PENATALAKSANAAN SYOK PADA ANAK

Moh. Supriatna TS

PENDAHULUAN

SINDROM KLINISKEGAGALAN 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 :

NutrisiOksigen

Pasokanutilisasi

Metabolisme Jaringan tubuh

Defisiensi 02 Seluler

FUNGSI SISTEM SIRKULASI

Jantung Pembuluh

Darah Volume

Darah

Curah jantung & adekuatAliran 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

KLASIFIKASI SYOK MENURUT ETIOLOGI

SYOK HIPOVOLEMIK SYOK DISTRIBUTIF SYOK KARDIOGENIK SYOK SEPTIK SYOK OBSTRUKTIF

PENGANGKUTAN OKSIGEN

Cardiac Out Put Blood flow

OxygenDelivery

Blood O2 Content

Hb Contentration

O2 Bound to Hb

O2 Dissolved in Plasma

STADIUM SYOKFASE 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 TrombositPembentukan Trombus

PendarahanPelepasan 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

Kesadaran AnuriaGMO

klinis

PERJALANAN PATOFISIOLOGIS DARI SYOK

Septic Shock

Cardiogenic ShockHypovolemic

ShockCapilary Leak

Mediators

Myocardial Depression

Preload Vasodilatation

Contractility

Cardiac Output Blood Pressure

Sympathetic Discharge

Vasoconstriction,

HR Contractility

Improved Cardiac output and blood pressure

COMPENSATED

UNCOMPENSATED

Myocardial perfusion Myocardial O2

Consumption

Cardiac Output

Mediator Release

Cell Function

Cell Death Death of Organism

Tissue Ischemia

Loss of Autoregulation

of Mycrocirculation

COMPENSATED

Vasoconstriction HR Contractility

DIAGNOSIS SYOK

1. Riwayat Penyakit2. 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 HipovolemiShunting Vaskuler Relatif

( a dan b ) Hipotensi Berat

ETIOLOGI SYOK DISTRIBUTIFPenyebab 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 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 Jantungb. Preload dan Afterloadc. 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 SEPTIKPATOFISIOLOGI SYOK SEPTIK

Sumber infeksi

Organisme

Sintesa NO Sel endotel Toksin

Makrofag

TNF , IL–1, IL-2

Sel T PMN

TH 1

INF

TNF

IL - 2

TH 2

IL – 4

IL – 5

IL - 10

PAF Metab. Asam arakidonat

Kebocoran kapiler

Depresi miokard

SVR

SYOK SEPTIK

SEPSIS DAN GANGGUAN KOAGULASI

Sepsis

Inflammatory cytokines

IL - 6 TNF -

Tissue factor Mediated activation

of coagulation

Inhibition of physiological anticoagulant

pathways

Depression of

fibrinolysis due to high levels of PAI

- 1Enhanced fibrin formation Impaired fibrin

removal

Microvascular thrombosis

CYTOKINE-MEDIATED PATHOGENETIC PATHWAYS of MICROVASCULAR THROMBOSIS

in SEPSIS

Sepsis

Activation of coagulation

Widespread fibrin

Deposition

Consumption of 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(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

1. 2.

Oksigenasi

CaO2 SaO2 95 – 100 %

Sistem K.V

a. Preload ( resusitasi volume )

b. Atasi Disritmiac. Koreksi keseimbangan

asam - basaJalan 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 / kristaloidb. Dipandu : respons klinis,perfusi, perifes, tvs, tekanan sistem,MAP

( SYOK KARDIOGENIK ) : Fluid Chalenge hati – hati :

a. memperbaiki kontraktilitas jantungb. dipantau ketat dengan TVS

Algoritme Terapi Cairan Pada Syok

Suspected shock

Hypovolemia, Hypoperfusion, Tachycardia

10 – 30 mL X.tal / kg / 6 – 10 min

Normotensive

Hypotensive

In Sepsis :

Antibiotics, Imunotheraphy

In Anaphylaksis :

Catekolamin, steroid, antihistamin

Urine > 1 ml/kg/hr

10-20 mL X.tal/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

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 (

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 exxesive, 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

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

TERAPI ANTIINFLAMASI PADA SYOK

1. KORTIKOSTEROIDPada 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 METACLOFORAMIDEMerubah respons inflamasi pada syok septik.

MONITORING

• State of Consiousness-Glasgow Coma Scale• Respiratory Rate and Character• Cardiovascular Parameters :

a. Skin and Core Temperature Differenceb. Pulse Rate and Volumec. Blood Pressured. Capillary Perfusion Timee. 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 ORGANA. 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 intravaskularb. COc. 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 volume2. Me kontraktilitas jantung dan 3. Me SVR

• Dengan pemahaman patofisiologi, diagnosis dini dan memperhatikan “ key management “ syok, diharapkan dapat me mortalitas syok