Pediatric Sepsis
Pediatric Critical CareDiponegoro University/Kariadi
HospitalSemarang - 2011SEPSISModule ofLearning ObjectivesHow to
diagnose pediatric sepsis How to manage pediatric sepsis How to
understand early detection in pediatric sepsis How to prevent
sepsis
Must to know key points to diagnose sepsisDifferential diagnosis
from clinical manifestations Laboratory interpretation: hematology,
serology and microbiology
(bacteriology)DefinitionClassificationEtiologyEpidemiologyPathogenesisDiagnosis
Must to know key points to manage sepsisProcedure of : fluid
resuscitation, Infection control, Nutrition and Bed restMedical
treatment : empirical antibiotic deescalating systemNonsurgical
critical care management : electrolyte disturbance, acid-base
imbalance, multiorgan dysfunctionSource of infection detection
Must to know key points to do early detection Communication
skillCorrelation between predisposing factors and onset of
sepsis
SEPSISIntroductionConsensus 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 admissionMortality 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
SIRS : At least 2 of the following (temp. or leukocyte
abnormality should be present): Core temperature > 38.5C or <
36CTachycardia, a mean HR > 2SD above normal for ageMean
Respiratory Rate > 2SD above normal for ageLeukocyte count or
for age or >10% immature neutrophilsINFECTION:Suspected or
proven infection by any pathogen or a clinical syndrome assoc. with
a high probability of infectionEvidence 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 infectionSEVERE SEPSIS Sepsis plus one of the
following : cardiovascular organ dysfunction or ARDS or two or more
other organ dysfunctionsSEPTIC SHOCK Sepsis and cardiovascular
organ dysfunction(Goldstein et al. Pediatr Crit Care 2005, 6 :
1)Correlation between SIRS, Infection and SepsisBacteria Fungi
Parasite Virus Other Infection Major surgery Trauma Burn Transplant
rejection Pancreatitis Myocard infarct SEPSIS SIRS (non infection)
Pathophysiology of Sepsis InfectionInitiationsPrimary
MediatorsPrimary SitesSecondary MediatorsSecondary SitesShock
MODSLPS, ExotoxinsTNF, IL-1, IFN, etcWBCS, Vascular CoagulationO2
Radicals, NO, PAF, TXA2, ILS, etcEndothelium, OrgansNew Concept
about SIRS, SEPSIS, CARS, MARSPro-inflammatory responseSystemic
spillover of pro-inflammatory mediatorsInitial insult (bacterial,
viral, traumatic, thermal)Anti-inflammatory responseSystemic
spillover of anti-inflammatory mediatorsSystemic reactionSIRS
(pro-inflammatory)CARS (anti-inflammatory)MARS
(mixed)Cardiovascular compromise shock, SIRS
predominatesHomeostasis CARS and SIRS balanced Apoptosis (cell
death) Death with minimal inflammationOrgan dysfunction SIRS
predominatesSuppression of the immune system CARS predominatesCARS
: Compensatory Antiinflammatory Response SyndromeMARS : Mixed
Antiinflammatory Response Syndrome
The Pathophysiological and Clinical Process of MODS
The Inflammatory Cascade Leading to MODSIntestinal Ischemia /
Reperfusion Injury Humoral MediatorsCellular MediatorsComplement
Endotoxin Cytokines PAF Eicosanoids OthersPMNS (acute) Macrophages
(chronic)Selectins IntegrinsPMNCellOxidants proteasesPulmonary
Microvascular Endothelial Endothelial Dysfunction Microvascular
Thrombosis Ec Blebbing, Focal Necrosis Increased microvascular
permeability Interstitial Edema Alveolar Hemorrhage / Edema Fibrin
Deposition Repair / Cell death Intestinal Ischemia / Reperfusion
Injury (contd)Splanchnic BedSystemic CirculationActivated
Complement TNF, IL-1, IL-6, LPS, PAFTxA2 LTB4 PAF TNF IL-2ODFRS
PGI2 NONeutrophilsMicrocirculatory PluggingTXA2
LTC4VasoconstrictionReduced Splanchnic PerfusionTXA2Activated
NeutrophilsDefinition of MODSOccurrence 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 OutcomeRespiratory system: PO2 /
FiO2 ratio.Renal system: serum creatinine concentration.Hepatic
system: serum bil. concentration.Haematological system: platelet
count.CNS: Glasgow Coma ScaleMODSMain 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:
Predisposition of infectionI: Infection (insult)R: Respons of
inflammatoryO: Organ dysfunctionDiagnosis of Septic ShockSepsis
with signs of shock Altered consciousnessLow Systolic BP < 5
percentile and low MAP according to ageDecreased peripheral
perfusion: cold extremities, prolong capillary refill time > 2
second, increase serum lactate, urine output < 1 ml/kgBW,
core-toe temperature different > 2 C ManagementBUNDLE
DEFINITIONA "bundle" isa 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 BundleEarly IdentificationEarly
Antibiotics and CulturesEarly Goal Directed Therapy
246 - hour Severe Sepsis/Septic Shock Bundle
1. Early Detection:Obtain serum lactate.
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 fluidTitrate
to MAP according to age.
