llND\H|l|\N

SINDROM KLINIS
KEGAGALAN SISTEM SIRKULASI
KEBUTUHAN OKSIGEN
NUTRIEN JARINGAN
DEFISIENSI AKUT
DITINGKAT SEL
: SYO| l\D\ \N\|
|cuduun uu! dururu!

/ mcrb!d!!us mcr!u!!!us
% 8O h!pcvc!cm!k
/ . Svck kcmpcnsus! su!!! d! D c k
mun!cs!us! k!!n!s !uk ]c!us
( rc!cks s!mpu!!s Rcd!s!r!bus!
. sc!ck!! u! ducruh dur! crun
pcr!cr ncn- , , v!!u! kc ]un!un puru
) c!uk
: Tu]uun lr!mcr lcnc!c!uun Svck

- ( ) lrc!cud rcsus!!us! vc!umc

- |cn!ruk!!!!!us

- Rcs!s!cns! pudu s!s!cm!k

DllTNTST SYO|
DllTNTST SYO|

STNDROM |lTNTS \|Tl\T |lG\G\l\N STSTlM
: STR||l\ST |NT|| MlNC|||lT

v
Nutrisi
vOksigen
Pasokan
utilisasi
Metabolisme
Jaringan tubuh
Defisiensi 02 Seluler
l|NGST STSTlM STR||l\ST
l|NGST STSTlM STR||l\ST

Jantung
Pembuluh Darah
Volume Darah

Curah jantung
&
adekuat
Aliran darah
Metabolisme
jaringan
Metab
olit
Eliminasi Di Organ
Pembuangan
llNG\T|R\N C|R\H J\NT|NG
llNG\T|R\N C|R\H J\NT|NG
D\N Tl|\N\N D\R\H
D\N Tl|\N\N D\R\H
PRELOAD CONTRACTILITY AFTERLOAD
HEART RATE STROKE VOLUME
CARDIAC OUTPUT SYSTEMIC VASCULAR RESISTANCE
BLOOD PRESSURE
llNG\NG||T\N O|STGlN
llNG\NG||T\N O|STGlN
Cardiac Out Put Blood flow
Oxygen
Delivery
Blood O
2
Content
Hb Contentration
O
2
Bound to Hb
O
2
Dissolved in Plasma
|l\STlT|\ST SYO|
|l\STlT|\ST SYO|
MlN|R|T lTTOlOGT
MlN|R|T lTTOlOGT
v SYO| HTlO\OllMT|
v SYO| DTSTRTl|TTl
v SYO| |\RDTOGlNT|
v SYO| SllTT|
v SYO| OlSTR||TTl
ST\DT|M SYO|
ST\DT|M SYO|
: l\Sl T |OMllNS\ST
: l\Sl T |OMllNS\ST
Mckun!smc |cmpcnsus! Tubuh rc!cks!
s!mpu!!s

- Rcs!s!cns! s!s!cm!k

: ; , , HR ku!!! d!n!n pucu!

. , , cup rc!!! !cr!umbu! nud! !cmuh
. !ck nud! scmp!!

( ) Tckunun duruh N

- Tckunun D!us!c!!k

- Rcs!s!cns! pcmbu!uh duruh

: ( <), sp!unkn!k G!n]u! D!urcs!s Su!urun
( , ) ccrnu mun!uh !!cus

: ( ) l\Sl TT Dl|OMllNS\ST !
: ( ) l\Sl TT Dl|OMllNS\ST !
- Mckun!smc kcmpcnsus! uu!
- Mc!ubc!!smc unucrcb!k
- \sum !uk!u! us!dcs!s >>
!crbcn!uk usum kurbcnu!
!n!rusc!u!cr
- |cn!ruk!!!!!us c!c! ]un!un
- lcmpu Nu | sc!

Tn!cr!!us mcmbrun sc!

|crusukun sc!
: ( ) l\Sl TT Dl|OMllNS\ST ?
: ( ) l\Sl TT Dl|OMllNS\ST ?
\!!run duruh !umbu!

