Sepsis or septicemia
in children
Definition
?Bacteremia：
Bacteria invade into blood temporarily with
flora <100 CFU/ml in blood
?Septicemia or Sepsis：
Pathogens(bacteria or fungi) invade into
blood,proliferate greatly,and release endotoxin
?Toxemia：
Endotoxin absorbed into blood with no bacteria
?Septicopyemia：
Sepsis with metastatic foci in organs,pyemia is
a status which no bacterium in blood is cultured
?Gram stain positive coci
?Gram stain negative bacilli
?Anaerobic bacteria
?Fungi
Pathogens
?virulence and quantity
Exotoxin,Endotoxin
?Defense mechanism
Immunologic function,age,etc
?Chronical diseases：
Nephropathy,Liver sclerosis,Connective tissue diseases,Diabetes
mellitus,Malignant tumor,and so on
?Medical factors：
long-term Steriods,Antibiotics,All kinds of instrumentation
such as invasive meauver,catheterization
Associated factors
?More than one bacterium isolated in the same
blood samples
?Associated with immnocompromised status
?Commonly occurs in patients with chronic
diseases or use of immnodepressors
Polymicrobial sepsis
?Clinical feature：
endotoxemia and shock
young baby is easy to suffer from sepsis,and
deteriorate to MODS.it can be asymptomatic
?Blood test,WBC elavates or drops
?Metastatic foci,more commonly
Features
vi rul ence f ever f eat ur e
Sh ock
or
D IC
MO SF
comm on
C omm on pathogen s
（ pn eumococcus,
E,col i ）
H i gh
f ever
comm on no no
acute
P athogens w i th
st r ong v
（ st aph yl ococcus
aur eus,pseud omonas,
kle bsi el l a ）
H i gh
fe ver
to dr op
Sever el y
ill
mor e mor e
suba cute
C ond i ti ona l
pathogen s
（ st aph yl ococcus
epi dermi dis ）
l o w ～
me dium
comm on no no
classification
Mechanism
Gram-negative
bacteria
Gram-positive bacteria
Endotoxin Lipoteichoic acid -peptidoglycan complex
SIRS
Inflmmatory
mediatorsACTH,RAS
endothe
Immno cell
Complement system、
coagulation cascades
Adrenocorticotrophic hormone
kallikrein-kinin system
MOSF
?Metastatic foci：
endocarditis,meningitis,oestoarthritis,and so on
?mulnutrition
?Disturbed hemostasis,such as acidosis
?Complications in organs:dysfunction
Complication
Clinial syndrome manefested with strong inflmmation
? over-responsiveness of inflmmatory
mediators
all over the body(cytokines Cascade）
? pathogenic factors：
infection:bacteria,virus,…
non-infection:injuries,burns,…
? outcome,organ and tissue injuries
Systemic Inflammatory Response Syndrome
-SIRS
Hypothesis associated with SIRS
? Over-responsiveness:inflmmatory mediators
? Disturbed microcirculation
? Injuried intestinal barrier
Pathophysiology of SIRS
? Excessive uncontrolled inflmmation
over-responsiveness to inflmmation,SIRS and CARS
cytokines and other mediators released
? Unstable circulation
peripheral vascular resistance reduced early,and
greatly elavated lately
abnormal oxigen delivery（ Ca-vO2 decresed）
? Permanent high metabolism
tissue oxigen consumption exceeds,BMR elavates
substance use disturbed
Correlation of SIRS and etiology
bacteria
fungi
parasites
virus
others
infections sepsis S I R S
others
injuries
burns
panceasitis
?principles：
?Antibiotics:Early,adequate,regulatory,combined
and through vein
?Clear up the infected foca
?Regulate inflmmatory responsivesness
?Keep intestine clean
?Ameliorate microcirculation
?Rest,nutrition and supportive measures
Treatment
Septic shock
Definition
?Septic shock：
Acute circulation dysfunction caused by
infection of bacteria,vira,fungi and
so on,which can develope from SIRS,
severe sepsis to MODS,it’s mortality is 40％
?multiple organ dysfunction
?Gram-negative bacilli：
commonly,cold shock at early stage
?Gram-positive coci：
warm shock
Pathogens
Mechanism
?Microciculation dysfunction
?Over-immunoinflammatory responsiveness
?Neuro-endocrinal mediators
Mechanism － microcirculation dysfunction
