STROKE

Dodik Tugasworo
PENYAKIT SARAF

NYERI
SAKIT KEPALA
MIGREN
VERTIGO
KESEMUTAN
PARKINSON
EPILEPSI
INFEKSI OTAK
GANGGUAN INGATAN
GANGGUAN PERKEMBANGAN ANAK
GANGGUAN GERAK
TUMOR OTAK
GEGAR OTAK
PIKUN BUYUTAN
STROKE
n KENAPA BISA STROKE ?
n BAGAIMANA GEJALA STROKE ?
n BAGAIMANA CARA
PENGOBATANNYA ?
n BAGAIMANA PERAWATAN SETELAH
STROKE ?
n BAGAIMANA HIDUP DENGAN STROKE
DAN HIDUP DENGAN PENDERITA
STROKE ?
APAKAH STROKE ?

SUHARTO
GUS DUR

MENDADAK

MENCEMASKAN KESEMBUHAN
MENAKUTKAN KECACATAN
MENGGELISAHKAN KEMATIAN
STROKE
n Penyakit dengan mortalitas tinggi
– ke 3 di AS (sesudah penyakit jantung & kanker)
(Laporan ke Presiden, 1964 - 65)
– mengenai (insidensi) hampir 400.000/thn (AS,
Whisnant, 1971)
– membunuh 200.000 orang/tahun (AS, Kurtzke,
1980)
– Di Indonesia 2008 Stroke penyebab kematian No
1
n INDONESIA & NEG. BERKEMBANG : PREVAL &
MORTALITAS MENINGKAT
STROKE adalah MASALAH KESH. MASYARAKAT
 Problems (United State)

 160.000 death / years

 730.000 new case and recurrent stroke (‘97)
 A new case stroke every minute
 Death case stroke every three minute
 direct-costs $ 27 billion
 indirect-costs $ 13 billion (1996)
 Out Come of Acute Stroke patients
Stroke Unit Dr Kariadi Hospital Semarang 2001

150

100

50

0
Ischaemic Haemorrhagic

Recovery Force discharge Death

 BATASAN STROKE
W.H.O 1986 memberikan batasan sbb ;
 Suatu TANDA-TANDA KLINIS yang
BERKEMBANG CEPAT akibat
GANGGUAN FUNGSI - OTAK FOKAL
atau GLOBAL dengan GEJALA– GEJALA
yg berlangsung 24 jam atau lebih /
menyebabkan KEMATIAN tanpa sebab
lain selain VASKULER
STROKE (BRAIN ATTACK)
(Adams Jr 2003)
S lurred speech, difficulty understanding others
L egs clumsy or numb
O ne side of body affected
W eakness
H eadache, unusually severe (or facial numbness)
E yes: loss of sight (in one eye or both eyes)
A rms clumsy or numb AND/OR
D izziness
INCIDENCE OF THE MAIN CAUSES OF STROKE
 Anatomi Otak Kita
 Otak kita terdiri atas 2 belahan, otak KIRI
dan otak KANAN
 Otak kiri berfungsi sebagai pemantau dan
pelaksana the three “R’s (Reading, wRiting
and aRhithmetic), bersifat logis – analistis
 Otak kanan pola kognitif yang intuitif holistik,
memproses segala informasi secara simultan,
memandang problem secara holistis, jauh
kedepan, mengenal wajah orang dan melihat
sifat – sifat secara keseluruhan. Imajinasi,
persepsi visual, orientasi tempat, emosi.
 ANATOMI DAN FUNGSI OTAK

O T A K BERAT :
1200 - 1400 GRAM
KUMPULAN (2 % BB)
PUSAT-PUSAT

TUGAS BERAT

PERLU MAKANAN YANG CUKUP

DAN TERATUR
TIAP MENIT : 800 CC OKSIGEN
100 MGR GLUKOSA

TERHENTI SEL TERGANGGU

30 DETIK
TERHENTI SEL MATI KECACATAN
3 MENIT
TERHENTI MENINGGAL
8 MENIT
n Gejala dan tanda yang timbul pada
stroke harus sesuai daerah yang
terkena.
n Cacat yang timbul pada stroke
umumnya terjadi akibat kerusakan pada
area motorik di otak.
n Gejala yang timbul pada stroke tidak
selalu nyata, kadang ringan dan
tersamar (misal bahasa, memori, emosi,
perilaku, demensia, dsb)
 ARTERIAL TERRITORRIES OF CEREBRAL HEMISPHERES
LEFT (FRONTAL); RIGHT (HORIZONTAL)