\rcus! Trcmbcs!!
lcmbcn!ukun Trcmbus
lcnduruhun
lc!cpusun Mcd!u!cr

\uscd!!u!us! \r!cr!u!

|cnu!kun lcrmcub!!!!us |up!!cr

\R
Fase dekompensasi
Perfusi jaringan indekuat disertai hipotensi

Kesadaran menurun krn perfusi ke otak

menurun

Hipotensi sebagai tanda terakhir dari syok

Untuk anak 1-10
th
: <70 mmHg +(umur/thn
x 2) mmHg
: l\Sl TTT TRl\lRSTlll
Kerusakan / Kematian Sel
Disfungsi sistem multi organ
Cadangan fostat E. Tinggi

( Hepar, Jantung )

Tckunun duruh !uk

!crukur

Nud! !uk !crubu

|csudurun

Anuria

GMO
klinis
llRJ\l\N\N l\TOlTSTOlOGT SYO|
llRJ\l\N\N l\TOlTSTOlOGT SYO|
Septic Shock Cardiogenic Shock
Hypovolemic Shock
Capillary Leak Mediators
Myocardial
Depression
Preload Vasodilatation Contractility
Cardiac Output
Blood Pressure
Sympathetic Discharge
Vasoconstriction,
HR Contractility
Improved Cardiac
output and blood
pressure
COMPENSATED
DECOMPENSATED
Myocardial perfusion
Myocardial O
2

Consumption
Cardiac
Output
Mediator Release
Cell Function
Cell Death Death of Organism
Tissue Ischemia
Loss of Auto
regulation of
Microcirculation
COMPENSATED
Vasoconstriction
HR Contractility
Syok Hipovolemik
Etiologi: Diare, perdarahan, muntah, intake
tak adekuat, diuresis osmotik, luka bakar

HYPO
VOL
SHOCK
PRELOAD
AFTERLOAD
CONTRACTILITY
N /
Syok hipovolemik

Primary Assessment: Finding

A

B Takhipneu tanpa pe WOB

C Takhikardi

Tek.Drh N/ hipotensi dgn

tek.nadi sempit

Nadi lemah,kecil /tak teraba

Pengisian kapiler lambat

kulit dingin,pucat

Kesadaran menurun

Oliguria

D Kesadaran menurun

Distributive Shock
Distributiv
e
shock
PRELOAD
N /
CONTRACTILITY
N /
AFTERLOAD
Variable
Findings of Distributive Shock
Primary Assessment Finding
A Patent airway, unless unconc.
B Tachypnea without WOB, except
caused by pneumonia, ARDS, pulm edema
C Tachycardia, Hypotension with wide
pulse pressure(warm shock) or narrow p.pressure(cold
shock) or normotension; Bounding perpheral pulse,
Delayed cap.refill, Warm&flush skin(warm shock) or
pale skin(cold shock): Changes in mental status;
oliguria
D Changes in mental status

Septic Shock
PRELOAD

CONTRACT
I-
LITY / N
AFTERLOAD
VARIABLE
Consensus Definitions and clinical
Characteristic of Ped.Sepsis
Systemic Inflammatory Response
Syndrome ( SIRS )
Sepsis
Severe Sepsis
Septic shock
SIRS
Core temp of >38.5C or <36C
Tachycardia >2SD above normal for age,
for chhildren <1 year bradycardia <10
th

percentile for age
Mean RR>2SD above normal for age
Leucocyte count or for age or 10%
immature neutrophils
( At least 2 of the 4 criteria )
SEPSIS :

SIRS in the presence of, or as a result of,

suspected or proven infection
Severe sepsis
Sepsis plus either cardiovascular
dysfunction or ARDS