Microcirculation
Capllary leakage,
sluge formationCell oxigen use obstacled,acdosis
Blood plates and endothellin
release mediators
（ 5-HT,Histamine）
WBC aggregation
complement activity
Capllary injuries and
leakage
Inflmmatory cell
activity
Tissue and cells
injuries
Organs and tissue
dysfunction
endotoxinhypovolume Over-reaction
Mechamism－ over-responsiveness
INF? IL-4 TNF? IL-5 IL-2 IL-10
IL-1 PAFTh-2Th-1IL-6TNF? 花生四烯酸
capllary leakage,
myocardiac inhibition,abnorminal vessel resistance
Septic syndrome
Septic shock
Macrophage T cell
LPS
Pathogens
Polyneuclear
Endotheline
NO synthase
kidney
Mechanism－ neuroendocrinal
交感 -肾
上腺素
More Blood return
to heart
Coronary
vessel
花生四
烯酸
Internal
organ
ET－ NOStress
steriods
Hypophysi
s-adrenal
axis
前列腺素
vessel
beta-
endorphl
in
内皮
细胞
others
儿茶酚胺
intestine
TXA2PGI2
vasoconstriction
Clinical manifestation
?compensatory shock,hypoperfusion,early
oliguria,unstable blood pressue
lactic acidosis,hypoxia
?Uncompensatory shock,organ dysfunction
capillary reperfusion
SBP/DBP descend
?Refractory shock,MODS,lately
difficult to treat
Clinical manifestation
?Mutiple organ dysfunction syndrome
?Fast onset,primary
?Delayed onset,secondary to infection commonly
Diagnosis
? respiratory system:shock lung/ARDS
? circulatory system:heart failure
? central nervous system:dysfunction
? blood system:DIC
? urinary system:acute renal failure
? gastrointestinal sysrem:dysfunction
? liver:hepatic failure
Clinical manefestation
?Hypoperfusion:lactic acidosis,
hypoxia,tachycardia
?uncompensatory,SBP/DBP drops,ARDS
?Late stage,MODS
principles：
?Early to identify,to diagnose,and to treat
?Oxigen supply and respiratory support
?Liquid resuscitation,acidosis and vaso-dilation drugs
?Heart function protection,organ perfusion and oxigen delivery
?Adrenal cortisol,LPS antibodies
?Infection control actively
?Hypothermal therapy
Treatment
in children
Definition
?Bacteremia：
Bacteria invade into blood temporarily with
flora <100 CFU/ml in blood
?Septicemia or Sepsis：
Pathogens(bacteria or fungi) invade into
blood,proliferate greatly,and release endotoxin
?Toxemia：
Endotoxin absorbed into blood with no bacteria
?Septicopyemia：
Sepsis with metastatic foci in organs,pyemia is
a status which no bacterium in blood is cultured
?Gram stain positive coci
?Gram stain negative bacilli
?Anaerobic bacteria
?Fungi
Pathogens
?virulence and quantity
Exotoxin,Endotoxin
?Defense mechanism
Immunologic function,age,etc
?Chronical diseases：
Nephropathy,Liver sclerosis,Connective tissue diseases,Diabetes
mellitus,Malignant tumor,and so on
?Medical factors：
long-term Steriods,Antibiotics,All kinds of instrumentation
such as invasive meauver,catheterization
Associated factors
?More than one bacterium isolated in the same
blood samples
?Associated with immnocompromised status
?Commonly occurs in patients with chronic
diseases or use of immnodepressors
Polymicrobial sepsis
?Clinical feature：
endotoxemia and shock
young baby is easy to suffer from sepsis,and
deteriorate to MODS.it can be asymptomatic
?Blood test,WBC elavates or drops
?Metastatic foci,more commonly
Features
vi rul ence f ever f eat ur e
Sh ock
or
D IC
MO SF
comm on
C omm on pathogen s
（ pn eumococcus,
E,col i ）
H i gh
f ever
comm on no no
acute
P athogens w i th
st r ong v
（ st aph yl ococcus
aur eus,pseud omonas,
kle bsi el l a ）
H i gh
fe ver
to dr op
Sever el y
ill
mor e mor e
suba cute
C ond i ti ona l
pathogen s
（ st aph yl ococcus
epi dermi dis ）
l o w ～
me dium
comm on no no
classification
Mechanism
Gram-negative
bacteria
Gram-positive bacteria
Endotoxin Lipoteichoic acid -peptidoglycan complex
SIRS
Inflmmatory
mediatorsACTH,RAS
endothe
Immno cell
Complement system、
coagulation cascades
Adrenocorticotrophic hormone
