Dr. Takdir Setiawan MSc, Sp.S

Bagian SarafRSUD AmbarawaKab. Semarang

Definisi StrokeStroke adalah gangguan fungsional otak fokal maupun global yang terjadi secara akut, berasal dari gangguan aliran darah otak. Termasuk di sini perdarahan subarachnoid, perdarahan intraserebral dan iskemik atau infark serebri. Tidak termasuk disini gangguan peredaran darah otak sepintas, tumor otak, infeksi atau stroke sekunder karena trauma (WHO, 1986)

Risk Factors for StrokeNon-Modifiable Risk Factors for StrokeAge Sex Race/ethnicity Family history

Modifiable Risk Factors for Stroke6HypertensionDiabetesSmokingHyperlipidemiaCarotid stenosisAtrial fibrillation

Perbedaan klinisAnamnesis

GejalaPerdarahanInfark Onset Saat onset Warning Nyeri Kepala Kejang Muntah Kesadaran Mendadak Sedang aktif - - + + + + + + + + Mendadak Istirahat + + (TIA) +/- - - +/-

Perbedaan klinisTanda-tanda

Tanda-tandaPerdarahanInfark Bradikardi Udem papil Kaku kuduk Tanda Kernig Brudzinski ++(dari permulaan) sering + + +++ +++ +/- - - - -

SCORE SIRIRAJS= kesadaran0=CM1= somnolen2= sopor/komaM= Muntah0=tidak ada1= adaN= nyeri kepala0= tidak ada1= adaD= DiastolikA=Ateroma0= tidak ada1=salahsatu atau lebih: DM, angina, penyakit pembuluh darah

Score SSS >1: perdarahan supratentorialScore SSS< -1: Infark serebriScore SSS -1 s/d 1: meragukan(2,5xS)+ (2xM)+ (2xN)+ (0,1D)- (3xA)- 12

PERBEDAAN STROKE HEMORAGIK DAN ISKEMIK

VARIABELPISPSATROMBOSISEMBOLIUsia40-60Tidak tentu40-70Semua umurOnsetAkut (dtk/mnt)Akut (mnt/jam)BertahapAkutSaatAktiitasAktivitasBangun tidurTidak tentuSakit kepala++++++--Muntah++++++--Prodromal--TIA+++-Kesadaran/Herniasi OtakCepat komaVariasi dapat koma/normalNormal/ ringan hari ke 3-5Normal/sedang hari 3-5Kaku Kuduk++ jarang++++ selalu--KelumpuhanCepat hemiplegi (mnt/jam)VariasiBertahapMendadak beratAfasia/Tanda Kortikal--SeringSeringArterial Sindrom-KadangSelaluSelaluKejang/RigiditasSering+++Kadang++JarangKadang

PERBEDAAN STROKE HEMORAGIK DAN ISKEMIKVARIABELPISPSATROMBOSISEMBOLIReflek PatologisSegeraVariasiLambatLambatHipertensiSelalu +VariasiKadang N/HipotensiJarangJantungHipertrofi LVVariasiNAritmia, AF,Infark miokard, asma kardial, angina pektorisRiwayatHipertensi-Hipotensi/ Diabetes/ DehidrasiLP/LCSN/darah++Darah++++JernihJernihBruit Arteri---SeringX FotoShift pineal++-Calcifikasi-CT scanHiperdernsHiperdernsHipodernsHipodensOptalmoskopRetinopati HTSub hyaloidSilver wireNArteriografiShiftAneurisma, AVMOklusi/stenosisOklusi/ stenosisDopplerNNAliran lambatAliran lambatHematologyNNHematokrit/ Diabetes/ hiperlipidemiaN

Multiple faktor risiko Aterotrombosis

Pembentukan Plak Aterosklerotik

Akumulasi lipoprotein pd tunika intimaStres oksidatifAktivasi CitokinePenetrasi MonocyteMigrasi makrofag foam cell Muscle Cell SmoothAkumulasi matriks ekstraselulerKalsifikasi dan fibrosis

