Implementation of the NICE prevention and treatment of early onset neonatal infection guideline: the Glasgow experience

Introduction: Ionised hypocalcemia (S-Ca2+) has been repeatedly observed in neonates with sepsis. Our aim was to evaluate total calcemia (S-Ca) and its relationship to laboratory markers of infection. Methods: We retrospectively evaluated total calcemia (S-Ca) and its relationship to laboratory markers of sepsis/infection (serum levels of C-reactive protein – S-CRP and procalcitonin – S-PCT) in 29 full-term neonates with early-onset neonatal infection hospitalized at our neonatology ward between 2012 and 2016. The control group consisted of 705 neonates without infection. Results: In neonates with early-onset infection , the S-Ca on day 1, 2 and 3 was significantly lower (p < 0.0001; p < 0.0001; p = 0.05 versus controls) same as the pooled S-Ca (p < 0.0001 versus controls). There was a weak negative correlation between pooled S-Ca and S-PCT, or pooled S-Ca and S-CRP (r = −0.22, p = 0.06; r = −0.19, p = 0.09). Conclusion: S-Ca was decreased in neonates with early-onset infection and did show a slight tendency to inverse correlation with S-CRP and S-PCT. Pediatricians must be aware of the fact that a drop in total S-Ca should alert their attention to the risk of neonatal infection, and, likewise, that the children with neonatal infection are at a higher risk of hypocalcemia with all its consequences.

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Group B Streptococcus (Streptococcus agalactiae)

10.1093/med/9780190604813.003.0019 ◽

2018 ◽

Author(s):

Kirsty Le Doare ◽

Christine E. Jones ◽

Paul T. Heath

Keyword(s):

Early Onset ◽

Late Onset ◽

Group B Streptococcus ◽

Significant Risk ◽

Neonatal Infection ◽

Significant Risk Factor ◽

Invasive Disease ◽

Neurodevelopmental Outcomes ◽

Intrapartum Antibiotic ◽

Group B

Group B Streptococcus (GBS) is a leading cause of early neonatal infection and neonatal mortality, with long-term adverse neurodevelopmental outcomes in up to 50% of survivors of GBS meningitis. GBS has a likely underappreciated role in causing preterm birth and stillbirth. GBS colonizes the vagina and gastrointestinal tract of the pregnant woman, and transmission to the infant occurs during or just before delivery. Although the majority of these infants do not develop invasive disease, maternal colonization is a prerequisite for early onset disease (0–6 days of life, most commonly associated with sepsis and respiratory distress) and a significant risk factor for late onset disease (7–89 days of life, most commonly associated with sepsis and meningitis). The introduction of intrapartum antibiotic prophylaxis has resulted in significant declines in the incidence of early onset disease but provides no protection against late onset disease.

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Epidemiology of invasive early-onset neonatal infection in a French administrative district: A 10-year population-based study

Archives de Pédiatrie ◽

10.1016/j.arcped.2020.07.011 ◽

2020 ◽

Vol 27 (7) ◽

pp. 356-361

Author(s):

C. Dain ◽

J.-C. Rozé ◽

J. Caillon ◽

C. Flamant ◽

J.-B. Muller ◽

...

Keyword(s):

Early Onset ◽

Neonatal Infection ◽

Population Based ◽

Administrative District ◽

Population Based Study

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Serial Measurements of C-Reactive Protein and Interleukin-6 in the Immediate Postnatal Period: Reference Intervals and Analysis of Maternal and Perinatal Confounders

Clinical Chemistry ◽

10.1093/clinchem/47.6.1016 ◽

2001 ◽

Vol 47 (6) ◽

pp. 1016-1022 ◽

Cited By ~ 66

Author(s):

Claudio Chiesa ◽

Fabrizio Signore ◽

Marcello Assumma ◽

Elsa Buffone ◽

Paola Tramontozzi ◽

...

Keyword(s):

Interleukin 6 ◽

Early Onset ◽

Gestational Hypertension ◽

Neonatal Infection ◽

Reference Intervals ◽

Postnatal Period ◽

C Reactive Protein ◽

Reactive Protein ◽

Wide Range ◽

Near Term

Abstract Background: There is a wide range of reported sensitivities and specificities for C-reactive protein (CRP) and interleukin-6 (IL-6) in the detection of early-onset neonatal infection. This prompted us to assess reference intervals for CRP and IL-6 during the 48-h period immediately after birth and to identify maternal and perinatal factors that may affect them. Methods: CRP and IL-6 values were prospectively obtained for 148 healthy babies (113 term, 35 near-term) at birth and at 24 and 48 h of life, and from their mothers at delivery. Results: Upper reference limits for CRP at each neonatal age were established. At birth, CRP was significantly lower than at 24 and 48 h of life. Rupture of membranes ≥18 h, perinatal distress, and gestational hypertension significantly affected the neonatal CRP dynamics, but at specific ages. There was no correlation between CRP concentrations in mothers and their offspring at birth. The IL-6 values observed in the delivering mothers and in their babies at all three neonatal ages were negatively associated with gestational age. In the immediate postnatal period, IL-6 dynamics for term babies were significantly different from those for near-term babies. Maternal IL-6 concentrations correlated with babies’ IL-6 concentrations only for term deliveries. Apgar score had a significant effect on babies’ IL-6 values at birth. Conclusions: The patterns of CRP and IL-6 responses in the healthy neonate should be taken into account to optimize their use in the diagnosis of early-onset neonatal sepsis.

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