kallikrein-kinin system
MOSF
?Metastatic foci：
endocarditis,meningitis,oestoarthritis,and so on
?mulnutrition
?Disturbed hemostasis,such as acidosis
?Complications in organs:dysfunction
Complication
Clinial syndrome manefested with strong inflmmation
? over-responsiveness of inflmmatory
mediators
all over the body(cytokines Cascade）
? pathogenic factors：
infection:bacteria,virus,…
non-infection:injuries,burns,…
? outcome,organ and tissue injuries
Systemic Inflammatory Response Syndrome
-SIRS
Hypothesis associated with SIRS
? Over-responsiveness:inflmmatory mediators
? Disturbed microcirculation
? Injuried intestinal barrier
Pathophysiology of SIRS
? Excessive uncontrolled inflmmation
over-responsiveness to inflmmation,SIRS and CARS
cytokines and other mediators released
? Unstable circulation
peripheral vascular resistance reduced early,and
greatly elavated lately
abnormal oxigen delivery（ Ca-vO2 decresed）
? Permanent high metabolism
tissue oxigen consumption exceeds,BMR elavates
substance use disturbed
Correlation of SIRS and etiology
bacteria
fungi
parasites
virus
others
infections sepsis S I R S
others
injuries
burns
panceasitis
?principles：
?Antibiotics:Early,adequate,regulatory,combined
and through vein
?Clear up the infected foca
?Regulate inflmmatory responsivesness
?Keep intestine clean
?Ameliorate microcirculation
?Rest,nutrition and supportive measures
Treatment
Septic shock
Definition
?Septic shock：
Acute circulation dysfunction caused by
infection of bacteria,vira,fungi and
so on,which can develope from SIRS,
severe sepsis to MODS,it’s mortality is 40％
?multiple organ dysfunction
?Gram-negative bacilli：
commonly,cold shock at early stage
?Gram-positive coci：
warm shock
Pathogens
Mechanism
?Microciculation dysfunction
?Over-immunoinflammatory responsiveness
?Neuro-endocrinal mediators
Mechanism － microcirculation dysfunction
Microcirculation
Capllary leakage,
sluge formationCell oxigen use obstacled,acdosis
Blood plates and endothellin
release mediators
（ 5-HT,Histamine）
WBC aggregation
complement activity
Capllary injuries and
leakage
Inflmmatory cell
activity
Tissue and cells
injuries
Organs and tissue
dysfunction
endotoxinhypovolume Over-reaction
Mechamism－ over-responsiveness
INF? IL-4 TNF? IL-5 IL-2 IL-10
IL-1 PAFTh-2Th-1IL-6TNF? 花生四烯酸
capllary leakage,
myocardiac inhibition,abnorminal vessel resistance
Septic syndrome
Septic shock
Macrophage T cell
LPS
Pathogens
Polyneuclear
Endotheline
NO synthase
kidney
Mechanism－ neuroendocrinal
交感 -肾
上腺素
More Blood return
to heart
Coronary
vessel
花生四
烯酸
Internal
organ
ET－ NOStress
steriods
Hypophysi
s-adrenal
axis
前列腺素
vessel
beta-
endorphl
in
内皮
细胞
others
儿茶酚胺
intestine
TXA2PGI2
vasoconstriction
Clinical manifestation
?compensatory shock,hypoperfusion,early
oliguria,unstable blood pressue
lactic acidosis,hypoxia
?Uncompensatory shock,organ dysfunction
capillary reperfusion
SBP/DBP descend
?Refractory shock,MODS,lately
difficult to treat
Clinical manifestation
?Mutiple organ dysfunction syndrome
?Fast onset,primary
?Delayed onset,secondary to infection commonly
Diagnosis
? respiratory system:shock lung/ARDS
? circulatory system:heart failure
? central nervous system:dysfunction
? blood system:DIC
? urinary system:acute renal failure
? gastrointestinal sysrem:dysfunction
? liver:hepatic failure
Clinical manefestation
?Hypoperfusion:lactic acidosis,
hypoxia,tachycardia
?uncompensatory,SBP/DBP drops,ARDS
?Late stage,MODS
principles：
?Early to identify,to diagnose,and to treat
?Oxigen supply and respiratory support
?Liquid resuscitation,acidosis and vaso-dilation drugs
?Heart function protection,organ perfusion and oxigen delivery
?Adrenal cortisol,LPS antibodies
?Infection control actively
?Hypothermal therapy
Treatment
