Penatalaksanaan Syok Dr.tatty

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    PENATALAKSANAAN SYOK PADA ANAK

    TATTY ERMIN SETIATI

    SUB. BAGIAN PEDIATRI GAWAT DARURAT FK. UNDIP/RSUP

    DR. KARIADI SEMARANG

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    PENDAHULUAN

    SINDROM KLINIS

    KEGAGALAN SISTEM SIRKULASI

    KEBUTUHAN OKSIGEN

    NUTRIEN JARINGAN

    DEFISIENSI AKUT

    DITINGKAT SEL

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    SYOK PADA ANAK :

    Keadaan gawat darurat

    morbiditas / mortalitas

    80 hipovolemik

    Syok kompensasisulit di D / o.k manifestasi klinis tak jelas ( refleks

    simpatis

    Redistribusi selektif al. daerah dari organ perifer non-vital ke

    jantung, paru, otak )

    Tujuan Primer Pengelolaan Syok :

    - Preload ( resusitasi volume )

    - Kontraktilitas

    - Resistensi pada sistemik

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    DEFINISI SYOK

    SINDROM KLINIS AKIBAT KEGAGALAN SISTEM SIRKULASI UNTUK

    MENCUKUPI :

    Nutrisi

    Oksigen

    Pasokan

    utilisasi

    Metabolisme

    Jaringan tubuh

    Defisiensi 02 Seluler

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    FUNGSI SISTEM SIRKULASI

    Jantung

    Pembuluh Darah

    Volume Darah

    Curah jantung

    & adekuatAliran darah

    Metabolisme

    jaringan

    Metabolit

    Eliminasi Di Organ

    Pembuangan

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    PENGATURAN CURAH JANTUNG

    DAN TEKANAN DARAH

    PRELOAD CONTRACTILITY AFTERLOAD

    HEART RATE STROKE VOLUME

    CARDIAC OUTPUT SYSTEMIC VASCULAR RESISTANCE

    BLOOD PRESSURE

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    PENGANGKUTAN OKSIGEN

    Cardiac Out Put Blood flow

    Oxygen

    Delivery

    Blood O2Content

    Hb Contentration

    O2Bound to Hb

    O2Dissolved in Plasma

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    KLASIFIKASI SYOK

    MENURUT ETIOLOGI

    SYOK HIPOVOLEMIK

    SYOK DISTRIBUTIF

    SYOK KARDIOGENIK

    SYOK SEPTIK

    SYOK OBSTRUKTIF

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    STADIUM SYOK

    FASE I : KOMPENSASI

    Mekanisme Kompensasi Tubuh refleksi simpatis

    - Resistensi sistemik

    : HR; kulit dingin, pucat, cap.refill terlambat, nadi lemah, tek.nadi

    sempit

    -

    Tekanan darah ( N )

    - Tekanan Diastolik

    - Resistensi pembuluh darah splanknik

    : Ginjal (Diuresis

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    FASE II : DEKOMPENSASI (1)

    -Mekanisme kompensasi gagal

    - Metabolisme anaerobik

    - Asam laktat

    asidosis>>

    terbentuk asam karbonat

    intraseluler

    - Kontraktilitas otot jantung

    - Pompa Na K sel

    Integritas membran sel

    Kerusakan sel

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    FASE II : DEKOMPENSASI (2)

    Aliran darah lambat

    Agregasi Trombosit

    Pembentukan Trombus

    Pendarahan

    Pelepasan Mediator

    Vasodilatasi Arterial

    Kenaikan Permeabilitas Kapiler

    VR

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    Fase dekompensasi

    Perfusi jaringan indekuat disertai hipotensi

    Kesadaran menurun krn perfusi ke otakmenurun

    Hipotensi sebagai tanda terakhir dari syok Untuk anak 1-10th:

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    FASE III : IREVERSIBEL

    Kerusakan / Kematian Sel

    Disfungsi sistem multi organ

    Cadangan fostat E. Tinggi

    ( Hepar, Jantung )

    Tekanan darah tak terukur

    Nadi tak teraba

    Kesadaran

    Anuria

    GMO

    klinis

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    PERJALANAN PATOFISIOLOGI SYOK

