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STROKEDodik Tugasworo

PENYAKIT SARAF

NYERISAKIT KEPALAMIGRENVERTIGOKESEMUTANPARKINSONEPILEPSIINFEKSI OTAKGANGGUAN INGATANGANGGUAN PERKEMBANGAN ANAKGANGGUAN GERAKTUMOR OTAKGEGAR OTAKPIKUN BUYUTANSTROKE

KENAPA BISA STROKE ?BAGAIMANA GEJALA STROKE ?BAGAIMANA CARA PENGOBATANNYA ?BAGAIMANA PERAWATAN SETELAH STROKE ?BAGAIMANA HIDUP DENGAN STROKE DAN HIDUP DENGAN PENDERITA STROKE ?

APAKAH STROKE ?SUHARTOGUS DUR

MENDADAK

MENCEMASKANKESEMBUHANMENAKUTKANKECACATANMENGGELISAHKANKEMATIAN

STROKEPenyakit 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 INDONESIA & NEG. BERKEMBANG : PREVAL & MORTALITAS MENINGKATSTROKE adalah MASALAH KESH. MASYARAKAT

Problems (United State)160.000 death / years730.000 new case and recurrent stroke (97)A new case stroke every minuteDeath case stroke every three minutedirect-costs $ 27 billionindirect-costs $ 13 billion (1996)

Out Come of Acute Stroke patientsStroke Unit Dr Kariadi Hospital Semarang 2001

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146916

721465

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Force discharge

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IschaemicHaemorrhagic

Recovery14672

Force discharge914

Death1665

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BATASAN STROKEW.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)Slurred speech, difficulty understanding others LOWHEADegs clumsy or numbne side of body affectedeaknesseadache, unusually severe (or facial numbness)yes: loss of sight (in one eye or both eyes)rms clumsy or numb AND/ORizziness

INCIDENCE OF THE MAIN CAUSES OF STROKE

Anatomi Otak KitaOtak kita terdiri atas 2 belahan, otak KIRI dan otak KANANOtak kiri berfungsi sebagai pemantau dan pelaksana the three Rs (Reading, wRiting and aRhithmetic), bersifat logis analistisOtak 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 OTAKO T A KKUMPULAN PUSAT-PUSATTUGAS BERATPERLU MAKANAN YANG CUKUPDAN TERATUR

TIAP MENIT : 800 CC OKSIGEN100 MGR GLUKOSATERHENTI30 DETIKTERHENTI3 MENITTERHENTI8 MENITSEL TERGANGGUKECACATANMENINGGALSEL MATIBERAT :1200 - 1400 GRAM(2 % BB)

Gejala dan tanda yang timbul pada stroke harus sesuai daerah yang terkena.Cacat yang timbul pada stroke umumnya terjadi akibat kerusakan pada area motorik di otak.Gejala yang timbul pada stroke tidak selalu nyata, kadang ringan dan tersamar (misal bahasa, memori, emosi, perilaku, demensia, dsb)

ARTERIAL TERRITORRIES OF CEREBRAL HEMISPHERESLEFT (FRONTAL); RIGHT (HORIZONTAL)3211231 = nucleus lentiformis; 2 = thalamus; 3 = nucleus caudatusRed =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) SyndromeLocalization ----------------------------------------------------------------------------------------------------------------- Anterior (carotid) artery syndromes Middle cerebral artery Expressive aphasia Dominant posterior frontal lobe Receptive aphasia 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(motoric)(sensoric)

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 STEMOR BRAINSTEM (LACUNAR STROKE)

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

CEREBELLUM- Ipsilateral limb ataxia.- Gait ataxia.

S T R O K E(GANGGUAN PEREDARAN DARAH OTAK)DOKTERSPESIALISSARAFSEMBUH SEMPURNAMENINGGALMENYANDANG CACATF A K T O RR I S I K OFAKTORPENCETUSTERGANTUNGPADA KECEPATANBEROBATNYA

bukan stroke..Dokter menyimpulkan : gangguan di otakstrokeKeluhan pasien : tentukan jenisnya SNH atau SH Cara : - anamnesis - pemeriksaan klinis neurologi - algoritma dan penilaian dgn skor stroke - pemeriksaan dgn menggunakan alat

Stroke PreventionRisk Factor Management

Risk Factors1Non modifiable Age Race Gender Family history of stroke.

Risk Factors-2Modifiable / treatableHypertension atrial fibrillationDiabetes mellitus hyperhomocysteinemiaHyperlipidemia hypercoagulabilityCigarette smoking oral contraceptiveInfection: chlamydia, helicobacter, viruses.Prior stroke/TIA carotid stenosis Physical inactivity, obesity, sleep apnea/ snoring.Alcohol abuse. (Stroke, February 2001)

Diagnosis jenis strok (SI, SH, PSA,PIS) sejak dahulu sulit, seringkali meragukan, lama sampai diterapkannya CT-Scanning dalam klinik (1972).

