Dr. Roezwir Azhary Sp.

SMF SARAF RSAM

Definisi
Dulu (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
Sekarang
Dianggap stroke bila ditemukan patologi
(infark atau perdarahan) di jaringan otak

Anatomi
2/3 otak bagian depan diperdarahi oleh
sistem karotis dan 1/3 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

Anatomi
Ke2 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
arteri

Klasifikasi
1.
2.

Stroke Non Hemoragik (iskemik / infark)

Stroke Hemoragik (perdarahan
intraserebral dan perdarahan subarakhnoid)

Faktor Resiko
1. Unmodifieable
Usia, jenis kelamin, ras
2. Modifieable
Hipertensi, DM, kelainan jantung, merokok,
dislipedemia, hiperuricemia,
hiperhomositeinemia, penyakit
imunnulogi dan kelainan pembuluh darah
(takayasu dan moya-moya disease)

Patogenesis &
Patofisiologi

Patogenesis & Patofisiologi

Autoregulasi
Kemampuan pembuluh darah otak untuk
menyesuaikan diri terhadap fluktuasi
tekanan darah sistemik, agar aliran
darah otak tetap dalam batas normal
Hukum Monroe Kelly
Tekanan intrakranial suatu saat akan
meningkat apabila terjadi perubahan
pada volume intrakranial

BRAIN INFARCTION
Normal metabolism and blood flow
Brain : A very metabolically active organ
Glucose as a sole substrate
Energy produced depends on oxygen presence
ATP as energy for
maintain neuronal integrity
keep Ca++ outside and K+ within the cells
Brain requirement
O2 500 mL
Each minute !!
Glucose 75-100 mg

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 Consumption
3.5 ml/mg/minute
Maximum compensation to maintain CMRO2
at CBF 20-25 ml/100 gm/min

BRAIN INFARCTION
Normal metabolism and blood flow
Cerebral Blood Flow (CBF) in 100mg/minute
If CBF decreases to 15-18 electrical failure
Below 15 change in somato-sensory evoked potential
Below 10 ionic failure
Extracellular K+ , Intracellular Ca++
Free fatty acid releases, ATP breakdown,
intracellular acidosis
neuronal death

BRAIN INFARCTION
Normal metabolism and blood flow
Cerebral Blood Flow (CBF) in 100mg/minute
In 10-15 ml (between electrical and ionic failure)
Neuron not functioning, but still viable(hidup)
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 !!.

BRAIN INFARCTION
Factors that determine CBF
Regional Cerebral Blood Flow (rCBF)
Auto-regulation
Microcirculation change
Metabolic and neuro-chemical control

BRAIN INFARCTION
Regional Cerebral Blood Flow (rCBF)
Hagen Poisseuille Law
V=
V
p
r4
n
l

p . r4 .

n.l.8
= velocity of blood flow to the brain
= intravascular pressure
= radius of the artery
= blood viscosity
= arterial length

Changes of these factors can lead to ischemia

tissue necrosis

BRAIN INFARCTION
Auto-regulation
The capacity of cerebral circulation to maintain
relatively constant level of CBF
despite changing pressure
CBF relatively constant in MABP 50-150 mmHg
Chronic hypertension : Upper and lower levels of
auto-regulation are raised.

BRAIN INFARCTION
Auto-regulation
CBF
75

50

25

50

100

150

200

MABP

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 constrict
and if blood pressure decreases, they will dilate.
Damage of auto-regulation and collateral system
decreased 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
death
Production of O2 free radicals peroxidation fatty
acid in cell organelles and plasma membrane
damage cell function
Anerobic 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 Hemorrhage
Bleeding 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 aneurysm
Most common site - basal ganglia.

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

Subarachnoid Bleeding
The causes :
Ruptured aneurysm
Ruptured AVM
Ruptured angioma
Blood dyscrasia
Aneurysm : found commonly in Willis circle and
its branches
Aneurysm ruptures blood fills in subarachnoid
space 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 SAH
Often occurs at day 2 to 12 after the onset.
Hydrocephalus
Rebleeding : occurs in a few weeks after the
onset
Hyponatremia
Seizures

Diagnosis
Anamnesis
Pemeriksaan fisik
Pemeriksaan penunjang

Penatalaksanaan

Atasi 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 kecuali ada gangguan pada target organ
Penurunan TD tidak boleh >20-25% terutama
pada jam pertama pasca onset stroke
Tekanan darah diturunkan pada stroke
hemoragik apabila TD sistemik >180/105 mmhg

Penatalaksanaan hiperglikemi
Gula darah harus diturunkan apabila
>180 mg%
Hati hati dengan hiperglikemi reaktif
Ada 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, dll
Neuroprotektan (kontroversi)
Antibiotik bila ada infeksi
Trombolisis (3 jam pasca onset)

Rehabilitasi
Dilakukan sedini mungkin
Pasif
Melakukan latihan lingkup gerak sendi (ROM),
mobilisasi bertahap
Aktif
Dilakukan apabila cardiovaskular stabil, dan
setelah fase akut terlewati pada stroke
hemoragik
Tujuannya : mencegah kontraktur dan
trombosis vena dalam

Pencegahan Stroke

Primer
Ditujukan pada orang yang belum kena stroke
tapi mempunyai faktor resiko
Sekunder
Pada Orang yang pernah mengalami TIA dan
stroke
Carotid stenting
pemasangan balon pada pembuluh karotis
yang mengalami stenosis >60%
(asimptomatik)