PELATIHAN RESUSITASI

PEDIATRIK TAHAP LANJUT

SYOK
KOMISI RESUSITASI PEDIATRIK
UKK PEDIATRI GAWAT DARURAT IDAI

APRC

DEFINISI SYOK

SINDROM KLINIS AKIBAT KEGAGALAN SISTEM

SIRKULASI UNTUK MENCUKUPI :

NUTRISI
PASOKAN
METABOLISME
OKSIGEN UTILISASI JARINGAN TUBUH

FASE:
KOMPENSASI
DEKOMPENSASI
IREVERSIBEL
DEFISIENSI O2 SELULER

Etiologi Syok
Type
Hypovolemic
Distributive

Primary Insult
Decreased circulating
blood vol
Vasodilation -> venous
pooling -> decreased preload

Obstructive

Obstruction of cardiac
filling/out flow

Cardiogenic

Decreased contractility

Dissociative

O2 not released from

hemoglobin

Common Causes
Dehydration, hemorrhage,
capilarry leaks
Sepsis, anaphylaxis,
drug intoxication,
spinal cord injury
Cardiac tamponade, tension
pneumothoracx, pulmonary
embolus
Congenital heart disease,
myocarditis, dysritmia
CO poisoning,
methemoglobinemia

STADIUM SYOK

KOMPENSASI

DEKOMPENSASI

IREVERSIBEL (PRETERMINAL)

PERJALANAN KLINIS BERSIFAT PROGRESIF

FASE I: KOMPENSASI

KOMPENSASI TEMPORER

SIMPATIS, TEKANAN NADI

DISTRIBUSI SELEKTIF ALIRAN DARAH

RETENSI NA & AIR

KLINIS :

* TAKHIKARDIA
* GADUH GELISAH
* KULIT PUCAT DINGIN
* A.DORSALIS PEDIS TERABA LEMBUT

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 DARAH

TAKIPNU
PERFUSI PERIFER
ASIDOSIS (+)
OLIGURI (+)
TINGKAT KESADARAN A.DORSALIS PEDIS TAK TERABA

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

Manifestasi Klinis Syok Hipovolemik

Clinical Signs

Compensated Uncompensated

Blood loss (%) Up to 25

25 - 40 > 40

Heart rate

Tachycardia +

Tachycardia ++

Systolic BP

Plummeting

N or falling

Pulse volume N/
Capillary refill
Skin

N/

Tachy/bradycardia

++

+ ++

Cool, pale Cold, mottled

Cold, deathly pale

Respiratory rate Tachypnoea + Tachypnoea ++

Mental state

Irreversible

Sighing rsp.

Mild agitation Lethargic Reacts only to pain

Uncooperative or unresponsive

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

TATALAKSANA RESUSITASI
SYOK AWAL
RESUSITASI

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

Monitoring

State of consiousness
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
Pulse oximetry

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

PEMANTAUAN LANJUT

CARI PENYEBAB SYOK

EVALUASI FUNGSI SIST. ORGAN LAIN :

ATN/PRE RENAL FAILURE

ARDS
CARDIAC FUNCTION
GGN. KOAGULASI/DIC
ORGAN-ORGAN LAIN

CHILD IN SHOCK

(1) OXYGEN

(2) CRYSTALLOID
20 ml/kg)

IMPROVEMENT

NO IMPROVEMENT

NO IMPROVEMENT

URINARY CATHETER

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

ESTABLISH CVP

CVP < 5 Torr

CRYSTALLOID INFUSION
UNTIL CVP - 5 Torr

IMPROVEMENT

ESTABLISH ETIOLOGY
CONFIRM SOURCE
OF FLUID LOSS

ESTABLISH ETIOLOGY,
ETIOLOGY,
OBSERVATION
CVP > 5 Torr
1. CORRECT
ACIDOSIS

NO IMPROVEMENT

2. Co. GLUCOSE

ABG, HT, NaK, GLUC Ca,

SWAN GANZ CATHETER

3. INTROPIC
SUPPORT

STROKE VOLUME

CENTRAL VENOUS PRESSURE

Stadium syok septik dan manifestasi klinis

Stadium Tanda Klinis Gang fisiologis

Biokimiawi

Warm Shock perfusi perifer (N) Smv O2 hipokarbia

(Hiperdinamik) kulit hangat kering
VO2 hopoxia
HR nadi bounding CO kadar laktat
suhu / (tak stabil) SVR hiperglikemia
RR , gg. kesadaran
Cold Shock sianosis CO hipoxia
(Hipodinamik)
kulit dingin lembab
SVR
nadi kecil, lemah CVP koagulopati
HR , Oliguria
Smv O2
hipoglikemi
shallow breathing
pe kesadaran
MOSF bergantung sistem
Koma
GI bleeding/DIC
organ failure

susai

asidosis metab

yang terkena ARDS, CHF, RF jenis

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

TATALAKSANA SYOK ANAFILAKTIK

STOP ALERGEN PENYEBAB + ADRENALIN (IM)

AIR WAY & RESPIRATION ADEKUAT

SIRKULASI & HEMODINAMIK

WHEEZING NEBULASI ADRENALIN/SALBUTAMOL

OBSTRUKSI INTUBASI/SURGICAL AIRWAY
VASO PRESOR
FLUID LOADING

: ADRENALIN (10 g/kg BB)

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

RE ASSESSMENT ABC RESUSITASI

WHEEZING (+)
NEBULASI SALBUTAMOL
BILA PERLU
(+) HIDROKORTISON (IV)
(+) AMINOPILIN/SALBUTAMOL DRIP
SYOK BERLANJUT :
KOLOID + INOTROPIK

TATALAKSANA SYOK
KARDIOGENIK
OKSIGENISASI ADEKUAT

KOREKSI GGN ASAM BASA & ELEKTROLIT

KURANGI RASA SAKIT & ANSIETAS

ATASI DISRITMIA JANTUNG

KELEBIHAN PRELOAD : DIURETIKA

KONTRAKTILITAS:

FLUID CHALLENGE SESUAI

CVP/POAP
OBAT INOTROPIK (+)

BEBAN AFTERLOAD (SVR ) : VASODILATOR

KOREKSI PENYEBAB PRIMER

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
appropriately