Penyebab sumbatanSumbatan aliran darah oleh ateroma, emboli, trombus(Aterosklerosis)

A small clot may break off from a larger thrombus and be carried to other places in the bloodstream. When the embolus reaches an artery too narrow to pass through and becomes lodged, blood flow distal to the fragment ceases, resulting in infarction of distal brain tissue due to lack of nutrients and oxygen.As a cause of stroke, embolism accounts for approximately 32% of cases.Cerebral Embolism Formation

HCT Scan Stroke Infark

Cerebral Infarct - 1 Week

Cerebral Infarct - 2 Weeks

Brain: Haemorrhagic infarct.

Oleh karena ruptur aneurisma, angioma, lesi aterosklerotik

Definition (ICH) :Intracerebral hemorrhage (ICH) results from the rupture of an intracerebral vessel leading to the development of a hematoma in the substance of the brain.

HYPERTENSION OTHERAV-MALFORMATIONANEURYSMOther causes: bleeding into tumor, hypocoagulable state,hemorrhagic infarction, iatrogenic, and traumaINTRACEREBRAL HEMORRHAGENON TRAUMATIC

Primary and SecondaryCauses of Intracerebral Hemorrhage

Primary SecondaryHypertensionAmyloid angiopathy AneurysmsArteriovenous malformations Neoplasms Trauma Anticoagulation Use of thrombolytics Hemorrhagic conversion of ischemic stroke

Penyebab tersering ketiga perdarahan intraserebral setelah hipertensi arterial dan aneurisma adalah angiopati amiloid, yaitu sekitar 10% dari seluruh perdarahan intraserebral spontan. Kelainan angiopati amiloid ini khas yaitu terbentuknya deposit fibril amiloid pada tunika media dan tunika intima pada arteria kecil dan sedang. Perdarahan terjadi akibat robeknya dinding pembuluh yang lemah atau mikroaneurisma (Kazui et al., 1997; Qureshi et al., 2001). Angiopati Amiloid Serebral

Klasifikasi Perdarahan SubarakhnoidPerdarahan IntraserebralPerdarahan intrakranial non spesifik dan yang lain misalnya perdarahan ekstradural atau epidural non traumatik; perdarahan atau hematoma subdural non traumatik dan perdarahan intrakranial nonspesifikWHO ICD-NA, 1987

INTRACEREBRAL HEMORRHAGE

Intraventricular Hemorrhage:

HCTS 10/ 9/07

Gejala KlinisOnset sewaktu aktivitasPenurunan kesadaran, 2/3 komaNyeri kepala dan muntah sebagai tanda peningkatan TIKKejang jarang

AnamnesisHistoryOnset: usually during daytime activity, with progressive (ie, minute to hours) development:Alteration in level of consciousness (appr 50%)Nausea and vomiting (appr 40-50%)Headache (appr 40%Seizure (appr 6-7%)Focal neurological deficit

Px FisikPhysical: Clinical manifestations of ICH are determined by the size and location of hemorrhage, but may include the following:Hypertension, fever, or cardiac arrhythmiaNuchal rigiditySubhyaloid retinal hemorrhagesAltered level of consciousnessAnisocoriaFocal neurological deficits

Imaging studiesCT scanHyperdense signal intensityHematoma volume (cc)Perihematomal edema and displacement of tissue with herniationMRIVessel imagingCT angiography: AVMs, vasculitis, and other arteriopathiesMR angiography

S A H

Subarachnoid Hemorrhage:

Tanda & gejala SAHNyeri kepala berat, acutPenurunan kesadaran sementara/lamaKejangNausea & vomitusDefisit neurologic focal (hemiparese,disfasia)Funduscopi : papiledema/vitreous haemorrhageReactive hypertensionPyrexiaMeningismus(Lindsay,1997)

