PENATALAKSANAAN SYOK PENATALAKSANAAN SYOK PADA ANAK PADA ANAK

PENDAHULUAN

SINDROM KLINISKEGAGALAN SISTEM SIRKULASI

KEBUTUHAN OKSIGEN NUTRIEN JARINGAN

DEFISIENSI AKUT DITINGKAT SEL

:SYOK PADA ANAKØ Keadaan gawat darurat / morbiditas mortalitas

Ø % 80 hipovolemikØ / . Syok kompensasi sulit di D o k

manifestasi klinis tak jelas( refleks simpatis Redistribusi

. selektif al daerah dari organ perifer non- , , vital ke jantung paru

)otakØ :Tujuan Primer Pengelolaan Syok - ( )Preload resusitasi volume - Kontraktilitas - Resistensi pada sistemik

DEFINISI SYOK DEFINISI SYOK

SINDROM KLINIS AKIBAT KEGAGALAN SISTEM :SIRKULASI UNTUK MENCUKUPI

vNutrisivOksigen

Pasokanutilisasi

Metabolisme Jaringan tubuh

Defisiensi 02 Seluler

FUNGSI SISTEM SIRKULASI FUNGSI SISTEM SIRKULASI

Ø JantungØ Pembuluh DarahØ Volume Darah

Ø

Curah jantung & adekuatAliran darah

Metabolismejaringan

Metabolit

Eliminasi Di OrganPembuangan

PENGATURAN CURAH JANTUNG PENGATURAN CURAH JANTUNG DAN TEKANAN DARAH DAN TEKANAN DARAH

PRELOAD CONTRACTILITY AFTERLOAD

HEART RATE STROKE VOLUME

CARDIAC OUTPUT SYSTEMIC VASCULAR RESISTANCE

BLOOD PRESSURE

PENGANGKUTAN OKSIGEN PENGANGKUTAN OKSIGEN

Cardiac Out Put Blood flow

OxygenDelivery

Blood O2 Content

Hb Contentration

O2 Bound to Hb

O2 Dissolved in Plasma

KLASIFIKASI SYOK KLASIFIKASI SYOK MENURUT ETIOLOGI MENURUT ETIOLOGI

v SYOK HIPOVOLEMIKv SYOK DISTRIBUTIFv SYOK KARDIOGENIKv SYOK SEPTIKv SYOK OBSTRUKTIF

STADIUM SYOK STADIUM SYOK : FASE I KOMPENSASI : 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 Saluran ( , )cerna muntah ileus

: ( )FASE II DEKOMPENSASI 1 : ( )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

: ( )FASE II DEKOMPENSASI 2 : ( )FASE II DEKOMPENSASI 2

Aliran darah lambat Agregasi Trombosit

Pembentukan TrombusPendarahan

Pelepasan Mediator

Vasodilatasi Arterial

Kenaikan Permeabilitas Kapiler VR

Fase dekompensasi

• Perfusi jaringan indekuat disertai hipotensi

•• Kesadaran menurun krn perfusi ke otak

menurun

•• Hipotensi sebagai tanda terakhir dari syok• Untuk anak 1-10th: <70 mmHg +(umur/thn

x 2) mmHg

: FASE III IREVERSIBEL

Ø Kerusakan / Kematian SelØ Disfungsi sistem multi organØ Cadangan fostat E. Tinggi ↓↓ ( Hepar, Jantung ) ↓ Tekanan darah tak

terukur Nadi tak teraba Kesadaran ↓↓ Anuria GMO

klinis

PERJALANAN PATOFISIOLOGI SYOK PERJALANAN PATOFISIOLOGI SYOK

Septic Shock Cardiogenic ShockHypovolemic Shock

Capillary Leak MediatorsMyocardial Depression

Preload Vasodilatation Contractility

Cardiac Output Blood Pressure

Sympathetic Discharge

Vasoconstriction,

HR Contractility

Improved Cardiac output and blood pressure

COMPENSATED

DECOMPENSATED Myocardial perfusion

Myocardial O 2 Consumption

Cardiac Output

Mediator Release

Cell Function

Cell Death Death of Organism

Tissue Ischemia

Loss of Auto regulation of

Microcirculation

COMPENSATED

Vasoconstriction HR Contractility

Syok Hipovolemik

• Etiologi: Diare, perdarahan, muntah, intake tak adekuat, diuresis osmotik, luka bakar

