shock in children

Silvia triratna
Divisi pediatri gawat darurat
Bagian Ilmu Kesehatan Anak FK UNSRI/ RSUP Moh Hoesin
Palembang

Shock is a clinical syndrome characterized by a

state of inadequate tissue perfusion where
nutrient delivery does not meet tissue demands

Shock is NOT
Hypotension
Shock may be present with a normal blood
pressure
Shock may even occur with normal heart rates

Three key elements of

cardiovascular system

=pump propels the

fluid
=tubing distributes
and collects
the fluid
=fluid.

The Cardiovascular System

3. Collection
System

1. Pump
2. Fluid
3. Tubing

3.1. Distributio
System

Q = Cardiac output
Heart Rate
Neuro humoral

Stroke Volume
Preload
After load
Contractility

Mekanisme kompensasi

aktifasi simpatis

sekresi renin-angiotensin-aldosteron

ungsi dan kemampuan organ berbeda

kompensasi berbeda

aktifasi simpatis

amin, epinefrin dan norepinefrin di

ingkatan resistensi arterial sistemik

mengkonstriksi vena perifer

mendistribusikan aliran darah

agar perfusi ke organ vital tetap d

meningkatkan denyut jantung

meningkatkan curah jantun

sekresi renin-angiotensin-aldosteron

retensi natrium klorida dan air

meningkatkan aliran darah balik ven

ke jantung

Common Clinical Signs

of Shock

Delayed capillary refill

Mottled skin appearance
Tachycardia to 200
Decreased tears, urine output
Irritability, sleepy appearance

STADIUM SYOK

KOMPENSASI
DEKOMPENSASI
IREVERSIBEL

KOMPENSASI
REFLEKS SIMPATIS
Resistensi sistemik
distribusi ke organ vital >>>.

Katekolamin
dilepaskan

TD Normal, gelisah, kulit pucat dan

dingin, capilary refill > 2 detik

KOMPENSASI CO
Takikardia
sekresi vasopressin, Renin agiotensin
retensi Na + air

KOMPENSASI
DEKOMPENSASI
Mulai gagal mempertahankan CO
Sistem sirkulasi menjadi tidak efisien
metabolisme anaerob penumpukan as laktat
Pelepasan mediator vaskular vasodilatasi

Takikardi bertambah, Hipotensi, perfusi

memburuk, oliguria, asidosis, penurunan
kesadaran

DEKOMPENSASI
IREVERSIBEL

TERJADI KERUSAKAN/ KEMATIAN SEL

DISFUNGSI SISTEM ORGAN LAIN
CADANGAN ATP <<<
Tekanan darah tidak terukur,
nadi tidak teraba,
anuria,
Kesadaran makin menurun
Gagal sistem organ lain

ETIOLOGI

Hypovolemic

Cardiogenic

Hemorrhage
Serum/Plasma loss
Drugs

Myocardial
Dysrrhythmia
CHD-(duct dependant)

Distributive
Analphylactic
Neurogenic
Septic

Obstructive
Pneumo, tamponade,
Dissection

Dissociative
Heat, CO, Cyanide
Endocrine

Hemodynamic Variables
Different Shock States

MANAGEMENT

ABCs
Judicious fluids
Electricity
Pharmacologic interventions
Inotropes
Vasodilators
Anti- arrhythmics

Bolus Therapy
Goal is to restore intravascular
volume rapidly
Immediate volume expansion is
imperative in shock to restore tissue
perfusion
Re-evaluate after each bolus and
repeat every 5 minutes until
perfusion is improved

Distributive Shock
Vasodilation

Venous Pooling

Decreased
Preload
Maldistribution of regional blood flow

Distributive Shock:
Causes

Sepsis
Anaphylaxis
Neurogenesis (spinal)
Drug intoxication (TCA,
calcium, Channel
blocker)

