Sepsis in Newborn 2011


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Sepsis in Newborn

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  • The differences between gender is less clear in preterm low-birthweight infants
  • Symptoms within 6h of birthMainly vertical transmission – neonate is exposed to potentially pathogenic bacteria until the membranes rupture and the infant passes through the birth canal and/or enters the extrauterine environment
  • The most important factor predisposing to infection is prematurity or Low Birth WeightThey have 3-10 fold higher incidence of infection than full-term, normal birth weight infantsPossible explanations: 1. maternal genital tract infection (cause of preterm labour) with increased risk of vertical transmission 2. premature infants have documented immune dysfunction 3. premature infants often require prolonged IV access, endotracheal intubation, or other invasive procedures
  • Staph: frequently due to intravascular devices (umbilical artery or vein catheters)
  • Gram +ve = environment and patient’s skinGram –ve = mainly from personnel ie. Crowding, handwashingCandida sepsis = prolonged (>10 days of central IV catheters, previous surgery, necrotizing enterocolitis, or abdominal pathology>
  • Fever is present in only 10-15% of cases, but when sustained (>1hr) it generally indicated infection.
  • Neurologic findings = seizures/jitterinessJaundice especially occurring within the first 24h without Rh or ABO blood group incompatibility and with a higher than expected direct bilirubin concentration
  • Omphalitis infection prevents obliteration of the umbilical vessels
  • Omphalitis infection prevents obliteration of the umbilical vessels
  • Other CBC: absolute band count is not sensitive enough to predict sepsis, but a ratio of immature:totalpolymorphonuclear leukocytes of <0.2 has high negative predictive valuePLT: may fall hours to days before the onset of clinical sepsis but more often remains elevated until a day or so after the neonate becomes ill.Urinalysis and culture: should be obtained by catheterization or suprapubic aspiration NOT by urine collection bags. If you see >5 WBCs/high power field is presumptive evidence of a UTILP: risk of increasing hypoxia during an LP in already hypoxemic neonates; thus supplement O2 is given before LP to prevent hypoxia.
  • Start empiric therapy, and then adjust drug according to sensitivities and site of infection. If no growth by 48h and neonate appears well, antibiotics are stopped
  • Start empiric therapy, and then adjust drug according to sensitivities and site of infection. If no growth by 48h and neonate appears well, antibiotics are stopped
  • Note: for penicillin-intolerant women, cefazolin should be usedErythromycin has shown up to 25% resistance in GBSClindamycin has shown up to 15% resistance in GBSFor penicillin-allergic women at high risk for anaphylaxi, clindamycin or erythromycin should be used if isolates are susceptible. If resistant, then Vancomycin should be used.
  • Incidence is higher in premies and LBW infants; however most cases occur in full-term infants
  • Incidence is higher in premies and LBW infants; however most cases occur in full-term infantsNote: other neonatal pathogens, such as E.coli or Listeria monocytogenes may produce illness that is clinically indistinguishable from that due to GBS
  • Note: RDS secondary to surfactant deficiency can coexist with bacterial pneumonia. Distinguishing between hyaline membrane disease and invasive neonatal GBS infection -severe apnea, early onset of shock, abnormalities in the peripheral leukocyte count, and greater lung compliance may be more likely in infants with GBS disease.