•

HYPOVOL

SHOCK

PRELOAD ↓

AFTERLOAD ↑

CONTRACTILITYN / ↑

Syok hipovolemik Primary Assessment: Finding• A

• B Takhipneu tanpa pe↑ WOB• 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

Distributive Shock

Distributive

shock

PRELOAD N / ↑

CONTRACTILITYN / ↓

AFTERLOADVariable

Findings of Distributive Shock

• Primary Assessment Finding• A Patent airway, unless unconc.• B Tachypnea without ↑WOB, except

caused by pneumonia, ARDS, pulm edema• C Tachycardia, Hypotension with wide

pulse pressure(warm shock) or narrow p.pressure(cold shock) or normotension; Bounding perpheral pulse, Delayed cap.refill, Warm&flush skin(warm shock) or pale skin(cold shock): Changes in mental status; oliguria

• D Changes in mental status

Septic Shock

PRELOAD↓↓

CONTRACTI-

LITY ↓/ N

AFTERLOAD VARIABLE

Consensus Definitions and clinical Characteristic of Ped.Sepsis

• Systemic Inflammatory Response Syndrome ( SIRS )

• Sepsis• Severe Sepsis• Septic shock

SIRS

• Core temp of >38.5°C or <36°C• Tachycardia >2SD above normal for age,

for chhildren <1 year bradycardia <10th percentile for age

• Mean RR>2SD above normal for age• Leucocyte count ↑ or ↓ for age or 10%

immature neutrophils• ( At least 2 of the 4 criteria )

• SEPSIS :

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

suspected or proven infection

Severe sepsis

• Sepsis plus either cardiovascular dysfunction or ARDS

Or• Sepsis plus 2 or more other organ failures

RF as sign of organ dysfunctionin sepsis

• PaO2/FiO2 <300 in absence of CHD or lung disease

• PaCO2 >65 mmHg or 20 mmHg above baseline

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

• Need nonelective MV (invasive or noninvasive)

Septic shock

• Sepsis and

•• Cardiovascular dysfunction despite

administration of isotonic iv boluses > 40 ml/kg in 1 hour

Cardiovascular dysfunction

• Hypotension (SBP <5th percentile for age or SBP <2SD below normal for age or

• Need for vasoactive drug to maintain BP in normal range or

•• Two of the following characteristic of inadequate

organ perfusion:

Inadequate organ perfusion

• Unexplained metabolic acidosis: base deficit < 5meq/l

• Increase arterial lactate > twice the upper limit of normal

• Oliguria: Urine output0.5 ml/kg/hour• Prolonged cap refill: > 5 second• Cor to peripheral temp gap > 3°C

SEPTICSHOCK

PRELOADDECREASE

CONTRACTILITYN / DECREASED

AFTERLOADVARIABLE

. III SYOK KARDIOGENIK. III SYOK KARDIOGENIK

:EtiologiØ Pasca Bedah Penyakit Jantung BawaanØ MiokarditisØ / Infark Iskemik JantungØ / Kardiomiopati Primer SekunderØ , Hipoglikemia Gangguan MetabolikØ , Asfiksia Sepsis

CARDIOGENIC

SHOCK

PRELOADVARIABLE

CONTRACTILITYDECREASED

AFTERLOADINCREASED

MEKANISME SYOK KARDIOGENIK MEKANISME SYOK KARDIOGENIK

Cardiogenic Shock

Contractility

CO BP

Metabolic acidosis, hypoxia,Myocardial depressant factor

Compensatory mech. Afterload SVR

SYOK KARDIOGENIK 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

Findings of Cardiogenic Shock• Primary Assessment Finding• A• B Tachypnea; WOB↑• C Tachycardia; N/low BP with

a narrow pulse pressure; weak or absent of peripheral 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••

Obstructive Shock

• Cardiac tamponade• Tension pneumothorax• Ductal – dependent congenital heart lesions• Massive pulmonary embolism

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

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

Pathogenesis and Pathophysiology of SepsisNew Concept about SIRS, SEPSIS, CARS, MARS

Pro-inflammatory

response

Anti-inflammatory

response

Systemic Reaction:SIRS (pro-

inflammatory)CARS (anti-

inflammatory)MARS (mixed)

Systemic spillover of pro-inflammatory

mediators

Systemic spillover of anti-inflammatory

mediators

Initial insult (bacteria, viral, traumatic, thc, mal)

Cardiovascular Compromise

shock, SIRS pre-dominates

Homeostasis

CARS and SIRS

balanced

Apoptosis (cell death)

