stroke umbrah
DESCRIPTION
NEUROLOGITRANSCRIPT
Dr. Syarif Indra, Sp.SDr. Syarif Indra, Sp.SBagian Neurologi FK-UnandBagian Neurologi FK-Unand
RS. DR. M DjamilRS. DR. M DjamilPadang Padang
DEFINISI Gangguan fungsi otak akut akibat ggn suplai darah diotak, atau perdarahan yang terjadi mendadak yang menyebabkan defisit neurologik (ringan-berat-kematian)
Arteri-Arteri Serebralis
FACTORS ASSOCIATED WITH AN INCREASED RISK OF FACTORS ASSOCIATED WITH AN INCREASED RISK OF STROKESTROKE
* Epidemiologi :* Epidemiologi :
- Age Elderly>middle-aged or young- Age Elderly>middle-aged or young
adult > childrenadult > children
- Gender Men > women in each age group- Gender Men > women in each age group
- Race Blacks > asians or Hispanics > whites- Race Blacks > asians or Hispanics > whites
- Geographic region Eastern Europe > Western Europe ;- Geographic region Eastern Europe > Western Europe ;
Asia > Europe or North AmericaAsia > Europe or North America
* Family History* Family History Stroke or heart disease < age 60 Stroke or heart disease < age 60
* Other* Other, , potentially modifiable, factors :#potentially modifiable, factors :#- Diastolic or isolated systolic hypertensionDiastolic or isolated systolic hypertension
- Diabetes melitus , type 1 or type 2Diabetes melitus , type 1 or type 2
- Hyperlipidemia (hypercholesterolemia)Hyperlipidemia (hypercholesterolemia)
- HyperhomocystenemiaHyperhomocystenemia
- SmokingSmoking
- Alkohol abuseAlkohol abuse
- Drug abuseDrug abuse
- Oral contraceptive useOral contraceptive use
I. Faktor Resiko Yang Dapat Dikendalikan1. HIPERTENSI
Pengaruh Hipertensi
1. Sebagai faktor sekunder :
- TIA (Transient Ischemic Attack)
- Trombosis serebri
2. Sebagai faktor primer
Arteriosklerosis mempengaruhi arteriol otak rapuh: perdarahan otak
2. Diabetes Melitus : memperlambat atherosklerotik dari arteri-arteri besar dan arteri kecil gejala lebih berat, outcome lebih buruk
3. Penyakit Jantung : atrium fibrilasi (yang lebih sering) , mitral stenosis, Coronary artery disease, Hypertensi Heart Disease, LVH, reumatik HD, endokarditis, protese katup jantung
4.4. HiperlipidemiaHiperlipidemia : kolesterol total : kolesterol total , LDL , LDL , HDL , HDL , , trigliserida trigliserida
5.5. ObesitasObesitas : hiperagregabilitas trombosit : hiperagregabilitas trombosit6.6. MerokokMerokok : : konsentrasi fibrinogen, penebalan konsentrasi fibrinogen, penebalan
dinding arteri, viskositas darah dinding arteri, viskositas darah 7.7. Obat anti hamilObat anti hamil dgn kadar estrogen dgn kadar estrogen 8.8. Polisetemia veraPolisetemia vera Hb Hb > 18 > 189.9. HyperhomocysteinemiaHyperhomocysteinemia10.10. Drug abuseDrug abuse11.11. Faktor resiko yang tak dapat dikendalikanFaktor resiko yang tak dapat dikendalikan Umur, Umur,
herediter, gender, raceherediter, gender, race
- Polycythemia rubra vera
- Protein C or S deficiency
- Antiphospholipid/ anticardiolipin antibodies
- Nephrotic syndrome
- Malignancy
- Oral contraceptives
- Dehydration
HEMATOLOGIC OR COAGULATION DISORDERS CAUSING ISCHEMIC STROKE
Persons with the following conditions are at Persons with the following conditions are at the highest risk ischemic stroke :the highest risk ischemic stroke :- Atrial FibrillationAtrial Fibrillation- Asymptomatic stenosis of the carotid Asymptomatic stenosis of the carotid
