NEONATAL SEPSIS

Joanne Ang

Pediatrics Rotation – Nursery

INTRODUCTION Infection – important cause of neonatal

and infant morbidity and mortality

2% of fetuses are infected in utero 10% of infants have infections in the 1st

month of life

INTRODUCTION Neonatal Infections are unique

1.)infectious agents can be transmitted from the mother- transplacentally -ascending bacterial infections – maternal chorioamnionitis, PROM, resuscitation at birth

2.)newborn are less capable of responding to infections

3.)clinical manifestation vary and include subclinical , mild to severe manifestations

INTRODUCTION Neonatal Infections are unique

4.)maternal infection is often undiagnosed during pregnancy

5.)Wide variety of etiologic agents

6.)Immature and Very Low Birth weight remain in hospital for a long time which puts them at continuous risk for acquired infections

- Maternal infection that is the source of transplacental infection is often undiagnosed during pregnancy because the mother was either asymptomatic or had nonspecific signs and symptoms.

- Bacteria, viruses, fungi, protozoans and mycoplasmas.

CHORIOAMNIONITIS Criteria

Fever (Temperature of > 37.8 C) plus two or more of the following Maternal tachycardia (>100 bpm) Fetal tachycardia (>160 bpm) Uterine tenderness Malodorous or cloudy amniotic fluid Maternal WBC count >15,000 cells/cubic mm

The neonate is unable to respond effectively to infectious hazards because of deficits in the physiological response to infectious agents!

The neonatal neutrophil or polymorphonuclear (PMN) cell, which is vital for effective killing of bacteria, is defective in chemotaxis and killing capacity.

Decreased adherence to the endothelial lining of blood vessels reduces their ability to marginate and leave the intravascular area to migrate into the tissues.

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Once in the tissues, they may fail to deaggregate in response to chemotactic factors.

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Also, neonatal PMNs are less deformable; therefore, they are less able to move through the extracellular matrix of tissues to reach the site of inflammation and infection.

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The limited ability of neonatal PMNs for phagocytosis and killing of bacteria is impaired when the infant is clinically ill.

Lastly, neutrophil reserves are depleted easily because of the diminished response of the bone marrow, especially in the premature infant.

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ETIOLOGY The following are transplacentally

transmitted:ToxoplasmosisSyphilisCytomegalovirusParvovirus B19Varicella

ETIOLOGY The following are transplacentally and

intrapartally transmitted:Herpes Simplex VirusHIVHepatitis B and C virusTuberculosis

CLINICAL MANIFESTATION OF TRANSPLACENTAL INFECTIONS

CLINICAL MANIFESTATION OF TRANSPLACENTAL INFECTIONS

CLINICAL MANIFESTATION OF TRANSPLACENTAL INFECTIONS

SIGNS AND SYMPTOMS OF INFECTION

MOST COMMON ETIOLOGIES OF SEPSIS IN THE NEWBORN E. Coli Group B Streptococcus Listeria monocytogenes

RISK FACTORS ASSOCIATED WITH NEONATAL SEPSIS

RISK FACTORS ASSOCIATED WITH NEONATAL SEPSIS

Neonatal Risk FactorsTerm male infants have 2x higher than

femalePre-term have a 3-10x higher incidence of

infection than termLow Birth weight

WHAT IS SEPSIS?

NEONATAL SEPSIS

NEONATAL SEPSIS – EARLY ONSET Predisposing factors:

*Maternal group B Streptococcus (GBS) colonization (especially if untreated during labor)

*Premature rupture of membranes (PROM), preterm rupture of membranes, prolonged rupture of membranes

*Prematurity*Maternal urinary tract infection (3rd trimester)*Maternal Chorioamnionitis (WBC>18)

PREDOMINANT PATHOGENS Early Onset Sepsis

E.coliGroup B streptococcusListeriaHemophilus influenzaEnterobacter aeruginosaKlebsiella pneumoniaPseudomas aeruginosaStaphylococcus aureus

NEONATAL SEPSIS – LATE ONSET occurs at 7-90 days of life Prematurity, prolonged hospitalization,

presence of foreign bodies like umbilical catheters, ET tube, parenteral alimentation, prior use of antibiotics

Predominant pathogens:coagulase negative Staphylococcus

epidermidis, Staphylococcus aureus, Candida, Enterococcus, E coli, Klebsiella, Pseudomonas aeroginosa, GBS, Serratia, Acinetobacter, Anaerobes

SIGNS AND SYMPTOMS OF SEPSIS Respiratory distress

TachypneaRetractionsGruntingNasal flaringApnea

Abnormal skin color perfusionPale color or gray colorDelayed capillary refill time jaundice

SIGNS AND SYMPTOMS OF SEPSIS Temperature instability

Hypothermia and rarely, hyperthermia Feeding intolerance

VomitingDiarrheaAbdominal distention

Abnormal HR and BPTachycardia, bradycardia, hypotension

Abnormal neurologic statusLethargy, hypotonia, seizures

DIAGNOSISThe diagnosis of systemic infection in the

newborn is difficult to establish on the basis of clinical findings alone.

Any infant who suddenly changes for the worse should be suspected for sepsis.

LABORATORY DIAGNOSISBlood cultureCSF cultureUrine cultureCBCAcute phase reactants: ESR and CRPChest X-ray

SEPSIS SCREEN Because none of the diagnostic tests for

sepsis is able to identify infants with proven sepsis with reasonable accuracy, investigators have used combinations of laboratory tests to enhance the identification of infected neonates.

Because of its high negative predictive accuracy, it can provide a greater reassurance that an infection is not present.

SEPSIS SCREEN A positive sepsis screen result was

defined as two or more abnormal test results.Sensitivity = 93%Positive predictive accuracy of 39%

< 2 abnormal results = 99% negative predictive accuracy

MANAGEMENT

RISK FACTORS ASSOCIATED WITH NEONATAL SEPSIS

RISK FACTORS ASSOCIATED WITH NEONATAL SEPSIS

Neonatal Risk FactorsTerm male infants have 2x higher than

femalePre-term have a 3-10x higher incidence of

infection than termLow Birth weight

MANAGEMENT

MANAGEMENT

TREATMENT Initial empiric therapy for early onset sepsis

Ampicillin plus aminoglycoside (usually gentamicin or cefotaxime)

Antibiotic therapy should be tailored according to its sensitivities L. monocytogenes -> Aminoglycoside + ampicillin Enterococci -> Amoxicillin + aminoglycoside or

vancomycin GBS -> Penicillin or ampicillin S. aureus -> Penicillase resistant penicillins or

cephalosporins; MRSA – vancomycin, clindamycin P. aeruginosa -> Ticarcillin, carbenicillin and an

aminoglycoside; Most are sensitive to Ceftazidime Gram negative enteric organisms ->Generally sensitive

to aminoglycoside

TREATMENT Initial empiric therapy for late onset

sepsisAmpicillin plus cefotaxime; vancomycin +

gentamicin; vancomycin+cefotaxime With minimal or no focal infection

usually 7-10 days With meningitis caused by group B

streptococcus or gram negative enteric bacilli at least 21 days

SUPPORTIVE MEASURES Maintenance of normal body

temperature Maintenance of adequate nutrition Proper hydration Monitoring of electrolytes and glucose Ventilatory support if needed

THANK YOU