PENATALAKSANAAN SYOK

PADA ANAK

Moh. Supriatna TS
 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 & adekuat jaringan
Darah Aliran darah
Volume 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
 KLASIFIKASI SYOK
MENURUT ETIOLOGI

SYOK HIPOVOLEMIK
SYOK DISTRIBUTIF
SYOK KARDIOGENIK
SYOK SEPTIK
SYOK OBSTRUKTIF
 PENGANGKUTAN OKSIGEN

Cardiac Out Put Blood flow

Oxygen
Hb Contentration Delivery

O2 Bound to Hb Blood O2 Content

O2 Dissolved in Plasma
 STADIUM SYOK
FASE I : KOMPENSASI

Mekanisme Kompensasi Tubuh refleksi simpatis

- Resistensi sistemik
- Tekanan darah ( N )
- Tekanan Diastolik
- Tekanan Nadi Sempit
FASE II : DEKOMPENSASI
- 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 : LANJUTAN
Aliran darah lambat

Agregasi Trombosit
Pembentukan Trombus
Pendarahan
Pelepasan Mediator

Vasodilatasi Arterial

Kenaikan Permeabilitas Kapiler

VR
 FASE III : IREVERSIBEL
Kerusakan / Kematian Sel
Disfungsi sistem multi organ
Cadangan fostat E. Tinggi
( Hepar, Jantung )

Tekanan darah tak terukur
Nadi tak teraba
klinis Kesadaran
Anuria
GMO
 PERJALANAN PATOFISIOLOGIS DARI SYOK
Septic Shock Cardiogenic Shock
Hypovolemic Shock
Myocardial
Capilary 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

UNCOMPENSATED
Myocardial perfusion
Myocardial O2 Consumption

Cardiac Output Tissue Ischemia

Mediator Release
Loss of
Cell Function Autoregulation of
Mycrocirculation

Cell Death Death of Organism

 DIAGNOSIS SYOK

1. Riwayat Penyakit
2. Pemeriksaan Klinis
a. Status KV
- Freq. Jantung
- Kualitas Nadi
- Perfusi Kulit
- Tekanan Darah
b. Gangguan Sirkulasi
Organ Vital
- Status Mentalis / Respirasi
- Produksi Urin
c. Penentuan B.B dan Estimasi
kehilangan Volume Darah
B.B ( kg ) = 2 x ( umur / th + 4 )
Estimasi Vol. Darah = 80 ml / kg
B.B
 I. SYOK HIPOVOLEMIK
a. Etiologi
- Kehilangan Air dan Elektrolit
- Kehilangan Plasma
- Tindakan Bedah
- Pendarahan Saluran Cerna
b. Manifestasi Klinis
- Aliran Darah ke Organ Vital
( SSP, jantung, med. Adrenal )
- ADH , Stim Renin Aldosteron

Syok stadium dini ( kompensasi )
 II. SYOK DISTRIBUTIF

a. Tonus Vasomotor Maldistribusi

Abnormal Vol. Sirkulasi

Syok

b. Pooling Perifer Hipovolemi

Shunting Vaskuler Relatif

( a dan b ) Hipotensi Berat

 ETIOLOGI SYOK DISTRIBUTIF
Penyebab Syok Distributif
Anafilakis :
- Vaksin
- Darah
- Anestesi lokal
Neurologik :
- Cedera kepala
- Syok spinal
Syok Septik
Obat - obatan :
- Barbiturat
- Fenotiazin
- Tranquilizer
- Anti hipotensi
 III. SYOK KARDIOGENIK

Etiologi :
Pasca Bedah Penyakit Jantung Bawaan
Miokarditis
Infark / Iskemik Jantung
Kardiomiopati Primer / Sekunder
Hipoglikemia, Gangguan Metabolik
Asfiksia, Sepsis
 MEKANISME SYOK KARDIOGENIK

Cardiogenik Contractility
Shock

CO Compensatory mech.
Metabolic acidosis, hypoxia,
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
 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
 SYOK SEPTIK
PATOFISIOLOGI SYOK SEPTIK
Sumber infeksi Organisme

Sintesa NO Sel endotel Toksin

Makrofag Sel T PMN

TNF , IL1, IL-2
TH 1 TH 2 PAF Metab.
Asam
INF IL 4
arakidonat
TNF IL 5
IL - 2 IL - 10
Kebocoran kapiler Depresi miokard SVR

SYOK SEPTIK
 SEPSIS DAN GANGGUAN KOAGULASI
Sepsis

Inflammatory cytokines

IL - 6 TNF -

Tissue factor Mediated Inhibition of physiological Depression of

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

Enhanced fibrin formation

Impaired fibrin 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 ( 6 - 7 menit )
KRISTALOID dan atau KOLOID
10 30 ml / kg B.B ( < 20 menit )

diulang 2 3 kali
SYOK SEPTIK 60 120 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
 ( SYOK KARDIOGENIK ) :
Fluid Chalenge hati hati :
a. memperbaiki kontraktilitas jantung
b. dipantau ketat dengan TVS
 Algoritme Terapi Cairan Pada Syok
Suspected shock
Hypovolemia, Hypoperfusion, Tachycardia

10 30 mL X.tal / kg / 6 10 min Hypotensive

Normotensive In Sepsis : In Anaphylaksis :

Antibiotics, Catekolamin, 10-20 mL
Imunotheraphy steroid, X.tal/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 1020 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
 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) -
 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 exxesive, 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
 TERAPI ANTIINFLAMASI PADA SYOK

1. KORTIKOSTEROID
Pada syok septik, bila ada INSUFISIENSI
ADRENAL : Hydrocortisone 12,5 mg/m2/hari
(dosis fisiologis) atau 50 100 mg/m2/hari
(dosis untuk stress).
2. CHLOROQUIN dan METACLOFORAMIDE
Merubah respons inflamasi pada syok septik.
 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 A
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
 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
Trombositopeni berat < 30.000 dengan pendarahan :
- 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 dan
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
- Doparmin dosis rendah (0,5 4 g/kg B.B/menit)
 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