Septic Shock

Decrease
d Volume

Decreased
Pump
Function

Abnormal
Vessel
Tone

Cardiac Output
C.O.=Heart Rate x Stroke Volume

Heart rate
Stroke volume:

Preload- volume of blood in

ventricle
Afterload- resistance to
contraction
Contractility- force applied

Clinical Assessment
Heart rate
Peripheral circulation

capillary refill
pulses
extremity temperature

Pulmonary
End organ perfusion

brain
kidney

Improving Stroke Volume:

Therapy for Cardiovascular Support

Preload
Contractility

Afterload

Volume
Inotropes

Vasodilators

Septic Shock
Early (Warm)
Decreased peripheral vascular
resistance
Increased cardiac output

Late (Cold)
Increased peripheral vascular
resistance
Decreased cardiac output

Assessment of Circulation

Heart Rate and Perfusion Pressure

(MAP-CVP) Parameters by Age

Assessment of Circulation

Goals of Resuscitation
Overall goal:
increase O2 delivery

decrease demand

O2 content

Cardiac
output

Treatment
Sedation/analgesia

Blood
pressure

Principles of Management
A: Airway

patent upper airway

B: Breathing

adequate ventilation and

oxygenation

C: Circulation

optimize
cardiac function

oxygenation

Act quickly,
Think
slowly.
Greek Proverb

Airway
Management
Patients in shock have:

O2 delivery
progressive

respiratory
fatigue/failure
energy shunted from vital
organs
afterload

Airway
Management
Early intubation provides:

O2 delivery and content

controlled ventilation which:

reduces metabolic demand
allows C.O. to vital organs

Therapy
Vagolysis
Chromotropy

Heart S tr o k e V o lu m e

Rate

P r e lo a d

A f te r lo a d

V o lu m e
CVP

V a s o d ila t o r s
V a s o c o n s tr ic to r s

C o n tr a c tility
C o rre c t
a c id o s is
h y p o x ia
h y p o g ly c e m ia

I n o tr o p ic
a g e n ts

Fluids, Fluids, Fluids

Key to most resuscitative
efforts
Give generously and reassess

Fluid Choices
Colloid

s
e
t !
s
Ta at
e
r
G

Crystalloid

s
s
Le
g
n
i
Fill

Crystalloids
Hypotonic Fluids
D 5, D 10, D5 NS, D5 1/4 NS,

No role in resuscitation
Maintenance fluids only

Crystalloids

Isotonic Fluids
Intravascular volume expansion
Hauser:

crystalloids rapidly redistribute

Lethal animal model

NS = good resuscitative fluid

4x blood volume to restore

hemodynamics

Crystalloids

Isotonic Fluids
2 trauma studies
crystalloids

= colloids but:

4x amount
longer time to resuscitation

Crystalloids

Complications
Under-resuscitation
renal failure

Over-resuscitation
pulmonary edema
peripheral edema

Crystalloids
Summary
Crystalloids less effective than
equal volume of colloids
Preferred when 1o deficit is water
and/or electrolytes
Good in initial resuscitation to
restore extracellular volume
Hypertonic solutions however, may
act as plasma volume expanders

Fluid
Transport
Oncotic pressure
(tendency to pull
unit)

Hydrostatic
pressure
(tendency to
drive unit)

Capillary

Colloids
Albumin

Hepatic production
MW = 69,000
80% of COP
Serum t1/2:
18 hours
16 hours

endogenous
exogenous

Colloids
Hydroxyethyl Starch (Hespan)

Synthetic
Derived from corn starch
Average MW = 69,000
Stable, nonantigenic
Used for volume expansion
Renal excretion

90% gone in 42 days

1/2

2-67 hours

Colloids
Hydroxyethyl Starch (Hespan)

Greater in COP than albumin

Longer duration of action
0.006% adverse reactions
No effect on blood typing
Prolongs PT, PTT and clotting
times
Dosage

20 ml/Kg/day
max 1500 ml/day

Fluid Choices
t!
a
e
Based on:
r
G
s
te
s
a
T
type of deficit
urgency of repletion
pathophysiology of
condition
plasma COP

g
n
i
l
l
i
F
Less

Fluid Choices
Crystalloids for initial
resuscitation
PRBCs to replace blood loss

Fluid Management in Pediatric

Septic Shock
Emphasis on the golden hour
Early aggressive use of fluids
may improve outcome
Titrate-Reassess!