Or
Sepsis plus 2 or more other organ failures
RF as sign of organ dysfunction
in sepsis
PaO2/FiO2 <300 in absence of CHD or
lung disease
PaCO2 >65 mmHg or 20 mmHg above
baseline
Proven need FiO2 >50% to maintain SaO2
>92%
Need nonelective MV (invasive or
noninvasive)
Septic shock
Sepsis and

Cardiovascular dysfunction despite

administration of isotonic iv boluses > 40
ml/kg in 1 hour
Cardiovascular dysfunction
Hypotension (SBP <5
th
percentile for age or SBP
<2SD below normal for age or

Need for vasoactive drug to maintain BP in

normal range or

Two of the following characteristic of inadequate

organ perfusion:

Inadequate organ perfusion

Unexplained metabolic acidosis: base
deficit < 5meq/l
Increase arterial lactate > twice the upper
limit of normal
Oliguria: Urine output0.5 ml/kg/hour
Prolonged cap refill: > 5 second
Cor to peripheral temp gap > 3C
SEPTIC
SHOCK
PRELOAD
DECREASE
CONTRACTILITY
N / DECREASED
AFTERLOAD
VARIABLE
. TTT SYO| |\RDTOGlNT|
. TTT SYO| |\RDTOGlNT|

: l!!c!c!
luscu lcduh lcnvuk!! Jun!un luuun
M!ckurd!!!s
/ Tnurk Tskcm!k Jun!un
/ |urd!cm!cpu!! lr!mcr Sckundcr
, H!pc!!kcm!u Gunuun Mc!ubc!!k
, \s!ks!u Scps!s
CARDIOGENI
C
SHOCK
PRELOAD
VARIABLE
CONTRACTILITY
DECREASED
AFTERLOAD
INCREASED
Ml|\NTSMl SYO| |\RDTOGlNT|
Ml|\NTSMl SYO| |\RDTOGlNT|
Cardiogenic
Shock
Contractility
CO
BP
Metabolic acidosis, hypoxia,
Myocardial depressant factor
Compensatory mech.
Afterload
SVR
SYO| |\RDTOGlNT|
SYO| |\RDTOGlNT|
Curd!uc \cn!r!cu!ur lcrcrmuncc
: luc!cr Dc!crm!nun!

. u lrckucns! dun Trumu Jun!un

. b lrc!cud dun \!cr!cud

. c |cn!ruk!!!!!us M!ckurd
|cmpcnsus! Tubuh Sc! lcrpc!uu!!n
Cvc!c

Svck lrcrcs!
Mcmburuk
Findings of Cardiogenic Shock
Primary Assessment Finding
A
B Tachypnea; WOB
C Tachycardia; N/low BP with
a narrow pulse pressure; weak or absent of
peripheral pulse; N and then weak central
pulses;Delayed cap refill with cool extremities;
Signs of CHF; cyanosis(CHD/pulm.edema);
End-organ Function ( Cold, pale skin, oliguria)
D Changes of mental status

