Dr. Roezwir Azhary Sp.

S
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. Stroke Non Hemoragik (iskemik / infark)

2. 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

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
p . r4 .
V=
n.l.8
V = velocity of blood flow to the brain
p = intravascular pressure
r4 = radius of the artery
n = blood viscosity
l = 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

MABP
50 100 150 200
 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)