Penggolongan SAHDerajat I : asimtomatik/sakit kepala minimal/kaku kudukDerajat II :hanya sakit kepala lebih hebat dan kaku kudukDerajat III :Mengantuk/bingung, mungkin dengan hemiparesis ringanDerajat IV :Stupor dalam, mungkin disertai hemiparesis sedang-berat, Reaksi awal deserebrasiDerajat V :Koma DalamHunt dan HessGreenberg,2001

SAH The case you could miss(Sokransky 2001)Well-appearing patient with previous headaches Presents with a sudden headache that is now better

Cerebral vasospasm

HaemorrhageIncreaseIntracranial pressInfluks Ca+NecrosisNeuronGlobal ischemicReleaseVasoconstrictor agenEffects of bloodtoxicInfluks Ca+VasospasmeFocal IschemicSerotonin, Prostaglandin,

Vasospasme Process on Haemorrhage

Classically described based on the angiographic appearance of narrowed arteries in one of several settings:Subarachnoid hemorrhage (usually, but not always, aneurysmal SAH)SAH from other causes seems less likely to be associated with arterial narrowingRuptured AVM causing SAHPerimesencephalic SAHTraumatic SAHWhat is cerebral vasospasm?

Insuffisiensi brain function which suplaied by vasospasm artery Local vasospasm around hematome at intact arteri (unrupture)Probable local vasospasm around central of haemorrhage change into diffuse vasospasm

Effects of Vasospasme

Regional cerebral blood flow in health people :50-70 mL/min per 100 mgSymptoms of cerebral ischemia: < 20 mL/min per 100 mgStructure damage and neuronal death: flow < 15mL/min per 100 mg

Cerebral Blood Flow

NEUROPROTEKTAN

Citicholine Mechanism (neuronal)Increase choline formation and alter degradation phosphatydilcholineIncrease glucose uptake, asetilkholine, prevention lipid radicalIncrease glutationDecrease lipid peroxidaNa/K ATPase modulationMechanism (vascular)Increase CBFIncrease O2 consumtionDecrease vasculer resistance

(Perdossi, 2004)

Piracetam Mechanism (neuronal)Repair cell membran fluidityRepair neurotransmissionStimulation adenylate kinaseMechanism (vascular)Increase eritrocyte deformabilityDecrease platelet hyperagregationRepair microcirculation

(Perdossi, 2004)

Piracetam mengurangi alir masuk Kalsium yang tidak normal ke dalam neuron & sel otot polos pembuluh darah. Oleh karena itu, Piracetam mempengaruhi sistem saraf dan sistem serebrovaskuler, dimana Piracetam memiliki efek sitoprotektif dan fungsional Mekanisme Kerja Ganda PiracetamMelindungi SelMemperbaiki FungsiJaringan NeuronPiracetamJaringan SerebrovaskulerMeningkatkan Aliran Darah OtakEfek Sitoprotektif Dalam Pembuluh Darah Otak

HIPERTENSI

HipertensiHipertensiAkutKronisPemb.drh kecilSpasmeEnsefalopatihipertensifPemb drh kecilPemb drh sedangLipohialinosisMikroaneurismaTrombosisPISInfarklakunarAterosklerosisTIA,trombosis,Emboli serebriFaktor resiko lainDM,hiperlipidemipecah

MANAJEMEN

ManagementMedical ManagementSurgical Management

Pencegahan & penanganan tekanan intrakranial yg meningkat :- mengatur posisi kepala penderita- osmoterapi- hiperventilasi yang dpt dilaksanakan sesuai fasilitas & kondisi penderita2. Mengontrol peningkatan tekanan darah3. Mencari dan mengobati penyebab4. Pemberian neuroprotektan5. Tindakan pembedahan6. Pencegahan dan penanganan komplikasi sistemikTatalaksana Perdarahan Intraserebral

