Division of Neonatology, Department of Pediatrics, Johns Hopkins University (JHU), Baltimore, MD, USA.
Neurosciences Intensive Care Nursery, JHU, Baltimore, MD, USA.
Pediatr Res. 2021 Jan;89(1):223-230. doi: 10.1038/s41390-020-0876-8. Epub 2020 Apr 8.
Cooling delays, temperature outside 33-34 °C, and blood pressure below the mean arterial blood pressure with optimal cerebral autoregulation (MAP) might diminish neuroprotection from therapeutic hypothermia in neonates with hypoxic-ischemic encephalopathy (HIE). We hypothesized that longer time to reach temperature <34 °C and having temperature outside 33-34 °C would be associated with worse autoregulation and greater brain injury.
Neonates with HIE had rectal temperature and near-infrared spectroscopy autoregulation monitoring during hypothermia (n = 63) and rewarming (n = 58). All underwent brain MRI, and a subset received diffusion tensor imaging MRI before day 10 (n = 41).
Most neonates reached <34 °C at 3-6 h of life. MAP was identified in 54/63 (86%) during hypothermia and in 53/58 (91%) during rewarming. Cooling time was not related to blood pressure deviation from MAP. Later cooling was associated with lower ADC scalar in unilateral posterior centrum semiovale but not in other regions. Temperatures >34 °C were associated with blood pressure above MAP but not with brain injury.
In neonates who were predominantly cooled after 3 h, cooling time was not associated with autoregulation or overall brain injury. Blood pressure deviation above MAP was associated with temperature >34 °C. Additional studies are needed in a more heterogeneous population.
Cooling time to reach target hypothermia temperature within 6 h of birth did not affect cerebral autoregulation measured by NIRS in neonates with hypoxic-ischemic encephalopathy (HIE). Temperature fluctuations >33-34 °C were associated with blood pressures that exceeded the range of optimal autoregulatory vasoreactivity. Cooling time within 6 h of birth and temperatures >33-34 °C were not associated with qualitative brain injury on MRI. Regional apparent diffusion coefficient scalars on diffusion tensor imaging MRI were not appreciably affected by cooling time or temperature >33-34 °C. Additional research in a larger and more heterogeneous population is needed to determine how delayed cooling and temperatures beyond the target hypothermia range affect autoregulation and brain injury.
在患有缺氧缺血性脑病（HIE）的新生儿中，冷却延迟、环境温度在 33-34°C 之间以及平均动脉压下的血压可能会降低治疗性低温的神经保护作用。我们假设，达到<34°C 的时间更长，环境温度在 33-34°C 之间与较差的自动调节和更大的脑损伤有关。
在低温（n=63）和复温（n=58）期间，患有 HIE 的新生儿有直肠温度和近红外光谱自动调节监测。所有患者均接受脑 MRI 检查，其中一部分在第 10 天之前接受弥散张量成像 MRI（n=41）。
大多数新生儿在生命的 3-6 小时达到<34°C。在低温期间，54/63（86%）和复温期间 53/58（91%）可以识别出平均动脉压。冷却时间与血压与平均动脉压的偏差无关。较晚的冷却与单侧后大脑半卵圆中心的 ADC 标度值较低有关，但与其他区域无关。温度>34°C 与血压高于平均动脉压有关，但与脑损伤无关。
在主要在 3 小时后冷却的新生儿中，冷却时间与自动调节或整体脑损伤无关。血压高于平均动脉压与温度>34°C 有关。在更多样化的人群中需要进一步的研究。
在出生后 6 小时内达到目标低温温度的冷却时间不会影响患有缺氧缺血性脑病（HIE）的新生儿的近红外光谱测量的脑自动调节。温度波动>33-34°C 与血压超过最佳自动调节血管反应性范围有关。出生后 6 小时内的冷却时间和温度>33-34°C 与 MRI 上的定性脑损伤无关。弥散张量成像 MRI 上的区域表观弥散系数标度值没有受到冷却时间或温度>33-34°C 的明显影响。需要在更大、更多样化的人群中进行更多的研究，以确定延迟冷却和超出目标低温范围的温度如何影响自动调节和脑损伤。
