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STROKE ISKEMIK

By :
Ignatius Letsoin, MD, Msi.Med, Neurointerventionist
INTERVENTIONAL NEUROLOGY AND
STROKE PROGRAM
MAJOR CLINICAL MANIFESTATIONS
OF ATHEROTHROMBOSIS
Ischemic Transient
stroke ischemic attack

Myocardial Angina:
infarction • Stable
• Unstable

Peripheral arterial
disease:
• Intermittent claudication
• Rest Pain
• Gangrene
• Necrosis

Adapted from: Drouet L. Cerebrovasc Dis 2002; 13(suppl 1): 1–6.


DEFINISI

 WHO :
Ggn fungsional otak yg terjadi secara
mendadak dg tanda & gejala klinik baik
fokal maupun global yg berlangsung lbh dr
24 jam, atau dpt menimbulkan kematian,
disebabkan oleh ggn peredaran darah otak
DEFINISI...

 CHANDRA B :
Ggn fungsi saraf akut yg disebabkan oleh
krn ggn peredaran darah otak, dimana scr
mendadak (detik) dan scr cepat (jam)
timbul gejala & tanda yg sesuai dg daerah
fokal di otak yg terganggu
Cerebrovascular Disease:
Stroke Subtype
Hemorrhagic stroke (15%) Ischemic stroke (85%)
Lacunar small vessel
disease (25%)
Intracerebral
hemorrhage (59%)

Atherothrombotic
disease (20%)

SAH (41%)
Embolism (20%)

Cryptogenic (30%)
HOMUNKULUS
Dasar-Dasar Vaskularisasi SSP

 Sepasang Arteri Karotis

 Sepasang Arteri Vertebralis

 Ke-2 sistem ini membentuk sist. kolateral


yg disebut “Sirkulus Willisi”
FAKTOR PEMBULUH DARAH PADA
GANGGUAN PEREDARAN DARAH OTAK

 Terjadi melalui 4 cara :


1. Penyumbatan oleh trombus/embolus
2. Penyakit-penyakit pembuluh darah
3. Ruptur dinding pembuluh darah
4. Ggn susunan normal komponen darah
KLASIFIKASI STROKE
 Berdasarkan penyebabnya :
1. Stroke Iskemik (trombosis & emboli)
2. Stroke Perdarahan (PIS & subarakhnoid)
 Berdasarkan stadium/waktu :
1. TIA
2. RIND & Stroke in evolution
3. Completed stroke
 Berdasarkan sistem pembuluh darah :
1. Sistem karotis
2. Sistem vertebrobasiler
Classification of Stroke by Mechanism
STROKE
15%
Primary Hemorrhage
• Intraparenchymal
85% • Subarachnoid
Ischemic Stroke

20% 25% 20% 30% 5%


Atherosclerotic Penetrating Cardiogenic Cryptogenic Other, Unusual
Thrombosis Artery Disease Embolism Stroke Causes
(“Lacunes”) • Prothrombic states
● Atrial Fibrillation • Dissections
● Valve disease • Arteritis
● Ventricular thrombi • Migraine/vasospasm
Arteriolgenic ● Many others • Drug Abuse
Hypoperfusion Emboli • Many more

Fifth ACCP Consensus Conference on


Antithrombotic Therapy Chest. 1998;114(5):480S
PATOGENESIS ISKEMIK & INFARK

 Ambang fungsional → ADO 50-60 cc/100 gr/mnt


→ tdk terpenuhi fungsi neuronal terhenti

 Ambang aktifitas listrik otak → 15-18 cc, bila tdk


tercapai aktifitas listrik neuronal terhenti

 Ambang kematian sel → kurang dari 15 cc, sel-2


otak mengalami kerusakan total
PROGRESSION OF ATHEROSCLEROSIS
BEGINS WITH ENDOTHELIAL DYSFUNCTION

Plaque rupture

Adhesion Macrophage
Oxidized
Monocyte LDL-C molecule
LDL-C
Foam cell
CRP

Smooth muscle
cells

Endothelial Plaque instability


Inflammation Oxidation
dysfunction and thrombus

Libby P. Circulation. 2001;104:365-372; Ross R. N Engl J Med. 1999;340:115-126.