DIAGNOSIS JENIS STROK

ANAMNESISTabel 1. Perbedaan stroke hemoragik dan stroke infark

Perbedaan Stroke Hemoragik dan Stroke Infark berdasarkan anamnesisGejala/SimtomStroke Stroke nonhemoragik hemoragikSaat onsetSedang aktifIstirahatPeringatan (warning) - +Nyeri kepala +++ +Kejang + -Muntah + -Penurunan kesadaran +++ +

Tanda (sign) Stroke Hemoragik Stroke Non HemoragikBradikardi ++ (dari awal) (hari ke-4)Udem papil Sering + -Kaku kuduk+ -Tanda Kernig,Brudzinski ++ -Perbedaan Stroke Hemoragik dan Stroke Infark berdasarkan tanda-tandanya

II. STROKE BERDASARKAN PENYEBABNYA 1. STROKE HEMORAGIK = STROKE PERDARAHAN PERDARAHAN OTAKKURANGDARAHKECACATANPUSAT KESADARANKEMATIANTIDAK SADARPUSAT NAFASPUSAT JANTUNG

2. STROKE NON HEMORAGIK = STROKE SUMBATAN = SUMBATAN OTAK

DAERAHMATIA.B.C.D.PENEBALAN DINDINGALIRAN DARAH LAMBATDARAH KENTALDAERAH PENUMBRA(DAERAH SETENGAH MATI)HARUS DISELAMATKANKECACATANKECACATAN DIKURANGISEMAKSIMAL MUNGKINFISIOTERAPISUMBATAN / EMBOLUS

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 TCDEFFEKTIVEMUDAH DIGUNAKANNON-INVASIVENON-RADIO AKTIVEPORTABLEMURAHDAPAT DIULANG DAN AMANReport of the American Academy of Neurology (1990)

KEKURANGAN TCDPOSISI 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 SUMBATANDAPAT EVALUASI DAN MENGIKUTI PASIEN DENGAN VASOKONSTRIKSI PADA SEMUA KASUS, KHUSUSNYA SETELAH SAHDETEKSI AVM DAN MELIHAT SUPPLY ARTERI DAN GAMBARAN ALIRAN DAPAT UNTUK MELIHAT KEMATIAN OTAKPUSING KRONIS, MIGREN, VERTIGO


KEGUNAAN TCD :DETEKSI STENOSIS BERAT (>65%) DI PEMBULUH DASAR OTAK DAPAT MEMBERI GAMBARAN SIRKULASI KOLATERAL DENGAN MENGETAHUI REGIO PADA STENOSIS BERAT OR SUMBATANDAPAT EVALUASI DAN MENGIKUTI PASIEN DENGAN VASOKONSTRIKSI PADA SEMUA KASUS, KHUSUSNYA SETELAH SAHDETEKSI AVM DAN MELIHAT SUPPLY ARTERI DAN GAMBARAN ALIRAN DAPAT UNTUK MELIHAT KEMATIAN OTAKPUSING KRONIS, MIGREN, VERTIGO


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 MRIKontra indikasi relatif :1. Artificial joint2. Middle ear protesis3. Corpus alienum/benda-benda logam4. Hamil muda

Kontra indikasi absolut1. Terhadap penderita dgn alat pemacu jantung2. terhadap pend. dgn hemostatic clip (cerebral aneurysma.

KELEBIHAN DAN KEKURANGAN MRIKelebihan :1. Non invasive2. Banyak potongan yg dpt dilakukan secara langsung 3. Dgn akurat sangat tinggi hampir semua jaringan4. Tdk memakai sinar-X5. Tdk merusak keshehatan pd penggunaannya yg tepat 6. Banyak pekerjaan yg dpt dikerjakan tanpa zat kontras7. 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 MRIKekurangan :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 STROKE5 BPenanganan Stroke AkutPenanganan Faktor risikoPenanganan KomplikasiRehabilitasiPenanganan Post Stroke

5 "NO" OF MEIER RUGE FOR ACUTE ISCHEMIC STROKE THERAPY (1990)1. No antihypertensives *, 2. No diuretics, 3. No dexamethasone, 4. No glucose infusion, 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.Rapidly stabilize the patient, insert an IV- line. No glucose.Make a quick but thorough neurological assessment: stroke or non stroke?Withdraw blood for the most urgent tests: blood glucose, CBC, electrolytes. Sent the patient for brain-scan.CDP-choline?

Common stroke mimics.HypoglycemiaPost-ictal stateDrug overdose Encephalopathies with focal signsHyponatremiaSubdural hematoma/empyemaConcussion with neck injuryFacial 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%74-year old.2 hours after onsetBP 155/70Normal platelets, etc..t-PA administeredStuporous after 9 hrs.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 formulate a more rational plan of treatment.

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.In the presence of disruption of the BBB, reperfusion may induce cerebral edema and hemorrhage.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.

The next three days.Watch out for brain edema!Repeat all necessary tests as often as necessary, including CT.Keep the patients energy metabolism and electrolytes in an optimal condition.Treat fever aggressively!

In case something goes wrong.Most common complications of acute stroke:Cerebral edemaFever Electrolytes imbalanceMalnutrition.ConvulsionsDVT.

Cerebral edema.May develop acutely, usually after second day.Strict attention to fluid balance, avoid the use of hypotonic solutions, such as 5% glucose.Use mannitol with caution.Albumin, 25% solution, helpful, especially if serum albumin < 3.6 g/dl.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. Increase lactic acidosis.

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 patients recovery.Laboratory tests may help to determine the patients 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-2Deficiency 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, Jan.2001)

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.

Labetolol: 5-100 mg/h by intermittent bolus doses of 10-40 mg or continuous drip (2-8 mg/min).Esmolol: 500 g/kg as a load, maintenance use, 50-200 g/kg/min.Hydralazine: 10-20 mg Q 4-6 hEnalapril: 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 steroidHyperventilation: - 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 CANDIDATES1. Small hemorrhages ( 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!

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