3
3 1
2
2 1

1 = nucleus lentiformis; 2 = thalamus; 3 = nucleus caudatus

Red =a.cerebri ant. Green =a.cerebri med. Yellow =a.cerebri post. Light blue =a.choroidea ant.
Dark green =a.choroidea post. Dark blue =a.commun.post
 ANTERIOR AND POSTERIOR
VASCULAR SYNDROMES (FELBERG 2003)
Syndrome Localization
-----------------------------------------------------------------------------------------------------------------
 Anterior (carotid) artery syndromes
 Middle cerebral artery
• Expressive aphasia(motoric) • Dominant posterior frontal lobe
• Receptive aphasia(sensoric) • Dominant superior temporal lobe
• Weakness of arm and/or leg • Contralateral (to weakness) parietal
lobe
• Loss of lateral visual fields • Contralateral parietal lobe

 Anterior cerebral artery

• Weakness of leg • Medial (parafalcine) parietal lobe

 Posterior (vertebrobasilar) artery syndromes

• Vertigo, nystagmus that changes with the direction • Cerebellum
of gaze, cranial nerve palsies, retropulsion
• Hemiparesis, hemisensory loss, of one-half of the • Brainstem
body, swallowing difficulty
 COMMON PATTERNS OF NEUROLOGIC
IMPAIRMENTS IN ACUTE ISCHEMIC STROKE (1)
(Adams 2003)
L. (DOMINANT) HEMISPHERE R. (NONDOMINANT) HEMISPHERE
(major or branch cortical infarction) (Major or branch cortical infarction)

- Aphasia - Left hemiparesis

- Right hemiparesis - Left sided sensory loss

- Right sided sensory loss - Left sided spatial neglect

- Right sided spatial neglect - Left homonymous hemianopia

- Right homonymous hemianopia - Impaired left conjugate gaze

- Impaired right conjugate gaze
 COMMON PATTERNS OF NEUROLOGIC
IMPAIRMENTS IN ACUTE ISCHEMIC STROKE (2)
(Adams 2003)
DEEP (SUBCORTICAL) HEMISPHERE BRAIN STEM
OR BRAINSTEM (LACUNAR STROKE)

- Hemiparesis (pure motor stroke) or - Motor or sensory loss in all

sensory loss (pure sensory stroke).
- Dysarthria, including dysarthria-
clumsy hand.
body).
- Ataxic-hemiparesis.
- No abnormalities of cognition,
language or vision.
four limbs.
- Crossed signs (signs on same
side of face/other side of
- Dysconjugate gaze.
- Nystagmus ; Ataxia.
- Dysarthria; Dysphagia.

CEREBELLUM
- Ipsilateral limb ataxia.
- Gait ataxia.
 FAK T O R
RISIKO
FAKTOR
PENCETUS
STROKE
(GANGGUAN PEREDARAN DARAH OTAK)
DOKTER TERGANTUNG
SPESIALIS PADA KECEPATAN
SARAF BEROBATNYA

SEMBUH MENYANDANG
SEMPURNA CACAT
MENINGGAL
 ……………..
Keluhan pasien :

Dokter menyimpulkan : gangguan di otak

stroke bukan stroke

tentukan jenisnya
SNH atau SH
Cara : - anamnesis
- pemeriksaan klinis neurologi
- algoritma dan penilaian dgn skor stroke
- pemeriksaan dgn menggunakan alat
Stroke Prevention
 Risk Factors1

Non modifiable
 Age
 Race
 Gender
 Family history of stroke.
 Risk Factors-2

Modifiable / treatable
 Hypertension  atrial fibrillation
 Diabetes mellitus  hyperhomocysteinemia
 Hyperlipidemia  hypercoagulability
 Cigarette smoking  oral contraceptive
 Infection: chlamydia, helicobacter, viruses.
 Prior stroke/TIA  carotid stenosis
 Physical inactivity, obesity, sleep apnea/
snoring.
 Alcohol abuse.
(Stroke, February 2001)
DIAGNOSIS JENIS STROK
Diagnosis jenis strok (SI, SH, PSA,PIS)
sejak dahulu sulit, seringkali meragukan,
lama sampai diterapkannya CT-Scanning
dalam klinik (1972).
ANAMNESIS
Tabel 1. Perbedaan stroke hemoragik dan stroke infark