  • Focal infections involving bone and joints, skin and soft tissues, urinary tract, or lungs. Cellulitis and adenitis are often localized to the submandibular or parotid regions
  • Ventriculitis
  • Sepsis in Newborn 2011

    1. 1. OutlineSepsis in Newborn Epidemiology and etiology Signs and symptoms Diagnostic tests Treatment
    2. 2. OutlineGBSIn Pregnant Women In Newborn Epidemiology Epidemiology Guidelines for screening Signs and symptoms of and prophylaxis GBS (early and late) Treatment
    3. 3. What is Neonatal Sepsis? Bacteremia with systemic signs and symptoms of infection in the first 4 weeks of life SIRS in neonate and pediatric patients (2 or more of the following): Temperature instability Respiratory dysfunction Cardiac dysfunction Perfusion abnormalities Sepsis = SIRS with confirmed infectious process
    4. 4. Epidemiology and Etiology 2% of fetuses are infected in utero 10% of infants have infections in the 1st month of life Incidence 1-4cases per 1,000 live births in developed countries Twofold higher incidence of sepsis in term males and term females
    5. 5. Epidemiology and Etiology Most common neonatal pathogens: GBS – group B streptococcus Escherichia coli Other common pathogens: Staphylococcus, Streptococcus pneumoniae/viridans, Enterococci, Clostridia (in developing countries)
    6. 6. Figure 1Bacterial Causes of Systemic Neonatal Infections
    7. 7. Early Onset Within 7 days of birth Most cases occur within 72h Common with maternal obstetric complications (mainly vertical transmission) Intrapartum acquired organisms
    8. 8. Early OnsetRisk factors: Prematurity PROM occuring ≥ 18h before birth Maternal bleeding (eg. Placenta previa, abruptio placentae) Preeclampsia Difficult or traumatic delivery Maternal infection
    9. 9. Late Onset After 7 days of birth Mainly horizontal transmission (acquired from the environment) Newborn nursery, neonatal intensive care unit, or community 30-60% Staphylococci Enterobacter cloacae, E. sakazakii suggest contaminated feedings
    10. 10. Late OnsetRisk factors: Prolonged use of intravascular catheters Prolonged hospitalization Preterm infants have prolonged hospitalizations Contaminated equipment
    11. 11. Signs and SymptomsCommon signs: Diminished spontaneous activity Feeding intolerance, less vigorous sucking Apnea, respiratory distress Tachycardia or bradycardia Hypotension, poor perfusion with pallor Temperature instability (hypo or hyperthermia)
    12. 12. Signs and SymptomsLater complications of Sepsis: Respiratory failure Pulmonary hypertension Cardiac failure Shock Renal failure Liver dysfunction Cerebral edema or thrombosis Adrenal hemorrhage and/or insufficiency DIC
    13. 13. Signs and SymptomsSpecific signs: Meningitis, encephalitis, or brain abscess coma, seizures, opisthotonos Omphalitis Periumbilical erythema, discharge, or bleeding without a hemorrhagic diathesis Peritonitis or necrotizing enterocolitis Unexplained abdominal distention, bloody diarrhea, fecal leukocytes
    14. 14. Signs and SymptomsSpecific signs: Early-onset GBS and L. monocytogenes Respiratory distress Osteomyelitis or pyogenic arthritis Decreased spontaneous movement or extremity, swelling, warmth, erythema, tenderness over a joint
    15. 15. Diagnostic Tests CBC/blood culture Urinalysis and culture Lumbar puncture Increased risk of hypoxia Supplemental O2 is given before
    16. 16. Treatment Antibiotic therapy Early-onset sepsis: Initial therapy should include ampicillin or penicillin G plus an aminoglycoside Cefotaxime may be added to or substituted for aminoglycoside if meningitis is suspected If foul-smelling amniotic fluid is present at birth, therapy for anaerobes, clindamycin, metronidazole should be added
    17. 17. Treatment Antibiotic therapy Late-onset sepsis of a previous well infant: Ampicillin plus gentamicin or ampicillin plus cefotaxime If gram –ve meningitis is suspected, ampicillin, cefotaxime and aminoglycoside Late-onset sepsis in hospital-acquired: Vancomycin plus aminoglycoside If P. aeruginosa is prevalent in nursery, ceftazidime is used instead of aminoglycoside
    18. 18. Treatment Supportive therapy Respiratory and hemodynamic management Other treatments Exchange transfusion in severely ill (hypotensive and metabolic acidotic neonates) can be used Fresh frozen plasma Can help reverse heat-stable and heat-labile opsonin deficiencies that occur in low birth weight infants Granulocyte transfusions have been used but have not improved outcome significantly IV immune globulin given at birth may prevent sepsis in high-risk low birth weight infants
    19. 19. What is GBS? Group B Streptococcus or Streptococcus agalactiae Gram +ve Catalase –ve Complete hemolysis (Beta) on blood agar Bacitracin and trimethoprim-sulfamethoxazole Resistant Facultative anaerobe Lancefield group B carbohydrate antigen
    20. 20. GBS in Pregnant WomenEpidemiology 30% of women at term have vaginal or rectal cultures 50% of their infants also become colonized 1-2% develop early-onset disease
    21. 21. Early Onset Disease Same risk factors as sepsis for newborn for early disease Specific major risk factor for GBS is maternal vaginal or rectal colonization by GBS Incidence of early onset GBS infection increases with the length of rupture of membranes Screening and intrapartum antibiotic prophylaxis for GBS have significantly decreased the rate of early-onset disease Decrease from 1.7 cases per 1,000 live births to 0.6 cases per 1,000
    22. 22. Late Onset Disease GBS acquired later from maternal or non- maternal sources (eg. Nursery) Rate of late-onset GBS remained unchanged with intrapartum screening and antibiotic prophylaxis (environment)
    23. 23. Figure 2 – Incidence of early onset and late onset invasive GBS disease, 1989 through 2000.
