PENATALAKSANAAN SYOK

PADA ANAK
 PENDAHULUAN

SINDROM KLINIS
KEGAGALAN SISTEM SIRKULASI

KEBUTUHAN  OKSIGEN 
NUTRIEN JARINGAN

DEFISIENSI AKUT
DITINGKAT SEL
 SYOK PADA ANAK :
 Keadaan gawat darurat
 morbiditas / mortalitas  
 80 % hipovolemik
 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, otak )
 Tujuan Primer Pengelolaan Syok :
- Preload  ( resusitasi volume )
- Kontraktilitas 
- Resistensi pada sistemik 
DEFINISI SYOK

SINDROM KLINIS AKIBAT KEGAGALAN SISTEM

SIRKULASI UNTUK MENCUKUPI :

 Nutrisi Pasokan Metabolisme

 Oksigen utilisasi Jaringan tubuh

Defisiensi 02 Seluler
 FUNGSI SISTEM SIRKULASI

 Jantung Curah jantung Metabolisme

 Pembuluh Darah & adekuat jaringan
 Volume Darah Aliran darah
Metabolit

Eliminasi Di Organ
Pembuangan
PENGATURAN CURAH JANTUNG
DAN TEKANAN DARAH
PRELOAD CONTRACTILITY AFTERLOAD

HEART RATE STROKE VOLUME

CARDIAC OUTPUT SYSTEMIC VASCULAR RESISTANCE

BLOOD PRESSURE
 PENGANGKUTAN OKSIGEN

Cardiac Out Put Blood flow

Oxygen
Hb Contentration Delivery

O2 Bound to Hb Blood O2 Content

O2 Dissolved in Plasma
 KLASIFIKASI SYOK
MENURUT ETIOLOGI

 SYOK HIPOVOLEMIK
 SYOK DISTRIBUTIF
 SYOK KARDIOGENIK
 SYOK SEPTIK
 SYOK OBSTRUKTIF
 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 <), Saluran cerna (muntah, ileus)
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)
Aliran darah lambat

Agregasi Trombosit
Pembentukan Trombus
Pendarahan
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
 Kerusakan / Kematian Sel
 Disfungsi sistem multi organ
 Cadangan fostat E. Tinggi 
( Hepar, Jantung )

Tekanan darah tak terukur
Nadi tak teraba
Kesadaran 
klinis
Anuria
GMO
PERJALANAN PATOFISIOLOGI SYOK
Septic Shock Cardiogenic Shock
Hypovolemic Shock
Myocardial
Capillary Leak Mediators Depression

 Preload Vasodilatation  Contractility

 Cardiac Output  Blood Pressure

Sympathetic Discharge

Improved Cardiac Vasoconstriction, 

output and blood  HR  Contractility
pressure

COMPENSATED
 Vasoconstriction
 HR  Contractility

COMPENSATED

DECOMPENSATED
 Myocardial perfusion
 Myocardial O2 Consumption

 Cardiac Output Tissue Ischemia

Mediator Release
Loss of Auto
 Cell Function regulation of
Microcirculation

Cell Death Death of Organism

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

PRELOAD ↓

HYPO
VOL CONTRACTILITY
SHOCK N/ ↑

AFTERLOAD ↑
 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

PRELOAD
N/↑

Distributive CONTRACTILITY
shock N/↓

AFTERLOAD
Variable
 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 <10 th
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 dysfunction
in 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
 PRELOAD
DECREASE

SEPTIC
CONTRACTILITY
SHOCK
N / DECREASED

AFTERLOAD
VARIABLE
 III. SYOK KARDIOGENIK

Etiologi :
 Pasca Bedah Penyakit Jantung Bawaan
 Miokarditis
 Infark / Iskemik Jantung
 Kardiomiopati Primer / Sekunder
 Hipoglikemia, Gangguan Metabolik
 Asfiksia, Sepsis
 PRELOAD
VARIABLE

