Ilsa Hunaifi

Neurologist
FK Universitas Mataram/RSUP NTB

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 WHO  15 juta menderita stroke di seluruh
dunia
 Stroke penyebab kecacatan dan kematian utama
di Indonesia
 Di RSDS  angka kematian mencapai 28,76 %
 Di AS
 Penyebab kematian No 4 , 22, 9%
 Prevalensi mencapai 6,8 juta orang  20 tahun dan
Insidens baru  795 rb per tahun
 87% stroke iskemik, 10 % ICH dan 3 % SAH
 Insidensi tertinggi pada usia  65 tahun dan laki-
laki > wanita
 Kecepatan dalam pengenalan, transport dan
terapi menentukan keberhasilan terapi

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 WHO  Gangguan fungsi otak,fokal(global) yang timbul
mendadak,berlangsung selama lebih 24 jam (kecuali bila
mengalami tindakan pembedahan atau meninggal
sebelum 24 jam) disebabkan oleh karena kelainan
peredaran darah otak
 Definisi baru  CNS infarction : adanya episode
disfungsi neurologis yang disebabkan oleh infark
serebri fokal, spinal atau retina, berdasarkan
patologi, imaging atau bukti obyektif adanya
iskemia serebri, medula spinalis atau retina sesuai
distribusi vaskuler dan adanya bukti klinis adanya
iskemia serebri, medula spinalis atau retina dengan
gejala yang menetap ≥ 24 jam atau sampai
meninggal dan penyebab lain telah disingkirkan
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 ICH  disfungsi neurologis yang berkembang
cepat akibat adanya darah dalam parenkim
otak atau sistem ventrikel yang bukan
disebabkan karena trauma
 SAH  disfungsi neurologis yang berkembang
cepat akibat dan atau sakit kepala akibat
perdarahan dalam ruang subarachnoid (ruang
antara membran arachnoid dan piameter
dalam otak maupun medula spinalis)

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 Stroke iskemik
 Stroke iskemik trombotik
 Stroke emboli
 Lacunar stroke
 Cryptogenic stroke
 Stroke perdarahan
 ICH
 SAH

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 Unmodifiable  HT
 DM
 Usia  resiko
meningkat 2x lipat  Dyslipidemia

setelah usia  55 th  AF

 Jenis kelamin  Laki  Sickle Cell Disease

> wanita  Terapi Hormonal

 Low birth weight <  Oral contraception

2500 gr  Diet

 Etnis/race   Obesitas

black/latin > white  Physical inactivity

 Genetik Well Documented Modifiable

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 Less documented
 Migraine
 Metabolic syndrome
 Konsumsi alkohol
 Drugs abuse
 SDB
 Hyperhomosistein
 Peningkatan Lp(a)
 Hiperkoagulasi (Thrombophilia)
 Inflamasi dan infeksi

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 Modifiable Risk
factor

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 Stroke iskemik  iskemia serebri fokal 
penurunan aliran darah  kerusakan
metabolisme neuron
 Stroke infark trombotik
 Iskemia serebri akibat oklusi atau penyempitan
PD dan clot  proses aterosclerosis/aterogenesis
 Aterogenesis
 Injury dinding PD  foam cell  oxidasi LDL
kholesterol  migrasi dan proliferasi sel otot polos
PD Proliferasi dan agegrasi/migrasi platelet 
trombus  oklusi PD
 Supply darah < 16-18 cc/100 gr/menit dalam 1 jam 
infark cerebri

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PATOFISIOLOGI
ISKEMIK KASKADE