Death with minimal

inflammation

Organ dysfunction

SIRSPre-

dominated

Suppression of the

immune systemCARS pre-

dominated

SEPSIS DAN GANGGUAN KOAGULASI SEPSIS DAN GANGGUAN KOAGULASI

Sepsis

Inflammatorycytokines

- IL 6 - TNF

Tissue factor Mediated activation of

coagulation

Inhibition of physiological anticoagulant

pathways

Depression of

fibrinolysis due to high

levels of-PAI 1

Enhanced fibrinformation

Impaired fibrinremoval

Microvascularthrombosis

- CYTOKINE MEDIATED PATHOGENETIC- CYTOKINE MEDIATED PATHOGENETIC PATHWAYS of MICROVASCULAR THROMBOSIS PATHWAYS of MICROVASCULAR THROMBOSIS

in SEPSIS in SEPSIS

Sepsis

Activation ofcoagulation

Widespread fibrin

Deposition

Consumption of platelets and clottingfactor

Microvascularthrombosis Bleeding

( )severe

MANIFESTASI KLINIS SYOK SEPTIK MANIFESTASI KLINIS SYOK SEPTIK

v STADIUM KOMPENSASI - Resistensi Vaskuler - Curah Jantung - Takhikardia - Ekstermitas Hangat - Divresis Normalv STADIUM DEKOMPENSASI - Volume Intravaskuler - Depresi Miokard - Eksternal Dingin - Gelisah, Anuria, Distres Respirasi - Resistensi Vaskuler - Curah Jantung v STADIUM IREVERSIBEL - GMO

Most Common Pathogens in Childhood Bacterial Most Common Pathogens in Childhood BacterialSepsisSepsis

Age Group Pathogens Antimicrobial(Pending culture)

Initial dose (mg/kg)

0 – 1 months Group B Strept. EnterobacteriaceaeStaph. AureusListeria meningtides

Ampiciline +GentamicinCefotaxime

502.55-0

1 – 24 months H. influenzae, Strept. PneumoniaeS. aureus, Neisseria meningtidisGroup B Streptococcus

CefotaximeAmpiciline +Chlorampenicol

505025

> 24 months S. PneumoniaeH. InfluenzaeS. AureusN. Meningtidis

CefotaximeCefriaxoneAmpiciline +Chlorampenicol

50505025

Immuno compromised

S. aureus, ProteusPseudomonasEnterobacteriaceae

Vancomycin +Ceftazidime +Ticarcillin

255075

PENATALAKSANAAN SYOK PENATALAKSANAAN SYOK

1. 2.

Oksigenasi

CaO2 ↑SaO2 95 – 100 %

Sistem K.V

a.Preload ↑( resusitasi volume )

b.Atasi Disritmiac.Koreksi keseimbangan

asam - basaJalan nafas Oksigen ↓ Α ν ξ ι ε τ α σ

TERAPI CAIRAN PADA SYOK TERAPI CAIRAN PADA SYOKØ AKSES VENA (90 detik); Tak berhasil IO

Ø KRISTALOID dan atau KOLOID 10 – 30 ml / kg B.B (6-10 menit) diulang 2 – 3 kaliØ SYOK SEPTIK 60 – 100 ml / kg B.B (dalam 6 jam pertama)Ø THE 1st CONSENSUS CONFERENCE on CCM 1997 (SYOK SEPTIK) a. Koloid terapi inisial, dilanjutkan

koloid/kristaloid b. Dipandu : respons klinis,perfusi, perifes, tvs,

tekanan sistem,MAP

Algoritme Terapi Cairan Pada Syok 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 mL crys or coll/kg/10 min

AnuriaUrine < 1 ml/kg/hr

Urine output < 1 ml/kg/hr

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

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

Early Goal DirectedEarly Goal DirectedTherapy pada Syok SeptikTherapy pada Syok Septik

• Early aggressive fluid therapy (Crystaloid or colloid) n U w t n i hi ours o m ss onh f ad i i

