Dr. Roezwir Azhary Sp. SSMF SARAF RSAM

DefinisiDulu (WHO) Sindrom Klinis berupa defisit neurologis fokal/global yang menetap lebih dari 24 jam, atau berakhir dengan kematian tanpa diketahui sebab lainnya, kecuali kelainan vaskular di otak

SekarangDianggap stroke bila ditemukan patologi (infark atau perdarahan) di jaringan otak

Anatomi4/5 otak bagian depan diperdarahi oleh sistem karotis dan 1/5 bagian belakang (batang otak, bagian oksipital dan bagian dalam otak) diperdarahi oleh sistem vertebro basiler Normal tiap 100gr jaringan otak harus mendapat darah 50 55 cc/menit = 1/5 dari kardiak output

AnatomiKe2 sistem arteri dihubungkan oleh sepasang arteri komunikan posterior, menghubungkan arteri karotis interna dengan arteri serebri posterior dan arteri komunikan anterior yang menghubungkan kedua arteri serebri anterior membentuk sirkulus arteriosus WILLISI

Klasifikasi1. Stroke Non Hemoragik (iskemik / infark)2. Stroke Hemoragik (perdarahan intraserebral dan perdarahan subarakhnoid)

Faktor Resiko1. Unmodifieable Usia, jenis kelamin, ras2. ModifieableHipertensi, DM, kelainan jantung, merokok, dislipedemia, hiperuricemia, hiperhomositeinemia, penyakit imunnulogi dan kelainan pembuluh darah (takayasu dan moya-moya disease)

PATOGENESIS BRAIN INFARCTIONNormal metabolism and blood flow

Brain :A very metabolically active organGlucose as a sole substrate Energy produced depends on oxygen presenceATP as energy for maintain neuronal integrity keep Ca++ outside and K+ within the cells Brain requirement O2 500 mLGlucose 75-100 mgEach minute !!

BRAIN INFARCTION Normal metabolism and blood flow

Cerebral Blood Flow (CBF) 53 ml/100 gm brain/minute (range 50-60)Cerebral Metabolism Rate for Oxygen (CMRO2) Cerebral O2 Consumption3.5 ml/mg/minute Maximum compensation to maintain CMRO2 at CBF 20-25 ml/100 gm/min

BRAIN INFARCTION

Cerebral Blood Flow (CBF) in 100mg/minuteIf CBF decreases to 15-18 electrical failure

Below 15 change in somato-sensory evoked potentialIn 10-15 ml (between electrical and ionic failure)Neuron not functioning, but still viable

BRAIN INFARCTION These neuron appear in the periphery, around infarcted area (perifocal area).Their existence is determined by collateral system.The area is called PENUMBRA.It is a target of intervention !!.

Below 10 ionic failureExtracellular K+ , Intracellular Ca++ Free fatty acid releases, ATP breakdown, intracellular acidosis neuronal death

BRAIN INFARCTION Factors that determine CBF Regional Cerebral Blood Flow (rCBF)Auto-regulationMicrocirculation changeMetabolic and neuro-chemical control

BRAIN INFARCTION Regional Cerebral Blood Flow (rCBF)Hagen Poisseuille Law

V =

V = velocity of blood flow to the brainp = intravascular pressurer4 = radius of the arteryn = blood viscosityl = arterial length

Changes of these factors can lead to ischemia tissue necrosisp . r4 . n . l . 8

BRAIN INFARCTION Auto-regulation

The capacity of cerebral circulation to maintainrelatively constant level of CBF despite changing pressure

CBF relatively constant in MABP 50-150 mmHg

Chronic hypertension : Upper and lower levels ofauto-regulation are raised.

BRAIN INFARCTION Auto-regulation25507550100150200CBFMABP

BRAIN INFARCTION Auto-regulation

The ability of auto-regulation and collateral system have a role in stroke attack.

If blood pressure increases, the vessels will constrictand if blood pressure decreases, they will dilate.

