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PENATALAKSANAAN SYOK PADA ANAK

TATTY ERMIN SETIATI
SUB. BAGIAN PEDIATRI GAWAT DARURAT FK. UNDIP/RSUP
DR. KARIADI SEMARANG
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
Oksigen
Pasokan
utilisasi
Metabolisme
Jaringan tubuh
Defisiensi 02 Seluler
FUNGSI SISTEM SIRKULASI

 Jantung
 Pembuluh Darah
 Volume Darah

Curah jantung
& adekuat
Aliran darah
Metabolisme
jaringan
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
Delivery
Blood O
2
Content
Hb Contentration
O
2
Bound to Hb
O
2
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 1-10
th
: <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 
Anuria
GMO
klinis
PERJALANAN PATOFISIOLOGI SYOK
Septic Shock Cardiogenic Shock
Hypovolemic Shock
Capillary Leak Mediators
Myocardial
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

HYPO
VOL
SHOCK
PRELOAD ↓
AFTERLOAD ↑
CONTRACTILITY
N / ↑
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 / Septic Shock

Distributive
shock
PRELOAD
N / ↑
CONTRACTILITY
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
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 <5
th
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
III. SYOK KARDIOGENIK
Etiologi :
 Pasca Bedah Penyakit Jantung Bawaan
 Miokarditis
 Infark / Iskemik Jantung
 Kardiomiopati Primer / Sekunder
 Hipoglikemia, Gangguan Metabolik
 Asfiksia, Sepsis

CARDIOGENIC
SHOCK
PRELOAD
VARIABLE
CONTRACTILITY
DECREASED
AFTERLOAD
INCREASED
MEKANISME SYOK KARDIOGENIK
Cardiogenic
Shock
Contractility
CO 
BP 
Metabolic acidosis, hypoxia,
Myocardial depressant factor
Compensatory mech.
 Afterload
 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
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

PENATALAKSANAAN SYOK
1. 2.
Oksigenasi
CaO
2

SaO
2
95 – 100 %
Sistem K.V
a. Preload 
( 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 1
st
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 –
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
Anuria
Urine < 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 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
Fluid Therapy
in Sepsis and Septic Shock
Type of Fluid
Colloid
Crystalloid
Volume
60 – 100 ml/kg
(6 hours)
CO , Restore BP
 MOF
Inotropic
Vasopressor
 (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
( ug/kg/min )
Comment
Inotropioc agents
Norephrine
(  - 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 hypertension
Dopamine
( - 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)
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
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 DO
2
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