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geriatri
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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 keduaDepkes 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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MedicalPneumoniaUrinary 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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NeurologicalElevated intracranial pressure
Herniation
Hemorrhagic transformationSeizures
Cerebral edema
Hydrocephalus
Recurrent stroke
DAMPAK SOSIAL STROKE
KEHILANGAN PEKERJAANMENURUNKAN PRODUKTIFITASMENJADI BEBAN KELUARGABEBAN NEGARAMERUSAK KEHARMONISAN KELUARGADEPRESI.BUNUH DIRI*
Tidak dapat dimodifikasi
UsiaJenis kelaminKeturunanRasDapat dimodifikasi
HipertensiPenyakit jantung Diabetes mellitusMerokokHipercholesterolemia*
PREVENSI PRIMER
PENCEGAHAN LEBIH PENTING !
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macdoc
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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 UnstableIschaemic
stroke
Myocardial infarction
Peripheral arterial
disease:
Intermittent claudication Rest Pain Gangrene Necrosis*
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
macdoc
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Thrombus
P
l
a
t
e
l
e
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 capUnstable plaque
Thin fibrous capThe 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 capUnstable plaque
Thin fibrous capThe 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)All patients:
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Terapi
Fase akut --> monitor di stroke unit1. 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
macdoc
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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*
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*
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*
5. ASPEK REHABILITASI MEDIK
Melibatkan :
1. FISIOTERAPI
2. SPEECH TERAPI
3. OKUPASI TERAPI
4. PSIKOLOGI
5. Petugas Sosial
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