    Septic Shock Cardiogenic Shock

    Hypovolemic Shock

    Capillary Leak MediatorsMyocardialDepression

    Preload Vasodilatation Contractility

    Cardiac OutputBlood Pressure

    Sympathetic Discharge

    Vasoconstriction,

    HR Contractility

    Improved Cardiacoutput and bloodpressure

    COMPENSATED

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    DECOMPENSATED

    Myocardial perfusion

    Myocardial O2Consumption

    Cardiac Output

    Mediator Release

    Cell Function

    Cell Death Death of Organism

    Tissue Ischemia

    Loss of Autoregulation of

    Microcirculation

    COMPENSATED

    VasoconstrictionHR Contractility

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    Syok hipovolemik

    Primary Assessment: Finding A

    B Takhipneu tanpa peWOB

    C Takhikardi

    Tek.Drh N/ hipotensi dgn

    tek.nadi sempit

    Nadi lemah,kecil /tak teraba

    Pengisian kapiler lambat

    kulit dingin,pucat

    Kesadaran menurun

    Oliguria

    D Kesadaran menurun

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    Distributive / Septic Shock

    Distributive

    shock

    PRELOAD

    N /

    CONTRACTILITY

    N /

    AFTERLOAD

    Variable

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    SIRS

    Core temp of >38.5C or 2SD above normal for age,

    for chhildren

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    SEPSIS :

    SIRS in the presence of, or as a result of,

    suspected or proven infection

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    Severe sepsis

    Sepsis plus either cardiovascular

    dysfunction or ARDS

    Or

    Sepsis plus 2 or more other organ failures

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    RF as sign of organ dysfunction

    in sepsis PaO2/FiO2 65 mmHg or 20 mmHg abovebaseline

    Proven need FiO2 >50% to maintain SaO2>92%

    Need nonelective MV (invasive ornoninvasive)

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    Septic shock

    Sepsis and

    Cardiovascular dysfunction despite

    administration of isotonic iv boluses > 40

    ml/kg in 1 hour

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    Cardiovascular dysfunction

    Hypotension (SBP

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    Inadequate organ perfusion

    Unexplained metabolic acidosis: base

    deficit < 5meq/l

    Increase arterial lactate > twice the upperlimit of normal

    Oliguria: Urine output0.5 ml/kg/hour

    Prolonged cap refill: > 5 second

    Cor to peripheral temp gap > 3C

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    III. SYOK KARDIOGENIK

    Etiologi :

    Pasca Bedah Penyakit Jantung Bawaan

    Miokarditis

    Infark / Iskemik Jantung

    Kardiomiopati Primer / Sekunder

    Hipoglikemia, Gangguan Metabolik

    Asfiksia, Sepsis

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    CARDIOGENICSHOCK

    PRELOADVARIABLE

    CONTRACTILITY

    DECREASED

    AFTERLOAD

    INCREASED

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    MEKANISME SYOK KARDIOGENIK

    Cardiogenic

    Shock

    Contractility

    CO

    BPMetabolic acidosis, hypoxia,

    Myocardial depressant factor

    Compensatory mech.

    Afterload

    SVR

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    SYOK KARDIOGENIK

    Cardiac Ventricular Performance

    Factor Determinant :

    a. Frekuensi dan Irama Jantung

    b. Preload dan Afterload

    c. Kontraktilitas Miokard

    Kompensasi Tubuh Self Perpetuating Cycle

    Syok Progresif Memburuk

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    Findings of Cardiogenic Shock

    Primary Assessment Finding

    A

    B Tachypnea; WOB

    C Tachycardia; N/low BP with

    a narrow pulse pressure; weak or absent ofperipheral pulse; N and then weak central

    pulses;Delayed cap refill with cool extremities;

    Signs of CHF; cyanosis(CHD/pulm.edema); End-

    organ Function ( Cold, pale skin, oliguria)

    D Changes of mental status

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    Cardiac tamponade

    Muffled or diminished heart sound

    Pulsus paradoxus(decrease in systolic BP by

    more than 10 mmHg during inspiration

    Distended neck vein

    Note: Children following cardiac surgery,

    D/ ndistinguishable from cardiogenic

    shock, Echo: important

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    Tension pneumothorax

    Patients with chest trauma, or any intubated child

    who deteorates suddenly during PPV

    Hyperresonance on the affected side Diminished breath sounds on the affected side

    Distended neck vein

    Tracheal deviation towards contralateral side Rapid deteoration in perfusion and rapi change

    from tachycardia to bradicardia

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    MANIFESTASI KLINIS SYOK SEPTIK

    STADIUM KOMPENSASI

    - Resistensi Vaskuler

    - Curah Jantung

    - Takhikardia

    - Ekstermitas Hangat

    - Divresis Normal

    STADIUM DEKOMPENSASI- Volume Intravaskuler

    - Depresi Miokard

    - Eksternal Dingin

    - Gelisah, Anuria, Distres Respirasi

    - Resistensi Vaskuler

    - Curah Jantung

    STADIUM IREVERSIBEL

    - GMO

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    PENATALAKSANAAN SYOK

    1. 2.

