Magnus Liljedahl1, L Bodin, J Schollin. 1. Department of Paediatrics, Orebro University Hospital, SE-70185 Orebro, Sweden. magnus.liljedahl@orebroll.se
Abstract
AIM: To determine whether sepsis caused by coagulase-negative staphylococci (CoNS) is a risk factor for developing bronchopulmonary dysplasia (BPD) in premature newborns. METHODS: All newborns born at < or = 30 wk of gestation at Orebro University Hospital during 1994-2001 with clinical sepsis caused by CoNS (group A, n = 22) or by other bacteria (group B, n = 17) were included and compared with premature newborns without sepsis (group C, n = 53). Clinical sepsis was defined as a positive blood culture (monoculture) plus clinical symptoms and laboratory findings. BPD was defined as treatment with oxygen > 21% for at least 28 d. RESULTS: The incidence of BPD differed between the three groups, as follows: CoNS sepsis (A) 64%, other sepsis (B) 41% and control (C) 24%. The difference between the control group and the sepsis groups was highly significant (p = 0.006). In a univariate model the crude estimates of relative risk (RR) for occurrence of BPD increased with presence of sepsis and particularly with presence of sepsis with CoNS (A: RR 2.6, 95% CI 1.5-4.6, p = 0.001; B: RR 1.7, CI 0.8-3.5, p = 0.17). When regression was performed with two additional predictive variables in multivariate models including sepsis, gestational age and mechanical ventilation (group A: RR 1.5, CI 1.1-2.0, p = 0.004; group B: RR 0.9, CI 0.6-1.4, p = 0.67), the estimates were lower. CONCLUSION: The relative risk for BPD is significantly increased in premature newborns with sepsis caused by CoNS compared with those with sepsis caused by other bacteria and compared with premature newborns with no sepsis.
AIM: To determine whether sepsis caused by coagulase-negative staphylococci (CoNS) is a risk factor for developing bronchopulmonary dysplasia (BPD) in premature newborns. METHODS: All newborns born at < or = 30 wk of gestation at Orebro University Hospital during 1994-2001 with clinical sepsis caused by CoNS (group A, n = 22) or by other bacteria (group B, n = 17) were included and compared with premature newborns without sepsis (group C, n = 53). Clinical sepsis was defined as a positive blood culture (monoculture) plus clinical symptoms and laboratory findings. BPD was defined as treatment with oxygen > 21% for at least 28 d. RESULTS: The incidence of BPD differed between the three groups, as follows: CoNS sepsis (A) 64%, other sepsis (B) 41% and control (C) 24%. The difference between the control group and the sepsis groups was highly significant (p = 0.006). In a univariate model the crude estimates of relative risk (RR) for occurrence of BPD increased with presence of sepsis and particularly with presence of sepsis with CoNS (A: RR 2.6, 95% CI 1.5-4.6, p = 0.001; B: RR 1.7, CI 0.8-3.5, p = 0.17). When regression was performed with two additional predictive variables in multivariate models including sepsis, gestational age and mechanical ventilation (group A: RR 1.5, CI 1.1-2.0, p = 0.004; group B: RR 0.9, CI 0.6-1.4, p = 0.67), the estimates were lower. CONCLUSION: The relative risk for BPD is significantly increased in premature newborns with sepsis caused by CoNS compared with those with sepsis caused by other bacteria and compared with premature newborns with no sepsis.
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