STROKE

Epidemiologi
Stroke is the fourth leading cause o death in the
United States (a ter heart disease, cancer, and
chronic lung disease)
and the most common disabling neurologic
disorder.
Approximately 800,000 new strokes occur and
approximately
130,000 people die rom stroke in the United
States
each year.
 Epidemiologi
Indonesia 15,4% kematian
Rata2 usia 58,8 th +- 13,3 th
FAKTOR RISIKO
FAKTOR RISIKO
 CIRI KHAS STROKE
Onset tiba-tiba
Keterlibatan fokal CNS
Tidak ada resolusi cepat
Penyebab vaskular
 TIA
Gejala stroke kurang dari 24 jam
Biasanya kurang dari 1 jam
TIA is now de ned as transient stroke
symptoms that resolve completely without
evidence o in arction on MRI.
ABCD2 Score
ABCD2 Score
DAERAH STROKE
GEJALA KLINIS
 KLASIFIKASI

ISKEMIK HEMORAGIK

EMBOLI EPIDURAL
TROMBOSIS SUBDURAL
SUBARAKNOID
INTRACEREBRAL
 PATOGENESIS ISKEMI
FAKTOR PEMBERAT FAKTOR PROTEKTIF
DEPLESI ENERGI Sirkulasi kolateral
PERUBAHAN GRADIEN ION(K ektraseluler Neuron inhibitorik
meningkat merangsang neuron sekitar)
Disregulasi kalsium Transcriptional Hypoxia Response
Eksitotoksisitas Neurogenesis
Stres oksidatif Angiogenesis
Inflamasi Ischemic Tolerance
Repair Mechanisms
SINDROMA BERDASARKAN ANATOMI
JENIS SINDROMA
SINDROMA
Arteri serebri anterior
Arteri serebri media
Arteri karotis interna
Arteri serebri posterior
CIRI
Hemiparesis hemiestesi kontralateral, terutama
kaki. Abulia, disconection syndrome,
inkontinensia uri,
Divisi superior: hemiparesis muka, tangan, dan
lengan, afasia broca
Divisi inferior: hemianopsia homonim,
terganggunya fungsi kortikal dan spasial, afasia
wernicke(di daerah otak dominan)
Oklusi percabangan
Oklusi pangkal: mengenai kaki juga
Bervariasi tergantung keparahan sumbatan
Supply the occipital cerebral cortex, medial
temporal lobes, posterior
corpus callosum, thalamus, and rostral
midbrain
Homonymous hemianopia
cortical blindness, memory impairment
( rom temporal lobe involvement), or inability
to recognize amiliar aces (prosopagnosia), as
well as a variety
o exotic visual and behavioral syndromes
SIRKULASI POSTERIOR
 SINDROMA
SINDROMA CIRI
BASILAR Gangguan fungsi batang otak luas
Penurunan kesadaran fatal
Cabang sirkumferensial panjang Posterior serebri: ataxia, sindrom horner,
defisit sensorik wajah, nistagmus, nausea,
vertigo, muntah, disfagia, disartria
Cegukan
a. Serebelli inferior anterior: ipsilateral
acial weakness, gaze palsy, dea ness,
and tinnitus
a. Serebelli inferior superior: resembles
anterior in eriorc erebellar artery lesions,
but impaired optokinetic nystagmus or
skew deviation o the eyes may
occur,auditory unction is una ected,
Cabang
 SINDROMA
SINDROMA CIRI
LONG PENETRATING PARAMEDIAN Perdarahan: medial portion o the cerebral
VERTEBROBASILAR BRANCHES peduncle, sensory pathways, red nucleus,
reticular ormation,
and midline cranial nerve nuclei (III, IV, VI,
XII)

SHORT BASAL VERTEBROBASILAR Cranial nerves (eg, III, VI, VII) that emerge
BRANCHES rom the ventral sur ace o the brainstem
may be a ected
 INFARK LAKUNAR
Small vessel occlusion a ecting penetrating
arteries deep
in the brain may cause in arcts in the putamen
or, less commonly, the thalamus, caudate
nucleus, pons, posterior
limb o the internal capsule, or other sites
 INFARK LAKUNAR
Pure motor hemiparesis
Pure sensory stroke
Ataxic hemiparesis
Dysarthria-clumsy hand syndrome
ETIOLOGI
 TROMBOSIS SINUS CAVERNOSUS
Trombosis septik dan steril
Gejala: nyeri kepala, papiledema, penurunan
kesadaran, kejang, defisit neurologis fokal
D-dimer naik, CSF meningkat
Terapi: antikoagulan, antibiotik
 Pendekatan Klinis
Anamnesis
Pf
Lab
Pencitraan

