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SEPSIS
Pediatric Critical Care
Diponegoro University/Kariadi Hospital
Semarang - 2011
Learning Objectives
1. How to diagnose pediatric sepsis
2. How to manage pediatric sepsis
3. How to understand early detection
in pediatric sepsis
How to prevent sepsis
Definition
Differential diagnosis
Classification
from clinical
Etiology
manifestations
Epidemiology Laboratory
interpretation:
Pathogenesis
hematology, serology
Diagnosis
and microbiology
(bacteriology)
Communication skill
Correlation between predisposing factors
and onset of sepsis
SEPSIS
Introduction
Consensus for pediatric sepsis was done (2005),
according to the age (Goldstein et al. Pediatr Crit Care
2005, 6 : 1) Update in 2007 (Crit Care Med 2009 vol
37 no 2)
The changes recommended were few
There was no change in emphasis (continued emphasis)
There are some new recommendations in the 2007
update
Epidemiology
Incidence of severe sepsis : 2-11% PICU
admission
Mortality rate of sepsis in developing country
still high
(50-70%);
in developed country decreased from 97% to
9% (DuPont HL. Medicine 1968;48:307-332) (Stoll
BJ, Holman RC, Shuchat A. Pediatrics 1998;102:E18)
Mortality rate for septic shock / MOF : 80%
Definition
INFECTION:
Suspected or proven infection by any pathogen or a clinical syndrome assoc. with
a high probability of infection
Evidence of infection : positive findings on clinical exam, imaging, laboratory test,
pneumonia (chest radiograph), petechial or purpuric rash, or purpura fulminans)
SEPSIS SIRS in the presence of or as a result of suspected or proven infection
Correlation between
SIRS, Infection and Sepsis
Bacteria
Major surgery
Fungi
Trauma
Infection
Parasite
SEPSIS
SIRS
(non
infectio
n)
Burn
Transplant
rejection
Pancreatitis
Virus
Other
Myocard infarct
Pathophysiology of Sepsis
Infection
Initiations
LPS, Exotoxins
Primary Mediators
Primary Sites
Secondary
Mediators
Secondary Sites
Shock MODS
Initial insult
(bacterial, viral,
traumatic, thermal)
Anti-inflammatory
response
Systemic spillover of
antiinflammatory
Systemic reaction
mediators
SIRS (pro-inflammatory)
CARS (anti-inflammatory)
MARS (mixed)
Systemic spillover of
proinflammatory mediators
Cardiovascular Homeostasis
compromise
CARS
shock, SIRS
and SIRS
predominates
balanced
Apoptosis (cell
death) Death
with minimal
inflammation
Organ
dysfunction
SIRS
predominates
CARS : Compensatory Antiinflammatory Response Syndrome
MARS : Mixed Antiinflammatory Response Syndrome
Suppression of
the immune
system CARS
predominates
Cellular Mediators
PMNS (acute)
Macrophages
(chronic)
Selectin
s
Integrin
s
Cel
l
Oxidants
protease
s
PMN
Splanchnic Bed
Activated Complement
TNF, IL-1, IL-6, LPS, PAF
ODFRS
TxA2
LTB4
Neutrophils
PAF
TNF
TXA2
LTC4
PGI2
NO
Microcirculatory
Plugging
Activated
Neutrophils
TXA2
Vasoconstriction
IL-2
Reduced Splanchnic Perfusion
Definition of MODS
Occurrence of 2 or more organ
dysfunction for minimum 24 48 hours.
Criteria by:
Marshall
Leteurte or Fischer & Fancony
(Pediatrics)
Goldstein (2005)
Marshall Descriptors
for MODS Outcome
Respiratory system: PO2 / FiO2 ratio.
Renal system: serum creatinine
concentration.
Hepatic system: serum bil.
concentration.
Haematological system: platelet count.
CNS: Glasgow Coma Scale
MODS
Main caused of death in the critically ill
patients in PICU.
The more MODS highest mortality.
1 organ failure 30 40 % mortality.
2 organ failure 50 60 % mortality.
3 organ failure 80 100 % mortality.
Diagnosis approach
P
I
R
O
:
:
:
:
Predisposition of infection
Infection (insult)
Respons of inflammatory
Organ dysfunction
Management
BUNDLE DEFINITION
A "bundle" is a group of interventions related
to a disease process that, when executed
together, result in better outcomes than
when implemented individually.
1. Sepsis Resuscitation Bundle
(To be accomplished as soon as possible and scored over first
6 hours):
2. Sepsis Management Bundle
(To be accomplished as soon as possible and scored over
first 24 hours):
6 Hours
Resuscitation Bundle
Early Identification
Early Antibiotics and Cultures
Early Goal Directed Therapy
2. Early Blood
Cx/Antibiotics:
within 3 hours of
presentation.