Clinical Practice Parameters,

Carcillo et al., CCM, 2002

Alpha-Beta Meter

Dopam
ine

Epineph
rine

N
hr ore
N in p
hr eo e ine
p
in sy
e ne
p

a
t
u
b
o e
D in
m

SURVIVING SEPSIS CAMPAIGN GUIDELINES

FOR MANAGEMENT OF
SEVERE SEPSIS AND SEPTIC SHOCK

PEDIATRIC CONSIDERATION

Phase 1 Barcelona declaration

Phase 2 Evidence based guidelines
Phase 3 Implementation and education
SSC Steering Committee:
Global Consensus

13 September 2004
Catania, Sicily
Steering Committee Met
6 hour bundle formed
24 hour bundle formed
STOP SEPSIS BUNDLE

PEDIATRIC SEPSIS AND

SEPTIC SHOCK

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%

Consensus on Pediatric Sepsis

Definition and Organ Dysfunction (2005)

SIRS
INFECTION:
SEPSIS
SEVERE SEPSIS
SEPTIC SHOCK

Consensus on Pediatric Sepsis

Definition and Organ Dysfunction (2005)

SIRS :
At least 2 of the following (temp. or leucocyte abnormality
should be present):

Core temperature > 38.5C or < 36C

Tachycardia, a mean HR > 2SD above normal for age
Mean Respiratory Rate > 2SD above normal for age
Leucocyte count or for age or >10% immature
neutrophils

Consensus on Pediatric Sepsis

Definition and Organ Dysfunction (2005)

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)

Consensus on Pediatric Sepsis

Definition and Organ Dysfunction (2005)

SEPSIS
SIRS in the presence of or as a result of
suspected or proven infection
SEVERE SEPSIS Sepsis plus one of the
following : cardiovascular organ dysfunction or
ARDS or two or more other organ dysfunctions
SEPTIC SHOCK Sepsis and cardiovascular
organ dysfunction
(Goldstein et al. Pediatr Crit Care 2005, 6 : 1)

sepsis
a spectrum of disorders that result from
infection by bacteria, viruses, fungi, or
parasites or the toxic products of these
microorganisms.
Bacteremia, viremia, fungemia, and
parasitemia
refer to bloodstream invasions that may be
associated with fever but have no other signs
or symptoms of circulatory compromise or
end-organ malperfusion or dysfunction.

Table 1. Age-specific vital signs and laboratory

variables
(HR, RR, leucocyte count, syst. BP for the 5th and 95th
percentile)
Heart rate, Beats/min b, c

Age group

0 days- 1
wk
1 wk - 1
mo
1 mo to 1
yr
2-5 yrs
6-12 yrs
13 to <18

Leukocyte count,
Leokocytes x
103/mm3 b, c

Systolic
blood
pressure,
mmHg b, c, e, f

Tachycardi
a

Bradycardi
a

Respiratory
rate,
Breaths/min d

>180

<100

>50

>34

<65

>180

<100

>40

>19.5 or <5

<75

>180

<90

>34

>17.5 or <5

<100

>140

NA

>22

>15.5 or <6

<94

>130

NA

>18

>13.5 or
<4.5

<105

Table 2. Organ Dysfunctions Criteria

Cardiovascular dysfunction
Despite administration of isotonic intravenous fluid bolus 40 mL/kg in
1 hr
Decrease in BP (hypotension) <5th percentile for age or systolic BP <2
SD below for age, OR