CONTRACTILITY
CARDIOGENIC
DECREASED
SHOCK

AFTERLOAD
INCREASED
 MEKANISME SYOK KARDIOGENIK

Cardiogenic Contractility
Shock

Compensatory mech.
Metabolic acidosis, hypoxia, CO 
 Afterload
Myocardial depressant factor BP   SVR
 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 Sepsis
New Concept about SIRS, SEPSIS, CARS, MARS
Pro-inflammatory Anti-inflammatory
response response
Initial insult
(bacteria, viral, traumatic, thc, mal)

Systemic spillover of Systemic spillover of

pro-inflammatory anti-inflammatory
mediators mediators
Systemic Reaction:
SIRS (pro-inflammatory)
CARS (anti-inflammatory)
MARS (mixed)

Apoptosis Organ Suppression

Cardiovascular Homeostasis (cell death) dysfunction of the immune
Compromise
system
shock, CARS and SIRS Death with
minimal SIRS CARS
SIRS pre-dominates balanced inflammation Pre-dominated pre-dominated
 SEPSIS DAN GANGGUAN KOAGULASI

Sepsis

Inflammatory cytokines

IL - 6 TNF - 

Tissue factor Mediated Inhibition of Depression of

activation of coagulation physiological fibrinolysis due
anticoagulant pathways to high levels of
PAI-1

Enhanced fibrin Impaired fibrin

formation removal

Microvascular
thrombosis
CYTOKINE-MEDIATED PATHOGENETIC
PATHWAYS of MICROVASCULAR
THROMBOSIS in SEPSIS
Sepsis

Activation of coagulation

Widespread fibrin Consumption of

Deposition platelets and
clotting factor

Microvascular
thrombosis Bleeding (severe)
 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
 Most Common Pathogens in Childhood Bacterial Sepsis
Age Group Pathogens Antimicrobial Initial
(Pending culture) dose
(mg/kg)
0 – 1 months Group B Strept. Enterobacteriaceae Ampiciline + 50
Staph. Aureus Gentamicin 2.5
Listeria meningtides Cefotaxime 5-0
1 – 24 months H. influenzae, Strept. Pneumoniae Cefotaxime 50
S. aureus, Neisseria meningtidis Ampiciline + 50
Group B Streptococcus Chlorampenicol 25
> 24 months S. Pneumoniae Cefotaxime 50
H. Influenzae Cefriaxone 50
S. Aureus Ampiciline + 50
N. Meningtidis Chlorampenicol 25

Immuno S. aureus, Proteus Vancomycin + 25

compromised Pseudomonas Ceftazidime + 50
Enterobacteriaceae Ticarcillin 75
 PENATALAKSANAAN SYOK
1. 2.

Oksigenasi Sistem K.V

CaO2  a. Preload 
SaO2 95 – 100 % ( resusitasi volume )
b. Atasi Disritmia
c. Koreksi keseimbangan
asam - basa
Jalan nafas Oksigen  Anxietas
 TERAPI CAIRAN PADA SYOK
 AKSES VENA (90 detik); Tak berhasil  IO
 KRISTALOID dan atau KOLOID
10 – 30 ml / kg B.B (6-10 menit)

diulang 2 – 3 kali
 SYOK SEPTIK  60 – 100 ml / kg B.B
(dalam 6 jam pertama)
 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
Suspected shock
Hypovolemia, Hypoperfusion, Tachycardia

10 – 30 mL Cryst/Colloid / kg / 6 – Hypotensive
10 min
Normotensive In Sepsis : In Anaphylaksis :
Antibiotics, Catekolamin, 10-20 mL
Imunotheraphy steroid, crys or
antihistamin coll/kg/10
min
Urine > 1 ml/kg/hr Urine < 1 ml/kg/hr Anuria

