BIKHA STROKE By Dr. Bikha Ram Devrajani FCPS, FACP, FRCP Professor Medicine Liaquat University of...

BIKHA

STROKE

By

Dr. Bikha Ram DevrajaniFCPS, FACP, FRCP

Professor MedicineLiaquat University of Medical & Health

Sciences, Jamshoro

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Definition of Stroke

Acute focal neurological deficit resulting from cerebrovascular disease and lasting more than 24-hours (or causing earlier death)

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Definition of Stroke

Stroke is not a diagnosis but a clinical syndrome with numerous causes

The main types of stroke and their relative occurrence are:

Cerebral infarction (85%) Intracerebral haemorrhage (10%) Subarachnoid haemorrhage (5%)

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Transient Ischaemic Attack (TIA)

Also defined as an acute focal neurological deficit resulting from cerebrovascular disease, but the symptoms and signs resolve within 24-hours

Most patients recover within 30-min No fundamental difference between TIA and

stroke except for the duration of the symptoms

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Epidemiology of Stroke Stroke is the third leading cause of death in

the United States and a leading cause of serious, long-term disability.

In the United States there is one stroke patient in every 45 seconds.

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Ischaemic85%

Haemorrhagic15%

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Large Vessels and others50%

Small Vessel Disease25%

Thromboembolism Heart25%

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Pathophysiology

Clinical Classification of Focal Stroke. Transient if the deficit recover within 24 h. Completed if the focal deficit is persistent. Evolving if focal deficit continues to worsen

after about 6 h from onset.

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Pathophysiology

Cerebral Infarction Infarction is a process which takes some

hours to complete.

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Pathophysiology

Cerebral Infarction

a. Occlusion of a cerebral artery, the opening of anastomatic channels from other arterial territories may restore perfusion.

b. Reduction in perfusion pressure leads to homeostatic changes to maintain oxygenation of brain vasodilation of cerebral artery.

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PathophysiologyCerebral Infarction

c. If homeostatic process fails ischaemia begins - ultimately leads to infarction.i. When the blood-flow falls below threshold for

maintenance of electrical activity neurological deficit appears – but neurons are still viable. At this stage if blood-flow restores then recovery will be definite (TIA).

ii. If flow further falls, then cell death process starts.

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Pathophysiology

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PathophysiologyCerebral Infarction

Final result of occlusion of a cerebral blood vessel depends upon:

i. Competence of the circulatory homeostatic mechanism.

ii. Severity of reduction of blood-flow.

iii. Duration of reduction of blood-flow.

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Pathophysiology

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PathophysiologyCerebral Infarction If ischaemic damage is affecting the

endothelium of vessel then there is chance of haemorrhage in the infarction by blood’s thrombolytic mechanism.

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PathophysiologyCerebral Infarction Radiologically infarct can be seen as a

lesion which is composed of:• Ischaemic.

• Swollen but recoverable (pnemubra).

• Finally infarcted area will be replaced fluid filled cavity (liquification necrosis).

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Ischaemia

Energy Failure

Depolarization

Glutamate Release

Na+/Ca++ Influx

Cellular Swelling

Mitochondrial Injury

Free Radical Generation

Enzyme Activity

Necrotic Cell DeathNecrotic Cell DeathNecrotic Cell DeathNecrotic Cell Death

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PathophysiologyIntracerebral Haemorrhage Cessation of functions of affected parts. As neurons are structurally distrupted and

white matter fibre tract split apart. Rim of cerebral oedema around

haemorrhage.

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PathophysiologyIntracerebral Haemorrhage If big haemorrhage the shifting of midline

and transtentorial causing rapid death. If survives then haemosidrin lined slit in

brain parenchyma.

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CT Scan of Intracerebral Haemorrhage

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Causes of Cerebral Infarction(75-80% of all strokes)

Large artery atherothromboembolism =50%• Extracranial (aorta, carotid, vertebral arteries)

= 40-45%

• Intracranial (ICA, MCA, ACA, vertebral, basilar, PCA) = 5-10%

Small artery diseases (microatheroma/lipohyalinosis) = 20-25%

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Causes of Cerebral Infarction(75-80% of all strokes) Contd:

Embolism from the heart = 20% Non-atheromatous arterial disease (e.g.

dissection, arteritis) = 5% Blood disease (thrombophilia) <5%

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Cardiac Sources of Embolism(in anatomical sequence)

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Cardiac Sources of Embolism(in anatomical sequence)

Right to left shunt (paradoxical emboli from the venous system) via:

Patent foramen ovale Atrial septal defect Ventricular septal defect Pulmonary arteriovenous malformation

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Cardiac Sources of Embolism(in anatomical sequence) Contd.

