Syok Pada Anak

PELATIHAN RESUSITASI PEDIATRIK TAHAP LANJUT

SYOK KOMISI RESUSITASI PEDIATRIK UKK PEDIATRI GAWAT DARURAT IDAI

APRC

1

DEFINISI SYOK   SINDROM KLINIS AKIBAT KEGAGALAN SISTEM SIRKULASI UNTUK MENCUKUPI :    NUTRISI PASOKAN METABOLISME  OKSIGEN UTILISASI JARINGAN TUBUH   FASE:

KOMPENSASI DEKOMPENSASI IREVERSIBEL

SELULER

DEFISIENSI O2

2

Etiologi Syok Type Primary Insult Common Causes Hypovolemic Decreased circulating Dehydration, hemorrhage, blood vol capilarry leaks Distributive Vasodilation -> venous Sepsis, anaphylaxis, pooling -> decreased preload drug intoxication, spinal cord injury Obstructive Obstruction of cardiac Cardiac tamponade, tension filling/out flow pneumothoracx, pulmonary embolus Cardiogenic Decreased contractility Congenital heart

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FUNGSI SISTEM SIRKULASI   

JANTUNG METABOLISME



PEMB. DARAH JARINGAN

ALIRAN DARAH



VOL. DARAH

O2 DELIVERY

CURAH JANTUNG

ADEKUAT

  METABOLIT

2 = CO x CaO2 O2   = (1,34 x Hb x sat O2) + (0,003 x PaO2) 4

Pengaturan curah jantung dan tekanan darah Preload Afterload    

Contractility

Heart rate

Stroke volume

    Cardiac output

Systemic vascular resistance

  Blood pressure

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6

Distribution of CO & VO2 in a Healthy Resting Normal Subject % Total Organ CO GI tract and liver 24 Skeletal muscle 21 Kidney 19 Brain 13 Skin 9 Heart 4 Other organs 10

AVDO2 vol % 4.1 8.0 1.3 6.3 1.0 11.4 3.0

% Total VO2 25 30 7 20 2 11 5 7

Adapted from Wade OL, Bishop JM: Cardiac output and regional blood flow, Oxford, Blackwell, 1962

Extracel. Fluid Volume

Intra vasc. Vol. due to

Low Output Cardiac Failure

Oncotic Pressure Capillary Permeability

Pericardial Tamponade Constrictive Pericarditis

  CARDIAC OUTPUT

 

Activation receptor of ventricular & arterial

Non-osmotic Stimulation of Activation of the Vasopressin Sympathetic Nervous Renin-AngiotensinStimulation System Aldosterone System

RENAL WATER RENAL SODIUM

PERIPHERAL & RENAL

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FRANK STARLING`S LAW 5

4

STROKE VOLUME

SYMPATHOMIMETIC AMINES

POSITIVE INOTROPY

XANTHINES GLUCAGON

D 3

C B

2

1

CARDIAC GLYCOSIDES

NEGATIVE INOTROPY

HYPOXEMIA ACIDOSIS

A

HYPOGLYCEMIA

VOLUME INFUSION 0

ENDOTOXEMIA 5

10

CENTRAL VENOUS PRESSURE (Toor)

DRUG TOXICITY

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Oxyhemoglobin saturation

The Oxygen-hemoglobin Dissociation Curve

H+ 2,3-DPG CO2 Pi H+ 2,3-DPG CO2 Pi

PaO2

10

Shock Hypotension  Preload

Cellular hypoxia  Intravasculer volume  Myocardial contractility Anaerobic metabolism  Membrane permeability

products:

depressant factor

Metabolic by- lactic acid - myocardial

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STADIUM SYOK 

KOMPENSASI



DEKOMPENSASI



IREVERSIBEL (PRETERMINAL)