Gejala (symptom) Stroke hemoragik Stroke infark

-Onset/awitan Mendadak Mendadak
-Saat onset Sedang aktif Istirahat
-Peringatan (-) (+)
-Nyeri kepala +++ ±
-Kejang (+) (-)
-Muntah (+) (-)
-Penurunan +++ ±
kesadaran
 Perbedaan Stroke Hemoragik dan
Stroke Infark berdasarkan anamnesis
Gejala/Simtom Stroke Stroke non
hemoragik hemoragik
Saat onset Sedang aktif Istirahat
Peringatan (warning) - +
Nyeri kepala +++ +
Kejang + -
Muntah + -
Penurunan kesadaran +++ +
 Perbedaan Stroke Hemoragik dan Stroke
Infark berdasarkan tanda-tandanya

Tanda (sign) Stroke Hemoragik Stroke Non

Hemoragik

Bradikardi ++ (dari awal) ± (hari ke-4)

Udem papil Sering + -

Kaku kuduk + -

Tanda Kernig,Brudzinski ++ -
II. STROKE BERDASARKAN PENYEBABNYA
1. STROKE HEMORAGIK = STROKE PERDARAHAN
PERDARAHAN OTAK

KURANG
DARAH

KECACATAN
PUSAT
KESADARAN

TIDAK SADAR
PUSAT NAFAS
KEMATIAN
PUSAT JANTUNG
2. STROKE NON HEMORAGIK = STROKE SUMBATAN
= SUMBATAN OTAK

KECACATAN
A. SUMBATAN / EMBOLUS

DAERAH
MATI

B. PENEBALAN DINDING

DAERAH PENUMBRA
C. ALIRAN DARAH LAMBAT (DAERAH SETENGAH MATI)

HARUS DISELAMATKAN
D. DARAH KENTAL
FISIOTERAPI

KECACATAN DIKURANGI
SEMAKSIMAL MUNGKIN
Diagnosis Stroke
- Berdasarkan temuan klinis
- Pemeriksaan Penunjang

PEMERIKSAAN PENUNJANG
Tujuan : -menegakkan diagnosis
-mencari faktor risiko
-mencari faktor penyulit
 LABORATORIUM
1. DARAH
- Rutin
- Hematokrit
- Masa perdarahan dan pembekuan
- Gula Darah I / II
- Kolesterol total, HDL, LDL
- Trigliserid
- Asam urat
- Ureum , Kreatinin
- Elektrolit
- Khusus : - Agregasi trombosit - Homocysteine
- APTT - Fibrinogen
- D-dimer - Protein C dan S
2. LUMBAL PUNGSI
- perdarahan sub arahnoid
3. X- FOTO TORAKS
- besar jantung, penyakit paru
4. EKG
- fibrilasi atrium, iskemik/infark jantung
EKOKARDIOGRAFI
- sumber emboli di jantung dan aorta proksimal
5. NEUROSONOGRAFI
- stenosis, vaso spasme
6. ANGIOGRAFI SEREBRAL
- AVM, anuerisma
Pemeriksaan Neuroimajing/neurosonologi (NINS)
selain dengan CT Scan & MRI ialah dengan
Angiografi serebral, PET, SPECT, dan sonografi
dopler (Transcranial Doppler Sonography = TCDS)
untuk mendeteksi stenosis vaskular ekstra dan
intrakranial untuk membantu evaluasi diagnostik,
etiologik, terapetik dan prognostik
KEUNTUNGAN TCD

EFFEKTIVE
MUDAH DIGUNAKAN
NON-INVASIVE
NON-RADIO AKTIVE
PORTABLE
MURAH
DAPAT DIULANG DAN AMAN

Report of the American Academy of Neurology (1990)

KEKURANGAN TCD

POSISI ANATOMI PEMBULUH DARAH BERBEDA, LETAK DARI

ARTERI SULIT DITEMUKAN

PENYAKIT BILATERAL SIMETRIS, VASOCONSTRICTION OR

STENOSIS PADA REGIO YANG LUAS, DAN ARTERI DISTAL DAN
ARTERI PENETRATING SULIT DIPERIKSA

SEBAGIAN PENDERITA TIDAK PUNYA WINDOW

Report of the American Academy of Neurology (1990)