Left Atrium Thrombus:

• atrial fibrillation*• sinoatrial disease (sick sinus syndrome)• atrial septal aneurysm

Myxoma and other tumours*

* substantial risk of embolism

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Cardiac Sources of Embolism(in anatomical sequence) Contd:

Mitral Valve Rheumatic endocarditis (stenosis* or

regurgitation) infective endocarditis* Mitral annulus calcification Mitral valve prolapse


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Mitral Valve Non-bacterial thrombotic (marantic)

endocarditis. Libman-Sacks endocarditis Prosthetic heart valve*


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Left Ventricle Mural thrombus:

• acute myocardial infarction (within previous few weeks)*

• left ventricular aneurysm or akinetic segment

• dilated cardiomyopathy*


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Left Ventricle Mural thrombus:

• mechanical ‘artificial’ heart*• blunt chest injury (myocardial contusion)

Myxoma and other tumours*


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Aortic Valve Rheumatic endocarditis (stenosis or

regurgitation). Infective endocarditis* Syphilis Non-infective thrombotic (marantic)

endocarditis* substantial risk of embolism

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Aortic Valve Libman-Sacks endocarditis Prosthetic heart valve* Calcific stenosis/sclerosis/calcification


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Cardiac Sources of Embolism(in anatomical sequence) Contd.

Congenital heart disease (particularly with right to left shunt)

Cardiac manipulation/ surgery/ catheterisation/ valvuloplasty/ angioplasty

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Causes of Intracerebral Haemorrhage (10-15% of all strokes)

A. Arterial Disease (anatomical factors) ‘Complex’ disease (fibrinoid necrosis) in

small, penetrating vessels:• most common cause in middle and old age

hypertensives• haemorrhages often deep in putamen (40%),

caudate nucleus (85%), thalamus (15%), cerebral hemispheres (lobar) (20%), cerebellum (8%), and brainstem (8%)

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A. Arterial Disease (anatomical factors) Amyloid (congophilic) angiopathy*

• most common cause in old age• haemorrhages often in lobes of cerebral

hemispheres• may be associated with dementia

* causes of multiple haemorrhages in the brain parenchyma

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A. Arterial Disease (anatomical factors) Vascular malformations (arteriovenous

and cavernous angiomas)• dural or brain• most common cause of ICH in young

normotensive people• seizures and headaches commonly antedate

haemorrhage• cavernous angiomas tend to be multiple and

familial


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A. Arterial Disease (anatomical factors) Caroticocavernous fistula Hereditary haemorrhagic telangiectasia Saccular aneurysms

• cause 1 in 13 intracerebral haemorrhages (2 in 13 <65 years old), usually in conjunction with subarachnoid haemorrhage


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A. Arterial Disease (anatomical factors) Atheromatous aneurysm Septic arteritis and mycotic aneurysms Necrotising angitis of the CNS* Arterial dissection


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A. Arterial Disease (anatomical factors) Intracerebral tumours

• primary (glioblastoma, oligodendroglioma, medulloblastoma, haemangioblastoma)

• metastases (melanoma, bronchial carcinoma, renal carcinoma, choriocarcinoma, endometrial carcinoma)

Intracranial venous thrombosis*


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A. Arterial Disease (anatomical factors) Moyamoya syndrome Occult head injury* Trauma Haemorrhagic brain infarction

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B. Raised Blood Pressure (haemodynamic factors)

Acute arterial hypertension Alcohol (also antiplatelet action, and

coexistent liver disease) Amphetamines (may also cause a

vasculitis) Cocaine and other sympathomimetic drugs

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Monoamine oxidase A inhibitors Exposure to extreme cold Trigeminal nerve stimulation Post carotic endarterectomy, heart

transplantation, or correction of congenital heart lesions

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Chronic arterial hypertension, causing complex small vessel disease (see above)

