Stroke
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)
150
100
50
0
Ischaemic Haemorrhagic
O T A K BERAT :
1200 - 1400 GRAM
KUMPULAN (2 % BB)
PUSAT-PUSAT
TUGAS BERAT
3
3 1
2
2 1
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 :
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
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
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.