TCD HAS ESTABLISHED VALUE IN :

DETEKSI STENOSIS BERAT (>65%) DI PEMBULUH DASAR

OTAK
DAPAT MEMBERI GAMBARAN SIRKULASI KOLATERAL DENGAN
MENGETAHUI REGIO PADA STENOSIS BERAT OR SUMBATAN
DAPAT EVALUASI DAN MENGIKUTI PASIEN DENGAN
VASOKONSTRIKSI PADA SEMUA KASUS, KHUSUSNYA SETELAH
SAH
DETEKSI AVM DAN MELIHAT SUPPLY ARTERI DAN GAMBARAN
ALIRAN
DAPAT UNTUK MELIHAT KEMATIAN OTAK
PUSING KRONIS, MIGREN, VERTIGO

Report of the American Academy of Neurology (1990)

KEGUNAAN TCD :

DETEKSI STENOSIS BERAT (>65%) DI PEMBULUH DASAR

OTAK
DAPAT MEMBERI GAMBARAN SIRKULASI KOLATERAL DENGAN
MENGETAHUI REGIO PADA STENOSIS BERAT OR SUMBATAN
DAPAT EVALUASI DAN MENGIKUTI PASIEN DENGAN
VASOKONSTRIKSI PADA SEMUA KASUS, KHUSUSNYA SETELAH
SAH
DETEKSI AVM DAN MELIHAT SUPPLY ARTERI DAN GAMBARAN
ALIRAN
DAPAT UNTUK MELIHAT KEMATIAN OTAK
PUSING KRONIS, MIGREN, VERTIGO

Report of the American Academy of Neurology (1990)

 CT Scanning tanpa kontras merupakan
pemeriksaan baku emas untuk menentukan
jenis patologi strok, lokasi dan ekstensi lesi,
serta menyingkirkan lesi non vaskular
(Konsensus Nasional 1999).
 Godfrey HOUNSFIELD (1971) ahli fisika dan
James AMBROSE (1972) dokter radiologi
Inggris, pada 1979 memperoleh anugrah
NOBEL untuk penemuan CT Scan, yang
dengan sinar-X diubah impuls listrik,
memproyeksi titik-titik tubuh menjadi gambar
2 dimensi dengan bantuan komputer
 Pemeriksaan MRI diindikasikan untuk
diagnosis jenis lesi patologik strok dengan
lebih tajam (Konsensus Nasional 1999).
 RaYmod DAMADIN (1960), menggunakan
MRI dalam riset; atas dasar interaksi
gelombang RADIO dgn inti PROTON dlm
MEDAN MAGNIT yg kuat tanpa sinar-X,
dgn gambar tajam; dan digunakan di RS
(1980 an)
KONTRA INDIKASI MRI
Kontra indikasi relatif :
1. Artificial joint
2. Middle ear protesis
3. Corpus alienum/benda-benda logam
4. Hamil muda

Kontra indikasi absolut

1. Terhadap penderita dgn alat pemacu
jantung
2. terhadap pend. dgn hemostatic clip
(cerebral aneurysma.
KELEBIHAN DAN KEKURANGAN MRI
Kelebihan :
1. Non invasive
2. Banyak potongan yg dpt dilakukan secara langsung
3. Dgn akurat sangat tinggi hampir semua jaringan
4. Tdk memakai sinar-X
5. Tdk merusak keshehatan pd penggunaannya yg tepat
6. Banyak pekerjaan yg dpt dikerjakan tanpa zat kontras
7. Potongan yg dihasilkan dpt 3 dimensi (aksial, frontal,
dan sagital) dan malah banyak potongan dapat dibuat
hanya dlm datu waktu (dpt membuat > 8 potongan
sekaligus)
KELEBIHAN DAN KEKURANGAN MRI
Kekurangan :
1.Tdk dpt digunakan u/penderita gawat
darurat/darurat akut, yg non koperatif / anak-
anak karena pem ini memerlukan wkt yg lama,
dan alat-alat bantu yg bersifat ferromagnetik tdk
dpt masuk ke ruang pemeriksaan (gantry)
2. Sementara pemeriksaan berlangsung ada suara
gaduh
3. Biaya pemeriksaan dan pemeliharaan lebih tinggi
dari biaya pemeriksaan radiologi lainnya.
 PENANGANAN STROKE