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C. Bleeding Diathesis (haemostatic factors)*

Anticoagulants• risk of intracerebral haemorrhage is about

1% per year• Increased risk if elderly, previous stroke,

hypertensive, small vessel disease, and if INR > 4.0


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Antiplatelet drugs: probably a relatively minor contributory factor

Thrombolytic treatment• 0.75% of patients with myocardial infarction

(>2% risk if elderly >65 years, low body weight <70-kg, hypertensive, and given alteplase as opposed to streptokinase; 0.3% risk if none of these risk factors)


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Thrombocytopenia Haemophilia & other hereditary

coagulation factor deficiencies (e.g. factor V) Leukaemia Diffuse intravascular coagulation


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Risk Factors for Cerebral InfarctionRelative

RiskEstimated age-

standardised prevalenceof exposure inpopulation (%)

Definite increasing age male gender increasing BP 2-4 30 cigarette smoking 2-4 25 diabetes mellitus 2 3 atrial fibrillation 6 1 ischaemic heart disease (IHD) 1-3 20 carotid bruit/stenosis 3-15 4 transient ischaemic attack or

previous stroke7 2

peripheral vascular disease(intermittent claudication)

1-4 3

increasing plasma fibrinogen

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Risk Factors for Cerebral InfarctionPossible

hyperlipidaemia* (definite for IHD) hyperhomocystinaemia activation of the renin-angiotensin-

aldosterone system high plasma factor VII coagulant activity low blood fibrinolytic activity raised haematocrit

* probable weak (or under-researched) positive association with ischaemic stroke, and possible weak inverse/negative association

with haemorrhagic stroke

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raised von-Willebrand factor antigen raised tissue plasminogen activity antigen plasma viscosity (largely determined by

plasma fibrinogen) physical inactivity obesity snoring and sleep apnoea



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recent infection family history of stroke diet (salt, fat) alcohol (none, or heavy drinking) race social deprivation stress



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Infarction

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Haemorrhage

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Focal Neurological and Ocular Symptoms

Motor Symptoms weakness or clumsiness of one side of

the body, in whole or in part (hemiparesis) simultaneous bilateral weakness

(paraparesis, quadriparesis)* difficulty swallowing (dysphagia)* imbalance (ataxia)*

* as an isolated symptom, this does not necessarily indicate focal brain ischaemia or haemorrhage because there are many other

potential causes

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Speech/Language Disturbances difficulty understanding or expressing

spoken language (dysphasia) difficulty reading (dyslexia) or writing

(dysgraphia) difficulty calculating (dyscalculia) slurred speech (dysarthria)*


potential causes

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Sensory Symptoms Somatosensory

• altered feeling on one side of the body, in whole or in part (hemisensory disturbance)


potential causes

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Sensory Symptoms Visual

• loss of vision in one eye, in whole or in part (monocular blindness)

• loss of vision in the left or the right half or quarter of the visual field (hemianopia, quadrantanopia)

• bilateral blindness• double vision (diplopia)*


potential causes

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Vestibular Symptoms a spinning sensation (vertigo)*

Behavioural/Cognitive Symptoms difficulty dressing, combing hair, cleaning

teeth etc.; geographical disorientation; difficulty copying diagrams such as a clock, flower, or intersecting cubes (visual-spatial-perceptual dysfunction)

forgetfulness (amnesia)** as an isolated symptom, this does not necessarily indicate focal

brain ischaemia or haemorrhage because there are many other potential causes

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Non-focal Neurological Symptoms

Generalised weakness and/or sensory disturbance‘Blackouts’ with altered or loss of consciousness or fainting, with or without impaired vision in both eyesIncontinence of urine or faecesConfusion

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Non-focal Neurological SymptomsAny of the following symptoms, if isolated:*

A spinning sensation (vertigo) Ringing in ears (tinnitus) Difficulty swallowing (dysphagia) Slurred speech (dysarthria) Double vision (diplopia) Loss of balance (ataxia)

* If these symptoms occur in combination, or with focal neurological symptoms, they may indicate focal cerebral ischaemia

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DIFFERENTIAL DIAGNOSIS OF ISCHEMIC STROKE & TIA

Clinical diagnosis of ischemic or hemorrhagic stroke depends upon clinicians understanding of brain function and pathology.