• V sopr ssors notrop a e ic ru s w n r s st n d g he e i a ce

to lu t r pf id he a • n po ntsd i oo G d

p r p r l p r us on e i he a e f i on ousn ss ci e

p ll r l n a i a fee i g t m < ” rm i e a xtr m t s e e i ie

uls pr ssur N e e e or f age CVP 8-12 mmHg, ur s s mlDi e i > g SvcO2 >

70%• Admission to PICU when stabilized

Supplemental oxygen endotracheal intubation and

mechanical ventilation

Central venous and arterial

catheterization

Sedation, paralysis (if intubated), or both

Goals achieve

d

ScvO2

MAP

CVP

Hospital admission

8-12 mmHg

≥ 65 and ≤ 90 mmHg

≥ 70%

Yes

No

Crystalloid

Colloid

< 8 mmHg

Vasoactive agents< 65 mmHg> 90 mmHg

Transfusion of red cells until hematocrit ≥ 30%

Inotropic agents

< 70%

Protocol for Early Goal-Directed

Therapy

Fluid Therapy in Sepsis and Septic Shock

Type of Type of Fluid Fluid

Colloid Colloid CrystalloiCrystalloi

dd

Volume Volume 60 – 100 60 – 100

ml/kgml/kg(6 hours)(6 hours)

CO , Restore BPCO , Restore BP

MOFMOF

InotropicVasopressor

Ø (SYOK KARDIOGENIK) : Fluid Chalenge hati – hati :

a. memperbaiki kontraktilitas jantungb. dipantau ketat dengan TVS

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

Larutan Vol. Plasma Vol. Inters I.IntraselAlbumin 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) -

ADRENAL INSUFFISIENSI ADRENAL INSUFFISIENSI PADA SYOK PADA SYOK

SEPTIKSEPTIK 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

TERAPI SUPORTIF TERAPI SUPORTIF

vSubstitusi faktor koagulasi (pada Hemodilusi/PIM) :

- Fresh Frozen Plasma - CyroprecipitatevTranfusi Masif setiap 5 – 6 unit PC ditambah 2

unit FFPvFibrinogen < 100 mg/dl (tak respons terhadap

FFP) : - Cyro precipitate 4 unit/10 kg BBvKonsentrat trombosit diberikan : Trombositopeni berat < 30.000 dengan

perdarahan atau tindakan invasif : - Konsentrat Trombosit

IMUNOTERAPIIMUNOTERAPI

• 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)

FUNGSI ORGAN 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

( )FUNGSI ORGAN lanjutan ( )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

TATALAKSANA SYOK KARDIOGENIK 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

Commonly Used Cardiovascular Drugs in Shock Commonly Used Cardiovascular Drugs in ShockSyndromesSyndromes

Drug Dose ( ug/kg/min )

Comment

Inotropioc agentsNorephrine( - adrenergic )

0.05 – 1.0 For profound hypotension not responding to fluid or other inotropic drugs

Ephinephrine( - and - adrenergic )

0.05 – 1.0 Dose related response, higher doses cause vasoconstriction. Useful in maintaining CO and BP inpatients unresponsive to dopamine or debutamine

Isoproterenol( - adrenergic )

0.05 – 0.5 Indicated in bradycardia unresponsive to atropine if increase in heart rate is not excessive, may be helpful in reactive pulmonary hypertensionDopamine

( - and - dopaminergic )

1 – 20 Cardiovascular effects are complex and dose related. Low dose infusion can restore cardiovascular stability and improve renal function

…( )Commonly Used Cardiovascular lanjutan …( )Commonly Used Cardiovascular lanjutan

Drug Dose( ug/kg/min )

Comment

Dobutamine( - and - adrenergic )

1 – 20 Positive inotropic effect with minimal changes in heart rate or systemic vascular resistance

Amrinone 1 – 10 Initial bolus infusion may be required. Limited data available in children

VasodilatorsNitroprusside 0.005 – 8 Balanced arterial and venous dilator.

May result in thiocyanate or cyanide toxicity

Phentolamine 1 – 20 Causes dilatation of arterial and venus beds. Indirect inotropic effect may cause compensatory tachycardia

Nitroglicerine 0.5 – 20 Venus dilator. Dose not well established for infants and children

MONITORINGMONITORING - 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 BodyWeight

Pulse Oximetry SvcO2

KEY POINTS IN MANAGEMENT KEY POINTS IN MANAGEMENT

Ø Remember BP and pulse are unreliable indicators in early septic shock

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

Ø Do not delay treatment, try to prevent the onset of hypotension, metabolic acidosis, and hypoxia

Ø Give adequate fluids early in treatment, especially colloids

Ø Do not use inotropic agents until the patients has received adequate fluid therapy

Ø Monitor blood glucose, gases, and PH, and treat appropriately

/RINGKASAN KESIMPULAN/RINGKASAN KESIMPULAN• Syok merupakan keadaan gawat darurat, sering ditemukan

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 melalui

pemahaman 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 dan memperhatikan “key management“ syok, diharapkan dapat me mortalitas syok