    Oksigenasi

    CaO2

    SaO295100 %

    Sistem K.V

    a. Preload

    ( resusitasi volume )

    b. Atasi Disritmia

    c. Koreksi keseimbanganasam - basa

    Jalan nafas Oksigen Anxietas

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    TERAPI CAIRAN PADA SYOK

    AKSES VENA (90 detik); Tak berhasil IO

    KRISTALOID dan atau KOLOID10 30 ml / kg B.B (6-10 menit)

    diulang 2 3 kali

    SYOK SEPTIK

    60

    100ml / kg B.B(dalam 6 jam pertama) THE 1st CONSENSUS CONFERENCE

    on CCM 1997(SYOK SEPTIK)a. Koloid

    terapi inisial, dilanjutkan koloid/kristaloidb. Dipandu : respons klinis,perfusi, perifes, tvs,

    tekanan sistem,MAP

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    Algoritme Terapi Cairan Pada Syok

    Suspected shock

    Hypovolemia, Hypoperfusion, Tachycardia

    10 30 mL Cryst/Colloid / kg / 6 10 min

    Normotensive

    Hypotensive

    In Sepsis :

    Antibiotics,Imunotheraphy

    In Anaphylaksis :

    Catekolamin,steroid,antihistamin

    Urine > 1 ml/kg/hr

    10-20 mLcrys orcoll/kg/10min

    AnuriaUrine < 1 ml/kg/hr

    Urine output < 1 ml/kg/hr

    Reevaluated 10 mL X.tal/kg 10 mL X.tal/kg 1020 mL X.tal/kg

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    Reevaluated 10 mL X.tal/kg 10 mL X.tal/kg 10-20 mL X.tal/kg

    Improved

    Reevaluated

    Improved

    Reevaluated

    Hypotensive, urine < 1 mL/kg/hr

    CVP < 10 mmHg CVP,Cardiac status,chest X-Ray,Echocardiography

    CVP > 10 mmHg

    Afterload reduction,inotropic support,consider pulmonary

    10-20 mL X.tal/kg

    Reevaluated

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    Early Goal Directed

    Therapy pada Syok Septik Early aggressive fluid therapy (Crystaloid or

    colloid)In EMU, within 6 hours of admission

    Vasopressors & Inotropic drugs when resistance tofluid therapy

    End points: Good peripheral perfusionConciousness, Capillary feeling time < 2, Warmextremities, MAP/Pulse pressure N for age, CVP8-12 mmHg, Diuresis > 2ml/kg SvcO2 > 70%

    Admission to PICU when stabilized

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    Fluid Therapy

    in Sepsis and Septic Shock

    Type of FluidColloid

    Crystalloid

    Volume60 100 ml/kg

    (6 hours)

    CO , Restore BPMOF

    Inotropic

    Vasopressor

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    Efek volume infus 1 L koloid pada kompartemen tubuh (70 kg)

    Larutan Vol. Plasma Vol. Inters I.Intrasel

    Albumin 5% 1000 - -

    Hemacel 700 300 -

    Gelafundin 1000 - -

    Plasmafusin 1000 - -

    Dextran 40 1600 (-260) (-340)

    Dextran 70 1300 (-130) (-170)

    Expafusin 1000 - -HAES steril 6% 1000 - -

    HAES steri10% 1450 (-450) -

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    ADRENAL INSUFFISIENSI PADA SYOK

    SEPTIK

    KORTIKOSTEROID

    Pada syok septik, bila refrakter thdp

    dopamin/adrenalin/nor-adrenalin

    mungkin terjadi INSUFISIENSI ADRENAL

    Hydrocortisone 50mg (bolus),

    dilanjutkan 1-2 mg/kgBB/ 24 jam; 5-7

    hari

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    IMUNOTERAPI

    Tranfusi tukar pada sepsis :

    - memperbaiki oksigenasi jantung

    - mengeluarkan mediator dan endotokin

    Immunoglobulin (I.V) pada sepsis

    Hemofiltrasi dan Plasmafiltrasi :

    mengeluarkan endotoksin, mediator

    mengurangi respons inflamasi sistemik (SIRS)