arteryartery- Amourosis FugaxAmourosis Fugax- TIATIA- Previous ischemic strokePrevious ischemic stroke
PATIENTS AT HIGHEST RISK
Berdasarkan lesi pada otak, stroke dibagi 2 :Berdasarkan lesi pada otak, stroke dibagi 2 :
1. Infark (non hemoragik1. Infark (non hemoragik stroke stroke))
- TIA / RIND- TIA / RIND
- Trombosis serebri- Trombosis serebri
- Emboli serebri- Emboli serebri
2. 2. Perdarahan otak (hemoragikPerdarahan otak (hemoragik stroke stroke))
- Perdarahan intraserebral- Perdarahan intraserebral/serebeller/serebeller
- Perdarahan subarachnoid- Perdarahan subarachnoid
PEMBAGIAN STROKE
Non Hemorhagik :Non Hemorhagik :
TIA (Transient Ischemic Attack)TIA (Transient Ischemic Attack) DefinisiDefinisiGangguan peredaran darah otak sepintas, yang Gangguan peredaran darah otak sepintas, yang menimbulkan ggn fungsi otak sebentar, membaik menimbulkan ggn fungsi otak sebentar, membaik sblm 24 jamsblm 24 jamPatogenese : lihat buku ajar neurologiPatogenese : lihat buku ajar neurologiEtio :Etio :- Spasme pembuluh darah yg sdh aterosklerotik- Spasme pembuluh darah yg sdh aterosklerotik- Mikroemboli dari jantung- Mikroemboli dari jantung- Polisitemia- Polisitemia- Kelainan paru - Kelainan paru - Steal sindrom (dari a. karotis ke subklavia )- Steal sindrom (dari a. karotis ke subklavia )
1.1. Sistem Carotis :Sistem Carotis : Amaorosis fugax, disartri, Amaorosis fugax, disartri, hemiparesis, reflek patologik+, hemihipestesia, afasia hemiparesis, reflek patologik+, hemihipestesia, afasia (hem dominan)(hem dominan)
2.2. Sistem VertebrobasilerSistem VertebrobasilerDrop attack (khas), parese sekitar mulut, buta Drop attack (khas), parese sekitar mulut, buta sepintas, diplopia, disfagia, disfungsi serebelum (dgn sepintas, diplopia, disfagia, disfungsi serebelum (dgn gejala spt ataksia , disartri, nistagmus, hipotoni, reflek gejala spt ataksia , disartri, nistagmus, hipotoni, reflek menurun, vertigo dlmenurun, vertigo dlll))
TerapiTerapi : :1.1. Anti platelet agregasi: Aspirin, dipiridamol, Anti platelet agregasi: Aspirin, dipiridamol,
pentoksifilin, indobufen, tiklopidin, cilostazol, pentoksifilin, indobufen, tiklopidin, cilostazol, clopidogrelclopidogrel
2.2. Obati faktor rObati faktor riisikosiko3.3. Pemberian obat jangka panjang (bisa bertahun-tahun)Pemberian obat jangka panjang (bisa bertahun-tahun)
Gejala Klinis : tergantung lokasi
Gejala klinik :Gejala klinik :• Defisit neurologik akut/sub akut/progresif, kesadaran Defisit neurologik akut/sub akut/progresif, kesadaran
biasa baikbiasa baik• Hemiparese/hemihipestesi/disartri/babinskiHemiparese/hemihipestesi/disartri/babinski ++• Neurogenic bladder (jenis un inhibited bladder)Neurogenic bladder (jenis un inhibited bladder)• Serangan waktu istirahat, sering usia tua >50 thSerangan waktu istirahat, sering usia tua >50 th• Bila infark luas Bila infark luas edema edema TIK TIK bisa herniasi bisa herniasi
tentorial dalam 72 jam atau lebih tentorial dalam 72 jam atau lebih kematian kematian• Nn kranial VII, XII terkena (dipersarafi oleh satu Nn kranial VII, XII terkena (dipersarafi oleh satu
hemisfer) nn kranialhemisfer) nn kranial lain tak kena (dipersarafi dua lain tak kena (dipersarafi dua hemisfer)hemisfer)
Diagnosis :Diagnosis :Cepat, tepat, bedakan dgn perdarahan periksa lab Cepat, tepat, bedakan dgn perdarahan periksa lab terkait , CTterkait , CT Scan kepala ( tampak bayangan Scan kepala ( tampak bayangan hipodens ), MRI, TC doppler, kalau perlu LPhipodens ), MRI, TC doppler, kalau perlu LP