3. EGDT:
Hypotension
or lactate > 4 mmol/L:
initial fluid bolus
20-40 ml of crystalloid (or
colloid equivalent) per kg of
body weight.
Vasopressors:
Hypotension not
responding to fluid
Titrate to MAP according
to age.
Septic shock or
lactate > 4 mmol/L:
ScvO2<70% with
CVP > 8 mmHg,
MAP > 65 mmHg:
Steroids:
for septic shock requiring continued use of
vasopressors for equal to or greater than 6 hours.
Early Antibiotic/Culture
Within the first hour
Culture should be made before
antibiotic
Empirical AB/ De-escalation of one
or more drugs that active against all
likely pathogen and that penetrate in
the presumed source of infection
20
Count
10
Jenis kelamin
perempuan
laki-laki
Jenis kelamin
Count
perempuan
0
laki-laki
Enterob. aerogenes
Pseudomonas aerugino
Staphylococcus epide
E. coli
Count
Jenis kelamin
perempuan
laki-laki
Enterob. aerogenes
Pseudomonas aerugino
Staphylococcus epide
E. coli
30
20
Count
10
tidak
0
ya
20
10
Count
ya
20
Count
10
Kulturdarah sensitif
tidak
ya
20
Count
10
ya
20
Count
10
ya
10
Count
ya
20
Count
10
ya
20
Count
10
ya
30
20
Count
10
ya
Source of infection
Common bugs
55% polymicrobial
JAMA 1995;274:639644
2005
2006
No.
Microorganisms
Rank
Rank
E.coli
28
19
K.pneum.
23
20
S.aureus/MRSA
17
21
P.aeruginosa
19
23
E.aerogenes
18
27
S.epid./MRSE
20
29
Proteus spp.
15
11
Candida
12
15
Acinetobac. spp
14
Antibiotics
Full- loading dose
AB/ regimen should be reassessed
daily to optimize activity, prevent
resistance, reduced toxicity, and cost
Combination th/ if known/suggest
pseudomonas
0 1 months
Pathogens
(Pending culture)
Initial
dose
(mg/kg)
Ampiciline +
50
Staph. Aureus
Gentamicin
2.5
Listeria meningtides
Cefotaxime
5-0
Cefotaxime
50
Ampiciline +
50
Group B Streptococcus
Chlorampenicol
25
S. Pneumoniae
Cefotaxime
50
H. Influenzae
Cefriaxone
50
S. Aureus
Ampiciline +
50
N. Meningtidis
Chlorampenicol
25
S. aureus, Proteus
Vancomycin +
25
Pseudomonas
Ceftazidime +
50
Enterobacteriaceae
Ticarcillin
75
> 24 months
Immuno
compromised
Antimicrobial
Antibiotic
Combination AB/ in neutropenic
patients
Empirical AB/ not more than 3 5
days
Duration of AB: 7 10 days
Negative cultured
Sepsis occurred
In > 50%
Decision to : continue,
Narrow, stop of AB
On the basis 0f
Clinical judgment
&
Clinical information
Stepwise management of hemodynamic support with goals of normal perfusion and perfusion pressure (MAP-CVP)
in infants and children with septic shock. Proceed to next step if shock persists.
Recognize
Recognize decreased
decreased mental
mental status
status and
and perfusion.
perfusion.
Maintain
Maintain airway
airway and
and establish
establish access
access according
according to
to PALS
PALS guidelines.
guidelines.
0 min
5 min
Push
Push 20cc/kg
20cc/kg isotonic
isotonic saline
saline or
or colloid
colloid boluses
boluses up
up to
to and
and over
over 60
60 cc/kg
cc/kg
Correct
Correct hypoglycemia
hypoglycemia and
and hypocalcemia
hypocalcemia
Fluid refractory shock
15 min
Fluid responsive
Establish
Establish central
central venous
venous access,
access, begin
begin
dopamine
dopamine therapy
therapy and
and establish
establish arterial
arterial monitoring
monitoring ..
Fluid refractory-dopamine resistant shock
Observe
Observe in
in PICU
PICU
Titrate
Titrate epinephrine
epinephrine for
for cold
cold shock,
shock, norepinephrine
norepinephrine for
for warm
warm
shock
shock to
to normal
normal MAP-CVP
MAP-CVP and
and SVC
SVC O2
O2 saturation
saturation >
> 70%
70%
Give
Give hydrocortisone
hydrocortisone
Normal Blood Pressure
Cold Shock
SVC O2 sat < 70%
Add vasodilator or Type III PDE inhibitor
with volume loading
Refractory shock
Consider
Consider ECMO
ECMO
k
g
n
e
r
a
r
a
T
iu ana
y
a
d
sa
3.