*ManagementIn emergency RoomABC rulesBP continuous monitoringContinuous ECG monitoringO2 pulse oxymetry2 IV lines (norma saline only)Blood (CBC, SMAC, RBS, PTT, INR)Save 6 ml of bloodFacilitate transfer to the operating room or ICU

*Hasil optimal terapi Stroke perdarahan sampai 96 jam setelah onsetPuncak vasospasme antara hari ke 5-10)

*Acute stroke care-General management (Ischemic Stroke)The mainstay of acute treatment (A,B,C)Treatment and stabilisation of general conditionSpecific therapyRecanalisation of a vessel occlusionPreventive of mecanism leading to neuronal death in the ischhemic brainEarly secondary preventionEarly rehabilitationProphylaxis and treatment of complications

(Lamsudin, 2004)

*Blood pressureThere are adequately sized randomized , controlled study guiding BP mangementElevated BP (sistolic>200mmHg or diastolic >110mmHg0 may tolerated in the acute phaseAvoid and treat hypotension or drastic reduction BPBP may be lowered if cardiac condition require itAcute stroke care-General management(Lamsudin, 2004)

*Blood pressure (BP)Indications for immediate AH therapy in acute strokeIntracerebral haemorrhageCardic failureAcute coronary syndromeAortic dissectionHypertensive enchephalophaty

Acute stroke care-General management(Lamsudin, 2004)

MEDICAL MANAGEMENT OF ICH (Pouratian 2003) Cardiopulmonary optimization ( Airway, Breathing, Circulation,skin, seizures) Reversing coagulation defects (coagulopathies and platelet disorders) Blood pressure control (Labetolol & nicardipine IV, nitroprusside not often used brain edema). ICP reduction: - Ventriculostomy as therapeutic means of reducing ICP - Head-of-bed elevated at 300, patients neck in neutral position maximize venous outflow. - Minimize agitation: sedatives - Hyperosmolar fluids (mannitol, hypertonic saline) - Hyperventilation used only as temporary measures - Barbiturate-induced coma : rarely - Vasogenic edema with mass effect: corticosteroids (controversial) Ultra-early hemostatic therapy: - Antifibrinolytic tranexamic acid, aprotinin, activated recombinant factor VII (rFVIIa)

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 ELEVATED 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.

Pemilihan cairan sebaiknya berdasarkan atas status hidrasi pasien, konsentrasi elektrolit,dan kelainan metabolik yang ada The American Heart Association sudah menganjurkan normal saline 50 ml/jam selama jam-jam pertama dari stroke iskemik akut. Metabolisme anaerobik yang dipicu oleh iskemia mengakibatkan asidosis laktat dan meninggikan PCO2 jaringan(tidak harus asidosis laktat sistemik),hal inilah yang menyebabkan banyak dokter enggan memakai RL selama fase akut stroke, kedua osmolaritas RL 273 dianggap hipotonik bila dibanding plasma (normal 285 + 5 mOsm/L) Pemilihan terapi untuk StrokeIyan Darmawan,md 2008

Ringer asetat (acetad ringer)Merupakan alternative yang lebih baik dari pada ringer laktat dan normal saline .RL dan AR berbeda pada sumber bikarbonat LR mengandung 28 mmol laktat per liter sedangkan AR 28 mmol asetat. Berbeda dengan laktat, yang metabolismenya terjadi terutama di dalam hati, asetat dimetabolisme terbanyak dalam otot dan sebagian kecil dalam ginjal dan jantung.