TROMBOSIS SEREBRI
TERAPITERAPIUmumUmum : : sesuai dengan penanganan pada stroke akut ; sesuai dengan penanganan pada stroke akut ;
jalan nafas, oksigenasi, atur intake cairan, jalan nafas, oksigenasi, atur intake cairan, sesuaikan sesuaikan kalori, elektrolit , atasi demam makanan kalori, elektrolit , atasi demam makanan tergantung tergantung kondisi umpama RG, diet rendah lemak dllkondisi umpama RG, diet rendah lemak dll
Khusus :Khusus :1.1. Antiedema : gliserol, manitol, kortikosteroidAntiedema : gliserol, manitol, kortikosteroid2.2. Obat sitoprotektif : utk melindungi jaringan penumbra Obat sitoprotektif : utk melindungi jaringan penumbra
gol Ca antagonis gol Ca antagonis3.3. Antiplatelet agregasiAntiplatelet agregasi4.4. Anti koagulan (trombolitik), Recombinant Tissue Anti koagulan (trombolitik), Recombinant Tissue
Plasminogen Activator (rTPA)Plasminogen Activator (rTPA)5.5. Metabolik aktivatorMetabolik aktivator6.6. Obati faktor resiko / peny penyertaObati faktor resiko / peny penyerta
- - Bila hipertensi : 3-5 hari pertama tak diturunkan Bila hipertensi : 3-5 hari pertama tak diturunkan kecuali hipertensi emergensi ( diast > 120 atau kecuali hipertensi emergensi ( diast > 120 atau MABP > 140 mmHg)MABP > 140 mmHg)
- Rehabilitasi, fisioterapi pasif/aktif - Rehabilitasi, fisioterapi pasif/aktif - ResosialisasiResosialisasi- Bila mengenai kedua hemisfere ( yg kiri disusul yg - Bila mengenai kedua hemisfere ( yg kiri disusul yg
kanan) kanan) hemiparese duplek hemiparese duplekLesi tract pyr ki Lesi tract pyr ki hemip ka Hemip hemip ka HemipLesi tract pyr ka Lesi tract pyr ka hemip ki duplex hemip ki duplexNn kranialis ki-ka ( VII,IX,X,XI,XII) ikut lesi Nn kranialis ki-ka ( VII,IX,X,XI,XII) ikut lesi gangguan menelan, bicara, mimik,gangguan menelan, bicara, mimik, afasia afasia muka muka topeng (pseudobulbertopeng (pseudobulber paralise)paralise) ………….. tipe UMN ………….. tipe UMNBedakan dengan bulber paralise Bedakan dengan bulber paralise !! ……………tipe ……………tipe UMNUMN
EMBOLI SEREBRIEMBOLI SEREBRI- > 90 % dari - > 90 % dari kelainan kelainan jantung jantung
-- Partikel/plaq trombus yg nempel di katup jantung lepas Partikel/plaq trombus yg nempel di katup jantung lepas
ke otak ke otak oklusi arteri otak oklusi arteri otak
Gejala klinisGejala klinis : : Gejala motorik / sensorik sesuai lesi dll Gejala motorik / sensorik sesuai lesi dll seperti pada trombosis serebri. Bila embolus besar seperti pada trombosis serebri. Bila embolus besar bisa delirium, pingsan, gelisah , kesadaran menurun, bisa delirium, pingsan, gelisah , kesadaran menurun, kejangkejang
Diagnosa Diagnosa - Ada sumber emboli Ada sumber emboli dari dari ( kelainan jantung )( kelainan jantung )- Gej waktu serangan sudah maksimalGej waktu serangan sudah maksimal;; ggambaran klinis ambaran klinis
spt trombosisspt trombosis- Tanda Tanda klinis klinis emboli pada organ lainemboli pada organ lain- CT Scan : infark multipel, sekitar infark tampak petechieCT Scan : infark multipel, sekitar infark tampak petechie- Mudah meluas menjadi infark hemoragik ( dgn gejala-Mudah meluas menjadi infark hemoragik ( dgn gejala-
gejala seperti perdarahan otak )gejala seperti perdarahan otak )
TTERAPIERAPI