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 Stroke emboli  Adanya material emboli
yang berasal dari proximal terutama dari
jantung, PD besar (aorta, A.karotis,
A.vertebralis, vena (paradoxical emboli))
 Lacunar stroke  aterosklerosis pada
cabang2 kecil PD di circulus willisi akibat
terjadinya penebalan lipohialinosis di PD 
infark 3 mm s/d 2 cm
 Cryptogenic stroke  penyebab belum
diketahui, diduga akibat PFO, ateroma arkus
aorta, Antiphosfolipid antibody syndrome dan
factor V Leiden gen mutation
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 Anamnesis  adanya faktor resiko, onset, gejala-
gejala lain
 Pemeriksaan umum dan neurologi  VS, defisit
kognitive, gangguan lapang pandang, hemiparesis,
occular palsy, defisit sensoris, ataxia
 Laboratorium  semua pasien dilakukan
pemeriksaan DL, FH, GDA, cardiac enzyme
(Troponin, CKMB), SE, BUN/creatinin, Faal hati,
toxicology urine (narkoba), EKG, LP, dSA,
 Radiology  CT scan kepala tanpa kontras, MRI
kepala, carotid duplex, TEE/TTE, DSA
 DDx

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CT awal 36 jam kemudian

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 Memperbaiki blood flow  rtPA
 Memperbaiki glikolisi aerob  oksigenasi dan
terapi insulin
 Mengurangi eksitotoksik  neuroprotektan
 Mengurangi inflamasi  inhibisi mikroglia
(riset)
 Regenerasi sel neuron  stem cell (riset)
 Melalui mekanisme multiple  albumin dan
hipotermia (riset)

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 ASA  dosis awal 325 mg dalam 24-48 jam
onset stroke, prevensi stroke 50-325 mg
 ASA 25 mg + dipiridamol 200 mg
 Clopidogrel  75 mg
 Ticlopidin  250 mg
 Cilostazol  2x50 mg

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 Tergantung beberapa faktor
 Beratnya defisit neurologis
 Usia
 Penyebab stroke
 Penyakit penyerta

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 Iskemia otak akibat emboli, emboli berasal dari
jantung atau non jantung
 Jantung
 AF
 Infark jantung
 Endokarditis bakterial akut
 Katup jantung protese
 Non jantung
 Aterosklerosis aorta
 Diseksi karotis
 Lemak, tumor, udara
 Komplikasi bedah thorak
 Tidak diketahui 31
 Defisit neurologis akut dan maksimal saat
onset

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 Lab
 EKG
 Echocardiografi
 CT scan/MRI

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3 fase
 Restorasi sirkulasi  rTPA < 3 jam – 4,5 jam
 Prevensi emboli berulang
 Antikoagulan
 KI mutlak  ICH, gangguan hemostasis, ulkus
peptikum aktif/perdarahan GIT aktif, gangguan hepar
dan ginjal berat, defesiensi AT III
 KI relatif  infark luas dengan midline shift, HT tidak
terkontrol, ulkus peptikum tidak aktif, riwayat
perdarahan oleh pemberian antikoagulan, ITP, alergi,
paska operasi
 Tx  LMWH dan Warfarin
 Terapi fisik dan rehabilitasi
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 10-15 % kasus stroke
 Laki-laki > wanita
 Faktor resiko  HT, merokok, alkohol,
genetik

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 Tempat yang tersering  kortek, basal
ganglia, kapsula interna, thalamus, brain
stem dan serebelum
 Faktor anatomik  AVM, AVF, CAA
 Faktor hemostatik  pemakaian
antikoagulan, Gangguan FH
 Faktor hemodinamik  HT

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 Defisitneurologis akut berat – koma
 Nyeri kepala, mual, muntah
 Pada orang tua  CAA
 Riwayat penggunaan
Antikoagulan/trombolitik
 Riwayat kejang

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 HT dengan kondisi klinis yang berat koma
sampai meninggal
 Defisit neurologis fokal dan efek
hematomnya
 Mungkin ada Kejang

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 Lab
 Radiologis
 Thorak
 Ct scan
 Angiografi dan venografi  usia < 50 tahun

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 Konservatif
 Umum  6 B
 Khusus  pengendalian HT, kejang dan
peningkatan TIK
 Operatif
 ICH serebelum > 3 cm atau < 3 cm dengan tanda
penekanan brain stem atau hidrosefalus
 ICH dengan lesi struktural
 ICH lobar < 1 cm permukaan korteks

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 Primary SAH :
Non traumatic SAH or spontaneous SAH is a
neurologic emergency characterizered by
the
extravasation of blood into the spaces
covering the central nervous system that are
filled with cerebrospinal fluid.

