seminar stroke.4th rotation medicine

8/6/2019 Seminar Stroke.4th Rotation Medicine

1/68

By

Siti Nur Shafiqah Binti FazilMohammad Hazim Fikri Bin Adnan

Mohd. Amirul Hafifi Bin KhairulzamanNor Akma Binti Sulaiman

Norashikin Binti Naim

Zafirah Hani Binti RamliAtika Azura Binti Abdul Rashed


2/68

Public: weakness, usually permanent on oneside, often with loss of speech.


3/68

Stroke is a clinical syndrome characterized by

rapidly developing clinical symptoms and/or signs of

focal, and at times global, loss of cerebral function,

with symptoms lasting more than 24 hours or leading

to death, with no apparent cause other than that of

vascular origin.

~ Academy of Medicine, Malaysia


4/68

Ischemic Hemorrhage

- Sudden loss of fx dt loss of bloodsupply to an area that controls thatfx.

- Usually caused bypartial/complete blockage of anartery that supplies the brain.

- results from a weakenedvessel that ruptures andbleeds into the surroundingbrain.

- blood accumulates andcompresses the surrounding


5/68

HemorrhagicIschemic

Corticol

Lacunar

Brainstem

(85%) (15%)

h ertension - Em olism- atheroma

Large vessel

- Throm osis- Em olism

- Su arachnoidhemorrhage

- Intracere ralhemorrhage

- Mesothelioma

Anteriorcirculation

Posteriorcirculation

Smallarteries


6/68

NON-MODIFIABLE MODIFIABLE

Age Hypertension (systolic and diastolic)

Sex Cigarette smoking

Ethnicity/race Diabetes Mellitus

Family history of stroke Atrial fibrillation

Coronary heart disease

Hyperlipidemia

Obesity and physical inactivity

Raised homocysteine levelHigh dietary salt intake

Heavy alcohol consumption

Previous stroke


7/68

Three main causes of ischaemic stroke are:

1. Atherothromboembolism (50%)

2. Intracranial small vessel disease (penetrating arterydisease) (25%)

3. Cardiogenic embolism (20%)

Other causes:

Arterial dissection

Trauma

Vasculitis

Metabolic disorder

Congenital disorder


8/68


9/68

Caused by :

Extracranial embolism

Intracranial thrombosis

Decreased cerebral blood

flow

Necrosis of brain tissue

Cerebral infarction

Stroke

Initiate ischaemic cascade


10/68

1- Embolism

May arise from the heart or extracranial arteries

Sources of cardiogenic emboli : Valvular thrombi (MS, IE, prosthetic valve)

Mural thrombi ( MI, AF)


11/68

2- Thrombosis

Large vessels (including carotid artery system) Small vessels (comprising intracerebral arteries,

including the Circle of Willis & posterior circulation)


12/68


13/68

3- Flow disturbances

Inadequate cerebral blood flow due to :

Decreased cerebral perfusion pressure

Hematologic hyperviscosity ( sickle cell disease,multiple myeloma, polycythemia vera)


14/68

Less common cause :

polycythemia, sickle cell anemia, protein C deficiency,fibromuscular dysplasia of the cerebral arteries, andprolonged vasoconstriction from migraine headachedisorders.

Any process that causes dissection of the cerebral arteries(trauma, thoracic aortic dissection, arteritis)


15/68

Loss of perfusion to a portion of the brain

unleashed the ischemic cascade

On cellular level :

Ischemic neurons become depolarized (ATP depleted)

Membrane ion-transport systems fail

Calcium influx release neurotransmitters (including

glutamate)

Activates N-methyl-D-Aspartate (NMDA) & otherexcitatory receptors on other neurons


16/68

Neurons become depolarized

Further calcium influx

Further glutamate release

Local amplification of initial ischemic insult

+ Massive calcium influx activates various degradative

enzymes

destruction of the cell membrane and otheressential neuronal structures

+ Free radicals, arachidonic acid, and nitric oxide aregenerated by this process further neuronal damage


17/68

Intracerebral and subarachnoid hemorrhage


18/68

Blood vessel ruptures

Explosive entry of blood into the brain parenchyma.

The extravasation forms a roughly circular or oval massthat disrupts the tissue and grows in volume as the

bleeding continues.

Swelling of brain tissue (cerebral edema)

Adjacent brain tissue is distorted and compressed.