Khusus : anti edema, antikoagulan (trombolitik), low Khusus : anti edema, antikoagulan (trombolitik), low moleculer weight heparin (nadroparin, enoxaperin), moleculer weight heparin (nadroparin, enoxaperin), streptokinase , rTPA, cegah emboli ulang, streptokinase , rTPA, cegah emboli ulang, obati obati penyakit jantung penyakit jantung lainlainnnya spt tromb serebriya spt tromb serebri
LESI BATANG OTAKLESI BATANG OTAK
- - Mesensefalon Mesensefalon Sindroma Weber : hemiplegi spast Sindroma Weber : hemiplegi spast kontralateral, parese N III ipsilateral kontralateral, parese N III ipsilateral ((tipetipe infrainfra nuklear)nuklear)
-- Pons Pons Sindroma Foville : hemiparese Sindroma Foville : hemiparese kontralateral, konjugasi kesisi lesi.kontralateral, konjugasi kesisi lesi.
Sindroma Millard Goebler : deviasi konjugae kesisi Sindroma Millard Goebler : deviasi konjugae kesisi lesi, Parese VII ipsilateral tipe lesi, Parese VII ipsilateral tipe infra nuklearinfra nuklear
- Medula Oblongata Medula Oblongata Sindroma Wallenberg Sindroma Wallenberg (tromb a. vertebral) atau a.serebelli post. (tromb a. vertebral) atau a.serebelli post. inferiorinferior
- vertigo, muntah, cekukan, disfagivertigo, muntah, cekukan, disfagi- Analgesi, termo anastesi wajah homo lateralAnalgesi, termo anastesi wajah homo lateral- Hemiparese kontralateralHemiparese kontralateral- Sindroma horner ( miosis, ptosis,enoptalmus)Sindroma horner ( miosis, ptosis,enoptalmus)- Gejala serebelum : ataxia, hipotoni, nistagmus, Gejala serebelum : ataxia, hipotoni, nistagmus,
vertigovertigo
Hemorhagik StrokeHemorhagik Stroke
1. 1. Perdarahan Intra SerebralPerdarahan Intra Serebral- Hemisfer (kortek atau subkortex 80%) Serebelum: Hemisfer (kortek atau subkortex 80%) Serebelum:
20%20%- Bila perdarahan kecil: bisa gejalanya spt tromb Bila perdarahan kecil: bisa gejalanya spt tromb
CT Scan baru ketahuan (tampak bayangan hiperdens)CT Scan baru ketahuan (tampak bayangan hiperdens)
Gejala KlinisGejala Klinis- Kesadaran menurun : 65% langsung koma, 23 % ½ - Kesadaran menurun : 65% langsung koma, 23 % ½ -
2 jam kemudian, 12% 2 jam – bbrp hari2 jam kemudian, 12% 2 jam – bbrp hari- Mual, muntah, nafas ngorok, kejangMual, muntah, nafas ngorok, kejang- Hemiparese/hemi hipestesi kontra lateralHemiparese/hemi hipestesi kontra lateral- Parese nn kranialis (sesuai topik lesi)Parese nn kranialis (sesuai topik lesi)
2. Perdarahan Intra Serebeller 2. Perdarahan Intra Serebeller - Darah mendesak di fossa posteriorDarah mendesak di fossa posterior- Peningkatan TIK, pusing, muntah, singultus, Peningkatan TIK, pusing, muntah, singultus,
ggn okulomotoriusggn okulomotorius- Gejala lesi serebeler : ataxi, nistagmus, Gejala lesi serebeler : ataxi, nistagmus,
reflek fisiologis reflek fisiologis menurun dll, hemiparese (-)menurun dll, hemiparese (-)- Penekanan pada pons: rigiditas, dekortikasi, Penekanan pada pons: rigiditas, dekortikasi,
pupil pin pointpupil pin point- Penekanan pada medula oblongata gejala Penekanan pada medula oblongata gejala
lebih berat lebih berat mengenai inti-inti nervi kranialis mengenai inti-inti nervi kranialis vital, rigiditas deserebrasi vital, rigiditas deserebrasi kematian kematian
Klinis, CT Scan, MRI, LP bila perluKlinis, CT Scan, MRI, LP bila perluleukosit meningkat 15-20000, hiperglikemik reactionleukosit meningkat 15-20000, hiperglikemik reaction