Obstructive Shock
Cardiac tamponade
Tension pneumothorax
Ductal dependent congenital heart lesions
Massive pulmonary embolism
Cardiac tamponade
Muffled or diminished heart sound
Pulsus paradoxus(decrease in systolic BP
by more than 10 mmHg during
inspiration
Distended neck vein
Note: Children following cardiac
surgery, D/ ndistinguishable from
cardiogenic shock, Echo: important
Tension pneumothorax
Patients with chest trauma, or any intubated child
who deteorates suddenly during PPV
Hyperresonance on the affected side
Diminished breath sounds on the affected side
Distended neck vein
Tracheal deviation towards contralateral side
Rapid deteoration in perfusion and rapi change
from tachycardia to bradicardia
Pathogenesis and Pathophysiology of Sepsis
New Concept about SIRS, SEPSIS, CARS, MARS
Pro-
inflammatory
response
Anti-
inflammatory
response
Systemic Reaction:
SIRS (pro-
inflammatory)
CARS (anti-
inflammatory)
MARS (mixed)
Systemic spillover of
pro-inflammatory
mediators
Systemic spillover of
anti-inflammatory
mediators
Initial insult
(bacteria, viral, traumatic, thc, mal)
Cardiovascular
Compromise
shock,
SIRS pre-
dominates
Homeostasis
CARS and
SIRS
balanced
Apoptosis
(cell death)
Death with
minimal
inflammation
Organ
dysfunction
SIRS
Pre-
dominated
Suppression
of the
immune
system
CARS
pre-
dominated
SllSTS D\N G\NGG|\N |O\G|l\ST SllSTS D\N G\NGG|\N |O\G|l\ST
Scps!s
Tn!ummu!crv
cv!ck!ncs
- Tl G - TNl
T!ssuc uc!cr
Mcd!u!cd
uc!!vu!!cn c
ccuu!u!!cn
Tnh!b!!!cn c
phvs!c!c!cu!
un!!ccuu!un!
pu!huvs
Dcprcss!cn
c
!br!nc!vs!s
duc !c h!h
!cvc!s c
- l\T !
lnhunccd !br!n
crmu!!cn
Tmpu!rcd !br!n
rcmcvu!
M!crcvuscu!ur
!hrcmbcs!s
- CYTO|TNl MlDT\TlD l\THOGlNlTTC - CYTO|TNl MlDT\TlD l\THOGlNlTTC
l\TH"\YS c MTCRO\\SC|l\R THROMlOSTS l\TH"\YS c MTCRO\\SC|l\R THROMlOSTS
!n SllSTS !n SllSTS
Scps!s
\c!!vu!!cn c
ccuu!u!!cn
"!dcsprcud
!br!n
Dcpcs!!!cn
Ccnsump!!cn
c p!u!c!c!s
und c!c!!!n
uc!cr
M!crcvuscu!ur
!hrcmbcs!s
l!ccd!n
( ) scvcrc
M\NTllST\ST |lTNTS SYO| SllTT|
M\NTllST\ST |lTNTS SYO| SllTT|
v STADIUM KOMPENSASI

- Resistensi Vaskuler

- Curah Jantung

- Takhikardia

- Ekstermitas Hangat

- Divresis Normal
v STADIUM DEKOMPENSASI

- Volume Intravaskuler

- Depresi Miokard

- Eksternal Dingin

- Gelisah, Anuria, Distres Respirasi

- Resistensi Vaskuler

- Curah Jantung
v STADIUM IREVERSIBEL

- GMO

Mcs! Ccmmcn lu!hccns !n Ch!!dhccd luc!cr!u! Mcs! Ccmmcn lu!hccns !n Ch!!dhccd luc!cr!u!
Scps!s Scps!s
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
llN\T\l\|S\N\\N SYO|
llN\T\l\|S\N\\N SYO|

1. 2.
Oksigenasi
CaO
2

SaO
2
95 100 %
Sistem
K.V
a.Preload
( resusitasi volume )
b.Atasi Disritmia
c.Koreksi keseimbangan
asam - basa
Jalan nafas Oksigen

TlR\lT C\TR\N l\D\ SYO|
TlR\lT C\TR\N l\D\ SYO|

AKSES VENA (90 detik); Tak berhasil IO

KRISTALOID dan atau KOLOID

10 30 ml / kg B.B (6-10 menit)

diulang 2 3 kali

SYOK SEPTIK 60 100 ml / kg B.B

(dalam 6 jam pertama)

THE 1
st
CONSENSUS CONFERENCE

on CCM 1997

(SYOK SEPTIK)