Neurological deficit


19/68

1- Intracranial hemorrhage

Common : chronic high BP Weakens the arteries burst

2- Subarachnoid hemorrhage

Common : ruptured

aneurysm


20/68


21/68

Presentation of patient of stroke varies frommild confusion to altered level ofconsciousness, coma and death.

The presentation are dependant on whatportion of the brain is damage.

The areas of the brain affected by the strokedepend on the particular artery that is affected.


22/68

Ischemic stroke

Cortical

Lacunar

Brainstem

Hemorrhagic stroke


23/68


24/68


25/68


26/68

Anterior (carotid) artery circulation

Middle cerebral arteryAphasia

Hemiparesis / plegia

Hemianopia

Anterior cerebral artery

personality changes


27/68


28/68

Symptoms:

Dizziness

Diplopia

Dysarthria

Dysphagia

Dystaxia


29/68

Aphasia

Agnosia

Apraxia hemineglect

Loss of consciousness

Drowsy


30/68


31/68

Definition:

strokes caused by the occlusion of a small branch ofa larger blood vessel. Because of the way bloodvessels divide in the brain, lacunar strokes tend tooccur in areas located away from the surface of thebrain, where many of the smaller blood vesselbranches are located.

Alert

Normal cognitive function (absence of cortical signs)


32/68

Pure motor stroke

Pure Sensory

Sensorimotor

Ataxic Hemiparesis

Dysarthria Clumsy-Hand Syndrome


33/68


34/68


35/68

- dangerous: small portion but have many functions.

: most patient die.

Wallenberg's syndrome Horners syndrome Hemiparesis : corticospinal tract Diplopia: occulomotor Facial numbness and weakness: 5th and 7th cranial

nerve Nystagmus and vertigo: vestibular Dysphagia and dysartria: 9th and 10th


36/68

Dangerous within 24 hours.

Clinical manifestation is almost the same, but usuallypatient with hemorrhagic stroke present with severe

headache which sometimes preceed with vomitting.

Differences between intracerebral and subarachnoidcan only be found radiologically. However, in severe

hemorrhage, its difficult to distinguish between thetwo.

Definite differences between hemorrhagic and

infarction can only be seen radiologically.


37/68

Metabolic/toxic encephalopathy Epileptic seizures ( Todds palsy) Hemiplegic migrain Structural intracranial lesion ( subdural

hematoma, brain tumor, AVM) Encephalitis Head injury Relapsing multiple sclerosis

Conversion disorder Hyperviscosity syndrome Peripheral nerves lesion ( guillaine barre

syndrome)


38/68

FBC, ESR, serumelectrolytes, serumcreatinine,liverfunctiontest, bloodglucose, lipidprofile,coagulationprofile, ABG

- to detect common vascular risk factor and

markers of rarer causes such as atherosclerosis,diabetis mellitus or blood clotting problem

ECG, echocardiography, chest X-ray

- should be considered if cardiac embolism is

suspected Ctbrain

-should be done as soon as possible in all patient

to exclude or confirm hemorrhage


39/68

MRI brainandMRA

- should be considered if CT is negative (CT scan

unable to differentiate ischemic andhemorrhagic stroke especially perfomed >10

days after stroke)

DopplerorDuplexultrasoundscan

- this is used to find out whether there has beena narrowing of the blood vessels in the neck (the

carotid arteries), which supply blood to the

brain.

Lumbarpuncture- should be done if subarachnoid hemorrhage is

suspected and CT brain is negative


40/68

Acute management

Long-term management


41/68

Airway check the patient can protect can protect his/her airway andswallow w/o evidence of aspiration

Breathing check that the patient is breathing adequately; check O2

saturation and give O2 if saturation < 95%Circulation check peripheral perfusion, pulse, and blood pressure

adequate and treat w fluid replacement, anti-arrhythmics drugand inotropic drug as appropriate

Hydration screen for sign of dehydration and give fluids parenterally orby nasogastric tube if necessary

Nutrition assess nutritional status and provide nutritional supplementsif necessary; if dysphagia persist for a day or two, start feedingvia a nasogastric tube

Medication if the patient is dysphagic, consider alternative routes foressential medications


42/68

BP unless there is heart failure or renal failure, evidence ofhypertensive encephalopathy or aortic dissection, do not lowerthe blood pressure in the fist few week since the cerebrelperfusion may decrease. BP often returns towards the patientsnormal level within the first few days

