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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