT FOR REHAB.

1. Patients must be medically stable (i.e. no aspiration pneumonia, AMI, DVT, etc…)

2. They have a functional disability3. They have the intellectual capability to learn4. There are defined goals to be achieved5. There are non or minimal co-morbidities, e.g. recurrent stroke,

AMI, COAD, etc…6. They are not clinically depressed (this can affect motivation to

rehabilitate)7. They didn’t suffer from a dense stroke or ones that causes hemi-

neglect (e.g. a right hemisphere stroke)

WHAT ARE SOME OF THE COMMON PREDICTORS OF POOR FUNCTIONAL OUTCOME AFTER A STROKE?

A dense stroke, a recurrent stroke, or a stroke resulting in hemi-neglect

Impairment of bladder and bowel function Depression or cognitive deficits Delayed acute medical care or delayed rehabilitation Co-morbidities and poor social support