Terapi Terapi -- Pencegahan TIK meningkat Pencegahan TIK meningkat herniasi (beri anti edema) herniasi (beri anti edema)- Anti konvulsi, bila TD meningkat Anti konvulsi, bila TD meningkat edema meningkat edema meningkat
TIK meningkat, hati-hati menurunkan TDTIK meningkat, hati-hati menurunkan TD- bila TD menurun bila TD menurun iskemik meningkat iskemik meningkat segera atasi segera atasi
menjaga kerusakan neuron menjaga kerusakan neuronObat hemostasis : tranexamic acid 6 gr/hr IV 3 mg/anti Obat hemostasis : tranexamic acid 6 gr/hr IV 3 mg/anti fibrinolitik, cegah perdarahan ulangfibrinolitik, cegah perdarahan ulang
-- Prognosis : 10 % meninggal sblm pengobatanPrognosis : 10 % meninggal sblm pengobatan 40 % meninggal tanpa perbaikan40 % meninggal tanpa perbaikan
- Mortalitas Mortalitas ++ 60 % penyebab terbanyak : perdarahan 60 % penyebab terbanyak : perdarahan ulangulang
Diagnosa
3. Perdarahan Subarahnoid3. Perdarahan Subarahnoid
EtioEtio :: - Aneurisma intrakranial yg pecah - Aneurisma intrakranial yg pecah - AV malformasi pecah- AV malformasi pecah- Sekunder terhadap PIS- Sekunder terhadap PIS
Gejala klinis Gejala klinis -- Aneurisma pesah Aneurisma pesah s.kep hebat, mual, muntah s.kep hebat, mual, muntah- Rgs meningen Rgs meningen kaku kuduk, brudzinski, kernig kaku kuduk, brudzinski, kernig- Funduskopi: perdarahan subhialoid (+), edema papil Funduskopi: perdarahan subhialoid (+), edema papil
10% 10% - Gejala motorik/sensorik sesuai lesiGejala motorik/sensorik sesuai lesi- Ggn kesadaran: variasi ringan-komaGgn kesadaran: variasi ringan-koma- Otonom: keringat meningkat, takikardiOtonom: keringat meningkat, takikardi- Stres ulcer Stres ulcer hematemesis hematemesis- Sekitar perdarahan Sekitar perdarahan vasospasme vasospasme iskemik iskemik infark infark
TerapiTerapi• Antispasme disekitar perdarahan, dpt diberikan Ca Antispasme disekitar perdarahan, dpt diberikan Ca
antagonisantagonis
• Cegah perdarahan ulang: (hemost agent/sbg Cegah perdarahan ulang: (hemost agent/sbg antifibrinolitik, anti konvulsan, atasi kegelisahan)antifibrinolitik, anti konvulsan, atasi kegelisahan)
• AntiedemaAntiedema
• AntikonvulsiAntikonvulsi
• Nyeri kepala + cemas : analg sedatifNyeri kepala + cemas : analg sedatif
• LaxansiaLaxansia
• Anti hipertensiAnti hipertensi
DiagnosisDiagnosis - KlinisKlinis- CT Scan kepala, bila perlu CT Scan kepala, bila perlu
LPLP
Information to be Taught to the Public :Information to be Taught to the Public :- Sudden onset of the symptomsSudden onset of the symptoms- Weakness, clumsiness, heaviness, or numbness one Weakness, clumsiness, heaviness, or numbness one
side of the body hand or faceside of the body hand or face- Drooping of one side of the faceDrooping of one side of the face- Slurred speech of difficulty understanding languageSlurred speech of difficulty understanding language- Loss of or blurred vision in one or both eyesLoss of or blurred vision in one or both eyes- Dizziness or in balanceDizziness or in balance- Unusually severe headacheUnusually severe headache
Public must learn the correct response to a stroke Public must learn the correct response to a stroke
to seek medical attention immediatelyto seek medical attention immediately
““BRAIN ATTACK” COMMON SYMPTOMS OF STROKEBRAIN ATTACK” COMMON SYMPTOMS OF STROKE
- Time of onset of neurologic symptomsTime of onset of neurologic symptoms- Determine nature of neurologic symptoms :Determine nature of neurologic symptoms :
