Article Text

  1. S Supcun1,
  2. P Kutz1,
  3. C Roll1
  1. 1Department of Neonatology and Pediatric Intensive Care, Vest Children’s Hospital, University Witten-Herdecke, Datteln, Germany


Background and Aim: Caffeine therapy for apnoea of prematurity improves the rate of survival without neurodevelopmental disability in infants with very low birth weight. The mechanisms leading to improved neurodevelopmental outcome, however, remain largely unexplained. Here, we investigated the acute effect of caffeine administration on cerebral cortical activity using amplitude-integrated electroencephalography (aEEG) in preterm infants.

Patients and Methods: In 58 preterm infants, gestational age 29 weeks (median, range 24–33), birth weight 1130 g (550–2435), a caffeine loading dose of 10 mg/kg was administered intravenously over 30 minutes and aEEG, heart rate, oxygen saturation and pCO2 were registered continuously from 2 h before to 2 h after administration. Infants with an aEEG impedance rise >5 kOhm were excluded. Means of aEEG amplitudes—mean amplitude, lower margin and upper margin of band of activity—were calculated for each infant for the 2-h period before and the 2-h period after caffeine infusion. Data before and after caffeine infusion were compared using the Wilcoxon signed rank test.

Results: Seven infants were excluded from analysis for a rise of impedance. In the remaining 51 infants, the mean aEEG amplitude increased from 9.8 μV (5.9–13.3) to 10.6 μV (6.6–14.9) (p<0.0001), the mean lower margin of band of activity increased from 5.1 μV (2.9–7.3) to 5.6 μV (3.1–8.3) (p<0.0001) and the mean upper margin increased from 18.5 μV (8.5–26.3) to 20.1 μV (9.6–27.6) (p<0.0001).

Conclusions: Caffeine increases cerebral cortical activity in preterm infants. We speculate that the caffeine-mediated increase in neuronal activity fosters neuronal cell growth and survival in the developing human brain.

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