5 B
 Penanganan Stroke Akut
 Penanganan Faktor risiko
 Penanganan Komplikasi
 Rehabilitasi
 Penanganan Post Stroke
 5 "NO" OF MEIER RUGE FOR ACUTE
ISCHEMIC STROKE THERAPY (1990)
n 1. No antihypertensives *,
n 2. No diuretics,
n 3. No dexamethasone,
n 4. No glucose infusion,
n 5. No anticoagulant 4 hours after onset of
stroke.
* Except aortic dissection, acute myocardial infarction,
heart failure, acute renal failure, hypertensive
encephalopathy, thrombolytic therapy (T  185/110
mm Hg) (Brott 2000).
APPROACH TO ACUTE ISCHEMIC STROKE
MANAGEMENT (5 P): (Felberg 2003)
 PARENCHYMA: Management of the ischemic cascade  neuroprotective
agents. Until now none is approved by the FDA.
 PIPES (BLOOD VESSEL) :
1. Antitrombotic
1.1 Anti-platelet  ASA 160-300 mg (IST 1997, CAST 1997)
1.2 Anti-coagulantia (LMWH no benefit) (Hommel 1998, TOAST 1998,
Adams
1999)
2. Trombolytic
2.1 Trombolysis IV rtPA (FDA 1996) (time window 3 hrs).
2.2 Trombolysis IA (1998) (prourokinase) time window 6 hrs.
 PERFUSION: Induced hypertension ? ; Crystalloid/colloid solution
(Pentastarch?)   in cardiac output  10% improved outcome;
Bed position < 300 angle.
 PENUMBRA: Management of the ischemic penumbra  neuroprotectors ?
 PREVENTING COMPLICATION: Control of fever; glycemic control; DVT
precautions; aspiration precaution; avoid indwelling catheters; bowel
regimen; early mobilization.
 The first 30 minutes.
n Rapidly stabilize the patient, insert an
IV- line. No glucose.
n Make a quick but thorough neurological
assessment: stroke or non stroke?
n Withdraw blood for the most urgent
tests: blood glucose, CBC, electrolytes.
n Sent the patient for brain-scan.
n CDP-choline?
Common stroke mimics.
 Hypoglycemia
 Post-ictal state
 Drug overdose
 Encephalopathies with focal signs
 Hyponatremia
 Subdural hematoma/empyema
 Concussion with neck injury
 Facial nerve palsy!
 Migraineous accompaniment.
 The next hour.
 CT-scan reveals no ICH, blood tests and
history no contra-indication for
thrombolytic therapy:  r-tPA. Follow
guidelines scrupulously! May induce
hemorrhagic transformation of infarct.
 Pentoxyfilline, nimodipine or piracetam ?
 Cerebrolysin ?……European Stroke Conference
2001.
 CDP-choline?
 LMWH in selected cases.
.r-tPA induced bleeding. - 7%
n 74-year old.
n 2 hours after onset
n BP 155/70
n Normal platelets, etc.
n .t-PA administered
n Stuporous after 9 hrs.
n Re-CT  bleeding
 The first 24 hours.
 Observe the patient closely for any signs of
deterioration. Repeat brain scan if
necessary.
 Do not lower blood pressure except in the
presence of impending cardiac
decompensation.
 Perform additional laboratory tests the next
day. Do not forget albumin, repeat every
few days.
 Special tests may be needed to help
Intravenous Pentoxyfilline.
 Can be given directly, as a bolus.
 Better if given at a constant rate, with a non-
glucose fluid.
 Dosage may be individualized for each patient.
 Duration: 5-7 days, followed by oral medication.
 Handschu et al: most German hospitals use
either Pentoxyfilline or piracetam for acute
ischemic stroke!

