Neonatal Sepsis

1. Neonatal Sepsis Joanne Ang Pediatrics Rotation – Nursery

2. 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

3. 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

4. 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

5. 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.

6. 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

7. The neonate is unable to respond effectively to infectious hazards because of deficits in the physiological response to infectious agents! 1 2 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. 4 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. 3 Once in the tissues, they may fail to deaggregate in response to chemotactic factors.

8. 5 The limited ability of neonatal PMNs for phagocytosis and killing of bacteria is impaired when the infant is clinically ill. 6 Lastly, neutrophil reserves are depleted easily because of the diminished response of the bone marrow, especially in the premature infant.

10. Etiology • The following are transplacentally transmitted: • Toxoplasmosis • Syphilis • Cytomegalovirus • Parvovirus B19 • Varicella

11. Etiology • The following are transplacentally and intrapartally transmitted: • Herpes Simplex Virus • HIV • Hepatitis B and C virus • Tuberculosis

12. Clinical Manifestation of Transplacental Infections

13. Clinical Manifestation of Transplacental Infections

14. Clinical Manifestation of Transplacental Infections

15. Signs and Symptoms of infection

16. Most common EtiologIES of sepsis in the newborn • E. Coli • Group B Streptococcus • Listeriamonocytogenes

17. Risk factors associated with neonatal sepsis

18. Risk factors associated with neonatal sepsis • Neonatal Risk Factors • Term male infants have 2x higher than female • Pre-term have a 3-10x higher incidence of infection than term • Low Birth weight

19. What is sepsis?

21. Neonatal Sepsis

22. 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)

23. Predominant pathogens • Early Onset Sepsis • E.coli • Group B streptococcus • Listeria • Hemophilus influenza • Enterobacteraeruginosa • Klebsiella pneumonia • Pseudomasaeruginosa • Staphylococcus aureus

24. 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

26. Signs and symptoms of sepsis • Respiratory distress • Tachypnea • Retractions • Grunting • Nasal flaring • Apnea • Abnormal skin color perfusion • Pale color or gray color • Delayed capillary refill time • jaundice

27. Signs and symptoms of sepsis • Temperature instability • Hypothermia and rarely, hyperthermia • Feeding intolerance • Vomiting • Diarrhea • Abdominal distention • Abnormal HR and BP • Tachycardia, bradycardia, hypotension • Abnormal neurologic status • Lethargy, hypotonia, seizures

28. Diagnosis The 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.

29. Laboratory Diagnosis • Blood culture • CSF culture • Urine culture • CBC • Acute phase reactants: ESR and CRP • Chest X-ray

30. 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.

32. 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

33. Management

34. Risk factors associated with neonatal sepsis

35. Risk factors associated with neonatal sepsis • Neonatal Risk Factors • Term male infants have 2x higher than female • Pre-term have a 3-10x higher incidence of infection than term • Low Birth weight

36. Management

37. Management

38. 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

39. Treatment • Initial empiric therapy for late onset sepsis • Ampicillin 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

40. Supportive measures • Maintenance of normal body temperature • Maintenance of adequate nutrition • Proper hydration • Monitoring of electrolytes and glucose • Ventilatory support if needed

41. THANK YOU