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Neonatal Sepsis
Neonatal Sepsis
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Review Articles
Neonatal Sepsis – A Review
CHANDAN KUMAR SHAHA1, SANJOY KUMER DEY2, KAMRUL HASSAN SHABUJ1, JUBAIR CHISTI3, M
A MANNAN4, MD. JASHIMUDDIN5, MD. TARIQUL ISLAM6, MOHAMMOD SHAHIDULLAH7
differentiate an illness of microbial origin from an work-up and antibiotic therapy; however, combinations
identical clinical syndrome that can arise in several of risk factors are clearly additive and should greatly
non-microbial conditions11. When accompanied by enhance the suspicion of sepsis.13
evidence of hypoperfusion or dysfunction of at least
• Prematurity and low birthweight
one organ system, this becomes ‘severe sepsis’.
Finally, where severe sepsis is accompanied by • Premature or prolonged rupture of membranes (>18 h)
hypotension or need for vasopressors, despite • Maternal peripartum fever (>100.40F) or infection
adequate fluid resuscitation, the term ‘septic shock’
• Resuscitation at birth
applies11. Within this terminology, the archaic term
‘septicemia’, which persists in the language of the • Multiple gestation
non-specialist and layman, straddles the definitions • Invasive procedures
of sepsis, severe sepsis, and septic shock11.
• Infants with galactosemia (predisposition to E. coli
Neonatal sepsis is a clinical syndrome of systemic sepsis), immune defects, or asplenia.
illness accompanied by bacteremia occurring in the
first month of life12. The condition may be defined both • Other factors: Male sex (four times more affected
clinically and/or microbiologically, by positive blood than females), bottle-feeding (as opposed to
and/or cerebrospinal fluid cultures5. breast-feeding), low socio-economic status,
improper handwashing practice of NICU staff and
Classification family members etc.
Neonatal sepsis may be classified according to the
time of onset of the disease: early onset (EOS) and Causative organisms
late onset (LOS). The distinction has clinical Pathogens causing neonatal infections and their
relevance, as EOS disease is mainly due to bacteria antibiotic susceptibility pattern may change over
acquired before and during delivery, and LOS disease time14-16 and differ between countries17.
to bacteria acquired after delivery (nosocomial or Neonatal surveillance in developed countries generally
community sources). In the literature, however, there identifies Group B Streptococcus (GBS) and E. coli
is little consensus as to what age limits apply. A few as the dominant EOS pathogens and coagulase-
papers distinguish between very early onset (within negative staphylococci (CONS) as the dominant LOS
24 hours), EOS (24 hours to six days), and LOS (more pathogen followed by GBS and Staph aureus. In
than six days) sepsis5. Very late onset sepsis is developing countries, overall, Gram negative organisms
demarcated by onset at >30 days of age. are more common and are mainly represented by
Klebsiella, E. coli and Pseudomonas. Of the Gram
Risk factors
positive organisms, Staph aureus, CONS,
Several obstetric and neonatal factors have been
Streptococcus pneumoniae, and Streptococcus
identified that may be associated with an increased
pyogenes are most commonly isolated.18 Agents that
risk of neonatal infection. The presence of any of these
commonly cause nosocomial infection are coagulase-
factors alone is not an indication for a complete sepsis
negative staphylococci, gram-negative bacilli (E. coli, • Gastrointestinal system: Abdominal distension,
Klebsiella pneumonia, Salmonella, Enterobacter, vomiting, diarrhea, hepatomegaly
Citrobacter, Pseudomonas aeruginosa, Serratia), • Respiratory system: Apnea, dyspnea, tachypnea,
Enterococci, and S. aureus3. retractions, flaring, grunting, cyanosis
Pathogenesis • Renal system: Oliguria
The pathophysiology of sepsis arises largely from the • Cardiovascular system: Pallor, mottling; cold,
response of the host’s innate immune system under clammy skin, tachycardia, hypotension,
the influence of genetic factors. Sepsis originates from bradycardia
a breach of integrity of the host barrier, either physical
or immunological, and direct penetration of the • Central nervous system: Irritability, lethargy,
pathogen into the bloodstream, creating the septic tremors, seizures, hyporeflexia, hypotonia,
state.11 abnormal Moro reflex, irregular respirations, full
fontanel, high-pitched cry
Pathophysiological pathways of sepsis:11
• Hematologic system: Jaundice, splenomegaly,
Clinical manifestations pallor, petechiae, purpura, bleeding
The signs and symptoms of sepsis are influenced by Early-onset sepsis is usually a multisystem illness
the virulence of the pathogen, the portal of entry, the with prominent respiratory symptoms. It is
susceptibility and response of the host, and the characterized by a sudden onset and fulminant course
temporal evolution of the condition.11 that can progress rapidly to septic shock and death.
Initial signs and symptoms of infection in newborn Late-onset sepsis is usually more insidious but it can
infants:3 be fulminant at times. In addition to bacteremia, these
• General: Fever, temperature instability, “not doing infants may have an identifiable focus, most often
well”, poor feeding, edema meningitis in addition to sepsis.12
BANGLADESH J CHILD HEALTH 2012; VOL 36 (2) : 85 CK Shaha, SK Dey, KH Shabuj et al
14. Stoll BJ, Hansen N. Infections in VLBW infants: 17. Zaidi AK, Huskins WC, Thaver D, et al. Hospital-
studies from the NICHD Neonatal Research acquired neonatal infections in developing
Network. Semin Perinatol 2003;27:293–301. countries. Lancet 2005; 365: 1175–88.
15. May M, Daley AJ, Donath S, et al. Early onset 18. Wattal C, Oberoi JK. Neonatal Sepsis. Indian J
Pediatr 2011;78(4):473–474.
neonatal meningitis in Australia and New
Zealand, 1992-2002. Arch Dis Child Fetal 19. Stoll BJ, Hansen N, Fanaroff AA, et al. Late-
Onset Sepsis in Very Low Birth Weight
Neonatal Ed 2005;90:F324–7.
Neonates: The Experience of the NICHD
16. Isaacs D. A ten year, multicentre study of Neonatal Research Network. Pediatrics 2002;
coagulase negative staphylococcal infections in 110: 285-291.
Australasian neonatal units. Arch Dis Child Fetal 20. Adams-Chapman I, Stoll BJ. Prevention of
Neonatal Ed 2003;88:F89–93. nosocomial infections in the neonatal intensive
care unit. Curr Opin Pediatr 2002; 14: 157-164.