Bloodglucose

check blood glucose and treat w insulin when levels are > 11.1mmol/L. monitor closely to avoid hypoglycemia

Temperature check for pyrexia and investigate and treat underlying cause ;

give antipyretics since raised brain temperature may increaseinfarct volume

Pressuresarea

check pressure areas and introduce measures to reduce the riskfor bedsores : treat infection, maintain nutrition, provide apressure-relieving mattress, turn immobile patient regularly


43/68

Incontinence

check for constipation and urinary retention and treatappropriately; avoid urinary catheterization unless the patient isin acute urinary retention or incontinence is threatening pressureareas

Investigation

CT/MRI, blood glucose, urea n electrolyte, FBC, INR, ESR, ECG


44/68


45/68

Medical therapy Risk factor should be identified and addressed Risk factor are :

HPT treat and monitor

Smoking stop Lifestyle more active (exercise) Alcohol moderate intake/stop High cholesterol statins, diet Raised hematocrit reduce Atrial fibrillation anticoagulate

Obesity weight reduction Diabetes good control Severe carotid stenosis - surgery Sleep apnoea - treat


46/68

Antihypertensive therapy Recognition and good control of high BP is the major factor in both 1st and

2nd stroke prevention. Transient HPT often seen following stroke usuallydoes not require treatment provided diastolic pressure does not rise > 100mmHg. Sustained severe HPT needs treatment. BP should be loweredslowly to avoid any sudden fall in perfusion.

Antiplatelet therapy Long-term soluble aspirin(75 mg daily) reduces substantially the incidence

of further infarction following thromboembolic TIA or stroke. Clopidogrel and dipyrimadole are also used Combined aspirin 75 mg daily and dipytidamole 200 mg twice daily

possibly provide optimal prophylaxis against further thromboembolic

stroke or TIA.

Anticoagulants Heparin and warfarin shoud be given when there is atrial fibrillation


47/68

Other measures Polycythaemia and any clotting abnormalities should be

treated. Statin therapy should be given for all

Surgical approaches Internal carotid endarterectomy

Surgery is recommended in TIA or stroke patient with internalcarotid stenosis >70%.

Successful surgery reduces the risk of further TIA/stroke byaround 75%.

Endarterectomy has a mortality around 3% and a similar risk of

stroke. Percutanous transluminal angioplasty (stenting) is an

alternative. The value of surgery for asymtomatic carotid stenosis is

debatable.


48/68

Rehabilitation after stroke

Optimal care is on a stroke rehabilitation unit that

provides multidisciplinary services, coordinatesdisability-related medical care and trains caregivers.

Physiotherapy*

Speech therapy*

Occupational therapy*


49/68

Is particularly useful in the few weeks inreducing spasticity, relieving contractures andteaching patients to use walking aids.

The benefits of physiotherapy for longer-termoutcome are still inadequately researched.

Baclofen and/or botulinum toxin aresometimes helpful in the management ofsevere spasticity.


50/68

Speech therapists have a vital understanding ofaphasic patients problem and frustration.

Return of speech is hastened by conversation

generally. If swallowing is unsafe because of the risk of

aspiration, either nasogastric feeding orpercutanous gastrostomy will be needed.

Video-fluoroscopy while attempting toswallow is helpful.


51/68

Following recovery, the occupational therapistsplay a valuable role in assessing therequirement for and arranging the provision of

various aids and modifications in the home,such as stair rails, hoists or wheelchairs.


52/68

Anti-platelet- aspirin, clopidogrel, ticlopidine

Anticoagulants-heparin, warfarin

Thrombolytics-streptokinase, urokinase,t-PA

Antihypertensiveagents

ACE inhibitors

Beta-blockers

Hydralazine Lipidloweringdrugs


53/68


54/68

ANTIPLATELETS

Inhibition of prostaglandin mechanism

Aspirin

Inhibition of ADP-induced platelet aggregation Ticlodipine, clopidogrel

Blockade of GP llb/llla receptors on platelets

Abciximab, integrelin


55/68

irreversibly inactivates platelet cyclooxygenase1 (through acetylation)and suppresses theproduction of thromboxane A2

