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STROKE

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Setelah menyelesaikan topik 6 ini, peserta didik diharapkan

mampu:

Menjelaskan tentang Definisi stroke

Menjelaskan tentang Epidemiologi stroke Menjelaskan tentang Etiologi dan factor resiko stroke

Menjelaskan tentang klasifikasi stroke

Menjelaskan tentang Manifestasi stroke

Menjelaskan tentang Patofisiologi stroke

Menjelaskan tentang Pemeriksaan Diagnostik stroke Menjelaskan tentang penatalaksanaan stroke

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Gangguan dalam sirkulasiserebral o/k adanyasumbatan pd pemb darahdi otak

/- aliran darah ke area

dlm otak < O2 kejaringan di otakkematian jaringan

infark

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TIME is brain

Intervensi sejak dini dpt me outcomepasien

Bbrp pemb darah besar yg rusak setiapmenit o/k stroke iskemik:

1,9 juta neuron

14 trilliun synaps

12 km jaringan mielin

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Pathogenesis

Hemorrhagic Stroke (17%)

IntracerebralHemorrhage(59%)

Subarachnoid

Hemorrhage(41%)

Ischemic Stroke (83%)

Large Artery(20%)

Embolism(20%)

Lacunar (25%)

Cryptogenic (30%)

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R Hemiplegia/paresis

Impaired speech(Aphasias)

Impaired discrimination(R/L)

Slow performance,Cautious

Aware of deficitsDepression, Anxiety

Impaired comprehension &Memory R/T language and mathLeft -Sided CVA:

LEFT BRAIN DAMAGEHemianopsia

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Right-sided CVA:RIGHT BRAIN DAMAGE Impaired judgment

Impulsive/Safetyproblems

Denies/Minimizesproblems

L hemiplegia/paresis

Left-sidedneglect

Spatial-perceptualdeficits

Rapid performanceShort attention

span

Hemianopsia

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Cerebrovascular Accident

Risk Factors

Nonmodifiable:

Age Occurrence doubles each decade >55 years

Gender Equal for men & women; women die more frequently than

men

Race African Americans, Hispanics, Native Americans, Asian

Americans -- higher incidence

Heredity family history, prior transient ischemic attack, or prior

stroke increases risk

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Risk Factors

Controllable Risks with Medical Treatment & Lifestyle

Changes:

High blood pressure Diabetes

Cigarette smoking TIA (Aspirin)

High blood cholesterol Obesity

Heart Disease Atrial fibrillationOral contraceptive use Physical inactivity

Sickle cell disease Asymptomatic carotid stenosis

Hypercoagulability

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CVA Risk Factors

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Anatomy of Cerebral Circulation

Blood Supply

Anterior: Carotid Arteries middle & anterior cerebralarteries frontal, parietal, temporal lobes; basal ganglion; part of the

diencephalon (thalamus & hypothalamus)

Posterior: Vertebral Arteries basilar artery

Mid and lower temporary & occipital lobes, cerebellum, brainstem, &part of the diencephalon

Circle of Willis connects the anterior & posterior cerebralcirculation

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Anatomy of Cerebral Circulation

Blood Supply

20% of cardiac output750-1000ml/min

>30 second interruption neurologic metabolism

is altered; metabolism stops in 2 minutes; braincell death < 5 mins.

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C b l A id

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Cerebrovascular AccidentPathophysiology

Atherosclerosis: major cause of CVA

Thrombus formation & emboli development

Abnormal filtration of lipids in the intimal layer of the arterial wall

Plaque develops & locations of increased turbulence of blood -bifurcations

Increased turbulence of blood or a tortuous area

Calcified plaques rupture or fissure

Platelets & fibrin adhere to the plaqueNarrowing or blockage of an artery by thrombus or emboli

Cerebral Infarction: blocked artery with blood supply cut off

beyond the blockage

C b l A id

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Cerebrovascular AccidentPathophysiology

Ischemic Cascade

Series of metabolic events

Inadequate ATP adenosine triphosphate production

Loss of ion homeostasisRelease of excitatory amino acids glutamate

Free radical formation

Cell death

Border Zone: reversible area that surrounds the core ischemicarea in which there is reduced blood flow but which can be

restored(3 hours +/-)

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CVA? - Call 911

Sudden numbness or weakness of face, arm, or leg, especially on

one side of the body.

Sudden confusion or trouble speaking or understanding speech.

Sudden trouble seeing in one or both eyes.

Sudden trouble walking, dizziness, or loss of balance or

coordination

Sudden severe headache with no known cause.