Weakness of arm or faceWeakness of arm or face
Slurring of speech or abnormal languageSlurring of speech or abnormal language- Rate GCS score :Rate GCS score :
LanguageLanguage
Eye movementEye movement
Motor responseMotor response- History of recent illness, surgery, or traumaHistory of recent illness, surgery, or trauma- Recent use of medicationsRecent use of medications
INFORMATION TO BE OBTAINED IN THE FIELD BY EMERGENCY MEDICAL SERVICES
LEVEL OF EVIDENCE USED AS GUIDELINES FOR TREATMENT OF LEVEL OF EVIDENCE USED AS GUIDELINES FOR TREATMENT OF CEREBROVASCULAR DISEASECEREBROVASCULAR DISEASE
Level ILevel I
Data collected from large, randomized, controlled clinical trials which provide Data collected from large, randomized, controlled clinical trials which provide clear evidence of treatment effect. Data from meta-analyses can be used as clear evidence of treatment effect. Data from meta-analyses can be used as supporting information. This level of evidence can be used as the basis for the supporting information. This level of evidence can be used as the basis for the strongest recommendations (grade A) strongest recommendations (grade A)
Level IILevel II
Data collected from randomized, controlled clinical trials which provide Data collected from randomized, controlled clinical trials which provide evidence of treatment effect. Data from meta-analyses can be used as evidence of treatment effect. Data from meta-analyses can be used as supporting information. This level of evidence can be used as the basis supporting information. This level of evidence can be used as the basis recommendations of intermediate strength (grade B) recommendations of intermediate strength (grade B)
Level IIILevel III
Data collected from nonrandomized studies that compare result of treatment Data collected from nonrandomized studies that compare result of treatment with concurrent patients who do not receive the treatment.with concurrent patients who do not receive the treatment.
Level IVLevel IV
Data collected from nonrandomized studies that compare result of treatment Data collected from nonrandomized studies that compare result of treatment with concurrent patients who did not receive the treatment in the past with concurrent patients who did not receive the treatment in the past (historical controls)(historical controls)
Level VLevel V
Data collected from case series or reports. The weakest recommendations Data collected from case series or reports. The weakest recommendations ( Grade C) are based on levels III-V evidence( Grade C) are based on levels III-V evidence
LiteraturLiteratur- Adams RD. Principles of neurology 6Adams RD. Principles of neurology 6thth ed Mc Graw Hill 1997 ed Mc Graw Hill 1997
- Caplan LR. Stroke. A Clinical Approach 2Caplan LR. Stroke. A Clinical Approach 2ndnd ed Butterworth ed Butterworth Heinemann 1993Heinemann 1993
- Guidelines Stroke 2004 (PERDOSSI)Guidelines Stroke 2004 (PERDOSSI)
- Harsono, Buku Ajar Neurologi, Bab IIHarsono, Buku Ajar Neurologi, Bab II
- Harsono, Kapita selekta neurologi, Bab IIHarsono, Kapita selekta neurologi, Bab II
- Simon RP, Aminof MJ, Clinical Neurologi Simon RP, Aminof MJ, Clinical Neurologi
- Adams HP. Jr et al. Management of Stroke 2 nd ed. Adams HP. Jr et al. Management of Stroke 2 nd ed. ProfessionalProfessional Communications. IncCommunications. Inc 2002 2002