Philipp K A Agyeman1, Luregn J Schlapbach2, Eric Giannoni3, Martin Stocker4, Klara M Posfay-Barbe5, Ulrich Heininger6, Matthias Schindler7, Insa Korten8, Gabriel Konetzny9, Anita Niederer-Loher10, Christian R Kahlert10, Alex Donas4, Antonio Leone11, Paul Hasters11, Christa Relly12, Walter Baer13, Claudia E Kuehni7, Christoph Aebi14, Christoph Berger12. 1. Department of Pediatrics, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland. Electronic address: philipp.agyeman@insel.ch. 2. Department of Pediatrics, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland; Paediatric Critical Care Research Group, Mater Research Institute, University of Queensland, Brisbane, QLD, Australia; Paediatric Intensive Care Unit, Lady Cilento Children's Hospital, Children's Health Queensland, Brisbane, QLD, Australia. Electronic address: l.schlapbach@uq.edu.au. 3. Department of Woman-Mother-Child, Clinic of Neonatology, Lausanne, Switzerland; Department of Medicine, Infectious Diseases Service, Lausanne University Hospital, Lausanne, Switzerland. 4. Department of Pediatrics, Children's Hospital Lucerne, Lucerne, Switzerland. 5. Pediatric Infectious Diseases Unit, Children's Hospital of Geneva, University Hospitals of Geneva and University of Geneva, Geneva, Switzerland. 6. Infectious Diseases and Vaccinology, University of Basel Children's Hospital, Basel, Switzerland. 7. Institute of Social and Preventive Medicine, University of Bern, Bern, Switzerland. 8. Department of Pediatrics, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland; Department of Pediatrics, University of Basel Children's Hospital, Basel, Switzerland. 9. Children's Hospital Aarau, Aarau, Switzerland. 10. Infectious Diseases and Hospital Epidemiology, Children's Hospital of Eastern Switzerland, St Gallen, Switzerland; Infectious Diseases and Hospital Epidemiology, Cantonal Hospital, St Gallen, Switzerland. 11. Department of Neonatology, University Hospital Zurich, Zurich, Switzerland. 12. Division of Infectious Diseases and Hospital Epidemiology, and Children's Research Centre, University Children's Hospital Zurich, Switzerland. 13. Children's Hospital Chur, Chur, Switzerland. 14. Department of Pediatrics, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
Abstract
BACKGROUND: Sepsis is a leading cause of childhood mortality worldwide. We assessed population-based incidence and outcomes of blood culture-proven bacterial sepsis in children in Switzerland. METHODS: We did a multicentre, prospective, cohort study at ten paediatric hospitals in Switzerland. We included neonates and children younger than 17 years with blood culture-proven bacterial sepsis. Children were eligible if they met criteria for systemic inflammatory response syndrome-according to 2005 paediatric consensus definition- at the time of blood culture sampling. Incidence was calculated by dividing the number of annual sepsis episodes in the study for the years 2012-15 by the end-of-year resident paediatric population in Switzerland. The primary outcome was in-hospital mortality in the first 30 days after sepsis onset. FINDINGS: Between Sept 1, 2011, and Dec 31, 2015, we enrolled 1096 children to our study. Of 1181 episodes of blood culture-proven bacterial sepsis, 382 (32%) occurred in 379 previously healthy children, 402 (34%) in 391 neonates, and 397 (34%) in 341 children with comorbidities. Incidence was 25·1 cases per 100 000 (95% CI 23·8-26·4) in children and 146·0 cases per 100 000 (133·2-159·6) in neonates. Central line-associated bloodstream infections and primary bloodstream infections accounted for 569 (48%) of 1181 episodes, and organ dysfunction was present in 455 (39%) of 1181 episodes. Escherichia coli (242 of 1181 [20%]), Staphylococcus aureus (177 of 1181 [15%]), coagulase-negative staphylococci (135 of 1181 [11%]), and Streptococcus pneumoniae (118 of 1181 [10%]) were the most prevalent pathogens in our study, accounting for 57% of episodes. The overall case-fatality ratio was 7% (82 of 1181 episodes; 95% CI 5·6-8·6), and it was higher in neonates (11%, 45 of 402 episodes; 8·4-14·8; adjusted odds ratio [OR] 4·41, 95% CI 1·75-11·1) and children with comorbidities (7%, 27 of 397 episodes; 4·6-9·9; OR 4·97, 1·84-13·4) compared with previously healthy children (3%, ten of 382 episodes; 1·3-4·9). The case-fatality ratio was 1% (five of 726 episodes [95% CI 0·3-1·7]) for children without organ dysfunction, which increased to 17% (77 of 455 episodes [13·7-20·8]) when organ dysfunction was present (adjusted OR 4·84, 95% CI 1·40-16·7). INTERPRETATION: The burden of blood culture-proven bacterial sepsis on child health remains considerable. We recorded key differences in predominant organisms, severity, and outcome between neonates, previously healthy children, and children with comorbidities. Although for most episodes of blood culture-proven bacterial sepsis, no organ dysfunction was seen, presence of organ dysfunction was strongly associated with mortality. FUNDING: Swiss National Science Foundation, Swiss Society of Intensive Care, Bangerter Foundation, Vinetum and Borer Foundation, and Foundation for the Health of Children and Adolescents.
