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. 2012 May;88 Suppl 2(Suppl 2):S92-7.
doi: 10.1016/S0378-3782(12)70025-7.

Sepsis in young infants with congenital heart disease

S B Ascher  1 , P B Smith, R H Clark, M Cohen-Wolkowiez, J S Li, K Watt, E Jacqz-Aigrain, F Kaguelidou, P Manzoni, D K Benjamin Jr
Affiliations

Sepsis in young infants with congenital heart disease

S B Ascher et al. Early Hum Dev. 2012 May.

Abstract

Background: We sought to describe the incidence, pathogen distribution, and mortality associated with blood culture-proven sepsis in young infants with congenital heart disease (CHD) admitted to a neonatal intensive care unit (NICU).

Methods: Cohort study of all blood cultures obtained from infants with CHD between 4 and 120 days of age cared for in 250 NICUs managed by the Pediatrix Medical Group in the United States between 1996 and 2007.

Results: Of 11,638 infants with CHD, 656 (6%) had 821 episodes of sepsis: a cumulative incidence of 71/1000 admissions. Gram-positive organisms were the most common cause (64%), and coagulase-negative Staphylococcus and Staphylococcus aureus were the most frequently isolated species. On multivariable regression, infants with sepsis were more likely to die compared to infants with sterile blood cultures (odds ratio [OR] = 1.53 [95% confidence interval: 1.09, 2.13]). Infants with Gram-negative bacteraemia and candidaemia were more likely to die than infants with sterile blood cultures (OR = 2.01 [1.20, 3.37], and OR = 3.18 [1.60, 6.34], respectively).

Conclusion: Infants with CHD have a high incidence of culture-proven sepsis, especially with staphylococcal organisms. Gram-negative bacteraemia and candidaemia are strongly associated with increased mortality in this group of young infants.

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Conflict of interest statement

Conflict of interest statement

D.K.B. Jr. receives support from the United States government for his work in pediatric and neonatal clinical pharmacology (1R01HD057956-02, 1R01FD003519-01, 1U10-HD45962-06, 1K24HD058735-01, and Government Contract HHSN267200700051C) and the nonprofit organization Thrasher Research Foundation for his work in neonatal candidiasis (www.thrasherresearch.org). He also is a consultant for Pfizer, Cerexa, Biosynexus, and Johnson & Johnson and a principal investigator for Astellas Pharma, AstraZeneca, and UCB Pharma. P.B.S. received support from NICHD 1K23HD060040-01 and DHHS-1R18AE000028-01; he is also a consultant for Pfizer, Cubist Pharmaceuticals, Pangen Biosystems, Johnson & Johnson, and Astellas Pharma and a principal investigator for Cubist Pharmaceuticals. M.C.W. received support from the U.S. government for his work in pediatric and neonatal clinical pharmacology (Government Contract HHSN267200700051C, PI: Benjamin), the nonprofit organization Thrasher Research Foundation, and from NICHD 1K23HD064814-01. He is also a consultant and a principal investigator for Pfizer. All other authors report no potential conflicts of interest relevant to this article.

This study used CTSA biostatistical services through the Division of Pediatric Quantitative Sciences (NIH-5UL-1RR024128-01).

The funding organizations played no role in the study design, collection, analysis, and interpretation of the data, the writing of the manuscript, and the decision to submit the manuscript for publication.

Figures

Fig. 1
Fig. 1
Study population. CHD, congenital heart disease; CoNS, coagulase-negative Staphylococcus.
See this image and copyright information in PMC

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