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
Reevaluated

Hypotensive, urine < 1 mL/kg/hr

Improved

CVP < 10 mmHg CVP, CVP > 10 mmHg

Cardiac status,
chest X-Ray,
10-20 mL X.tal/kg Echocardiography

Afterload reduction,
Reevaluated inotropic support,
consider pulmonary
 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 to
fluid therapy
• End points : Good peripheral perfusion 
Conciousness, Capillary feeling time < 2”, Warm
extremities, MAP/Pulse pressure N for age, CVP
8-12 mmHg, Diuresis > 2ml/kg SvcO2 > 70%
• Admission to PICU when stabilized
 Supplemental oxygen 
endotracheal intubation and
mechanical ventilation
Protocol for Early
Central venous and
arterial
Goal-Directed
catheterization
Therapy
Sedation, paralysis
(if intubated), or both
Crystalloid
< 8 mmHg
CVP
Colloid
8-12 mmHg
< 65 mmHg
MAP Vasoactive agents
> 90 mmHg
≥ 65 and ≤ 90 mmHg
Transfusion of red cells
ScvO2 until hematocrit ≥ 30% < 70%
≥ 70% Inotropic agents

No
Goals achieved
Yes
Hospital admission
 Fluid Therapy
in Sepsis and Septic Shock

Volume Type of Fluid

60 – 100 ml/kg Colloid
(6 hours) Crystalloid

Inotropic
Vasopressor

CO , Restore BP
 MOF
 (SYOK KARDIOGENIK) :
Fluid Chalenge  hati – hati :
a. memperbaiki kontraktilitas jantung
b. dipantau ketat dengan TVS
 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) -
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
 TERAPI SUPORTIF
 Substitusi faktor koagulasi (pada Hemodilusi/PIM) :
- Fresh Frozen Plasma
- Cyroprecipitate
 Tranfusi Masif  setiap 5 – 6 unit PC ditambah 2
unit FFP
 Fibrinogen < 100 mg/dl (tak respons terhadap FFP) :
- Cyro precipitate 4 unit/10 kg BB
 Konsentrat trombosit diberikan :
Trombositopeni berat < 30.000 dengan perdarahan
atau tindakan invasif : - Konsentrat Trombosit
 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)

 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)
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
• 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 Syndromes
Drug Dose Comment
( ug/kg/min )
Inotropioc agents
Norephrine 0.05 – 1.0 For profound hypotension not
(  - adrenergic ) responding to fluid or other inotropic
drugs
Ephinephrine 0.05 – 1.0 Dose related response, higher doses
(  - and  - adrenergic ) cause vasoconstriction. Useful in
maintaining CO and BP inpatients
unresponsive to dopamine or
debutamine
Isoproterenol 0.05 – 0.5 Indicated in bradycardia unresponsive
(  - adrenergic ) to atropine if increase in heart rate is
not excessive, may be helpful in
reactive pulmonary hypertension
Dopamine 1 – 20 Cardiovascular effects are complex and
( - and  - dose related. Low dose infusion can
dopaminergic ) restore cardiovascular stability and
improve renal function
 Commonly Used Cardiovascular …(lanjutan)
Drug Dose Comment
( ug/kg/min )
Dobutamine 1 – 20 Positive inotropic effect with
(  - and  - adrenergic ) minimal changes in heart rate or
systemic vascular resistance
Amrinone 1 – 10 Initial bolus infusion may be
required. Limited data available in
children
Vasodilators
Nitroprusside 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
 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
 KEY POINTS IN MANAGEMENT
 Remember BP and pulse are unreliable indicators in
early septic shock
 Look for minor degrees of mental impairment
(anxiety,restlessness)
 Do not delay treatment, try to prevent the onset of
hypotension, metabolic acidosis, and hypoxia
 Give adequate fluids early in treatment, especially
colloids
 Do not use inotropic agents until the patients has
received adequate fluid therapy
 Monitor blood glucose, gases, and PH, and treat
appropriately
 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