a. Koloid terapi inisial, dilanjutkan

koloid/kristaloid

b. Dipandu : respons klinis,perfusi, perifes, tvs,

tekanan sistem,MAP
\!cr!!mc Tcrup! Cu!run ludu Svck \!cr!!mc Tcrup! Cu!run ludu Svck
Suspected shock
Hypovolemia, Hypoperfusion, Tachycardia
10 30 mL Cryst/Colloid / kg / 6
10 min
Normotensive
Hypotensive
In Sepsis :
Antibiotics,
Imunotheraphy
In Anaphylaksis :
Catekolamin,
steroid,
antihistamin
Urine > 1 ml/kg/hr
10-20 mL
crys or
coll/kg/10
min
Anuria
Urine < 1 ml/kg/hr
Urine output < 1 ml/kg/hr
Reevaluated 10 mL X.tal/kg 10 mL X.tal/kg 1020 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
Early Goal Directed
Early Goal Directed
Therapy pada Syok Septik
Therapy pada Syok Septik
Early aggressive fluid therapy (Crystaloid or
colloid) n U w t n
ours o m ss on
V sopr ssors notrop
ru s w n r s st n
to lu t r p
n po nts oo
p r p r l p r us on
on ousn ss
p ll r l n
t m < rm
xtr m t s
uls pr ssur N
or CVP 8-12 mmHg,
ur s s ml SvcO2 >
70%
Admission to PICU when stabilized
Supplemental oxygen
endotracheal intubation and
mechanical ventilation
Central venous and
arterial
catheterization
Sedation, paralysis
(if intubated), or both
Goals
achieve
d
ScvO2
MAP
CVP
Hospital admission
8-12 mmHg
65 and 90 mmHg
70%
Yes
No
Crystalloid
Colloid
< 8 mmHg
Vasoactive agents
< 65 mmHg
> 90 mmHg
Transfusion of red cells
until hematocrit 30%
Inotropic agents
< 70%
Protocol for Early
Goal-Directed
Therapy
Fluid Therapy
in Sepsis and Septic Shock
Type of
Type of
Fluid
Fluid
Colloid
Colloid
Crystalloi
Crystalloi
d
d
Volume
Volume
60 100
60 100
ml/kg
ml/kg
(6 hours)
(6 hours)
CO , Restore BP
CO , Restore BP
MOF
MOF
Inotropic
Vasopressor

(SYOK KARDIOGENIK) :
Fluid Chalenge hati hati :
a. memperbaiki kontraktilitas jantung
b. dipantau ketat dengan TVS
lck vc!umc !nus ! l kc!c!d pudu
lck vc!umc !nus ! l kc!c!d pudu
( ) kcmpur!cmcn !ubuh O k
( ) kcmpur!cmcn !ubuh O k
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) -
\DRlN\l TNS|llTSTlNST
\DRlN\l TNS|llTSTlNST
l\D\ SYO|
l\D\ SYO|

SllTT|
SllTT|

KORTIKOSTEROID

Pada syok septik, bila refrakter thdp

dopamin/adrenalin/nor-adrenalin
mungkin terjadi INSUFISIENSI ADRENAL
Hydrocortisone 50mg (bolus),
dilanjutkan 1-2 mg/kgBB/ 24 jam; 5-7 hari

TlR\lT S|lORTTl
TlR\lT S|lORTTl
v
Substitusi faktor koagulasi (pada
Hemodilusi/PIM) :

- Fresh Frozen Plasma

- Cyroprecipitate
v
Tranfusi Masif setiap 5 6 unit PC ditambah 2
unit FFP
v
Fibrinogen < 100 mg/dl (tak respons terhadap
FFP) : - Cyro precipitate 4 unit/10 kg BB
v
Konsentrat trombosit diberikan :

Trombositopeni berat < 30.000 dengan

perdarahan atau tindakan invasif : - Konsentrat
Trombosit

TM|NOTlR\lT
TM|NOTlR\lT
Tranfusi tukar pada sepsis :

- memperbaiki oksigenasi jantung

- mengeluarkan mediator dan endotokin

Immunoglobulin (I.V) pada sepsis
Hemofiltrasi dan Plasmafiltrasi :
mengeluarkan endotoksin, mediator


mengurangi respons inflamasi sistemik
(SIRS)
l|NGST ORG\N
l|NGST ORG\N
. \ : l\R|

Sup!u! Oks!cn udckuu!

