Cerebral Lactate Concentration in Neonatal Hypoxic-Ischemic Encephalopathy: In Relation to Time, Characteristic of Injury, and Serum Lactate Concentration

Tai-Wei Wu; Benita Tamrazi; Kai-Hsiang Hsu; Eugenia Ho; Aaron J Reitman; Matthew Borzage; Stefan Blüml; Jessica L Wisnowski

doi:10.3389/fneur.2018.00293

Cerebral Lactate Concentration in Neonatal Hypoxic-Ischemic Encephalopathy: In Relation to Time, Characteristic of Injury, and Serum Lactate Concentration

Front Neurol. 2018 May 11:9:293. doi: 10.3389/fneur.2018.00293. eCollection 2018.

Authors

Tai-Wei Wu¹, Benita Tamrazi², Kai-Hsiang Hsu^{1

3}, Eugenia Ho⁴, Aaron J Reitman⁵, Matthew Borzage¹, Stefan Blüml^{2

6}, Jessica L Wisnowski^{1

2

6}

Affiliations

¹ Department of Pediatrics, Keck School of Medicine, Fetal and Neonatal Institute, Division of Neonatology, Children's Hospital Los Angeles, University of Southern California, Los Angeles, CA, United States.
² Department of Radiology, Children's Hospital Los Angeles, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
³ Division of Neonatology, Department of Pediatrics, Chang Gung Memorial Hospital Linkou Branch, Taoyuan, Taiwan.
⁴ Department of Neurology, Children's Hospital Los Angeles, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
⁵ Division of Neonatology, Department of Pediatrics, LAC + USC Medical Center, Keck School of Medicine, University of Southern California, Los Angeles, CA, United States.
⁶ Rudi Schulte Research Institute, Santa Barbara, CA, United States.

Abstract

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 + MR spectroscopy) were performed during and after TH at 54.6 ± 15.0 and 156 ± 57.6 h 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), gray matter (GM), and white matter. 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 were no longer observed after TH. There was a weak correlation between serum lactate and cerebral lactate concentration at the BG (r_s = 0.3, p = 0.04) and Thal (r_s = 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 (r_s = 0.7, p = 0.03), Thal (r_s = 0.9 p = 0.001), and GM (r_s = 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 gray nuclei during TH. Differences in injury and altered regional cerebral metabolism may account for these differences.

Keywords: cerebral lactate; hypoxic-ischemic encephalopathy; lactate; magnetic resonance spectroscopy; neonatal asphyxia.