Septic shock or lactate > 4 mmol/L:CVP and ScvO2 measured.CVP
maintain >8 mmHg.MAP maintain >65 mmHg.
ScvO2 8 mmHg, MAP > 65 mmHg:PRBCs if Ht < 30%.
Inotropes.
2524 - hour Severe Sepsis and Septic Shock Bundle
Glucose control (insulin):maintained on average 24 monthsS.
PneumoniaeH. InfluenzaeS. AureusN. Meningtidis
CefotaximeCefriaxoneAmpiciline +Chlorampenicol50505025Immuno
compromisedS. aureus,
ProteusPseudomonasEnterobacteriaceaeVancomycin +Ceftazidime
+Ticarcillin255075Antibiotic Combination AB/ in neutropenic
patientsEmpirical AB/ not more than 3 5 daysDuration of AB: 7 10
daysNegative culturedSepsis occurredIn > 50%Decision to :
continue,Narrow, stop of ABOn the basis 0f Clinical
judgment&Clinical information4 basic principles of
empiricalAntibiotic TherapyAdequate and accurate antibiotic
therapy
Therapeutic effect of antibiotic
Antibiotic effect and negative effect of antibiotic
Accurate time of antibiotic therapy
Fluid responsiveRefractory shockPlace pulmonary artery catheter
and direct fluid, inotrope,vasopressor,vasodilator, and hormonal
therapies to attain normal MAP-CVP and CI > 3.3 and < 6.0
L/min/m2Stepwise 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.Give hydrocortisoneAt Risk of Adrenal Insufficiency?
Catecholamine -resistant shock Not at Risk?Titrate epinephrine for
cold shock, norepinephrine for warm shock to normal MAP-CVP and SVC
O2 saturation > 70% Fluid refractory-dopamine resistant
shockEstablish central venous access, begin dopamine therapy and
establish arterial monitoring .Fluid refractory shockPush 20cc/kg
isotonic saline or colloid boluses up to and over 60 cc/kgCorrect
hypoglycemia and hypocalcemiaRecognize decreased mental status and
perfusion.Maintain airway and establish access according to PALS
guidelines.Observe in PICUConsider ECMOPersistent
Catecholamine-resistant shock 0 min 5 min60 min15 min Normal Blood
Pressure Low Blood Pressure Low Blood Pressure Cold Shock Cold
Shock Warm Shock SVC O2 sat < 70% SVC O2 sat < 70% Add
vasodilator or Type III PDE inhibitor Volume and Epinephrine Volume
and Norepinephrine with volume loading (?vasopressin or
angiotensin)Do not give hydrocortisoneTararengkiu sadayanaSoal
latihan MCQPernyataan yang benar tentang sepsis :Sindrom klinis
akibat respons proinflamasi sistemik masif terhadap infeksiTidak
terjadi pada penderita imunodefisiensiDisebabkan oleh bakteri gram
negatif tetapi tidak oleh bakteri gram positifBukan disebabkan oleh
virus ataupun parasit2.Metronidazole perlu diberikan dalam terapi
antibiotik empiris pada penderita sepsis dengan dugaan fokus
infeksi di daerah :Rongga mulutMuskuloskeletalRongga
abdomenParu-paru3. Seorang bayi berusia 7 bulan dengan sepsis
disertai adanya tanda inflamasi dan hematoma di kedua kelopak mata
dan jaringan muskulokutaneus. Mikroorganisme yang paling mungkin
sebagai penyebab :StaphylococcusStreptococcus
hemoliticusPseudomonas aerogenosaHaemophilus influenzae4. Pemberian
cairan initial pada penderita sepsis berat adalah :Cairan 20
ml/kgBB/jamCairan rumatanCairan 20-40 ml/kgBB/jamCairan 20-60
ml/kgBB/secepatnya
5. Pada penderita HIV, penyebab sepsis tersering adalah
:Trepanoma pallidumStreptococcus pneumoniaeMycobacterium
tuberculosisPneumocystis jiroveci
6. Seorang anak dengan sepsis disertai adanya hipotensi dan
penurunan kesadaran, memberikan respons hemodinamik yang baik
setelah inisiasi cairan resusitasi, diklasifikasikan sebagai
penderita :SepsisSepsis beratSyok sepsisKegagalan organ
multipel
7. Pemberian kortikosteroid pada penderita sepsis menunjukkan
manfaat yang baik bila diberikan pada :Syok septikAcute Respiratory
Distress SyndromeSepsis dini disertai perdarahan korteks
adrenalKegagalan organ multipel disertai pankreatitis akut
