Update of
Stroke Management

Fx. Soetedjo Widjojo, dr. SpS(K)

Bagian Neurologi FK UNS/RSUD Dr. Moewardi

Surakarta

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Stroke

Stroke

Suatu sindrom klinis dengan gejala berupa gangguan fungsi otak secara fokal maupun global, yang dapat menimbulkan kematian, atau kecacatan yang menetap lebih dari 24 jam, tanpa penyebab lain kecuali gangguan vaskuler

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Epidemiologi Stroke

Global (WHO, 2004)

15 juta orang diseluruh dunia menderita stroke (2002)

Satu orang meninggal oleh karena stroke tiap 3 menit

5 juta cacat permanen

Stroke adalah penyebab kematian ketiga terbanyak di dunia

2009,WHO : Stroke menjadi penyebab kematian kedua

Depkes 2008 menjadi stroke menjadi salah satu penyebab kematian utama di beberapa rumah sakit

Rata rata tiap pasien menghabiskan US$ 15.000 dalam 90 hari pertama pasca stroke

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KOMPLIKASI STROKE AKUT/SUBAKUT

BANYAK PROBLEM !!!

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MedicalPneumonia

Urinary tract infection

Airway obstruction

Cardiac arrhythmias

Hypertension

Decubitus ulcers

Dehydration

Joint problems

Electrolyte disturbances

Stress hyperglycemia

Pulmonary embolism

Stress ulcers (gastrointestinal)

Deep venous thrombosis

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Neurological

Elevated intracranial pressure

Herniation

Hemorrhagic transformation

Seizures

Cerebral edema

Hydrocephalus

Recurrent stroke

DAMPAK SOSIAL STROKE

KEHILANGAN PEKERJAANMENURUNKAN PRODUKTIFITASMENJADI BEBAN KELUARGABEBAN NEGARAMERUSAK KEHARMONISAN KELUARGADEPRESI.BUNUH DIRI

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Tidak dapat dimodifikasi

UsiaJenis kelaminKeturunanRas

Dapat dimodifikasi

HipertensiPenyakit jantung Diabetes mellitusMerokokHipercholesterolemia

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PREVENSI PRIMER

PENCEGAHAN LEBIH PENTING !

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40%

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Types of Stroke

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Brain Attack

Sudden Onset of:

Slurred speech, difficulty understanding others
Legs clumsy or numb
One side of body affected
Weakness

Headache, unusually severe (or facial numbness)
Eyes: loss of sight (in one eye or both eyes)
Arms clumsy or numb AND/OR
Dizziness

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Major Clinical Manifestations
of Atherothrombosis

Adapted from: Drouet L. Cerebrovasc Dis 2002; 13(suppl 1): 16.

Transient ischaemic attack

Angina:

Stable Unstable

Ischaemic

stroke

Myocardial infarction

Peripheral arterial

disease:

Intermittent claudication Rest Pain Gangrene Necrosis

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Atherothrombosis can be an extensive vascular disease affecting the coronary, cerebral and peripheral circulation.

It is a progressive, generalized disorder with many clinical manifestations either acute or chronic and often multiple in any single patient.

Stenosis in an atherosclerotic artery may give rise to angina, a transient ischemic attack (TIA) or intermittent claudication.

Atherothrombosis in the coronary arteries is the major cause of acute
coronary syndrome (ACS), defined as unstable angina and non Qwave myocardial infarction.

Atherothrombosis of the cerebral arteries may also result in TIA or
ischemic stroke.

In the peripheral arteries, thrombosis superimposed on atherosclerosis can contribute to the progression of peripheral arterial disease, producing intermittent claudication (leg pain on walking that is relieved by rest) as well as ischemic necrosis and, potentially, loss of the limb.

Reference:

1. Drouet L. Cereobrovasc Dis 2002; 13(suppl 1): 16.

Atherothrombosis can be an extensive vascular disease affecting the coronary, cerebral and peripheral circulation.

It is a progressive, generalized disorder with many clinical manifestations either acute or chronic and often multiple in any single patient.

Stenosis in an atherosclerotic artery may give rise to angina, a transient ischemic attack (TIA) or intermittent claudication.

Atherothrombosis in the coronary arteries is the major cause of acute
coronary syndrome (ACS), defined as unstable angina and non Qwave myocardial infarction.

Atherothrombosis of the cerebral arteries may also result in TIA or
ischemic stroke.

In the peripheral arteries, thrombosis superimposed on atherosclerosis can contribute to the progression of peripheral arterial disease, producing intermittent claudication (leg pain on walking that is relieved by rest) as well as ischemic necrosis and, potentially, loss of the limb.

Lumen

Lipid Rich Core

Endothelium

Thick
Fibrous Cap

Unstable

Stable

Thin

Fibrous Cap

Falk E et al. Circulation. 1995;92:657671.

Atherosclerotic Plaque

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Thrombus

P

l

a

t

e

l

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t

s

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1. Ideally the fibrous cap should be protective separating the lipid rich core from blood born agents.

