INTRODUCTION: Both systemic inflammation and impaired cerebral autoregulation (CA) have been associated with brain injury in preterm infants. We hypothesized that impaired CA represents a hemodynamic link between inflammation and brain injury. RESULTS: Neither fetal vasculitis nor interleukin-6 (IL-6) affected CA significantly. A high level of IL-6 was associated with hypotension (P = 0.03) irrespective of dopamine therapy. The magnitude of impairment in CA increased with decreasing mean arterial blood pressure (MAP) (P = 0.02). No significant associations were found between these parameters and either intraventricular hemorrhage (IVH) (n = 10) or neonatal mortality (n = 8). DISCUSSION: In conclusion, postnatal inflammation was weakly associated with arterial hypotension, and hypotension was weakly associated with impaired autoregulation. There was no direct association, however, between autoregulation and antenatal or postnatal signs of inflammation. METHODS: In our study, 60 infants (mean (±SD) of gestational age (GA) 27 (±1.3) wk) underwent continuous recording of MAP and cerebral oxygenation index (OI) by means of near-infrared spectroscopy (NIRS) for 2.3 ± 0.5 h, starting 18 ± 9 h after birth. Coherence and transfer function gain between MAP and OI represented the presence and degree of impairment of CA, respectively. We considered fetal vasculitis (placenta histology) to be an antenatal marker of inflammation, and used the level of IL-6 in blood, measured at 18 ± 10 h after birth, as a postnatal marker of inflammation. Definition of hypotension was MAP (mm Hg) ≤ GA (wk).
INTRODUCTION: Both systemic inflammation and impaired cerebral autoregulation (CA) have been associated with brain injury in preterm infants. We hypothesized that impaired CA represents a hemodynamic link between inflammation and brain injury. RESULTS: Neither fetal vasculitis nor interleukin-6 (IL-6) affected CA significantly. A high level of IL-6 was associated with hypotension (P = 0.03) irrespective of dopamine therapy. The magnitude of impairment in CA increased with decreasing mean arterial blood pressure (MAP) (P = 0.02). No significant associations were found between these parameters and either intraventricular hemorrhage (IVH) (n = 10) or neonatal mortality (n = 8). DISCUSSION: In conclusion, postnatal inflammation was weakly associated with arterial hypotension, and hypotension was weakly associated with impaired autoregulation. There was no direct association, however, between autoregulation and antenatal or postnatal signs of inflammation. METHODS: In our study, 60 infants (mean (±SD) of gestational age (GA) 27 (±1.3) wk) underwent continuous recording of MAP and cerebral oxygenation index (OI) by means of near-infrared spectroscopy (NIRS) for 2.3 ± 0.5 h, starting 18 ± 9 h after birth. Coherence and transfer function gain between MAP and OI represented the presence and degree of impairment of CA, respectively. We considered fetal vasculitis (placenta histology) to be an antenatal marker of inflammation, and used the level of IL-6 in blood, measured at 18 ± 10 h after birth, as a postnatal marker of inflammation. Definition of hypotension was MAP (mm Hg) ≤ GA (wk).
Authors: Anne M Plomgaard; Thomas Alderliesten; Topun Austin; Frank van Bel; Manon Benders; Olivier Claris; Eugene Dempsey; Monica Fumagalli; Christian Gluud; Cornelia Hagmann; Simon Hyttel-Sorensen; Petra Lemmers; Wim van Oeveren; Adelina Pellicer; Tue H Petersen; Gerhard Pichler; Per Winkel; Gorm Greisen Journal: PLoS One Date: 2017-03-22 Impact factor: 3.240
Authors: Liesbeth Thewissen; Alexander Caicedo; Petra Lemmers; Frank Van Bel; Sabine Van Huffel; Gunnar Naulaers Journal: Front Pediatr Date: 2018-05-14 Impact factor: 3.418