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Transient Ischemic Attack

Temporary focal loss of neurologic function

Caused by ischemia of one of the vascular territories of

the brainMicroemboli with temporary blockage of blood flow

Lasts less than 24 hrs often less than 15 mins

Most resolve within 3 hours

Warning sign of progressive cerebrovascular disease

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Transient Ischemic Attack

Diagnosis:

CT without contrast

Confirm that TIA is not related to brain lesions

Cardiac EvaluationRule out cardiac mural thrombi

Treatment:Medications that prevent platelet aggregation

ASA, Plavix

Oral anticoagulants

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Classifications

Based on underlying pathophysiologic findings

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Classifications

Ischemic Stroke

Thrombotic

Embolic

Hemorrhagic Stroke

Intracerebral HemorrhageSubarachnoid Hemorrhage

Aneurysm

Berry or Saccular

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Classifications

Ischemic Strokeinadequate blood flow to the brain from partial orcomplete occlusions of an artery--85% of all strokes

Extent of a stroke depends on:

Rapidity of onset

Size of the lesion

Presence of collateral circulation

Symptoms may progress in the first 72 hours as infarction & cerebral

edema increase

Types of Ischemic Stroke:

Thrombotic Stroke Embolic Stroke

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CVA Recognition

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Ischemic Thrombotic Stroke

Lumen of the blood vessels narrow then

becomes occluded infarction

Associated with HTN and Diabetes Mellitus

>60% of strokes

50% are preceded by TIA

Lacunar Stroke: development of cavity in place ofinfarcted brain tissue results in considerable deficits

motor hemiplegia, contralateral loss of sensation or

motor ability

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Thrombotic Stroke

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Common Sites of Atherosclerosis

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Ischemic Embolic Stroke

Embolus lodges in and occludes a cerebral artery Results in infarction & cerebral edema of the area supplied by

the vessel

Second most common cause of stroke 24%

Emboli originate in endocardial layer of the heart atrial

fibrillation, MI, infective endocarditis, rheumatic heart disease,

valvular prostheses

Rapid occurrence with severe symptoms body does not havetime to develop collateral circulation

Any age group

Recurrence common if underlying cause not treated

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Embolic Stroke

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Goals for Management

Immediate assess & stabilize ABCs, VS

Neurologic screening

Oxygen if hypoxic

IV access

Check glucose Activate stroke team CODE GREEN

12-lead EKG

Immediate Neuro Assessment Establish symptom onset

Review hx

Stroke Scale

Facial droop; arm drift; abnormal speech

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CT Scan No hemorrhage:

Consider Fibrinolytic therapy Check for exclusions

tPA

No anticoagulants or antiplatelet therapy for 24 hours

If not a candidate: Antiplatelet Therapy

CT Scan Hemorrhage:

Neurosurgery?

If no surgery: Stroke Unit Monitor BP and treat Hypertension

Monitor Neuro status

Monitor blood glucose and treat as needed

Supportive therapy

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Immediate assess & stabilize ABCs, VS Neurologic screening

Oxygen if hypoxic

IV access

Check glucose

Active stroke team

Emergent CT scan of brain

12-lead EKG

Immediate Neuro Assessment Establish symptom onset

Review hx

Stroke Scale

Facial droop; arm drift; abnormal speech

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Hemorrhagic Stroke

Hemorrhagic Stroke

15% of all strokes

Result from bleeding into the brain tissue itself

Intracerebral

Subarachnoid


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Cerebrovascular AccidentHemorrhage Stroke

Intracerebral Hemorrhage

Rupture of a vessel

Hypertension most important cause

Others: vascular malformations, coagulation disorders,anticoagulation, trauma, brain tumor, ruptured aneurysms

Sudden onset of symptoms with progression

Neurological deficits, headache, nausea, vomiting,decreased LOC, and hypertension

Prognosis: poor 50% die within weeks

20% functionally independent at 6 months


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Cerebrovascular AccidentHemorrhage Stroke

Intracerebral Hemorrhage

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C A

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Hemorrhagic-Subarachnoid

Hemorrhagic StrokeSubarachnoid Hemorrhage

Intracranial bleeding into the cerebrospinal fluid-filled space

between the arachnoid and pia mater membranes on the

surface of the brain

C b l A d

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Commonly caused by rupture of cerebral aneurysm

(congenital or acquired)

Saccular or berry few to 20-30 mm in size

Majority occur in the Circle of Willis

Other causes: Arteriovenous malformation (AVM), trauma,

illicit drug abuse Incidence: 6-16/100,000

Increases with age and more common in women


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Cerebrovascular AccidentHemorrhagic-Subarachnoid

Cerebral Aneurysm

Warning Symptoms: sudden onset of a severe

headache worst headache of ones life

Change of LOC, Neurological deficits, nausea, vomiting,seizures, stiff neck

Despite improvements in surgical techniques, manypatients die or left with significant cognitive difficulties

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H h i S b h id

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Cerebral Aneurysm

Surgical Treatment:

Clipping the aneurysm prevents rebleed

Coiling platinum coil inserted into the lumen of the

aneurysm to occlude the sac

Postop: Vasospasm prevention Calcium Channel Blockers

H h i S b h id

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Cerebral Aneurysm Surgical Tx

H h i S b h id

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Cerebral Aneurysm Coiling

C b l A id t

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Classification

C b l A d

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Clinical Manifestations

Middle Cerebral Artery Involvement Contralateral weakness

Hemiparesis; hemiplegia

Contralateral hemianesthesia Loss of proprioception, fine touch and localization

Dominant hemisphere: aphasia

Nondominant hemisphere neglect of opposite side;

anosognosia unaware or denial of neuro deficit

Homonymous hemianopsia defective vision or blindness

right or left halves of visual fields of both eyes

C b l A id t

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Anterior Cerebral Artery InvolvementBrain stem occlusion

Contralateral

weakness of proximal upper extremity

sensory & motor deficits of lower extremities

Urinary incontinence

Sensory loss (discrimination, proprioception)

Contralateral grasp & sucking reflexes may be present

Apraxia loss of ability to carry out familiar purposefulmovements in the absence of sensory or motor impairment

Personality change: flat affect, loss of spontaneity, loss ofinterest in surroundings

Cognitive impairment


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Cerebrovascular AccidentClinical Manifestations

Posterior Cerebral Artery &

Vertebrobasilar Involvement

Alert to comatose

Unilateral or bilateral sensory loss

Contralateral or bilateral weakness

Dysarthria impaired speech articulation

Dysphagia difficulty in swallowing

Hoarseness Ataxia, Vertigo

Unilateral hearing loss

Visual disturbances (blindness, homonymous hemianopsia

nystagmus, diplopia)

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Ce eb ovascu a cc deClinical Manifestations

Right Brain Left Brain Damage

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Affect

Difficulty controlling emotions

Exaggerated or unpredictable emotional response Depression / feelings regarding changed body image

and loss of function


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Intellectual Function

Memory and judgment

Left-brain stroke: cautious in making judgmentsRight-brain stroke: impulsive & moves quickly to decisions

Difficulties in learning new skills


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Communication

Left hemisphere dominant for language skills in theright-handed person & most left-handed persons --Aphasia/Dysphasia

Involvement Expression & ComprehensionReceptive Aphasia (Wernickes area): sounds of speech nor

its meaning can be understood spoken & written

Expressive Aphasia (Brocas area): difficulty in speakingand writing

Dysarthria: Affects the mechanics of speech due to musclecontrol disturbances pronunciation, articulation, andphonation


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Spatial-Perceptual Alterations 4 categories:

1. Incorrect perception of self & illness

2. Erroneous perception of self in space may neglect allinput from the affected side (worsened by homonymous

hemianopsia)

3. Agnosia: Inability to recognize an object by sight, touch or

hearing

4. Apraxia: Inability to carry out learned sequential

movements on command

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Homonymous Hemianopsia


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Elimination

Most problems occur initially and are temporary

One hemisphere stroke: prognosis is excellent fornormal bladder function

Bowel elimination: motor control not a problem

constipation associated with immobility, weak

abdominal muscles, dehydration, diminished response tothe defecation reflex

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Treatment Goals

Prevention Health Maintenance Focus:

Healthy diet

Weight control

Regular exercise No smoking

Limit alcohol consumption

Route health assessment

Control of risk factors


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Treatment Goals

Prevention

Drug Therapy

Surgical Therapy

Rehabilitation


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Diagnostic Studies

Done to confirm CVA and identify cause

PE: Neuro Assessment; Carotid bruit

Carotid doppler studies (ultrasound study)

CT primary identifies size, location, differentiates betweenischemic and hemorrhagic

CTA CT Angiography visualizes vasculature

MRI greater specificity than CT

May not be able to be used on all patients (metal, claustrophobia)

Angiography: gold standard for imaging carotid arteries


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Treatment Goals

Drug Therapy Thrombotic CVA to reestablish bloodflow through a blocked artery

Thrombolytic Drugs: tPA (tissue plasminogen activator)produce localized fibrinolysis by binding to the fibrin in the thrombi

Plasminogen is converted to plasmin (fibrinolysin)Enzymatic action digests fibrin & fibrinogen

Results is clot lysis

Administered within 3 hours of symptoms of ischemic

CVAConfirmed DX with CT

Patient anticoagulated

ASA, Calcium Channel Blockers

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CVA - Treatment Goals

Surgical Treatment

Carotid endarterectomy preventive > 100,000/year

removal of atheromatous lesions

Clipping, wrapping, coiling Aneurysm

Evacuation of aneurysm-induced hematomas larger than 3

cm.