 Secondary SAH :
Craniocerebral Trauma

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1-7 % of acute cerebrovascular episodes.
USA : 2 - 5 % of all new Dx Strokes
USA : 21.000 - 33.000 people each year
Incidence in different countries : variable
Incidence in the world : 10,5/100.000/yr
Prevalence 0,2 – 7,9%, greater in older px

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Sex :
Male : Female = 2 : 3.
Age :
Incidence increases with age
Age : 40 – 60 yrs ; peak : 55 - 65 yrs.
40 yrs : Male >
> 50 yrs : Female >
Rupture 70 - 90 % SAH, age 50 - 60 yrs.
Blacks : White = 2,1 : 1

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Major factors ass. with poor outcome :
 Level of consciousness on admission
 Age
 Amount of blood on initial head CT scan.

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 SAH 5 % of deaths from stroke, but for
27 % of all strokes before the age of 65.
 Most deaths occur within 2 weeks after ictus, 10 %
before receiving medical att,
25 % within 24 hours.
 Mortality : 75 % in 2 years.
 2/3 : die or significantly disabled
 1/3 of px admitted : moribund

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 Craniocerebral Trauma
 Non Traumatic Ruptured Intracranial Aneurysm
(80 %)
 Bleeding AVM
 Ruptured Mycotic Aneurysm
 Multiple aneurysm : 15 -20 %.

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 Inherited or congenital weakness of the arterial
wall.
 Atherosclerosis is postulated as the most
important factor in the development and
subsequent rupture of saccular aneurysms.

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 Congenital
20 % have a positive family history F1,
Rupture 4 times from general population.
Saccular aneurysm associated with connective
tissue disease .
 Acquired

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- Hypertension is a general risk factor

Other risk factors :

 - Recent heavy alcohol consumption
 - Smoking
 - Aneurysm size
 - Family history SAH

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Based on Location:
 Anterior circulation (80-90 %)
1. Internal carotid artery
2. Anterior cerebral artery
3. Medial cerebral artery
 Posterior circulation (10-20%)
1. Vertebral artery
2. Basilar artery
3. Posterior cerebral artery

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Symptoms and signs :
 Severe generalized headache,sudden onset. “The
worst headache I ever had in my life”,
Thunderclap headache, warning leaks, Sentinel
headache.
 Loss of consciousness
 Nausea, Vomiting
 Diplopia, Photophobia

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 Nuchal rigidity
 Subhyaloid hemorrhage
 Hypertension
 Vital signs abnormal

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Grading Clinical Appearance

Grade I Asymptomatic or mild headache and slight

nuchal rigidity
Grade II Moderate to severe headache and nuchal
rigidity without neurological deficit other than
cranial nerve palsy
Grade III Drowsiness,Confusion or mild focal neuro
logical deficit
Grade IV Stupor,moderate to severe hemiparesis,
possibly early decerebrate rigidity and
vegetative disturbances
Grade V Deep Coma and decerebrate rigidity
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 Fischer Group Blood on CT

1 No subarachnoid blood detected

2 Diffuse deposits or a thin layer < 1

mm in fissures and vertical cysterns
3 Localized clots and/or thick layer
>1mm or > 5 x 3 mm in the
horizontal plane
4 Intracerebral or intraventricular
clot but with only diffuse or no SAH

For prediction of vasospasm

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 1. Head CT scan : first study within 12 hrs
 2. Lumbar puncture : xanthochrom, >12 hrs
 3. CT angiography of the head
 4. Cerebral angiography
 5. Three dimensional DSA
 6. Head MRI
 7. MRA
 8. TCD (transcranial doppler ultrasonography)