BACKGROUND:Sepsis is a leading cause of childhood mortality worldwide. We assessed population-based incidence and outcomes of blood culture-proven bacterial sepsis in children in Switzerland. METHODS: We did a multicentre, prospective, cohort study at ten paediatric hospitals in Switzerland. We included neonates and children younger than 17 years with blood culture-proven bacterial sepsis. Children were eligible if they met criteria for systemic inflammatory response syndrome-according to 2005 paediatric consensus definition- at the time of blood culture sampling. Incidence was calculated by dividing the number of annual sepsis episodes in the study for the years 2012-15 by the end-of-year resident paediatric population in Switzerland. The primary outcome was in-hospital mortality in the first 30 days after sepsis onset. FINDINGS: Between Sept 1, 2011, and Dec 31, 2015, we enrolled 1096 children to our study. Of 1181 episodes of blood culture-proven bacterial sepsis, 382 (32%) occurred in 379 previously healthy children, 402 (34%) in 391 neonates, and 397 (34%) in 341 children with comorbidities. Incidence was 25·1 cases per 100 000 (95% CI 23·8-26·4) in children and 146·0 cases per 100 000 (133·2-159·6) in neonates. Central line-associated bloodstream infections and primary bloodstream infections accounted for 569 (48%) of 1181 episodes, and organ dysfunction was present in 455 (39%) of 1181 episodes. Escherichia coli (242 of 1181 [20%]), Staphylococcus aureus (177 of 1181 [15%]), coagulase-negative staphylococci (135 of 1181 [11%]), and Streptococcus pneumoniae (118 of 1181 [10%]) were the most prevalent pathogens in our study, accounting for 57% of episodes. The overall case-fatality ratio was 7% (82 of 1181 episodes; 95% CI 5·6-8·6), and it was higher in neonates (11%, 45 of 402 episodes; 8·4-14·8; adjusted odds ratio [OR] 4·41, 95% CI 1·75-11·1) and children with comorbidities (7%, 27 of 397 episodes; 4·6-9·9; OR 4·97, 1·84-13·4) compared with previously healthy children (3%, ten of 382 episodes; 1·3-4·9). The case-fatality ratio was 1% (five of 726 episodes [95% CI 0·3-1·7]) for children without organ dysfunction, which increased to 17% (77 of 455 episodes [13·7-20·8]) when organ dysfunction was present (adjusted OR 4·84, 95% CI 1·40-16·7). INTERPRETATION: The burden of blood culture-proven bacterial sepsis on child health remains considerable. We recorded key differences in predominant organisms, severity, and outcome between neonates, previously healthy children, and children with comorbidities. Although for most episodes of blood culture-proven bacterial sepsis, no organ dysfunction was seen, presence of organ dysfunction was strongly associated with mortality. FUNDING: Swiss National Science Foundation, Swiss Society of Intensive Care, Bangerter Foundation, Vinetum and Borer Foundation, and Foundation for the Health of Children and Adolescents.
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