Memastikan diagnosis stroke dan mencari

penyebab
 Anamnesis
Gejala
Onset
Faktor resiko
Penyakit terkait
 PF
Umum
Neurologis
Primary survey secondary survey
 LAB
Mencari etiologi dan dd
DPL: TE/PV/leukositosis
GDS: hipo-hiperglikemia
Koagulasi: penyebab dan pertimbangan
antikoagulan
LED: arteritis
Sifilis
Troponin: jika dicurigai infark miokardium
 PENCITRAAN
Diagnosis
Paling cepat: CT scan non contrast. MRI lebih
superior untuk infark
Mencari etiologi
USG Dopler
DSA
MRA
CT Angiography
ekokardiografi
 PENCEGAHAN PRIMER
Gaya hidup: olahraga
Statin
With or without dyslipidemia, who are at increased
(>10%) 10-year risk or cardiovascular events. http://
my.americanheart.org/cvriskcalculator
Tekanan darah
Kendali GDS
Antiplatelet, indikasi sama dengan statin
Antikoagulan
 TERAPI STROKE ISKEMIK AKUT
Investigasi awal: Primary survey secondary,
pencitraan
TERAPI MEDIS
INVASIF
PEMBEDAHAN
 MEDIS
Kontrol TD: Hipertensi permisif. Guidelines
suggest allowing autoregulation up to 220/120
mm Hg i thrombolytic therapy is not given, or up
to 180/105 mm
Hyperthermia, which may adversely af ect
outcome, should be corrected, and any in ectious
cause identi ed.
Hypoxia (oxygen saturation 94%) should be
treated with supplemental oxygen.
Hypoglycemia (blood glucose <60 mg/dL) should
be corrected.
 MEDIS
Anticoagulation with heparin, given by continuous
intravenous in usion to achieve an activated partial
thromboplastin time (aP ) 1.5 to 2.5 times control, followed
by warfarin, given orally daily to achieve an INR o 2.50.5,
or another oral anticoagulant (see able 13-6), is indicated i
a cardiac embolic source (eg, atrial brillation, mitral
stenosis, or mechanical valve replacement) appears to be
responsible or IA or acute ischemic stroke.
Antiplatelet therapy with aspirin (325 mg orally once,
followed by 81-325 mg orally daily) is recommended or
presumed noncardiogenic IA or acute ischemic stroke,
unless the patient is to undergo thrombolysis.
Statins should be continued or patients receiving longterm
statin treatment.
 MANAJEMEN HT PADA stroke iskemik
Indikasi: TDS > 180/TDD >110
Bila TDS> 230 dan/atau TDD 121-140:
labetalol iv 10-20 mg selama 1-2 menit dapat
diulang tiap 10-20 menit. Maks 300 mg
Bila TDS 180-230 dan/atau TDD 105-120 terapi
darurat ditunda kecuali ada perdarahan
intraserebral, gagal jantung kiri, diseksi aorta,
ensefalopati ht
Batas penurunan 20-25 % MAP
 INTERVENSI-TROMBOLISIS
Intravenous thrombolysisIntravenous administration
o recombinant tissue plasminogen activator (rtPA
or alteplase) within 4.5 hours o the onset o symptoms
reduces disability and mortality rom acute ischemic
stroke. he drug is administered at a dose o 0.9 mg/
kg, up to a maximum total dose o 90 mg; 10% o the
dose is given as an intravenous bolus and the remainder
as a continuous intravenous in usion over 60 minutes.
reatment should be started within 60 minutes o
the patients arrival at the hospital, which provides time or
diagnosis and evaluation o possible contraindications.
 KONTRAINDIKASI
bleeding complications
include recent trauma, surgery, or hemorrhage;
blood
pressure greater than 185 mm Hg systolic or
greater
than 110 mm Hg diastolic pressure; and impaired
coagulation (INR >1.7, elevated aP , or platelet
count <100,000/L).
 Waspada
Within the irst 24 hours a ter administration o
rtPA, anticoagulants and antiplatelet agents
should not
be given, blood pressure should be care ully
monitored,
and arterial puncture and placement o central
venous
lines, bladder catheters, and nasogastric tubes