Ischemic Cascade (Cellular changes)
50 Normal CELLULAR CHANGES
CBF :
- O2 extraction
cc/100gr/min Oligemia - CMRO2 Normal
30 - Anaerobic Glycolysis
Lactoacidosis, pH
Mild Ischemia - Protein Synthesis
disturbed
20 - “ELECTRICAL FAILURE”
Moderate * Pump failure
* Ischemic Penumbra”
Ischemia - Glutamate release
10 - Ca influx
- Free Radicals
Severe
“IONIC FAILURE”
Ischemia - Energy Failure CELL
0 DEATH/Pannecrosis
 Viskositas darah dipengaruhi oleh :
1. Hematokrit
- Nilai Hm 45% → faktor risiko
2. Fibrinogen darah
- Media interaksi eritrosit & platelet
3. Rigiditas eritrosit
- Ǿ 7-8 μm dpt melewati Ǿ kapiler 3-5 μm
4. Agregasi trombosit
- Pd stroke terjadi hiperagregasi trombosit
BRAIN ATTACK...!!!

PE
Y
LUXUR S

LUX SION
RF
SION
PERFU

U
UR
Y
INFARK

S
IK
PE

EM
NU
M BR

K
A

IS
INFARK
PENUMBRA ISKEMIK
LUXURY PERFUSIONS
FAKTOR RISIKO KONVENSIONAL

Tidak dapat dikontrol :


- Usia
- Ras
- Jenis kelamin
- Herediter
Faktor Risiko...

Dapat dikontrol :
- Hipertensi - Merokok
- D.M - Sleep apnea
- Peny. Jantung - Kontrasepsi oral
- Riwayat stroke - Alcohol abuse
- Dislipidemia - Infection
- Obesitas - Pe ↑↑ fibrinogen
- Hiperuricemia
Faktor Risiko...

FAKTOR RISIKO GENERASI BARU

Kriptogenik
- Homosistein - Def estrogen
- Protein C & S - Plasma
fibrino
- Anti trombin III gen
- Antifosfolipid antibodi - Infeksi
DIAGNOSTIK STROKE

 Dasar diagnosis :
1. Anamnesis
- Onset timbul sangat mendadak
- Saat onset sedang bekerja atau istirahat
- Ditanyakan adanya faktor-2 risiko
2. Pemeriksaan fisik
- GCS dan tanda vital
- Mata : refl. & Ǿ pupil, gerakan bola mata
DIAGNOSTIK STROKE...

- Leher : kaku kuduk


- Saraf kraniales
- Motorik, sensibilitas & vegetatif
- Skor konvensional (SSS atau Gajah Mada)
3. Gejala klinik :
- Tergantung daerah otak yg terkena
- Stroke pd sistem karotis
- Stroke pd sistem verebro-basiler
4. Pemeriksaan penunjang :
- Laboratorium darah & urine
- Pemeriksaan foto thoraks & EKG
- Pemeriksaan funduskopi mata
- Pemeriksaan CT Scan/MRI → ‘gold standar’
SIRIRAJ STROKE SCORE (SSS)

1. Kesadaran : - komposmentis (0), somnolen (1)


& semi koma/koma (2) → dikalikan 2,5
2. Muntah : - tidak (0), ya (1) → dikalikan 2
3. Nyeri kepala : - tidak (0), ya (1) → dikalikan 2
4. Tekanan darah : - diastolik → dikalikan 10%
5. Ateroma : DM, klaudikatio intermiten & angina
pektoris - tidak (0), ya (1) → dikalikan -3
6. Konstanta : - dikurangi dg 12
Catatan : SSS > 1 → SH ; SSS < 1 → SNH
SKOR GAJAH MADA

1. Penurunan kesadaran
2. Nyeri kepala
3. Refleks babinski
Catatan :
- 1,2,3 (+) → Stroke Hemoragik (SH)
- 1,2 (+) → Stroke Hemoragik (SH)
- 1 atau 2 (+) → Stroke Hemoragik (SH)
- 1,2,3 (-) → Stroke Non Hemoragik (SNH)
- 3 (+) → Stroke Non Hemoragik (SNH)
Presentasi Klinis Stroke Akut

Kelumpuhan wajah / anggota gerak


Ggn sensibilitas pd satu sisi tubuh
Perubahan mendadak status mental
Bicara tdk lancar (afasia)
Bicara pelo / cadel (disatria)
Ggn penglihatan (hemianopia)
Gerakan tdk terkontrol (ataksia)
Vertigo, nyeri kepala & muntah
BRAIN INJURY
PENGELOLAAN