PERJALANAN KLINIS BERSIFAT PROGRESIF

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FASE I: KOMPENSASI 

KOMPENSASI TEMPORER



 SIMPATIS,  SVR,  TEKANAN NADI



DISTRIBUSI SELEKTIF ALIRAN DARAH



 RETENSI NA & AIR



KLINIS :

* TAKHIKARDIA * GADUH GELISAH * KULIT PUCAT DINGIN * PENGISIAN KAPILER >>13

FASE 2: DEKOMPENSASI 

KOMPENSASI MULAI GAGAL



HIPOPERFUSI  HIPOKSIA JAR.  METAB. ANAEROBIK  GGN. METAB. SELULER PELEPASAN MEDIATOR : * VASODILATASI 



PERMEABILITAS  DEPRESI MIOKARD  GGN KOAGULASI  

KLINIS : TAKHIKARDIA 

* * *

TEKANAN DARAH14

FASE 3: IREVERSIBEL 

KOMPENSASI GAGAL



CADANGAN ENERGI TUBUH 



KERUSAKAN/KEMATIAN SEL  DISFUNGSI ORGAN MULTIPEL



KLINIS : * T.D TAK TERUKUR

* NADI TAK TERABA * TINGKAT KESADARAN * ANURIA (+) * GAGAL MULTI ORGAN DAN KEMATIAN 15

Manifestasi Klinis Syok Clinical Signs Irreversible Blood loss (%)

Compensated

Up to 25

25 - 40

Heart rate Tachycardia + Tachy/bradycardia Systolic BP Pulse volume Capillary refill Skin Respiratory rate rsp. Mental state

N N/ 

> 40 Tachycardia ++

N or falling Plummeting +

N/  Cool, pale

Uncompensated

 ++ +

Cold, mottled

Tachypnoea +

 ++ Cold, deathly pale

Tachypnoea ++

Sighing 16

Mild agitation

Lethargic

Reacts only to pain

GANGGUAN PERFUSI PERIFER CORE > PERIFER TEMP. ~ > 2O C  CAPILLARY REFILL >> : 

* NAIL BED PRESS * BLANCHING SKIN TEST 

PRODUKSI URIN  (N) BAYI = 2 ml/kg/jam ANAK = 1 ml/kg/jam

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TATALAKSANA RESUSITASI SYOK

RESUSITASI AWAL  OKSIGEN 100% + VENTILATORY SUPPORT  PASANG AKSES VASKULER (90 DETIK)  FLUID CHALLENGE (20 ml/kg BB)   

SECEPATNYA < 10 MENIT DPT DIULANGI 2-3 KALI KRISTALOID/KOLOID

PEMANTAUAN AWAL  RESPON THD FLUID CHALLENGE  PANTAU PROD. URIN (KATETER)  STAT. LAB/PENUNJANG

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Monitoring   

State of consiousness-Glasgow Coma Scale Respiratory rate and character Cardiovascular parameters     



Skin and core temperature difference Pulse rate and volume Blood pressure Capillary perfusion time 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

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RESUSITASI LANJUT BILA FLUID CHALLENGE NON RESPONSIVE 

INTUBASI & VENT. MEKANIK

PASANG CVP & LOADING HATI-HATI  KOREKSI EFEK INOTROPIK NEGATIF 

Hb < 5 g/dl  PRC 10 ml/kg BB (Ht 40-50 vol %)



OBAT INOTROPIK 20

PEMANTAUAN LANJUT 

CARI PENYEBAB SYOK (CXR, KONSULTASI)



EVALUASI FUNGSI SIST. ORGAN LAIN :     

ATN/PRE RENAL FAILURE ARDS CARDIAC FUNCTION GGN. KOAGULASI/DIC ORGAN-ORGAN LAIN

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CHILD IN SHOCK     (1) OXYGEN

(2) CRYSTALLOID 20 ml/kg)  

IMPROVEMENT

NO IMPROVEMENT

 