Stroke, 2001
 Reperfusion injury.
n In the presence of disruption of the
BBB, reperfusion may induce cerebral
edema and hemorrhage.
n After a prolonged period of occlusion
leading to cellular injury: reperfusion
may result in increased production of
free radicals, gene expression and
inflammatory events  augmentation
of cellular damage.
 LMWH.
 Usually not used as monotherapy.
 Personal preference: give together with
another drug to selected stroke
patients.
 Start early, continue for 5-7 days.
 Avoid LMWH if:
- systolic blood pressure > 180 mmHg.
- very large infarct or even a tiny
bleed.
 LMWH.
 Usually not used as monotherapy.
 Personal preference: give together with
another drug to selected stroke
patients.
 Start early, continue for 5-7 days.
 Avoid LMWH if:
- systolic blood pressure > 180 mmHg.
- very large infarct or even a tiny
bleed.
 The next three days.
 Watch out for brain edema!
 Repeat all necessary tests as often as
necessary, including CT.
 Keep the patient’s energy metabolism
and electrolytes in an optimal condition.
 Treat fever aggressively!
 In case something goes
wrong.
Most common complications of acute
stroke:
 Cerebral edema
 Fever
 Electrolytes imbalance
 Malnutrition.
 Convulsions
 DVT.
 Cerebral edema.
n May develop acutely, usually after second
day.
n Strict attention to fluid balance, avoid the
use of hypotonic solutions, such as 5%
glucose.
n Use mannitol with caution.
n Albumin, 25% solution, helpful, especially if
serum albumin < 3.6 g/dl.
n Surgical help in case everything else fails.
 Fever.
 May be annoying and is bad for recovery.
 Prevention is better than cure: meticulous
attention to good nursing practice.
 Try to determine exact cause and eradicate it.
 Use suitable antibiotics as necessary.
 Use water bed!
 If possible treat the patient in an air-conditioned
room.
 Fever is bad for stroke
patients!
 Increases the release of excitotoxic
transmitters
 Increases production of free radicals
 Induces more damage to BBB
 Increases post-ischemic depolarization in
the
penumbra.
 Harmful to the recovery of cellular
metabolism.
 Electrolyte imbalance.
 Bad for recovery, may be life-
threatening!
 Repeat electrolyte test as often as
needed.
 Treat promptly, do not rely on “clinical
judgment” alone!
 Enlist the help of a good “internist”.
 Proceed with caution, do not “over-
treat”.
 Malnutrition.
 Remember to feed the patient!
 Fluid infusions alone is not enough.
 Starvation is very bad for the patient.
 A well balanced diet is important to the
patient’s recovery.
 Laboratory tests may help to determine
the patient’s nutritional status.
 Convulsions.
 Occur in approximately 10-20% of
stroke patients, especially those with
large infarct.
 Use parenteral dilantin except if contra-
indicated.
 Oral route is too slow!
 Control drug level and possible side
effects.
 Routine administration of an
anticonvulsant is not recommended.
 Deep vein thrombosis.
 Not frequent in Indonesia.
 Can be prevented by early mobilization.
 Use of LMWH or heparin may be
indicated.
 Often overlooked unless inspected
daily!
Inspect the patients leg, daily!
 Increased level of
Homocysteine.
 Harmful effects due to impairment of
endothelial
function through production of hydrogen
peroxide and consumption of NO to form
nitrosohomocysteine.
 Aggravates atherosclerosis and coagulation.
 Provokes neuropathy, retinopathy,
nephropathy
and cerebral vasospasm in SAH
 Homocysteine-2
 Deficiency of folic acid, vitamin B-12, B-6,
genetic defects of certain enzymes:
methionine- synthetase,
methylenetetrahydrofolate-reductase (folic
acid), and cystathione -synthetase (B6).
 Indication to treat when homocysteine levels
> 14 mol/L. (folic acid + vitamins B-6 + B-
12).
 New data: hyper-homocysteinemia may just
be a result of the ischemic event. (Stroke,
 BLOOD PRESSURE MANAGEMENT
IN ICH (Broderick 1999)
- If SBP > 230 mm Hg or DBP > 140 mm Hg on 2 readings
5 minutes apart  nitroprusside 0.5-10 g/kg/min.
- If SBP is 180-230 mm Hg, DBP 105-140 mm Hg, or mean
arterial BP  130 mm Hg on 2 readings 20 minutes apart
 labetolol, esmolol, enalapril, or other smaller doses
of titrabble IV medications eg diltiazem, lisinopril, or
verapamil.
- If SBP is < 180 mm Hg and DBP < 105 mm Hg, defer
antihypertensive therapy.
- If ICP monitoring is available, cerebral perfusion
pressure should be kept at > 70 mm Hg.
n Labetolol: 5-100 mg/h by intermittent bolus doses of 10-40 mg or continuous drip (2-8
mg/min).
n Esmolol: 500 g/kg as a load, maintenance use, 50-200 g/kg/min.
n Hydralazine: 10-20 mg Q 4-6 h
n Enalapril: 0.625-1.2 mg Q 6 h as needed.
 MANAGEMENT OF ICP
(Broderick 1999)
Osmotherapy:
- Mannitol 20% (0.25-0.5 g/kg every 4 h), for only  5 d.
- Furosemide (10 mg Q 2-8 h) simultaneously with mannitol.
- Serum osmolality  310 mOsm/L, measured 2 X daily.
No steroid
Hyperventilation:
- Reduction of pCO2 to 35-30 mm Hg, by raising ventilation rate
at constant tidal volume (12-14 mL/kg), lowers ICP 25%-30%.
Muscle relaxants:
- Neuromuscular paralysis in combination with adequate
sedation can reduce elevated ICP.
- Vecuronium or pancuronium, with only minor histamine
liberation and ganglion-blocking effects are preferred.
 RECOMMENDATIONS FOR SURGICAL
TREATMENT OF ICH (Broderick 1999)
NON SURGICAL CANDIDATES
1. Small hemorrhages (<10 cm3) or minimal neurological
deficits.
2. GCS score  4. Except for cerebellar hemorrhage with
brainstem compression for livesaving surgery.