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N Engl J Med 2006;354;390

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 Typical Presentation
•Severe headache with nausea and vomiting
•Meningismus
•Diminish level of conciousness
•Focal neurologic signs
Atypical presentation
•Thunderclap headache
•Confusional state
•Associated head trauma

Head CT without contrast

SAH No SAH

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 SAH No SAH

LP

Abnormal, N
Xanthochrom,
CTA or CA but equivocal (RBC
RBC elevated
elevated
unchanged
Xanthochrom
from tube 1-4 Stop
Aneurysm N
found CTA or CA
Repeat
CTA 1-3
week
Aneurysm found N

Imaging
of brainstem
Prompt Tx and myelum Prompt Tx Stop
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 Hypertensive intracerebral hemorrhage
 Migraine
 Bacterial Meningitis
 Ruptured mycotic aneurysm
 Traumatic spinal puncture

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 Hunt and Hess grade 1-3 should undergo early
surgery to prevent rebleeding.
 Clipping of the neck of the aneurysm, has
a mortality of 2,6%,morbidity 10,5 %.
 Endovascular coiling with platinum coil.
Disadvantage more often incomplete and carry a
risk for reopening.

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 Hunt & Hess grade I – II within 96 hours of SAH were
found to have a significantly better outcome when
treated with prophylactic nimodipine.
 Hunt & Hess grade III – IV improve neurol deficits.
 Hunt & Hess grade V showed no benefit.

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Management Recommendation
of Condition

Airway and Monitor closely in intensive care unit or

cardiovascular preferably in neurologic critical care unit
system

Environment Maintain reduced noise level and limit visitors

until aneurysm is treated

Pain Administer morphine sulfate (2–4 mg IV every

2–4 hr) or codeine (30–60 mg IM every 4 hr)

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Management of Recommendation
condition
Gastrointestinal Administer ranitidine (150 mg PO twice daily or 50
prophylaxis mg IV every 8–12 hr) or lansoprazole (30 mg PO daily)

Deep venous Use thigh-high stockings and sequential compression

thrombosis pneumatic devices; administer heparin (5000 U SC
prophylaxis three times daily) after treatment of aneurysm
Blood pressure
Keep systolic blood pressure at 90–140 mm Hg
before aneurysm treatment, then allow hypertension
to keep systolic blood pressure <200 mm Hg

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Management of Recommendation
condition
Serum glucose Maintain level at 80–120 mg/dl; use sliding scale or
continuous infusion of insulin if necessary

Core body Keep at ≤37.2°C; administer acetaminophen (325–650

temperature mg PO every 4–6 hr) and use cooling devices if
necessary
Calcium antagonist Administer nimodipine (60 mg PO every 4 hr for 21
days)
Antifibrinolytic Administer aminocaproic acid (first 24–48 hr, 5 g IV,
therapy (optional) followed by infusion at 1.5 g/hr)

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Management of Recommendation
condition
Anticonvulsants Administer phenytoin (3–5 mg/kg/day PO or IV) or
valproic acid (15–45 mg/kg/day PO or IV)

Fluids and hydration Maintain euvolemia (CVP, 5–8 mm Hg); if cerebral

vasospasm is present, maintain hypervolemia (CVP, 8–
12 mm Hg, or PCWP, 12–16 mm Hg)
Nutrition Try oral intake (after evaluation of swallowing); for
alternative routes, enteral feeding preferred

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Management of Recommendation
condition
Surgical clipping Perform procedure within first 72 hr

Endovascular coiling Perform procedure within first 72 hr

Hydrocephalus Insert external ventricular or lumbar drain

Rebleeding Provide supportive care and emergency treatment of

aneurysm
Cerebral vasospasm Maintain hypervolemia or induced hypertension with
phenylephrine, norepinephrine, or dopamine;
provide endovascular treatment (transluminal
angioplasty or direct vasodilators)

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Management of Recommendation
condition