  NO IMPROVEMENT

(3) CRYSTALLOID - INCREASE MABP (20 ml/kg) - NORMALIZATION HR - IMPROVED PERFUSION - URINE OUTPUT > 1 ml/kg/hr

URINARY CATHETER   ESTABLISH CVP

IMPROVEMENT   ESTABLISH ETIOLOGY CONFIRM SOURCE OF FLUID LOSS

CVP > 5 Torr 1. CORRECT ACIDOSIS

NO IMPROVEMENT

2. Co. GLUCOSE

ABG, HT, NaK, GLUC Ca, SWAN GANZ CATHETER CO, RAP, PAP, POAP

STROKE VOLUME

  CVP < 5 Torr     CRYSTALLOID INFUSION UNTIL CVP - 5 Torr  

ESTABLISH ETIOLOGY, OBSERVATION

3. INTROPIC SUPPORT

CENTRAL VENOUS PRESSURE

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Stadium syok septik dan manifestasi klinis Stadium

Tanda Klinis

Gang fisiologis Biokimiawi

Warm Shock perfusi perifer (N) O2 hipokarbia (Hiperdinamik) kulit hangat kering hopoxia HR  nadi bounding   suhu / (tak stabil) hiperglikemia RR  , gg. kesadaran

 Smv  VO2  CO kadar laktat  SVR

Cold Shock sianosis  CO hipoxia (Hipodinamik) kulit dingin lembab  SVR asidosis metab nadi kecil, lemah  CVP koagulopati HR  , Oliguria  Smv O2 hipoglikemi shallow breathing 23 pe  kesadaran

TATALAKSANA SYOK SEPTIK 

AB BROAD SPECTRUM

 SESUAI KULTUR

RESUSITASI CAIRAN : KOLOID/KRISTALOID  OBAT INOTROPIK : DOBUTAMIN + DOPAMIN 

ISOPRENALIN/ADRENALIN

 SVR  VASODILATASI PERIFER  KOREKSI : - HIPO/HIPERGLIKEMI 

- ASAM BASA - ELEKTROLIT 24

TATALAKSANA SYOK ANAFILAKTIK  

STOP ALERGEN PENYEBAB + ADRENALIN (IM) AIR WAY & RESPIRATION ADEKUAT 





SIRKULASI & HEMODINAMIK  



WHEEZING  NEBULASI ADRENALIN/SALBUTAMOL OBSTRUKSI  INTUBASI/SURGICAL AIRWAY VASOPRESOR FLUID LOADING

: ADRENALIN (10 µg/kg BB) : KRISTALOID (20 ml/kg BB/IV-IO)

RE ASSESSMENT ABC RESUSITASI 

WHEEZING (+)  NEBULASI SALBUTAMOL BILA PERLU (+) HIDROKORTISON (IV) (+) AMINOPILIN/SALBUTAMOL 25 DRIP

TATALAKSANA SYOK KARDIOGENIK 

OKSIGENASI ADEKUAT



KOREKSI GGN ASAM BASA & ELEKTROLIT



KURANGI RASA SAKIT & ANSIETAS

 

ATASI DISRITMIA JANTUNG KELEBIHAN PRELOAD : DIURETIKA



KONTRAKTILITAS:

FLUID CHALLENGE SESUAI

CVP/POAP

INOTROPIK (+)  

OBAT

 BEBAN AFTERLOAD (SVR ) : VASODILATOR KOREKSI PENYEBAB PRIMER

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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 patient has received adequate fluid therapy Monitor blood glucose, gases, and pH, and treat 27 appropriately

SEQUENCE OF THERAPEUTIC MANEUVERS (VIPPS) Priority Mnemonic Therapy 1 V Ventilate 2

I

Infuse

3

P

Pump

4

P

Pharmacologic

5

S

Specific/ Surgical

Purpose Adequate O2&CO2 exchange Vascular Access Blood, fluid & electrolite balance Restoration cardiac performance Improved perfusion by vasoactive agents Medical & surgical management of 28 primary causes