Tara Benton, MD Pediatric Critical Care Fellow October 24, 2011 Sepsis
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- Tara Benton, MD Pediatric Critical Care Fellow October 24, 2011
Sepsis
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- Objectives Definitions Epidemiology Microbiology
Pathophysiology Guidelines for treatment Prevention
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- Sepsis clinical syndrome that complicates severe infection and
is characterized by systemic inflammation and widespread tissue
injury
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- Definitions SIRS (systemic inflammatory response syndrome) At
least 2 of the 4 following criteria (abnormal temp or WBC must be
one of them) Temperature >38.5 or 2 SD above normal for age in
absence of external stimulus, chronic drugs or painful stimuli) OR
otherwise unexplained persistent elevation over a 0.5-4 hr period
OR for children 10% neutrophils International Consensus Conference
on Pediatric Sepsis 2005
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- Definitions Infection defined as a suspected or proven (by
positive culture, tissue stain or PCR test) infection caused by any
pathogen OR a clinical syndrome associated with a high probability
of infection Sepsis = SIRS + infection Severe Sepsis = SEPSIS + CV
dysfunction OR ARDS OR 2 other organ dysfunctions Septic Shock =
SEPSIS + CV dysfunction International Consensus Conference on
Pediatric Sepsis 2005
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- Definitions Shock Inadequate perfusion and oxygenation of the
body and its organs Delivery of substrate demand
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- Epidemiology Bacterial sepsis is the leading cause of medical
admissions to the PICU Worldwide, sepsis is the most common cause
of death in infants In 1995 Watson et al published a large
population based study evaluating severe sepsis - 0.56 cases per
1000 children (total of 40,000 cases each year) More common in
infants especially low-birth-weight, least common in 10-14yr Half
of all patients in this study had underlying medical conditions
Respiratory infection and primary bacteremia encompasses >40% of
all causes
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- Epidemiology Mortality is consistent at ~10% across age groups
Severity of illness does correlate with mortality (in adults) SIRS
7% Sepsis 16% Severe Sepsis 20% Septic Shock - 46%
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- Microbiology Most common pathogen overall is Staphylococcus of
all types In the population study previously discussed, 18% of
cases overall and 26% of neonatal infections An international study
from 2007, 44% of all cases were caused by Staph Most common
isolate overall is Staph aureus Other organisms noted in above
studies: Streptococcus and Pseudomonas aeruginosa Viral sepsis may
be indistinguishable from bacterial sepsis HSV in neonates
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- Risk factors Genetic Study in adopted children by Sorensen et
all in 1988 more likely to die from an infectious etiology if
biologic parent died from infection before age 50. Not associated
with death from infection in adoptive parents Polymorphisms
identified in multiple inflammatory molecules but unclear effect on
host response Gender: M>F
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- Risk Factors Comorbidity Nearly half of all children with sever
sepsis have an underlying comorbidity (neuromuscular, CV,
respiratory) Neoplasm associated with greatest number of
sepsiis-related deaths among all children In older children, CV
conditions have the highest case fatality rate of all comorbid
conditions Risk of death increases with increasing number of organ
dysfunction
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- Risk Factors Environmental risk factors Surgical site
infections 1/3 most commonly reported infection (~15%) Contaminated
procedure, surgery >2hrs, abd or thoracic procedure, present of
3 discharge diagnoses Central venous lines Most often gram +
bacteria (staph aureus, staph epi) GNR 21% Very young, chronically
ill, poor nutritional status, loss of skin integrity, neutropenia
Endocarditis, Urosepsis, Hemodialysis, Osteomyelitis
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- Pathophysiology Widespread tissue injury Massive and
uncontrolled release of proinflammatory mediators Host inflammatory
response
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- Pathophysiology What the bacteria do to us: Depends on the
bacteria Gram-negative Lipopolysaccharide (LPS) endotoxin found in
cell wall Rapidly triggers an inflammatory response from host
Gram-positive Exotoxins (tetanus, diptheria, botulism) Endotoxin