Interfere with platelet aggregation

Anuclear platelet cannot synthesize newenzyme during its 10 day lifetime


56/68

Irreversibly inhibit binding of ADP to itsreceptors on platelets

Thus, inhibit activation of GP llb/IIIa receptors

required for platelets to bind to fibrinogen andto each other


57/68

ANTICOAGULANTS

Heparin

serve as a calatytic template to accelerate the

antithrombin reaction antithrombin inhibits clotting factor proteases by

forming stable complexes with them

it interacts with activated factors (thrombin)IIa,

IXa,Xa, providing anticoagulant effect withinminutes


58/68

Warfarin

Antagonist of vitamin K

inhibit the synthesis of Vitamin K dependent clotting

factors: factor II

factor VII

factor IX

factor X


59/68

THROMBOLYTICS

Streptokinase

Combines with ciculating plasminogen to form an

activator complex: convert plasminogenplasmin t-PA (Alteplase, Reteplase)

Preferentially activate plasminogen bound to fibrin confines fibrinolysis to the formed thrombus and

avoids systemic activation


60/68

ANTIHYPERTESIVE AGENTS

IV betablockers

hydralazine are recommended

ACE inhibitors

limited effect on cerebral circulation


61/68

angiotensinogen

Angiotensin 1

Angiotensin 2

Angiotensin 2 receptor

vasoconstriction Aldosterone secretion

Increase peripheral

vascular resistanceIncreased sodium,

Increase water retention

Increased blood pressure

ACE inhibitors

Captopril, enapril, lisinopril, ramipril

Inhibit peptidyl dipeptidase enzymeDecreased formation of angiotensin 2

Decreased breakdown of bradykinin

Angiotension

receptor blocker

Losartan, valsartan, irbesartan,candesarta

Block angiotensin 2 receptorDo not have effect on bradykinin

Similar benefits like ACE inhibitor


62/68

Labetalol


63/68

This drug causes direct vasodilation, actingprimarily on arteries and arterioles.

This results in a decreased peripheral

resistance, which in turn prompts a reflexelevation in heart rate and cardiac output.


64/68

LIPID LOWERING DRUGS

HMG CoA Reductase Inhibitor Bile acids binding resin

Nicotinic acid

Fibric acid derivatives

Cholesterol absorption inhibitors


65/68

HMG CoA reductase inhibitor

Lovastatin, simvastatin, pravastatin, fluvastatin

MOA: - analogs of 3-hydroxy-3-methylglutarate-competitive inhibitors of 3-H-3-M coenzyme A (HMG

CoA reductase) which catalyze mevalonate biosynthesis

HMG CoA mevalonate

HMG CoA re uctase ihibitor

Decreased de novo synthesis of cholesterol

Increase LDL receptor number

Increased LDL uptake by hepatocytes

Decreased plasma LDL


66/68

Bileacidbindingresin(cholestyramine,cholestipol,colesevelam)

Nicotinic acid(niacin)

Fibrates (clofibrate,benzafibrate,gemfibrozil)

Cholesterolabsoprtioninhibitor(ezetimibe)

MOA: binds to bileacid in the intestineand preventsreabsorbtion ;

Enterohepaticcycling interuptedMore cholesterolneede to form bileacidOutcome:

Increased de novesynthesis ofcholesterolIncreased LDL

MOA: -decreasedintracellular lipaseactivityIncreased

lipoprotein lipaseactivityDecrease catabolicrate of HDL

MOA: - activateperoxixomeproliferator-activated receptor

-Increasedexpression oflipoprotein lipase-Increasedcatabolism of VLDL

MOA: inhibitintestinal absorptionof dietry and biliarycholesterol

-reduce hepaticcholesterol stores-increase hepaticuptake of LDL fromplasma.


67/68

Phychosocial Financial

Sexual relationships changed.

Most of the females lost interest intheir appearance, regardless of their

age.

felt unable to prevent outbursts andthis compounded their feelings ofguilt, low-esteem and despair.

increase anger and feelings offrustration.

Loss of self esteem makes depressioncommon

Need to buy some equipment for thepatients for example, wheel chair, airbed, medication, pampers.

The fees for physiotherapy andspeech therapist treatment.

Many become unemployable, loseindependence and are financiallyembarrassed


68/68

Family members must be educated about howto take care of stroke patient

Both the family and stroke patient must go for

counseling in order to over come the problem Physiotherapy and speech therapy have an

important psychological role, as it will increaseconfidence of stroke patients to live their life.

seminar stroke.4th rotation medicine

Documents