Elavazhagan Chakkarapani1, Jonathan Davis1, Marianne Thoresen2. 1. Neonatal Neuroscience, School of Clinical Medicine, St Michael's Hospital, University of Bristol, Bristol, UK. 2. Neonatal Neuroscience, School of Clinical Medicine, St Michael's Hospital, University of Bristol, Bristol, UK Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway.
Abstract
BACKGROUND: Therapeutic hypothermia (HT) delays the cytokine response in infants with neonatal encephalopathy (NE). OBJECTIVE: To determine if HT delayed the C-reactive protein (CRP) response and altered white blood cell (WBC), neutrophil and platelet count course during the first week of life in infants with NE. DESIGN: Retrospective cohort study. SETTING: Regional neonatal intensive care unit, UK. PATIENTS: 104 term infants with NE (38 normothermia (NT) and 66 HT) born between 1998 and 2010. Infants not exposed to prenatal sepsis risk factors were classified as group 'A' and exposed infants to group 'B'. CRP >10 mg/L was defined as significant response. MAIN OUTCOME MEASURES: Time to CRP >10 mg/L, peak CRP, WBC, neutrophil and platelet count. RESULTS: Blood cultures were negative in all the infants. In babies who had CRP response, HT delayed time to CRP >10 mg/L (median (95% CI): group A, HT: 36 h (28.3 to 48.0); NT: 24 h (0.0 to 24.0); p=0.001; group B, HT: 30 h (15.2 to 56.8); NT: 12 h (0.0 to 24.0); p=0.009) and time to peak CRP (median (95% CI): group A, HT: 60 h (60.0 to 72.0); NT: 36 h (0.0 to 48.0); p=0.001; group B, HT: 84 h (62.1 to 120.0); NT: 24 h (0.0 to 36.0); p=0.001). Compared with NT, HT was associated with reduction in slope of CRP elevation by 0.5 (95% CI 0.04 to 0.97), WBC by 2.18×10(9)/L (95% CI 0.002 to 4.35) and platelet count by 32.3×10(9)/L (95% CI 2.75 to 61.8) independent of exposure to sepsis risk, meconium aspiration and severity of asphyxia. CONCLUSIONS: Therapeutic hypothermia delayed the initiation of CRP and its peak response, and depressed the WBC and platelet count compared with NT. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
BACKGROUND: Therapeutic hypothermia (HT) delays the cytokine response in infants with neonatal encephalopathy (NE). OBJECTIVE: To determine if HT delayed the C-reactive protein (CRP) response and altered white blood cell (WBC), neutrophil and platelet count course during the first week of life in infants with NE. DESIGN: Retrospective cohort study. SETTING: Regional neonatal intensive care unit, UK. PATIENTS: 104 term infants with NE (38 normothermia (NT) and 66 HT) born between 1998 and 2010. Infants not exposed to prenatal sepsis risk factors were classified as group 'A' and exposed infants to group 'B'. CRP >10 mg/L was defined as significant response. MAIN OUTCOME MEASURES: Time to CRP >10 mg/L, peak CRP, WBC, neutrophil and platelet count. RESULTS: Blood cultures were negative in all the infants. In babies who had CRP response, HT delayed time to CRP >10 mg/L (median (95% CI): group A, HT: 36 h (28.3 to 48.0); NT: 24 h (0.0 to 24.0); p=0.001; group B, HT: 30 h (15.2 to 56.8); NT: 12 h (0.0 to 24.0); p=0.009) and time to peak CRP (median (95% CI): group A, HT: 60 h (60.0 to 72.0); NT: 36 h (0.0 to 48.0); p=0.001; group B, HT: 84 h (62.1 to 120.0); NT: 24 h (0.0 to 36.0); p=0.001). Compared with NT, HT was associated with reduction in slope of CRP elevation by 0.5 (95% CI 0.04 to 0.97), WBC by 2.18×10(9)/L (95% CI 0.002 to 4.35) and platelet count by 32.3×10(9)/L (95% CI 2.75 to 61.8) independent of exposure to sepsis risk, meconium aspiration and severity of asphyxia. CONCLUSIONS: Therapeutic hypothermia delayed the initiation of CRP and its peak response, and depressed the WBC and platelet count compared with NT. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
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