Treatment of AV Malformations

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Carotid Artery Disease

C A

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Carotid Artery Disease

Carotid artery disease is the leading cause of strokes.

More than 50% of stroke victims present no warning signs.

After age 55, the risk of stroke doubles every 10 years.

97% of the adult population cannot name a single

warning sign of a stroke.

50% of nursing home admissions are stroke victims

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C d A S

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Carotid Artery Stents

C id E d

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Carotid Endarterectomy

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Treatment Goals

Drug Therapy

Measures to prevent the development of a thrombus orembolus for At Risk patients:

Antiplatelet Agents

Aspirin

Plavix

Combination

Oral anticoagulation Coumadin

Treatment of choice for individuals with atrial fibrillation who have had aTIA


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Ce eb ovascu a cc de

Nursing Diagnoses

Ineffective tissue perfusion r/t decreased cerebrovascular

blood flow

Ineffective airway clearance

Impaired physical mobility Impaired verbal communication

Impaired swallowing

Unilateral neglect r/t visual field cut & sensory loss Impaired urinary elimination

Situational low self-esteem r/t actual or perceived loss of

function


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Nursing Goals

Maintain stable or improved LOC Attain maximum physical functioning

Attain maximum self-care activities & skills

Maintain stable body functions Maximize communication abilities

Maintain adequate nutrition

Avoid complications of stroke Maintain effective personal & family coping


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Warning Signs of Stroke

Sudden weakness, paralysis, or numbness of the face,arm, or leg, especially on one side of the body

Sudden dimness or loss of vision in one or both eyes

Sudden loss of speech, confusion, or difficulty speakingor understanding speech

Unexplained sudden dizziness, unsteadiness, loss ofbalance, or coordination

Sudden severe headache


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Acute Phase

Assess: Frequently to assess CVA evolutionNeuro Glascow Coma Scale -- mental status, LOC,

pupillary response, extremity movement, strength,sensation; ICP; Communicationspeaking &

understanding; sensory-perceptual alterationsCV cardiac monitoring; VS, PO, hemodynamic monitoring;

Resp airway/air exchange/aspiration;

GI swallowinggag reflex; bowel sounds; bowel

movement regularityGU urinary continence

Integumentary skin integrity, hygiene

Coping individual and family


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Acute Phase

Nsg Action:

Supportive Care

Respiratory spans from intubation to breathing on own

Musculoskeletal -- Positioning side-to-side; HOB elevated;PROM exercise; splints; shoes/footboard

GI enteral feedings initially

GU foley catheter

Skin preventive care

Meds: anti platelet


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Acute Phase

Patient Education:

Clear explanations for all care/treatments

Focus on improvementsregained abilities

Include family


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Rehabilitation

Assess: Swallowing; Communication; Complications;motor and sensory function

Nsg Action: Coordinate resources: Speech Therapyassess swallowing

Physical Therapyambulation/strengthening

Bowel/Bladder Appropriate self-help resources

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Rehabilitation

Comprehensive plan Physical Medicine & Rehabilitation / Inpatient Rehab

Learn techniques to self-monitor & maintain physicalwellness

Demonstrate self-care skills

Exhibit problem-solving skills with self-care

Avoid complications of stroke

Communication Maintain nutrition & hydration

Use community resources

Family cohesiveness


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Rehabilitation

Resources

American Stroke Association

Association of Rehabilitation Nurses

National Institute of Neurological Disorders & Stroke National Stroke Association

Society for Neuroscience

Stroke Clubs International

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(1) Supportive measures

(2) Antiplatelet agents

(3) Thrombolysis

(4) Anticoagulation

(5) Secondary prevention

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Tangani komplikasi setelah pasien tirah baringlama (pneumonia, UTI, bowel and bladder care,pencegahan deep vein trombosis)

Tdk dpt menelan/regurgitate or aspiratenasogastric tube

Kontrol tekanan darah:Lanjutkan th/ regular anti-hypertensive drugs

Kontrol gula darah, pertahankan keseimbangancairan

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Anti-platelet agents

Aspirin 325 mg per day K.Indikasi pd hemorrhage

Active bleeding lesion (e.g. bleeding peptic ulcer)

Anticoagulasi u/ cardiac emboli dgn atrial fibrillation/thrombus pd

ventrikel kiri

Mulai dgn heparin dan warfarin (target INR=2-3)

Komplikasi :hemorrhagic

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Thrombolysis Dpt menyebabkan hemorrhagic

Dpt diberikan dlm 6 jam awal, tdk ada HTN , tanpakontraindikasi.

Obat: streptokinase dan Rt-PA.

Secondary prevention

Kontrol faktor resiko

Antiplatelet agent ( aspirin, ticlopidine, Dipyridamole,clopidogrel)

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