SURGICAL CANDIDATES
1. Cerebellar hemorrhage > 3 cm who are neurologically
deteriorating or who have brainstem compression and
hydrocepahalus from ventricular obstruction.
2. ICH with structural lesion eg aneurysm, AVM, or
cavernous angioma.
3. Young patients with a moderate or large lobar
hemorrhage who are clinically deteriorating.
 MANAGEMENT OF SAH (1)
1. BEDREST + tranquilizers + head position horizontal.

2. PREVENTION OF REBLEEDING
- Antihypertensive medications (controversial)
- Antifibrinolytics:
- Tranexamic acid 6 X 1gr (7-14 days)   40% in rebleeding offset by
 43% in focal ischemic deficits (Kassell 1984).
- Tranexamic acid + nimodipine   ischemic deficits (van Gijn 1992).
- Carotid ligation (indeterminate value)
- Intraluminal coils & balloons (experimental)

3. PREVENTION OF VASOSPASM
- Hypertension/hypervolemia/hemodilition (experimental)
- Calcium ch.antagonists : Nimodipine 6 X 60 mg p.o./infuse 1-2 mg/hr for 5-
14 ds.
- Intracisternal fibrinolysis +antioxidant+ antiinflammatory agents 
uncertain value
- Transluminal angioplasty in whom conventional therapy has failed.
 MANAGEMENT OF SAH (2)
4. HYDROCEPHALUS
- Acute (obstructive) hydrocephalus  ventriculostomy.
- Chronic (communicating) hydrocephalus  temporary/permanent CSF diversion.

5. PREVENTION OF HYPONATREMIA
- Intravascular administration of isotonic fluids.
- Monitoring CVP, pulmonary capillary wedge pressure, fluid balance & body weight.
- Volume contraction should be corrected by increasing the volume of fluids.

6. PREVENTION OF SEIZURES
- Prophylactic anticonvulsants is recommended.
- Longterm anticonvulsants not routinely recommended.

7. SURGICAL INDICATION
- RUPTURED ANEURYSMS
WFNS grade 1-3 (good-intermediate grade)  surgery strongly indicated.
- UNRUPTURED ANEURYSMS
Surgery recommended
- ASYMPTOMATIC ANEURYSMS
> 1 cm  operate; < 1 cm  do not operate (consensus).
STROK penyakit gawat dan akut
Emergency :
Diagnosa yang tepat dan segera sangat
menentukan TERAPI yang cepat & terarah
Morbiditas dan Mortalitas dapat
diturunkan
 The Ideal Stroke team.

The team should consist of:

 neurologists with special interest in stroke
 neuro-radiologists, well-trained to do angiograms +
Doppler evaluation of vessels supplying the brain
 A neurosurgeon, with special training in vascular surgery.
 Well-trained team of nursing personnel, physiotherapists.
 Other related specialists: social worker, psychiatrists….
 A well-run hospital with lab and imaging facilities,
available 24 hours a day, seven days a week.
Yin Yang
Thank you – Terima kasih!