Need for vasoactive drug to maintain BP in normal range (dopamine

>5 g/kg/min or dobutamine, epinephrine, or norepinephrine at any
dose), OR

Two of the following

Unexplained metabolic acidosis : base deficit >5.0 mEq/L

Increased arterial lactate >2 times upper limit of normal

Oliguria : urine output <0.5 mL/kg/hr

Prolonged capillary refill : >5 secs

Core to peripheral temperature gap >3oC

Respiratory
PaO2/FiO2 <300 in absence of cyanotic heart disease or preexisting
lung disease, OR

Table 2. Organ Dysfunction Criteria

(contd)
Neurologic

Glasgow Coma Scale 11 , OR

Acute change in mental status with a decrease in Glasgow Coma Score

3 points from abnormal baseline

Hematologic
Platelet count <80,000/mm3 or a decline of 50% in platelet count from
highest value recorded over the past 3 days (for chronic
hematology/oncology patients), OR

International normalized ratio >2

Renal
Serum creatinine 2 times upper limit of normal for age 2-fold increase
in baseline creatinine

Hepatic

Total bilirubin 4 mg/dL (not applicable for newborn), OR

ALT 2 times upper limit of normal for age

Pediatric Hypotension :
Systolic blood pressure > 2SD under average
It is advised to use
mean arterial blood pressure [MAP]
Because MAP reflex organ perfusion pressure

Mean arterial blood

pressure [MAP]
MAP
MAP
MAP
MAP
MAP
MAP

<
<
<
<
<
<

40
45
50
55
60
65

mmHg
mmHg
mmHg
mmHg
mmHg
mmHg

for
for
for
for
for
for

age
age
age
age
age
age

of
of
of
of
of
of

3 6 1 4 10 14 -

6
12
4
10
14
18

months
months
years
years
years
years

MAP can be straight measured or

calculated as follow:

MAP = [(Systolic) + ( 2 x
diastolic)] : 3

SEVERE SEPSIS BUNDLES

S
R
U
O
H
6
S
R
U
O
H
4
2

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 Hour Resuscitation
Bundle
Early Identification
Early Antibiotics and Cultures
Early Goal Directed Therapy

6 - hour Severe Sepsis/

Septic Shock Bundle
Early Detection:

Obtain serum lactate.

Early Blood
Cx/Antibiotics:

within 3 hours of presentation.

Early EGDT:
Hypotension
(SBP < 90, MAP <
65) or lactate > 4
mmol/L:

initial fluid bolus

20-40 ml of crystalloid (or
colloid equivalent) per kg of
body weight.

Vasopressors:

Septic shock or
lactate > 4 mmol/L:

Hypotension not
responding to fluid
Titrate to MAP >65 mmHg.

CVP and ScvO2 measured.

CVP maintain >8 mmHg.
MAP maintain >65 mmHg.

ScvO2<70% with
CVP > 8 mmHg,
MAP > 65 mmHg:

PRBCs if Ht < 30%.

Inotropes.

6 - HOURS SEPSIS BUNDLE

Supplemental oxygen
endotracheal intubation and
mechanical ventilation
Central venous and
arterial
catheterization
Sedation, paralysis
(if intubated), or both
CVP

Protocol for
Early Goal-Directed
Therapy

< 8 mmHg

Crystalloid
Colloid

8-12 mmHg
MAP

< 65 mmHg
> 90 mmHg

Vasoactive agents

65 and 90 mmHg
ScvO2
70%
No

Goals achieved
Yes
Hospital admission

Transfusion of red cells

until hematocrit 30%
Inotropic agents

< 70%

24 - hour Severe Sepsis and Septic

Shock Bundle

Glucose control (insulin):

maintained on average <150 mg/dL (8.3 mmol/L)

Drotrecogin alfa (activated):

administered in accordance with hospital guidelines

Steroids:
for septic shock requiring continued use of
vasopressors for equal to or greater than 6 hours.

