Original Research ARTICLE
Cerebral lactate concentration in neonatal hypoxic-ischemic encephalopathy: in relation to time, characteristic of injury, and serum lactate concentration
- 1Fetal and Neonatal Institute, Division of Neonatology, Children's Hospital Los Angeles, Department of Pediatrics, Keck School of Medicine of USC, University of Southern California, United States
- 2Department of Radiology, Children's Hospital Los Angeles, Keck School of Medicine of USC, University of Southern California, United States
- 3Department of Pediatrics, Division of Neonatology, Linkou Chang Gung Memorial Hospital, Taiwan
- 4Division of Neonatology, Department of Pediatrics, LAC+USC Medical Center, Keck School of Medicine of USC, University of Southern California, United States
- 5Department of Neurology, Children's Hospital Los Angeles, Keck School of Medicine of USC, University of Southern California, United States
- 6Rudi Schulte Research Institute, United States
Background: Cerebral lactate concentration can remain detectable in neonatal hypoxic-ischemic encephalopathy(HIE) after hemodynamic stability. The temporal resolution of regional cerebral lactate concentration in relation to the severity or area of injury is unclear. Furthermore, the interplay between serum and cerebral lactate in neonatal HIE has not been well-defined. The study aims to describe cerebral lactate concentration in neonatal HIE in relation to time, injury, and serum lactate.
Design/Methods: Fifty-two newborns with HIE undergoing therapeutic hypothermia(TH) were enrolled. Magnetic resonance imaging and spectroscopy (MRI+MRS) were performed during and after TH at 54.6 ± 15.0 and 156 ± 57.6 hours of life, respectively. Severity and predominant pattern of injury was scored radiographically. Single-voxel 1H MR spectra were acquired using short-echo (35 ms) PRESS sequence localized to the basal ganglia(BG), thalamus(Thal), grey matter(GM), and white matter(WM). Cerebral lactate concentration was quantified by LCModel software. Serum and cerebral lactate concentrations were plotted based on age at time of measurement. Multiple comparisons of regional cerebral lactate concentration based on severity and predominant pattern of injury were performed. Spearman’s Rho was computed to determine correlation between serum lactate and cerebral lactate concentration at the respective regions of interest.
Results: Overall, serum lactate concentration decreased over time. Cerebral lactate concentration remained low for less severe injury and decreased over time for more severe injury. Cerebral lactate remained detectable even after TH. During TH, there was a significant higher concentration of cerebral lactate at the areas of injury and also when injury was more severe. However, these differences was no longer observed after TH. There was a weak correlation between serum lactate and cerebral lactate concentration at the BG(rs =0.3,p=0.04) and Thal(rs =0.35, p=0.02). However, in infants with moderate-severe brain injury, a very strong correlation exists between serum lactate and cerebral lactate concentration at the BG(rs=0.7,p=0.03), Thal(rs=0.9p=0.001), and GM(rs=0.6,p=0.04) regions.
Conclusion: Cerebral lactate is most significantly different between regions and severity of injury during TH. There is a moderate correlation between serum and cerebral lactate concentration measured in the deep grey nuclei during TH. Differences in injury and altered regional cerebral metabolism may account for these differences.
Keywords: Lactate, Cerebral metabolites, MR spectroscopy, hypoxic-ischemic encephalopathy, Neonatal asphyxia
Received: 07 Feb 2018;
Accepted: 16 Apr 2018.
Edited by:Masahiro Tsuji, National Cerebral and Cardiovascular Center, Japan
Reviewed by:Tomoki Arichi, King's College London, United Kingdom
Eric S. Peeples, University of Nebraska Medical Center, United States
Copyright: © 2018 Wu, Tamrazi, Hsu, Reitman, Ho, Borzage, Bluml and Wisnowski. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: MD. Tai-Wei Wu, Keck School of Medicine of USC, University of Southern California, Fetal and Neonatal Institute, Division of Neonatology, Children's Hospital Los Angeles, Department of Pediatrics, Los Angeles, United States, email@example.com