Damage of auto-regulation and collateral systemdecreased regional CBF ischemic-infarction

BRAIN INFARCTION Micro-circulation change

Vessel occlusion result in Low shear stress blood aggregation blood viscosity and resistency Vasoconstriction caused by extracellular K

BRAIN INFARCTION Metabolic and neuro-chemical changes

K+ moves across the cell membrane into the extracellular space potentiate and enhance cell deathProduction of O2 free radicals peroxidation fatty acid in cell organelles and plasma membrane damage cell functionAnerobic glycolysis accumulation of lactic acid and lowering pH acidosis impaire cell metabolic function

BRAIN INFARCTION Metabolic and neuro-chemical changes

Production of excitatory neurotransmitter (glutamate, aspartate, kainic acid) Na+ and Ca++ influx into cells Water and Cl- follow Na+ cytotoxic edema

Intracerebral HemorrhageBleeding into the brain results from rupture of one of the cerebral vessels. In many cases, derives from a ruptured arteriosclerotic vessel. Major cause -- rupture of microaneurysms. (end result of longstanding arterial hypertension)at penetrating arteries.Atherosclerosis (in aging or chronic HTN) microaneurysms at penetrating arteries + 1mm : Charcot-Bouchard aneurysmMost common site - basal ganglia.

Intracerebral HemorrhageBrain hematoma : Compressive effect Extend to ventricular system or subarachnoid space

Subarachnoid Bleeding The causes :Ruptured aneurysmRuptured AVMRuptured angiomaBlood dyscrasia

Aneurysm : found commonly in Willis circle and its branchesAneurysm ruptures blood fills in subarachnoidspace and brain parenchym close to it.

Subarachnoid Bleeding Complications Associated With Subarachnoid Hemorrhage Vasospasm : Delayed narrowing of large capacitance arteries at the base of the brain after SAHOften occurs at day 2 to 12 after the onset. HydrocephalusRebleeding : occurs in a few weeks after the onsetHyponatremiaSeizures

Patogenesis & Patofisiologi

DiagnosisAnamnesis Pemeriksaan fisik Pemeriksaan penunjang

PenatalaksanaanAtasi kegawat daruratan bila ada (Resusitasi)Pemeriksaan laboratorium (DL, Fungsi Ginjal, Gula darah, asam urat, lipid profile, fungsi liver, analisa gas darah, elektrolit, dan pemeriksaan lainnya sesuai indikasi)Pemeriksaan Radiologi Pemeriksaan Jantung (EKG dan echo cardiografi sesuai indikasi)

Jaga jalan nafas tetap baik bila perlu berikan oksigen (nasal, sungkup, endotrakeal) Jaga keseimbangan cairan dan elektrolit Nutrisi : jaga jangan sampai terjadi under nutrisi (katabolisme)

Penatalaksanaan hipertensi pada stroke Fase akut Tekanan darah tidak diturunkan pada stroke non hemoragik apabila TD sistemik tidak melewati MABP yg ditetapkan kecuali ada gangguan pada target organ Penurunan TD tidak boleh >20-25% terutama pada jam pertama pasca onset strokeTekanan darah diturunkan pada stroke hemoragik apabila TD sistemik >180/105 mmhg

Penatalaksanaan hiperglikemiGula darah harus diturunkan apabila >180 mg%Hati hati dengan hiperglikemi reaktifAda bermacam cara menurunkan kadar gula darah

Anti platelat agregasi Aspirin dosis rendah 325 mg/hari pada hari pertama dan kedua, selanjutnya 80 mg/hari Cilostazol, clopidogrel, dipiridamol, dllNeuroprotektan (kontroversi)Antibiotik bila ada infeksiTrombolisis (3 jam pasca onset)

RehabilitasiDilakukan sedini mungkin PasifMelakukan latihan lingkup gerak sendi (ROM), mobilisasi bertahap AktifDilakukan apabila cardiovaskular stabil, dan setelah fase akut terlewati pada stroke hemoragik

Tujuannya : mencegah kontraktur dan trombosis vena dalam

Pencegahan StrokePrimerDitujukan pada orang yang belum kena stroke tapi mempunyai faktor resikoSekunderPada Orang yang pernah mengalami TIA dan strokeCarotid stentingpemasangan balon pada pembuluh karotis yang mengalami stenosis >60% (asimptomatik)

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