Abstract
A hemodynamically important patent ductus arteriosus is a common problem in the first week of life in the preterm infant. Although patent ductus arteriosus induces alterations in organ perfusion, scarce information is available of the impact of patent ductus arteriosus and its subsequent treatment on the oxygen supply and oxygen extraction of the brain. We investigated the impact of patent ductus arteriosus and its treatment with indomethacin on regional cerebral oxygen saturation and fractional tissue oxygen extraction by using near-infrared spectroscopy. Twenty infants with patent ductus arteriosus (gestational age: <32 weeks), subsequently treated with indomethacin, were monitored for mean arterial blood pressure, arterial oxygen saturation, near-infrared spectroscopy-determined regional cerebral oxygen saturation, and fractional tissue oxygen extraction ([arterial oxygen saturation - regional cerebral oxygen saturation]/arterial oxygen saturation). Ten-minute periods were selected and averaged during patent ductus arteriosus, at 10, 20, 30, 60, and 120 minutes, and at 6,12, 24, and 36 hours after starting indomethacin treatment (to ductal closure) for mean arterial blood pressure, arterial oxygen saturation, regional cerebral oxygen saturation, and fractional tissue oxygen extraction. The patients with patent ductus arteriosus were matched for gestational age, birth weight, postnatal age, and severity of respiratory distress syndrome with infants without patent ductus arteriosus, who served as control subjects. Mean arterial blood pressure and regional cerebral oxygen saturation were significantly lower and fractional tissue oxygen extraction significantly higher compared with the control infants during patent ductus arteriosus (mean arterial blood pressure: 33 +/- 5 vs 38 +/- 6 mmHg; regional cerebral oxygen saturation: 62% +/- 9% vs 72% +/- 10%; fractional tissue oxygen extraction: 0.34 +/- 0.1 vs 0.25 +/- 0.1, respectively). Regional cerebral oxygen saturation and fractional tissue oxygen extraction were lower and higher, respectively, up to 24 hours after the start of indomethacin but normalized to control values afterward. Indomethacin had no additional negative effect on cerebral oxygenation. A hemodynamically significant patent ductus arteriosus has a negative effect on cerebral oxygenation in the premature infant. Subsequent and adequate treatment of a patent ductus arteriosus may prevent diminished cerebral perfusion and subsequent decreased oxygen delivery, which reduces the change of damage to the vulnerable immature brain.
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