Lung protective strategy:

Maintain plateau pressures < 30 cm H2O for
mechanically ventilated patients

24 HOURS BUNDLE

Pediatric
Surviving Sepsis Campaign (2004)
Initial Fluid
Resuscitation
Mechanical ventilation
Antibiotic therapy
Source control
Vasopressors,
inotropic, and
vasodilators

Steroids
rhAPC (-), IVIG (?)
Blood product
Oxygen Therapy
Glucose control
Renal replacement
Bicarbonate therapy
Deep vein thrombosis and
stress ulcer prophylaxis
Antihrombin (AT III) (-)

5. Aproach
to Pediatric
Septic Shock

0 min
0 min
55min
min

Recognized decreased mental status and perfusion

Maintain airway and establish access according to PALS guidelines
Push 20 cc/kg isotonic saline or colloid boluses up to and over 60 cc/kg
Correct hypoglycemia and hypocalemia

15 minutes
15 min

Fluid refractory shock **

Fluid responsive *

Establish central venous access, begin dopamine or dobutamine

therapy and establish arterial monitoring

Fluid refractory-dopamine/dobutamine resistant shock

Titrate epinephrine for cold shock, norepinephrine for warm shock to
normal MAP-CVP difference for age and SVCO2 saturation > 70%

Observe in PICU

Catecholamine-resistance shock
At risk of adrenal insufficiency??

60 minutes
60 min

Draw baseline cortisol level

then
give hydrocortisone

Normal blood pressure, cold

shock SVCO2 sat < 70%

Not at risk??
Draw baseline cortisol level or perform
ACTH stim test. Do not give hydrocortisone

Low blood pressure, cold

shock SVCO2 sat < 70%

Low blood pressure, warm

shock SVCO2 sat < 70%

Add vasodilator or
Titrate volume resuscitation Titrate volume and NorEpinephrne
and Epinephrine
type III PDE inhibitor (Milrinone)
with volume loading
Persistent catecholamine-resistant shock
Start cardiac output measurement and direct fluid, inotrope,
vasopressor, vasodilator, and hormonal therapies to attain
normal MAP-CVP and CI > 3.3 and < 6.0 L/min/m2

Refractory shock
Consider ECMO

ACCM Recommendations for

neonatal and pediatric septic shock management.
0 min - Recognize mental status, poor perfusion
5 min - Maintain airway, establish access push 20ml/kg
up to 60ml/kg fluid. Observe in picu if positive response
15min - Recognize fluid refractory shock, start central
line, dopamine, establish arterial monitoring.
I f fluid refractory dopamine resistant shock (10mic/kg/min),
start epinephrine for cold, norepinephrine for warm shock.
If Risk of adrenal insufficiency (38-39) give hydrocortisone.
Normal BP, Cold shock SVC O2 sat <70 add vasodilator,
consider volume
Low BP, Cold shock, SVC O2 sat <70 - Titrate volume and
Epinephrine
Low BP, Warm shock : give Norepinephrine, fluid, consider
Vasopressin
EGDT keep the minimum cost and duration of hospital stay

SURVIVING SEPSIS MANAGEMENT

1. INITIAL RESUSCITATION

Early recognition and early intervention

is the key!
During the first 6 hours:
Early Goal Directed Therapy (EGDT)

Rivers (2001): Stabilization within 6 hours

hospital admission, before ICU admission

Aggressive fluid therapy, inotropic,

vasopressor, vasodilator

SURVIVING SEPSIS MANAGEMENT

MECHANICAL VENTILATION

MECHANICAL VENTILATION

EARLY IN YOUNG NFANT Due to low

functional residual capacity

SURVIVING SEPSIS MANAGEMENT

MECHANICAL VENTILATION

LUNG PROTECTIVE STRATEGY:

Low TV 6-8 ml/kgBW,

permissive hypercapnea,

sufficient PEEP prevent alveolar

collapse & reopening:
ventilator-induced lung injury
(VILI)

Inspiratory Plateau Pressure < 30

cm H2O

Prone & Recumbent position good tissue

SURVIVING SEPSIS MANAGEMENT

DIAGNOSIS and ANTIBIOTIC

SERUM LACTATE, CULTURES OBTAINED

BEFORE ANTIMICROBIAL THERAPY IS
INITIATED
I.V. ANTIBIOTIC STARTED WITHIN FIRST
HOUR
(AT LEAST THREE HOURS) OF
RECOGNITION OF SEVERE SEPSIS

Empirical anti-infective therapy within first

hour of recognition of sepsis

Reassessed after 48-72 hour, using narrow

SURVIVING SEPSIS MANAGEMENT

SOURCE CONTROL

Early recognition and early intervention

is the key!

PRESENCE OF FOCUS OF INFECTION

DRAINAGE,
DEBRIDEMENT OF NECROTIC TISSUE,
REMOVAL OF INFECTED DEVICE,
CONTROL OF INFECTION: hand
hygiene!

SURVIVING SEPSIS MANAGEMENT

2. Aggressive Fluid Resuscitation

Initial resuscitation :
rapid bolus of 20 ml/kg within 5-10
minutes, x3
(60-80 ml maybe more [100-200 ml]
within 6 hours)

Crystalloid and/or colloid

In cases with narrow Pulse Pressure (PP <10
mmHg): Colloid - more effective than
crystalloid in restoring PP

SURVIVING SEPSIS MANAGEMENT

3. Vasopressor, Inotropic, Vasodilator

Fluid refractory shock, MAP below normal

for age vasopressor (Dopamine) to
maintain normal MAP/age
Dopamine refractory shock, reverse with
Epinephrine or Norepinephrine
Low CO Dobutamine
MAP > for age, SVR despite fluid
resuscitation vasodilator
(Nitroprusside or Nitroglycerin)
Low CO, normotensive, SVR

SURVIVING SEPSIS MANAGEMENT

4. Therapeutic End Point

Capillary refill time < 2 seconds
Normal pulses, no different between
peripheral and central pulses, warm
extremities
Urine output > 1 ml/kg/hr
Normal mental status, decrease serum
lactate,
ScvO2 > 70%
Normal Pulse Pressure for age

SURVIVING SEPSIS MANAGEMENT

5. Steroids Therapy

Annane (2002) : In adult septic shock,

Hydrocortisone 50 mg/kg (200-300 mg)
i.v., with Fludrocortisone 50ug/kgbw p.o. for
7 days conflicting result

SSC (2004) recommended hydrocortisone

1-2 mg 50mg/kg for 24 hr infusion

No consensus doses for children available

Grade C

activation of 1KB-
Inhibition of NFK-B
Inhibition
of iNOS
Reversal of adrenergic
receptor desensitization

Hemodynamic
improvement

Decreased
transcription for
proinflammatory
cytokines, Cox-2,
ICAM-1,
VCAM-1
Increased
transcription
for IL1-ra

Decrease in the
dosage of
catecholamines
Potential mechanisms of benefit from steroid
therapy

SURVIVING SEPSIS MANAGEMENT

Activated Protein C
in Pediatric Sepsis
6.

Only one dose finding, placebo-controlled

study performed using APC in children

The powerful of study was very low, and

failed to show an effect on reducing
mortality

Study of rhAPC in pediatric sepsis

discontinued because of no benefit effects
(SCCM)

SURVIVING SEPSIS MANAGEMENT

7.