like cell wall components (lipoteichoic acid (LTA), peptidoglycan)
Soluble toxins (super antigens) toxic shock syndrome
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- Pathophysiology What we do to fight the bacteria: First the
pathogen is identified by our innate immune system (macrophages,
neutrophils) by specific receptors (Toll- like receptors) These
receptors trigger production of proinflammatory gene elements
Activation of innate immune cells and enhancement of pathogen
internalization and intracellular killing
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- Pathophysiology What we do to fight the bacteria: Release of
cytokines (TNF- , IL-1) and chemokines which modulate the
inflammatory response Of interest anti-inflammatory cytokines are
produced as well (TGF- , IL-1 receptor antagonist, IL10 )
Activation of adaptive immune system (T- and B-lymphocytes) More
cytokines released (able to produce both pro- and
anti-inflammatory) Activation of the endothelium results in more
cytokine release
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- Pathophysiology End organ results Endothelium Increase in
vascular permeability -> capillary leak Vasodilation Coagulation
cascade DIC both bleeding and microvascular clots Myocardial
dysfunction Temperature regulation Fever
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- Clinical presentation of Sepsis Classically early sepsis
presents as: Hyperdynamic and high cardiac output Warm extremities
Flash cap refill Widened pulse pressure Fever Ill appearing
Progression to shock will have findings of end organ dysfunction
Mental status changes (may just be irritability in infants)
Grunting or other signs of impending respiratory failure Poor urine
output Physical exam and history can give you clues to sites of
infection
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- Clinical presentation of septic shock Surviving Sepsis Campaign
2007 Guidelines for Pediatric Septic Shock
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- Treatment of sepsis Early recognition Goal directed therapy to
restore tissue perfusion In 2002 the first set of clinical practice
parameters were published Updated guidelines were published in 2007
and are what we use today
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- Goal Directed Therapy pediatric patients
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- Goal Directed Therapy
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- Goal directed therapy - neonates
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- Initial Antimicrobial Therapy As noted in the algorithm,
antimicrobial therapy should be initiated EARLY Complex decision
for choosing antibiotics and history of child is key Overall need
to start broad spectrum Should cover MRSA for all children now If
immunosuppressed or at risk like CF, should cover for Pseudomonas
Listeria monocytogenes and HSV coverage for infants
- Initial Antimicrobial Therapy Children >28 days of age and
normal hosts Vancomycin PLUS cefotaxime Consider clinda or
metronidazole if suspected GI/GU source Children >28 days and
immunosuppressed Vancomycin PLUS ceftazidime (or cefepime) Consider
adding aminoglycoside like tobramycin For Penicillin allergic:
Vancomycin PLUS meropenem For infants
- Initial Inotropic Therapy No one right answer for this Warm,
vasodilated, no known cardiac disease -> NOREPI or EPI Cool,
mottled -> DOPAMINE or EPINEPHRINE Cardiac disease ->
DOPAMINE OR EPINEPHRINE If one isnt working, add another Think
about vasopressin if not responding to the catecholamines (Dopa,
Epi, Norepi)
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- Summary of therapy Keep in mind goals up front SvO2 70%
Perfusion pressure CVP ~10-12 Follow lactate Early antibiotics
Fluid Inotrope Additional Inotrope Hydrocortisone ECMO
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- ICU monitoring and continued care Intubation with lung
protective mechanical ventilation if necessary Fluid removal
Diruetics CRRT or PD Hemoglobin - >10gm/dl Now being debated
Glycemic control start insulin if necessary to keep glucose 100-
200 Nutritional support utilizing enteral route if possible
(transpyloric if gastroparesis) Identifying source of infection and
addressing this if possible
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- Prevention Vaccination Following recommendations for reducing
CLABSI Insertion bundle Meticulous sterile technique went entering
line GET THE LINE OUT Follow VAP prevention bundle while intubated
Remove all plastic as soon as possible Talk about
lines/tubes/drains every day on rounds and engage bedside nursing
to facilitate the above
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- THANK YOU