Deficit that evolve over weeks are usually caused by:• Brain mass either primary or metastatic

brain tumor.• Brain abscess.• Sub-dural hematoma.

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TIA may be confused with classic or

complicated:

• Migraine.

• Seizures.

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Hemorrhagic stroke often enters in

differential diagnosis:

• Ischemic strokes.

• Verterobasillary ischemia.

• Non-specific dizziness.

• Meinier’s disease.

• Peripheral vestibulopathy.

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Differential Diagnosis of Stroke (in order of frequency of occurrence in general practice)

Metabolic/toxic encephalopathy (hypoglycaemia, non-ketotic hyperglycaemia, hyponatraemia, Wernicke-Korsakoff syndrome, hepatic encephalopathy, alcohol and drug intoxication)

Functional/non-neurological (e.g. hysteria) Epileptic seizure (postictal Todd’s paresis)

or non-convulsive seizures

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Elements of Patient Management within a Specialist Stroke Unit

Standardised (protocol driven) investigation and management

Risk assessment for swallowing Active treatment of contributory factors Early rehabilitation Multidisciplinary team Rationalise medication Research opportunities Discharge planning

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Tips on Triples in Acute Stroke: Some Points Worth Remembering

3 h window for safe and effective thrombolysis

Avoid thrombolyis if infarction already affects more than 1/3 of MCA territory

Control blood sugar tightly for 3 days Start blood pressure treatment after 3

days Take decision on tube feeding at 3 days

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Tips on Triples in Acute Stroke: Some Points Worth Remembering

Three complications to avoid: aspiration, venous thrombosis, infection

Three groups of patients (atherothrombotic, cardioembolic and haemorrhagic) get three different treatment: aspirin, warfarin or neither

Delay warfarin for 3 weeks after significant embolic infarct

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The 7 D’s of Stroke Care

Detection: Dispatch Delivery Door DataDecision Drugs

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Algorithm for Suspected Stroke:Goals for Management of Stroke

Critical EMS assessments and actions : Support ABCs; give oxygen if needed Perform prehospital stroke assessment Establish time when patient last known normal (Note: therapies

may be available beyond 3 hours from onset) Transport; consider triage to a center with a stroke unit if

appropriate; consider bringing a witness, family member or caregiver

Alert hospital Check glucose if possible

Identify signs of possible stroke

Continued

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Immediate general assessment and stabilization: Assess ABCs, vital signs Provide oxygen if hypoxemic Obtain IV access and blood samples Check glucose; treat if indicated Perform neurologic screening assessment Activate stroke team Order emergent CT scan of brain Obtain 12-lead ECG

Immediate neurologic assessment by stroke team or designee Review patient history Establish symptom onset Perform neurologic examination (NIH Stroke Scale or Canadian

Neurologic scale)

Continued

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Does CT scan show any hemorrhage?

Probable acute ischemic stroke; consider

fibrinolytic therapy:

Check for fibrinolytic exclusions Repeat neurologic exam: are deficits

rapidly improving to normal

Consult neurologist or neurosurgeon;

consider transfer if not available

HemorrhageNo Hemorrhage

Patient remains candidate for fibrinolytic therapy

Administer aspirin

Not a Candidate

Begin stroke pathway Admit to stroke unit if available Monitor BP; treat if indicated Monitor neurologic status; emergent CT if

deterioration Monitor blood glucose; treat if needed Initiate supportive therapy; treat comorbidities

Review risks / benefits with patient and family: If

acceptable Give tPA No anticoagulants or antiplatelet treatment for

24 hours

Candidate

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Critical Time Periods

Immediate general assessment 10 minutes

Immediate neurologic assessment 25 minutes

Acquisition of head CT 25 minutes

Interpretation of the CT Scan 45 minutes

Administration of fibrinolytics, timed from ED arrival 60 minutes

Administration of fibrinolytics, timed from onset of symptoms 3 hours

Admission to a monitored bed 3 hours

BIKHA STROKE By Dr. Bikha Ram Devrajani FCPS, FACP, FRCP Professor Medicine Liaquat University of...

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