Granulocyte Macrophage Colony Stimulating Factor (GM-CSF)

GM-CSF 1.0-10 g/kg 7 days

course

in neonate with

sepsis and
an absolute neutrophil count
(ANC) < 1500/ L improve
outcome

SURVIVING SEPSIS MANAGEMENT

8. Deep Vein Thrombosis (DVT) Prophylaxis

Most DVTs in young children

are associated with central
venous catheters (25% in
femoral CVLs)
No data on use of heparin
prophylaxis to prevent DVT in

SURVIVING SEPSIS MANAGEMENT

9. Stress Ulcers Prophylaxis

Commonly used in mechanical

ventilated children, coagulopathy and
hypotension but no studies have been
performed in children

H2 receptor blockers

Role of proton pump inhibitors (PPI)

Its effect is not known

Grade C

SURVIVING SEPSIS MANAGEMENT

10. Renal dysfunction

Correcting volume deficits and hypotension

reverses oliguria

The benefit of dopamine, diuretics, or fluid

loading to prevent renal dysfunction has
not been proved

The efficacy of CVVH in meningococcal

septic shock have convincingly
demonstrated

CVVH maybe useful in children with

SURVIVING SEPSIS MANAGEMENT

11. Glycemic Control

Infants in general are at risk

developing hypoglycemia when
depend on IV fluids

Glucose intake of 4-6 mg/kg/min

D10% in NaCl 0.45% (maintenance)

No studies in pediatric patients

analyzing the effect of rigid glycemic

SURVIVING SEPSIS MANAGEMENT

12. Sedation/Analgesia

Apropriate sedation and analgesia for

children with mechanical
ventilation are the standard

No data supporting any drugs or

regiments

Midazolam, profofol, etc

Grade B

SURVIVING SEPSIS MANAGEMENT

13. Blood Products

Maintain Hb within normal range

for age

( > 10 gr/dl) RBC

transfusion
Grade B
Do not use erythropoeitin
Do not use antithrombin

Blood Product: Coagulation

Dysfunction
Platelet concentrate

15 ml/kg

- < 50,000/mm3 if active bleeding , or preprocedure/surgical - 5,000-30,000/mm3 with

significant bleeding risk

- <5,000/mm3

regardless of bleeding
Fresh Frozen Plasma - planned invasive
procedure
FFP should not be used for fluid
replacement in shock
Cryoprecipitate when fibrinogen level <
1.0 g/L

SURVIVING SEPSIS MANAGEMENT

14.

Intravenous Immunoglobulin

Polyclonal IVIG reducing mortality rate

in adult sepsis

It is promising adjuvant in sepsis and

septic shock

In children all trials have been small,

insufficient to support a conclusion of
benefit

Monoclonal IVIG remains experimental

SURVIVING SEPSIS MANAGEMENT

15.

ECMO in Sepsis

In children with septic shock its impact is

not clear

Survival from refractory shock :

80% in neonates and 50% in children

12 meningococcus sepsis on ECMO

8 patients survived with normal lives at a
median of 1 yr

Children with sepsis on ECMO do not

SURVIVING SEPSIS MANAGEMENT

16. Bicarbonate Therapy

Using bicarbonate is not

recommended for treatment of
hypoperfusion- induced acidemia
with pH > 7.15

Bicarbonate did not improved

hemodynamics nor did it improve
responsiveness to catecholamines
(Cooper DJ, Walley KR, Wiggs BR, et al. Ann Intern Med 1990;
112:492)

PEDIATRIC CONSIDERATIONS
Parker MM; Hazelzet JA; Carcillo JA. Crit Care Med. 2004; 32(11
Suppl):S591-4

CONCLUSION:
Pediatric considerations include
a more likely need for intubation due to low functional
residual capacity,
more difficult intravenous access,
fluid resuscitation based on weight wit 40-60 mL/kg or
higher needed,
decreased cardiac output, and increased systemic
vascular resistant as the most common hemodynamic
profile,
greater use of physical examination therapeutic
endpoints,
the unsettled issue of high-dose steroids for therapy of
septic shock, and greater risk of hypoglycemia with

THANK YOU FOR LISTENING!