Pemilhan terapi cairan untuk stroke

ANTI HT

Blood Pressure (BP) Management Protocol in Acute StrokeAntihypertensive treatment should await the spontaneous decline in BP (within 1st to 10th days). If increased BP persist after 7-10 days, start treatment.Patients already on antihypertensive medication prior to stroke, drugs should be held or reduced for 7-10 days (except B-blockers, should be gradually over 5-6 days)

Treat If:BP is > 220/140 or MAP >130 mmHgMalignant or hypertensive encephalopathyAcute MIAortic dissection is suspectedBP is >180/100 and patient is for thrombolytic therapy24 hours following thrombolytic therapy (>185/110)Blood Pressure (BP) Management Protocol in Acute Stroke

The Following medications can be used, if needed:Esmolol bolus (500 ug/kg IV)Esmolol infusion (50-150 ug/kg/min) IV, (Body weight x 60 mg of esmolol diluted in 100 ml of saline, in a rate of 5-15 ml/hour)Labetalol infusion (15-35 ug/kg/ml) IV, (Body weight x 6 mg of labetalol diluted in 100 ml of saline, in a rate of 15-35 ml/hour)Labetalol 100-200 mg bid-tid. POAnalaprilat 1,25-5 mg IV, 6 hourlyLasix 20-40 mg iv tid-qidNicardipin 5 mg/hour IVClonidine 150-300 mg iv bolus (maximum of 750 mg per day)Sodium nitroprusside 0,25-0,5 mg/kg/minAvoid the use of calcium channel blockers and sodium nitropusside as possibleBlood Pressure (BP) Management Protocol in Acute Stroke

If SBP is > 200mmHg or MAP >150mmHg, then consider aggressive reduction of blood pressure with intravenous infusion, with frequent blood presure monitoring every 5 minutes. If SBP is > 180mmHg or MAP > 130mmHg and there is evidence of or suspicion of elevated ICP, then consider monitoring ICP and reducing blood pressure using intermittent or continuous intravenous medications to keep cerebral blood flow >60 to 80 mmHg

Guidelines for treating elevating Blood Pressure in ICH (1)

3. If SBP is > 180 mmHg or MAP > 130mmHg and there is no evidence of or suspicion of elevated ICP, then consider a modest reduction of blood pressure (eg, MAP of 110 mmHg or target blood pressure of 160/90mmHg) using intrmittent or continuous intravenous medications to control blood pressure, and clinically reexamine the patient every 15 minutes. Guidelines for treating elevating Blood Pressure in ICH (2)

Pembedahan Bukan tindakan rutinGCS 7-10Pemulihan fungsional tetap jelekDilakukan bila gagal mengendalikan peningkatan TIKPerdarahan serebeler sering dilakukan pembedahan

Kandidat yang tidak dioperasi1. Perdarahan dengan volume

Atherosclerosis is a disease that develops over several decades. Risk factors such as smoking or hypertension, hyperlipidemia, and hyperglycemia, with or without obesity, can promote its development.1Risk factors such as age, sex, race or ethnicity, and heredity are not modifiable. Yet, they are important risk factors.2Stroke incidence doubles each decade after age 55 years, and age is the single most important risk factor for stroke.2Sex and race, ethnicity, or both are also important risk factors, with the incidence of stroke greater in men and some Hispanic and African American groups being at a greater risk for stroke compared with whites.2Relative risk is greater if a parent has a history of stroke or a transient ischemic attack, and paternal history carries a greater risk than maternal history.2Local factors in arterial territoriesincluding blood flow parameters, vessel diameter, and arterial wall structureparticipate in atherothrombotic disease manifestation.1-2 Advances in pathophysiological insight into atherosclerosis have provided markers of inflammation that are targets for measurement to assess risk. Potential targets that should be measured to assess risk include C-reactive peptide, interleukin-6, prothrombic factors, and fibrinogen.1-2The presentation of the multiple risk factors for atherothrombosis simply highlights the importance of a disease that is the leading cause of death worldwide.

References1Yusuf S, Reddy S, Ounpuu S, et al. Global burden of cardiovascular diseases: part I: general considerations, the epidemiologic transition, risk factors, and impact of urbanization. Circulation. 2001;104:2746-2753.2Drouet L. Atherothrombosis as a systemic disease. Cerebrovasc Dis. 2002;13(suppl 1):1-6.