Penatalaksanaan Syok Pada Anak

SINDROM KLINIS KEGAGALAN SISTEM SIRKULASI

KEBUTUHAN NUTRIEN

OKSIGEN JARINGAN

DEFISIENSI AKUT DITINGKAT SEL

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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

HEART RATE

CARDIAC OUTPUT

CONTRACTILITY

AFTERLOAD

STROKE VOLUME

SYSTEMIC VASCULAR RESISTANCE

BLOOD PRESSURE

KLASIFIKASI SYOK MENURUT ETIOLOGI     

PENGANGKUTAN OKSIGEN

Cardiac Out Put

Hb Contentration

O2 Bound to Hb

O2 Dissolved in Plasma

Blood flow

Oxygen Delivery

Blood O2 Content

STADIUM SYOK FASE I : KOMPENSASI

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Mekanisme Kompensasi Tubuh - Resistensi sistemik - Tekanan darah ( N ) - Tekanan Diastolik - Tekanan Nadi Sempit

refleksi simpatis

FASE II : DEKOMPENSASI -

FASE II : LANJUTAN

FASE III : IREVERSIBEL 

Kerusakan / Kematian Sel  Disfungsi sistem multi organ  Cadangan fostat E. Tinggi ( Hepar, Jantung )

klinis

Tekanan darah tak terukur Nadi tak teraba Kesadaran Anuria GMO

PERJALANAN PATOFISIOLOGIS DARI SYOK Septic Shock

Cardiogenic Shock

Hypovolemic Shock Capilary Leak Preload

Mediators

Myocardial Depression

Vasodilatation Cardiac Output Sympathetic Discharge

Improved Cardiac output and blood pressure COMPENSATED

Vasoconstriction, HR

Contractility

Contractility Blood Pressure

Vasoconstriction HR Contractility COMPENSATED UNCOMPENSATED Myocardial perfusion Myocardial O2 Consumption Cardiac Output

Tissue Ischemia

Mediator Release Cell Function Cell Death

Loss of Autoregulation of Mycrocirculation 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 Abnormal

Maldistribusi Vol. Sirkulasi Syok

b. Pooling Perifer Shunting Vaskuler ( a dan b )

Hipovolemi Relatif

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  Shock 

Metabolic acidosis, hypoxia, Myocardial depressant factor

Contractility

CO BP

Compensatory mech.  Afterload SVR

SYOK KARDIOGENIK • •

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TATALAKSANA SYOK KARDIOGENIK • • • • • •

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SYOK SEPTIK PATOFISIOLOGI SYOK SEPTIK Sumber infeksi Sintesa NO

Organisme Sel endotel

Makrofag

Toksin

Sel T

PMN

TNF , IL–1, IL-2

Kebocoran kapiler

TH 1

TH 2

INF

IL

–

4

TNF

IL

–

5

IL - 2

IL - 10

Depresi miokard

SYOK SEPTIK

PAF

Metab. Asam arakidonat

SVR

SEPSIS DAN GANGGUAN KOAGULASI

CYTOKINE-MEDIATED PATHOGENETIC PATHWAYS of  MICROVASCULAR THROMBOSIS in SEPSIS

MANIFESTASI KLINIS SYOK SEPTIK 

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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. Enterobacteriaceae Staph. Aureus Listeria meningtides

Ampiciline + Gentamicin Cefotaxime

50 2.5 5-0

1 24 months

H. influenzae, Strept. Pneumoniae S. aureus, Neisseria meningtidis Group B Streptococcus

Cefotaxime Ampiciline + Chlorampenicol

50 50 25

> 24 months

S. Pneumoniae H. Influenzae S. Aureus N. Meningtidis

Cefotaxime Cefriaxone Ampiciline + Chlorampenicol

50 50 50 25

Immuno compromised

S. aureus, Proteus Pseudomonas Enterobacteriaceae

Vancomycin + Ceftazidime + Ticarcillin

25 50 75

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PENATALAKSANAAN SYOK

1.

2.

Sistem K.V

Oksigenasi

CaO2 SaO2 95 – 100 %

Jalan nafas Oksigen

Anxietas

a. Preload ( resusitasi volume ) b. Atasi Disritmia c. Koreksi keseimbangan asam - basa

TERAPI CAIRAN PADA SYOK  

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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

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( 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 Normotensive

–

30 mL X.tal / kg / 6

–

10 min

Hypotensive

In Sepsis :

In Anaphylaksis :

Antibiotics, Imunotheraphy

Catekolamin, steroid, antihistamin

Urine > 1 ml/kg/hr

Urine < 1 ml/kg/hr

10-20 mL X.tal/kg/10 min 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

10-20 mL X.tal/kg

Reevaluated

CVP, Cardiac status, chest X-Ray, Echocardiography

CVP > 10 mmHg

Afterload reduction, 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 ( ug/kg/min )

Comment

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

 Inotropioc agents Norephrine ( - adrenergic )

(

Commonly Used Cardiovascular …(lanjutan)

Drug

(

Dose ( ug/kg/min )

Comment

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

Dobutamine - and - adrenergic )

TERAPI ANTIINFLAMASI PADA SYOK 1.

2.

KORTIKOSTEROID Pada syok septik, bila ada INSUFISIENSI ADRENAL : Hydrocortisone 12,5 mg/m 2/hari (dosis fisiologis) atau 50  –  100 mg/m2/hari (dosis untuk stress). CHLOROQUIN dan METACLOFORAMIDE Merubah respons inflamasi pada syok septik.

MONITORING • • •

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TERAPI SUPORTIF 

Substitusi faktor koagulasi (pada Hemodilusi / PIM) : - Fresh Frozen Plasma - Cyroprecipitate

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Tranfusi Masif  FFP

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Fibrinogen < 100 mg/dl (tak respons terhadap FFP) : - Cyro precipitate 4 unit/10 kg BB

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Trombositopeni berat < 30.000 dengan pendarahan : - Konsentrat Trombosit

setiap 5  –  6 unit PC ditambah 2 unit

IMUNOTERAPI •

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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

FUNGSI ORGAN (lanjutan)

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 •

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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

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