should be avoided.
 Intraarterial thrombolysis
Intraarterial administration
o rtPA may be bene icial in patients with acute
ischemic stroke who are not candidates or intravenous
thrombolysis, such as those treated 4.5 to 6 hours a ter
the onset o symptoms or with a recent history o major
surgery, and in patients in whom intravenous therapy is
unsuccess ul.
 Clot retrieval
Mechanical thrombectomy with stent or coil retrievers (eg,
Solitaire FR, revo or Merci), alone or in combination with
rtPA, may also be use ul
or treating acute ischemic stroke, especially in patients
who are not candidates or or who ail intravenous
thrombolytic therapy. For example, the combination o
intravenous rtPA and intraarterial treatment with a
retrievable stent within 6 hours a ter onset o symptoms
can improve unctional outcome at 3 months in
patients with occlusion o the distal intracranial internal
carotid or proximal middle or anterior cerebral
artery.
 BEDAH
Carotid endarterectomy
Carotid artery stenting
Posterior fossa decompression with
evacuation of infarcted cerebellar tissue
Decompressive craniectomy
 ICH
10 persen stroke
Penyebab plg sering: hipertensi
AUTOREGULASI
 TATALAKSANA
ABCDE
SUPORTIF
Kontrol tekanan darah
Cari etiologi
Perhatikan indikasi bedah
 MANAJEMEN HT PADA ICH
Bila TDS> 180 dan/atau TDD>105 labetalol
nicardipin, diltiazem, nimodipin
Target MAP 20-25 persen
Bila TDS kurang 90 mmhg berikan vasopresor
 ETIOLOGI ICH
Chronic hypertension. Hypertensive hemorrhage has a predilection or the deep brain structures (basal ganglia,
thalamus, and deep subcortical white matter), the anterior pons, and the cerebellum. T ese are sites o per orating vessels
that appear particularly susceptible to damage due to chronic hypertension. Lobar hemorrhage may also be caused by
hypertension.
Cerebral amyloid angiopathy (CAA): CAA-related hemorrhages
are most commonly lobar (
Head trauma.
Coagulopathy (inherited, acquired, or due to anticoagulant
use) or thrombocytopenia (e.g., disseminated intravascular
coagulation [DIC], thrombotic thrombocytopenia purpura
[ P], acute leukemia).
Rupture o a vascular mal ormation (e.g., aneurysm, arteriovenous
mal ormation, cavernous mal ormation).
Hemorrhage into an ischemic stroke (hemorrhagic conversion),
which is more common with embolic strokes, septic emboli in endocarditis, and stroke in the PCA territory.
Cerebral venous sinus thrombosis (see Cerebral Venous
Sinus T rombosis and Cortical Vein T rombosis below).
Cocaine (due to acute hypertension).
Hemorrhagic cerebral metastases.
 INDIKASI BEDAH
1. Cerebellar hemorrhageNeurologic deterioration,
brainstem compression, and hydrocephalus are indicationsor
decompressive posterior ossa surgery, which may avert a atal
outcome. Results are best in conscious patients.
2. Lobar hemorrhageSurgical evacuation can also be
use ul or lobar hematomas, especially those larger than 30 mL
in volume and located within approximately 1 cm o the brain
sur ace. Patients with good neurologic Function who begin to
deteriorate are optimal candidates.
Prognosis is related to the level o consciousness be ore
surgery.
3. Deep hemorrhageSurgery is not bene cial or pontine
or deep cerebral hypertensive hemorrhage.
 PROGNOSIS
Considerable return o neurologic unction can
occur a ter
intracerebral hemorrhage, depending on its
location and
size. Mortality is 30% to 40%, most o which
occurs within
the irst ew days. At discharge rom the
hospital, about
75% o patients have signi icant disability.