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    FUNGSI ORGAN

    A. PARU :

    Suplai Oksigen adekuat

    - Intubasi/pemasangan V. mekanik dini pada syok

    septik

    - Pemberian cairan resusitasi, bila terlalu banyak/

    agresif

    resiko tinggi edema paru

    B. OTAK :

    - Hindari hipoksia, hipoglikemia

    - Hindari hiperkapnea dengan ventilator)

    - Pertahankan perfusi serebral :

    a. volume intravaskular

    b. CO

    c. Hb/tekanan darah adekuat

    - Pemantauan kadar Na serum, koreksi hati-hati

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    FUNGSI ORGAN (lanjutan)

    C. SIRKULASI SPLANKHNIK / SALURAN CERNA

    - Resusitasi volume, optimalisai CO, tekanan darah

    - Koreksi hipotensi vasopresor/inotropik)

    - NUTRISI ENTERAL DINI

    D. GINJAL

    - Resusitasi volume, optimalisasi CO, tekanan darah

    - Koreksi hipotensi

    - Koreksi hipoksia dan anemia berat

    - Hindari obat-obatan nefrotoksik

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    TATALAKSANA SYOK KARDIOGENIK

    Oksigenasi Adekuat

    Koreksi GGN Asam Basa dan Elektrolit

    Kurangi Rasa Sakit dan Ansietas

    Atasi Disritmia Jantung

    Kelebihan Preload : Diuretika

    Kontraktilitas : Fluid Challenge Sesuai CVP/POAP

    Obat Inotropik +)

    Beban Afterload SVR

    ) : Vasodilator

    Koreksi Penyebab Primer

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    Commonly Used Cardiovascular lanjutan)

    Drug Dose

    ( ug/kg/min )

    Comment

    Dobutamine( - and - adrenergic )

    1

    20 Positive inotropic effect withminimal changes in heart rate orsystemic vascular resistance

    Amrinone 1 10 Initial bolus infusion may berequired. Limited data available in

    childrenVasodilators

    Nitroprusside 0.005 8 Balanced arterial and venous dilator.May result in thiocyanate or cyanidetoxicity

    Phentolamine 1

    20 Causes dilatation of arterial andvenus beds. Indirect inotropic effectmay cause compensatory tachycardia

    Nitroglicerine 0.5 20 Venus dilator. Dose not wellestablished for infants and children

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    MONITORING

    State of Consiousness-Glasgow Coma Scale

    Respiratory Rate and Character

    Cardiovascular Parameters :

    a. Skin and Core Temperature Difference

    b. Pulse Rate and Volume

    c. Blood Pressure

    d. Capillary Perfusion Time

    e. Central Venous Pressure Should Be Monitored in

    Patient Where There Has Been Poor Response

    To Fluid Therapy Or With Established Shock

    Urinary Output-Urine Bag, Or Preferably Catheter; Output

    Should Be 1-2 ml/kg Body Weight

    Pulse Oximetry

    SvcO2

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    KEY POINTS IN MANAGEMENT

    Remember BP and pulse are unreliable indicators inearly septic shock

    Look for minor degrees of mental impairment(anxiety,restlessness)

    Do not delay treatment, try to prevent the onset ofhypotension, metabolic acidosis, and hypoxia

    Give adequate fluids early in treatment, especiallycolloids

    Do not use inotropic agents until the patients hasreceived adequate fluid therapy

    Monitor blood glucose, gases, and PH, and treatappropriately

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    RINGKASAN/KESIMPULAN

    Syok merupakan keadaan gawat darurat, seringditemukan pada anak

    Morbiditas dan mortalitas syok masih tinggi Syok hipovolemik, paling sering terjadi pada anak

    (80%), sisanya syok kardiogenik

    Diagnosis syok dini sulit, tetapi penting diketahui melaluipemahaman patofisiologi syok (stadium kompensasi,

    dekompensasi dan ireversibel) Pengelolaan syok bertujuan meningkatkan DO2 melalui

    pe

    CO yaitu :

    1. Memperbaiki prabeban dengan resusitasi volume

    2. Me

    kontraktilitas jantung dan

    3. Me SVR

    Dengan pemahaman patofisiologi, diagnosis dini danmemperhatikan key management syok, diharapkandapat me mortalitas syok

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