1. Umum : 5 B (Blood, Breath, Brain, Bowel dan


Bladder)
2. Faktor risiko : Hipertensi, Dislipidemia, DM, dll
3. Khusus : Trombolitik, Anti-koagulan & platelet,
Anti-edema & Neuroprotektan
4. Fisioterapi (rehabilitasi medik)
5. Pembedahan (surgery)
6. Pencegahan sekunder : Rubah life-style, diet
sabu-2, olah-raga, obat anti-koagulan & platelet)
THROMBOLYSIS

 Tissue Plasminogen Activator (t-PA)

ANTI-KOAGULAN

 Heparin
 Warfarin
NEUROPROTEKTOR

 Piracetam :
- Hr 1-3 12 gr/hr iv
- Hr 4-akhir minggu 4 4800 mg tab/hr
- Minggu ke-5 s/d 12 2400 mg tab/hr

 Citicoline :
- Hr 1 – akhir minggu 12 1000 mg/hr
ANTI-AGREGASI (PLATELET)

1. Gol. Salisilat : Aspilet, Aspirin


2. Gol. Clopidogrel
3. Gol. Ticlopidin
4. Gol. Cilostazol
OBAT DISLIPIDEMIA

1. Gol. Statin : simvastatin, atrovastatin


2. Gol. Fibrat : fenofibrat

Gol. Statin → “efek upstream & downstream”

“Upstream” : stabilkan aterosklerosis


“Downstream” : perbaiki enos (anti-oksidan,
anti-inflamasi & anti-trombus)
OBAT ANTI HIPERTENSI

1. Ace-Inhibitor : kaptopril, lisinopril


2. Beta-blocker : propanolol, atenolol
3. Calsium-antagonis : nifedipin, diltiazem
4. Diuretik : furosemid, hidroklortiazid
Stroke Classification (Bamford)

• Total Anterior Circulation Infarct (TACI)


Combination of new higher cerebral dysfunction (eg,
dysphasia); homonymous visual field defect; and
ipsilateral motor and/or sensory deficit of at least
two areas of face, arm and leg.

• Partial Anterior Circulation Infarct (PACI)


Two of the three components of the TACI syndrome
with higher cerebral dysfunction alone, or with a
motor/sensory deficit more restricted than those
classified as LACI
Stroke Classification (Bamford)...

• Posterior Circulation Infarct (POCI)


Ipsilateral cranial nerve palsy with contralateral
motor and/or sensory deficit; bilateral motor and/or
sensory deficit; disorder of conjugate eye movement;
cerebellar dysfunction without ipsilateral long tract
deficits; or isolated homonymous visual field defect

• Lacunar Infarct (LACI)


Pure motor > 2/3 face, arm, leg; pure sensory > 2/3
face, arm, leg; pure sensorimotor > 2/3 face, arm,
leg; ataxic hemiparesis; no higher dysphasia or
visuospatial or hemianopia or vertebrobasilar
problems
Sindrom Batang Otak
 Sindrom Weber (lesi pd pedunkulus serebri) :
- Parese N.III homolateral LMN
- Paresis N.VII & XII kontralateral UMN
- Hemiparesis ekstr. kontralateral UMN
 Sindrom Claude (lesi pd nukleus ruber) :
- Parese N.III homolateral LMN
- Ataksia, tremor & hipokinesia ekstr. kontralateral
 Sindrom Benedikt (lesi pd lemniskus medialis &
pedunkulus serebri) :
- Gejala spt sindr. Claude ditambah hemiparese &
hemihipestesia ekstr. kontralateral UMN
Sindrom Batang Otak...

 Sindrom Millard Gubler (lesi pd pons) :


- Paresis N.VI & VII homolateral LMN
- Hemiplegi ekstr. kontralateral UMN

 Sindrom Parinaud (lesi pd kolikulus superior) :


- Kelumpuhan gerakan kedua bola mata keatas

 Sindrom Foville (lesi pd lateral pons) :


- Parese N.VII homolateral LMN
- Hemiplegi ekstr. kontralateral UMN
PERBEDAAN SROKE

STROKE ISKEMIK STROKE PERDARAHAN


• Onset mendadak • Onset mendadak
• Saat onset istirahat • Saat onset sdg aktif
• Peringatan (+) • Peringatan (-)
• Nyeri kepala (±) • Nyeri kepala (+++)
• Kejang (-) • Kejang (+)
• Muntah (-) • Muntah (+)
• Kesadaran me↓ (±) • Kesadaran me↓ (+++)
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