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Syok pada Anak

Syok pada Anak

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Published by: Taufik Abidin on Mar 07, 2009
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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

3

FUNGSI SISTEM SIRKULASI
 

JANTUNG METABOLISME PEMB. DARAH JARINGAN VOL. DARAH

CURAH JANTUNG ALIRAN DARAH O2 DELIVERY

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         Cardiac output   Blood pressure
5

Contractility

Heart rate

Stroke volume

Systemic vascular resistance

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 Pericardial Tamponade Constrictive Pericarditis

Oncotic Pressure Capillary Permeability

  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

8

FRANK STARLING`S LAW
5

4

POSITIVE INOTROPY D

SYMPATHOMIMETIC AMINES XANTHINES GLUCAGON CARDIAC GLYCOSIDES

STROKE VOLUME

3

C B NEGATIVE INOTROPY A
VOLUME INFUSION
0 5 10

2

HYPOXEMIA ACIDOSIS HYPOGLYCEMIA ENDOTOXEMIA DRUG TOXICITY
9

1

CENTRAL VENOUS PRESSURE (Toor)

The Oxygen-hemoglobin Dissociation Curve
Oxyhemoglobin saturation

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 Metabolic by- lactic acid - myocardial

products:

depressant factor

11

STADIUM SYOK
  

KOMPENSASI DEKOMPENSASI IREVERSIBEL (PRETERMINAL)

PERJALANAN KLINIS BERSIFAT PROGRESIF

12

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 Uncompensated

Up to 25

25 - 40

> 40 Tachycardia ++

Heart rate Tachycardia + Tachy/bradycardia Systolic BP Pulse volume Capillary refill Skin Respiratory rate rsp. Mental state N N/  N/  Cool, pale Tachypnoea + Mild agitation +

N or falling Plummeting  ++ + Cold, mottled  ++ Cold, deathly pale Sighing
16

Tachypnoea ++

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

17

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

TATALAKSANA RESUSITASI SYOK

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

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

18

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

19

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

21

CHILD IN SHOCK     (1) OXYGEN (2) CRYSTALLOID 20 ml/kg)   NO IMPROVEMENT   NO IMPROVEMENT (3) CRYSTALLOID - INCREASE MABP (20 ml/kg) - NORMALIZATION HR - IMPROVED PERFUSION - URINE OUTPUT > 1 ml/kg/hr IMPROVEMENT  

URINARY CATHETER   ESTABLISH CVP   CVP < 5 Torr     CRYSTALLOID INFUSION UNTIL CVP - 5 Torr   IMPROVEMENT   ESTABLISH ETIOLOGY CONFIRM SOURCE OF FLUID LOSS CVP > 5 Torr NO IMPROVEMENT
1. CORRECT ACIDOSIS 2. Co. GLUCOSE
STROKE VOLUME

ESTABLISH ETIOLOGY, OBSERVATION

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

3. INTROPIC SUPPORT

CENTRAL VENOUS PRESSURE

22

Stadium syok septik dan manifestasi klinis
Stadium Tanda Klinis Gang fisiologis Biokimiawi  Smv  VO2  CO kadar laktat  SVR

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

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
 

WHEEZING  NEBULASI ADRENALIN/SALBUTAMOL OBSTRUKSI  INTUBASI/SURGICAL AIRWAY VASOPRESOR FLUID LOADING : ADRENALIN (10 µg/kg BB) : KRISTALOID (20 ml/kg BB/IV-IO)

SIRKULASI & HEMODINAMIK
 

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:
CVP/POAP INOTROPIK (+) FLUID CHALLENGE SESUAI OBAT

 

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

26

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 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

3 4 5

P P S

Pump Pharmacologic Specific/ Surgical

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