Astana Medical University.

V.G.Korpachev Department of pathological physiology.

IWS

Theme: “Sepsis in neonates”.

Prepared by: Yessenbekkyzy N.

General Medicine faculty,

2^nd course, 226 – group.

Faculty member: Kalizatova A.S.

2013.

Contents.

1. Introduction…………………………………………………………….....….3

2. Literature review

1. Etiology.………………………………………………………......4-5

2. Pathogenesis…………………………………………………........5-6

3. Treatment.........................................................................................6-7

2. Conclusion………………………………………………………..........8

3. List of references…………………………………………..............9

Introduction

Neonatal sepsis occurs in 1 to 8 per 1000 live births with the highest incidence occurring among infants of very low birth weight and gestation. It is mandatory to have a high index of suspicion for the possibility of sepsis, as well as a low threshold for commencing antibiotic treatment. While more babies are treated than are infected the consequences of untreated sepsis are devastating.Neonatal sepsis is invasive infection, usually bacterial, occurring during the neonatal period. Signs are multiple and include diminished spontaneous activity, less vigorous sucking, apnea, bradycardia, temperature instability, respiratory distress, vomiting, diarrhea, abdominal distention, jitteriness, seizures, and jaundice. Diagnosis is clinical and based on culture results. Treatment is initially with ampicillin plus either gentamicin or cefotaxime, narrowed to organism-specific drugs as soon as possible.

Early onset sepsis (within the first 48 hours of life)

• often manifests with pneumonia and/or septicaemia

• equal male and female incidence

• characterised by high risk of mortality (10 to 30%)

• predominantly due to organisms acquired from the birth canal

• occasionally intrapartum haematogenous spread occurs eg Listeria

• over 80% of cases are due to GBS and gram negative bacteria

Late onset sepsis (after the first 48 hours)

• due to organisms acquired either around the time of birth or in hospital eg Coagulase Negative Staphylococcus during hospitalisation in the NICU

• male predominance

• infants < 1000gms are particularly at risk

• mortality rate approximately 5%

• > 70% due to Coagulase Negative Staphylococcus and Staphylococcus aureus, 10 - 15% due to Gram negatives. Candida is an important pathogen, particularly among extremely low birth weight infants

• gram negatives and GBS predominate among infections acquired outside the NICU setting

2. Literature review.

2.1. Etiology.

Neonatal sepsis can be early onset (within 7 days of birth) or late onset (after 7 days). Early onset: Early-onset sepsis usually results from organisms acquired intrapartum. Most infants have symptoms within 6 h of birth, and almost all cases occur within 72 h. Group B streptococcus (GBS) and gram-negative enteric organisms (predominantly Escherichia coli) account for most cases of early-onset sepsis. Vaginal or rectal cultures of women at term may show GBS colonization rates of up to 30%. At least 35% of their infants also become colonized. The density of infant colonization determines the risk of early-onset invasive disease, which is 40 times higher with heavy colonization. Although only 1/100 of infants colonized develop invasive disease due to GBS, > 50% of those present within the first 6 h of life. Nontypeable Haemophilus influenzae sepsis has been increasingly identified in neonates, especially premature neonates.

Other gram-negative enteric bacilli (eg, Klebsiella sp) and gram-positive organisms—Listeria monocytogenes, enterococci (eg, Enterococcus faecalis, Enterococcus faecium), group D streptococci (eg, Streptococcus bovis), α-hemolytic streptococci, and staphylococci—account for most other cases. Streptococcus pneumoniae, H. influenzae type b, and, less commonly, Neisseria meningitidis have been isolated. Asymptomatic gonorrhea occurs occasionally in pregnancy, so Neisseria gonorrhoeae may be a pathogen.

Late onset: Late-onset sepsis is usually acquired from the environment . Staphylococci account for 30 to 60% of late-onset cases and are most frequently due to intravascular devices (particularly umbilical artery or vein catheters). E. coli is also becoming increasingly recognized as a significant cause of late-onset sepsis, especially in very LBW infants. Isolation of Enterobacter cloacae or E. sakazakii from blood or CSF suggests contaminated feedings. Contaminated respiratory equipment is suspected in outbreaks of hospital-acquired Pseudomonas aeruginosa pneumonia or sepsis. Although universal screening and intrapartum antibiotic prophylaxis for GBS have significantly decreased the rate of early-onset disease due to this organism, the rate of late-onset GBS sepsis has remained unchanged, which is consistent with the hypothesis that late-onset disease is usually acquired from the environment.

The role of anaerobes (particularly Bacteroides fragilis) in late-onset sepsis remains unclear, although deaths have been attributed to Bacteroides bacteremia. Anaerobes may account for some culture-negative cases in which autopsy findings indicate sepsis.

Candida sp are increasingly important causes of late-onset sepsis, occurring in 12 to 13% of very LBW infants.

Early and late onset: Certain viral infections (eg, disseminated herpes simplex, enterovirus, adenovirus, respiratory syncytial virus) may manifest as early-onset or late-onset sepsis.