    24. 24. CDC Guidelines Vaginorectal GBS screening cultures should be preformed for all pregnant women at 35-37weeks gestation Any woman with positive prenatal screening culture, GBS bacteriuria during pregnancy, or a previous infant with invasive GBS should receive intrapartum antibiotics Any woman with unknown status (culture not done, incomplete, or results unknown) and who deliver prematurely (<37weeks gestation) or experience prolonged rupture of membranes (>18hr) or intrapartum fever (>38oC) should also receive intrapartum antibiotics If amnionitis; replace GBS prophylaxis with broad-spectrum antibiotic therapy that includes an agent active against GBS Routine intrapartum prophylaxis is not recommended for women with GBS colonization undergoing planned cesarean delivery who have not begun labour or had rupture of membranes
    25. 25. Figure 3ScreeningGuidelines
    26. 26. GBS in NewbornEpidemiology Incidence higher in premature and low-birthweight infants Density of infant colonization determines the risk of early-onset invasive disease 40 times higher with heavy colonization 1/100 infants colonized develop invasive disease
    27. 27. Clinical ManifestationsEarly onset: Most infants become ill within the first 24hr of birth Most common manifestation is sepsis (50%), pneumonia (30%) and meningitis (15%) Asymptomatic bacteremia is uncommon but can occur Case fatality rate 4.7%
    28. 28. Clinical ManifestationsEarly onset: Respiratory symptoms are prominent regardless of the presence of pneumonia and include Cyanosis, apnea, tachypnea, grunting, flaring, and retractions Clinically and radiographically, pneumonia associated with early onset GBS disease is difficult to distinguish from hyaline membrane disease
    29. 29. Clinical ManifestationsLate onset: Most commonly manifests as bacteremia (45- 60%), meningitis (25-35%), focal infections (20%) Infants are often less severely ill on presentation than infants with early onset disease No increase risk after obstetric complications Case fatality rate 2.8%
    30. 30. Treatment Initial treatment should include ampicillin and aminoglycoside pending organism identification Penicillin G is treatment of choice of confirmed GBS infection In case of meningitis, high dose penicillin (450,000-500,000U/kg/24hr) and ampicillin (300- 400mg/kg/24hr) are recommended
    31. 31. Treatment Duration of therapy: Bacteremia without a focus – 10days Meningitis – 2-4weeks Ventriculitis – 4weeks Osteomyelitis – 4weeks
    32. 32. ReferencesCaserta, Mary. October 2009. Merck Manual for Health Care Professionals.“Infections in Neonates”.Figure 1. “Bacterial Causes of Systemic Neonatal Infections”. Nelson Textbook ofPediatrics. 19th ed. pp 267.Figure 2. Schrag SJ, Zywicki S, Farley MM, et al: Group B streptococcal disease inthe era of intrapartum antibiotic prophylaxis. N Engl J Med 2000;342:15-20.Figure 3. Schrag SJ, Gorwitz,. “Prevention of Perinatal Group BStreptococcal Disease”. Morbidity and Mortality Weekly Report 51(RR-11): 1-22, 2002.Lachenauer, C.S., Wessels, M.R.“Group B Streptococcus”. Nelson Textbook ofPediatrics.19th ed. pp879-883.