PENATALAKSANAAN SYOK

PADA ANAK
 PENDAHULUAN

SINDROM KLINIS
KEGAGALAN SISTEM SIRKULASI

KEBUTUHAN  OKSIGEN 
NUTRIEN JARINGAN

DEFISIENSI AKUT
DITINGKAT SEL
 SYOK PADA ANAK :
Ø Keadaan gawat darurat
  morbiditas / mortalitas  
Ø 80 % hipovolemik
Ø 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 )
Ø Tujuan Primer Pengelolaan Syok :
 - Preload  ( resusitasi volume )
 - Kontraktilitas 
 - Resistensi pada sistemik 
DEFINISI SYOK
SINDROM KLINIS AKIBAT KEGAGALAN SISTEM
SIRKULASI UNTUK MENCUKUPI :

v Nutrisi Pasokan Metabolisme

v Oksigen utilisasi Jaringan tubuh

Defisiensi 02 Seluler
 FUNGSI SISTEM SIRKULASI

Ø Jantung Curah jantung

Metabolisme
Ø Pembuluh Darah &
jaringan
Ø Volume Darah adekuat
Aliran darah
Ø Metab
olit

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

v SYOK HIPOVOLEMIK
v SYOK DISTRIBUTIF
v SYOK KARDIOGENIK
v SYOK SEPTIK
v 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
Ø Kerusakan / Kematian Sel
Ø Disfungsi sistem multi organ
Ø Cadangan fostat E. Tinggi ↓↓
 ( Hepar, Jantung )
 ↓
 Tekanan darah tak
terukur
 Nadi tak teraba
 klinis Kesadaran ↓↓
 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 
pressure
 HR  Contractility
COMPENSATED
 Vasoconstriction
 HR  Contractility

COMPENSATED

DECOMPENSATED
 Myocardial perfusion
 Myocardial O2
Consumption
 Cardiac Tissue Ischemia
Output
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/↑

Distributiv
e 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

CONTRACT
PRELOAD
I-
↓↓
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 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 :
Ø Pasca Bedah Penyakit Jantung Bawaan
Ø Miokarditis
Ø Infark / Iskemik Jantung
Ø Kardiomiopati Primer / Sekunder
Ø Hipoglikemia , Gangguan Metabolik
Ø Asfiksia , Sepsis
 PRELOAD
VARIABLE

CARDIOGENI CONTRACTILITY
C 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- Anti-
inflammatory inflammatory
response response
Initial insult
(bacteria, viral, traumatic, thc, mal)

Systemic spillover of Systemic spillover of

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

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

Inflammatory
cytokines
IL - 6 TNF - 

Tissue factor Inhibition of Depression

Mediated physiological of
activation of anticoagulant fibrinolysis
coagulation pathways due 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 Consumption
fibrin of platelets
Deposition and clotting
factor
Microvascular
thrombosis Bleeding
( severe )
 MANIFESTASI KLINIS SYOK SEPTIK
v STADIUM KOMPENSASI
 - Resistensi Vaskuler 
 - Curah Jantung 
 - Takhikardia
 - Ekstermitas Hangat
 - Divresis Normal
v 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
Sepsis
Age Group Pathogens Antimicrobial Initial dose
(Pending culture) (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.
Sistem
Oksigenasi K.V

CaO2 ↑ a.Preload ↑
SaO2 95 – 100 % ( resusitasi volume )
b.Atasi Disritmia
c.Koreksi keseimbangan
asam - basa
Jalan nafas Oksigen ↓
Αν ξ ι ε τ α σ
 TERAPI CAIRAN PADA SYOK
Ø AKSES VENA (90 detik); Tak berhasil  IO
Ø KRISTALOID dan atau KOLOID

10 – 30 ml / kg B.B (6-10 menit)



diulang 2 – 3 kali
Ø 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
Suspected shock
Hypovolemia, Hypoperfusion, Tachycardia

10 – 30 mL Cryst/Colloid / kg / 6 – Hypotensive
10 min
Normotensive In Sepsis : In Anaphylaksis :
10-20 mL
Antibiotics, Catekolamin,
crys or
Imunotheraphy steroid,
coll/kg/10
antihistamin
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)  n U within 
hours of admission
• Vasopressors  notropic
drugs when resistance
to fluid therap
• nd points  Good
peripheral perfusion
 onciousness
apillar feeling
time <  ”  arm
extremities
     ulse pressure N
for age CVP 8-12 mmHg,
 Supplemental oxygen 
endotracheal intubation and
mechanical ventilation Protocol for Early
Central venous and Goal-Directed
arterial
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

ScvO2 Transfusion of red cells

until hematocrit ≥ 30% < 70%
≥ 70% Inotropic agents
No Goals
achieve
Yes d
Hospital admission
 Fluid Therapy
in Sepsis and Septic Shock

Volume Type of
60 – 100 Fluid
ml/kg Colloid
(6 hours) Crystalloi
d
Inotropic
Vasopressor

CO , Restore BP
 MOF
Ø (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
v Substitusi faktor koagulasi (pada
Hemodilusi/PIM) :
 - Fresh Frozen Plasma
 - Cyroprecipitate
v Tranfusi Masif  setiap 5 – 6 unit PC ditambah 2
unit FFP
v Fibrinogen < 100 mg/dl (tak respons terhadap
FFP) : - Cyro precipitate 4 unit/10 kg BB
v 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 responding
(  - adrenergic ) to fluid or other inotropic drugs
Ephinephrine 0.05 – 1.0 Dose related response, higher doses cause
(  - and  - adrenergic ) vasoconstriction. Useful in maintaining CO
and BP inpatients unresponsive to
dopamine or debutamine
Isoproterenol 0.05 – 0.5 Indicated in bradycardia unresponsive to
(  - adrenergic ) atropine if increase in heart rate is not
excessive, may be helpful in reactive
Dopamine 1 – 20 Cardiovascular effects are complex and
pulmonary hypertension
(  - and  - dose related. Low dose infusion can restore
dopaminergic ) cardiovascular stability and improve renal
function
 Commonly Used Cardiovascular …( lanjutan )
Drug Dose Comment
( ug/kg/min )
Dobutamine 1 – 20 Positive inotropic effect with minimal
(  - and  - adrenergic ) 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
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
• 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