2. Endothelial dysfunction.Increased leukocyte recruitmentleukocytes take up oxidized lipids.smooth muscle cells and macrophages enhance lesion growth.rupture

3. Lumen preserved till later stagesby preserving lumen the arterial outer wall dilates

Stable plaque

Thicker fibrous cap

Unstable plaque

Thin fibrous cap

The clinical presentation and prognosis of coronary atherosclerosis depend more on plaque type than on plaque size. Stable plaques may narrow the arterial lumen and cause stable angina pectoris but are, otherwise, relatively harmless. In contrast, vulnerable plaques may rupture and thrombose, which is a potentially life-threatening event, being responsible for the development of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden death. Gradual lipid accumulation and ongoing inflammation may destabilize a plaque, increasing the risk of sudden plaque disruption and thrombosis. External factors such as mechanical and hemodynamic stresses may be important in precipitating, or 'triggering', disruption of vulnerable plaques. It is, however, the ensuing thrombotic response that makes plaque disruption dangerous. The thrombotic response is dynamic with simultaneously ongoing thrombosis and thrombolysis, frequently causing intermittent flow obstruction leading to an unstable coronary syndrome. The challenge of today is to stabilize the vulnerable plaques, to prevent new formation of vulnerable plaques, and to prevent thrombosis on intact and disrupted plaques.

1. Ideally the fibrous cap should be protective separating the lipid rich core from blood born agents.

2. Endothelial dysfunction.Increased leukocyte recruitmentleukocytes take up oxidized lipids.smooth muscle cells and macrophages enhance lesion growth.rupture

3. Lumen preserved till later stagesby preserving lumen the arterial outer wall dilates

Stable plaque

Thicker fibrous cap

Unstable plaque

Thin fibrous cap

The clinical presentation and prognosis of coronary atherosclerosis depend more on plaque type than on plaque size. Stable plaques may narrow the arterial lumen and cause stable angina pectoris but are, otherwise, relatively harmless. In contrast, vulnerable plaques may rupture and thrombose, which is a potentially life-threatening event, being responsible for the development of the acute coronary syndromes of unstable angina, myocardial infarction, and sudden death. Gradual lipid accumulation and ongoing inflammation may destabilize a plaque, increasing the risk of sudden plaque disruption and thrombosis. External factors such as mechanical and hemodynamic stresses may be important in precipitating, or 'triggering', disruption of vulnerable plaques. It is, however, the ensuing thrombotic response that makes plaque disruption dangerous. The thrombotic response is dynamic with simultaneously ongoing thrombosis and thrombolysis, frequently causing intermittent flow obstruction leading to an unstable coronary syndrome. The challenge of today is to stabilize the vulnerable plaques, to prevent new formation of vulnerable plaques, and to prevent thrombosis on intact and disrupted plaques.

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Ischemic core

Penumbra

Luxury perfusion

Normal

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Immediate Diagnostic Studies: Evaluation of a Patient With Suspected Acute Ischemic Stroke

Brain CT (brain MRI could be considered at qualified centers)
Electrocardiogram
Blood glucose
Serum electrolytes
Renal function tests
Complete blood count, including platelet count
Prothrombin time/international normalized ratio [INR]
Activated partial thromboplastin time [aPTT]

All patients:

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Terapi

Fase akut --> monitor di stroke unit

1. Mengembalikan sirkulasi stroke infark;

a.r-tPA

Intra arterial --> mengembalikan defisit dlm bbrp jam..NEUROINTERVENSI

Intravenous--> mengembalikan defisit dlm 3 jam.

Resiko perdarahan 1%

Dosis 0,9 mg/kg. 10% bolus sisa drip/24jam

b. Bedah revaskuler

Dilakukan < 12 jam

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STROKE AKUT

Sistolik >230 mmHg

Diastolik > 140 mmHg

Sistolik >230 mmHg

Diastolik 121-140 mmHg

Sistolik 180-230 mmHg

Diastolik 105-120 mmHg

Sistolik 230mmHg

Diastolik 121-140 mmHg

ukur ulang 15

Perdarahan intraserebral atau gangguan end organ

Obat AH parenteral

Obsevasi

Obat AH oral setelah 7-10 hari

Ya

Tidak

2. Penatalaksanaan hipertensi

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3. a.Pemberian antitrombotik pada stroke infark

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3.b. Pemberian antikoagulan pada stroke tromboemboli

Parenteral :Heparin, Low Molecule Heparin Weight (LMWH)Oral : Warfarin

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4. Pengelolaan edema otak dan peningkatan TIK

Oksigen dan patensi air wayHead up kepala 30 derajatHipotermi : ruangan AC, kompres /sungkup dingin, obat antipiretikBila kejang diberi antikonvulsan parenteralMannitol 0,25-0,5g/kg diberikan tiap 4 jam (pemberian > 6 jam onset)Hiperventilasi untuk menguras CO2BarbituratOperasi bedah (pada Stroke Perdarahan) untuk Dekompresi

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Indikasi Operasi stroke perdarahan

Volume perdarahan 30-60 cc

Lokasi lobar < 1-2 cm dari tepi

Perdarahan serebelum, lebar > 3 cm

Kesadaran : GCS > 4

Pada kasus Aneurisma, untuk mencegah perdarahan ulang

Clipping (dengan operasi)

Coiling (dengan intervensi endovaskuler)

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4. Komplikasi trombosis dan ulkus dekubitus

Menghindari imobilisasi/perubahan posisiPemakaian stockingPemberian heparin

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5. ASPEK REHABILITASI MEDIK

Melibatkan :

1. FISIOTERAPI

2. SPEECH TERAPI

3. OKUPASI TERAPI

4. PSIKOLOGI

5. Petugas Sosial

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