- / . Tn!ubus! pcmusunun \ mckun!k d!n! pudu

svck

scp!!k

- , lcmbcr!un cu!run rcsus!!us! b!!u !cr!u!u

/ bunvuk

urcs! rcs!kc !!n! cdcmu puru

. l : OT\|

- , H!ndur! h!pcks!u h!pc!!kcm!u

- ( ) H!ndur! h!pcrkupncu dcnun vcn!!!u!cr

- : lcr!uhunkun pcrus! scrcbru!

. u vc!umc !n!ruvusku!ur

. b CO

. / c Hb !ckunun duruh udckuu!

- , - lcmun!uuun kudur Nu scrum kcrcks! hu!!

hu!!
( ) l|NGST ORG\N !un]u!un
( ) l|NGST ORG\N !un]u!un
. C / STR||l\ST Sll\N|HNT| S\l|R\N ClRN\

- , , Rcsus!!us! vc!umc cp!!mu!!su! CO

!ckunun duruh

- ( / ) |crcks! h!pc!cns! vuscprcscr !nc!rcp!k

- N|TRTST lNTlR\l DTNT

. D GTNJ\l

- , , Rcsus!!us! vc!umc cp!!mu!!sus! CO

!ckunun duruh

- |crcks! h!pc!cns!

- |crcks! h!pcks!u dun uncm!u bcru!

- H!ndur! cbu!- cbu!un ncrc!cks!k

T\T\l\|S\N\ SYO| |\RDTOGlNT|

T\T\l\|S\N\ SYO| |\RDTOGlNT|
Oks!cnus! \dckuu!
|crcks! GGN \sum lusu dun l!ck!rc!!!
|urun! Rusu Suk!! dun \ns!c!us
\!us! D!sr!!m!u Jun!un
: |c!cb!hun lrc!cud D!urc!!ku
: |cn!ruk!!!!!us l!u!d Chu!!cnc
/ (+) Scsuu! C\l lO\l Obu! Tnc!rcp!k
( ) : lcbun \!cr!cud S\R \uscd!!u!cr
|crcks! lcnvcbub lr!mcr
Ccmmcn!v |scd Curd!cvuscu!ur Drus !n Shcck Ccmmcn!v |scd Curd!cvuscu!ur Drus !n Shcck
Svndrcmcs Svndrcmcs
Drug Dose
( ug/kg/min )
Comment
Inotropioc agents
Norephrine
( - 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
excessive, 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
( ) Ccmmcn!v |scd Curd!cvuscu!ur !un]u!un ( ) Ccmmcn!v |scd Curd!cvuscu!ur !un]u!un
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
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
MONTTORTNG
MONTTORTNG
- S!u!c c Ccns!cusncss G!usc Ccmu Scu!c
Rcsp!ru!crv Ru!c und Churuc!cr
: Curd!cvuscu!ur lurumc!crs

. u Sk!n und Ccrc Tcmpcru!urc D!crcncc

. b lu!sc Ru!c und \c!umc

. c l!ccd lrcssurc

. d Cup!!!urv lcrus!cn T!mc

. c Ccn!ru! \cncus lrcssurc Shcu!d lc

Mcn!!crcd !n

lu!!cn! "hcrc Thcrc Hus lccn lccr

Rcspcnsc

Tc l!u!d Thcrupv Or "!!h ls!ub!!shcd

Shcck
|r!nurv Ou!pu!- , |r!nc lu Or lrccrub!v
; - / Cu!hc!cr Ou!pu! Shcu!d lc ! ? m! k lcdv
"c!h!
lu!sc Ox!mc!rv
SvcO?
|lY lOTNTS TN M\N\GlMlNT
|lY lOTNTS TN M\N\GlMlNT

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
/ RTNG|\S\N |lSTMl|l\N
/ RTNG|\S\N |lSTMl|l\N
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
Dengan pemahaman patofisiologi, diagnosis dini dan
memperhatikan key management syok, diharapkan
dapat me mortalitas syok