Seizures Administer lorazepam (0.1 mg/kg, at a rate of 2

mg/min), followed by phenytoin (20 mg/kg IV bolus
at <50 mg/min, up to 30 mg/kg)

Hyponatremia With SIADH, restrict fluids; with cerebral salt-wasting

syndrome, aggressively replace fluids with 0.9%
saline or hypertonic saline solution

Myocardial injury and Administer metoprolol (12.5–100 mg PO twice daily);

arrhythmias evaluate ventricular function; treat arrhythmia

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Management of Recommendation
condition

Pulmonary edema Provide supplemental oxygen or mechanical

ventilation if necessary; monitor PCWP and
ventricular function; distinguish cardiogenic vs.
neurogenic pulmonary edema
Rehabilitation Provide physical, occupational, and speech therapies

Neuropsychological Perform global and domain-specific testing; provide

evaluation cognitive rehabilitation

Depression Administer antidepressant medications and provide

psychotherapy

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Management of Recommendation
condition
Chronic headaches Administer NSAIDs, tricyclic antidepressants, or SSRIs;
gabapentin

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 Arterialvasospasm : 60 -70 % in 4 weeks
 Rebleeding: max first 24 hrs, 20 % in 2 wks
 Acute hydrocephalus : > 50 % in 30 days
 Intracerebral hematoma
 Subdural hematoma

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 Epilepsy : 9 %, in 4 weeks
 Cardiac arrhytmia and myocardial inj
(35 %)
 SIADH
 Pulmonary and UTI
 Gastrointestinal bleeding

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 Maximum in the first 24 hours with a
cumulative risk of about 20 % in the next 14
days. Mortality 40 – 78%.
 Early surgery < 72 hrs, may improve outcome,
35 % rebleeding.
 Short-term Antifibrinolytic prevent rebleeding
and may improve outcome.

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 Blood in the subarachnoid space triggers a
pathological process that results in spasm of
the vessels of the major branches of the
circle of Willis  decrease vessel caliber 
decrease cerebral blood flow  ischaemic
complication 24 - 32%.
 Etiology is obscure.
 5 days after SAH. Vasospasm develops, lasts
for 1 – 2 weeks or more.

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 Consequence of vasospasm evolve more
slowly, more predictable, preventable and
treatable.
 Related to an inhibition of reuptake of Ca,
which leads to continued vasc smooth muscle
contraction.

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 Head CT scan within 4 days correlated
with the location and severity of vasospasm.
 TCD bedside evaluation for blood flow
velocity.
 PET
 SPECT
 Xenon CT

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 Nimodipine , selective cerebral
vasculature and block Calcium entry into
neurons by a direct action on L-type
voltage sensitive Calcium
channels.Intravenous route followed by
oral.
 Nimodipine in aneurysmal SAH reduce the
incidence of poor outcome due to delayed
cerebral ischemia associated with
vasospasm by 24 %.
 Nimodipine IV inhibits platelet
thromboxane B2 release.

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 Start as soon as possible in 4 days after Dx SAH was
established.
 Initial dose 15 ug/ kg/hour or 5 ml/ hour in the first
2 hours by continuous infusion administered via a
three-way stopcock infusion pump.
Co-infusion rate 20 ml/ hour.
Maintenance dose :30 ug/kg/hour or 10 ml/hour.
Co-infusion rate : 40 ml/hour.
 Tx continued for at least 1 week until 10 days.
 Oral nimodipine 6 dd 60 mg (2 tablet) may be
substituted for a further week or up to 21 days.
 Infusion fluids : normal saline, RL, dextran 40.

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 Hypotension (4,4%)
 Rash
 Others
: diarrhoea, headache,flushing,
nausea, myalgia.

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 Factors
that contributed most to variation in
outcome :
 Cerebral infarction
 Neurological grade
 Age
 Intraventricular hemorrhage
 Vasospasm
 Intracerebral hematoma
 History of hypertension
 Elevated glucose levels on admission

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 Simon RP et al. 2009. clinical neurology 7 ed.
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