Brain Perfusion in Asphyxiated Newborns Treated with Therapeutic Hypothermia

Abstract

Background and Purpose Induced hypothermia is thought to work partly by mitigating reperfusion injury in asphyxiated term newborns. The purpose of this study is to assess brain perfusion in the first week of life in these newborns. Patients and Methods In this prospective cohort study, magnetic resonance imaging (MRI) and perfusion imaging by arterial spin labeling (ASL-PI) was used to assess brain perfusion in these newborns. We measured regional cerebral blood flow values on 1–2 MRIs obtained during the first week of life and compared them to values obtained in control term newborns. The same or later MRI scans were obtained to define the extent of brain injury. Results Eighteen asphyxiated and four control term newborns were enrolled; eleven asphyxiated newborns were treated with hypothermia. Those developing brain injury despite being treated with induced hypothermia usually displayed hypoperfusion on day of life (DOL) 1, and then hyperperfusion on DOL 2–3 in brain areas subsequently exhibiting injury. Asphyxiated newborns not treated with hypothermia who developed brain injury also displayed hyperperfusion on DOL 1–6 in brain areas displaying injury. Conclusions Our data show that ASL-PI may be useful for identifying asphyxiated newborns at risk of developing brain injury, whether or not hypothermia is administered. Since hypothermia for 72 hours may not prevent brain injury when hyperperfusion is found early in the course of neonatal hypoxic-ischemic encephalopathy, such newborns may be candidates for adjustments in their hypothermia therapy or for adjunctive neuroprotective therapies.

Preferential Cephalic Redistribution of Left Ventricular Cardiac Output during Therapeutic Hypothermia for Perinatal Hypoxic-Ischemic Encephalopathy

“…Although our sample size is small, our data are consistent with two other studies reporting an increased cerebral blood flow beyond 24 hours after the initial insult in TH-treated newborns with HIE who develop more severe brain injury (23,24). Two explanations may account for this cephalic redistribution of LVCO in TH-treated newborns with brain injury.…”

Cerebral Oxygen Metabolism in Neonatal Hypoxic Ischemic Encephalopathy during and after Therapeutic Hypothermia

“…This observation was also consistent with a previous MRI study that showed decreased cerebral perfusion in acute neonatal HIE with hypothermia. 26 Although MRI methods for estimating CMRO 2 have been published in the adult literature, [27][28][29][30][31] there is currently little data on the MRI measurement of CMRO 2 in neonates. One recent abstract reported results for 6 normothermic preterm infants without acute brain injury.…”

Ultrafast Doppler Reveals the Mapping of Cerebral Vascular Resistivity in Neonates

“…First of all, most of these modalities require a contrast agent, which qualifies it as invasive: gadolinium derivatives in the case of MRI, iodine or barium compounds in the case of computed tomography angiography. Some modalities such as Arterial Spin Labeling, 27 Phase-contrast MR Angiography, or Cineangiography by MR global coherent-free precession 29 avoid the use of contrast agent but their resolution is limited (800 mm for the last one) compared with our 250 mm Ultrafast Doppler resolution. The rapidity of the acquisition process must be underlined: a decent quality Power Doppler Image is obtained with 400 ms of acquisition (one preterm infant cardiac cycle), and 1 second of acquisition gives a very good quality image (the quality of the Doppler images generally increases with the duration of the acquisition, but after 1.5 seconds of acquisition movement artifact can occur and blur the vascular paths).…”

“…On each ROI, the mean value of the resistivity and its standard deviation Effect of Therapeutic Hypothermia (for Hypoxo Ischemic Encephalopathy) and Rewarming on the Cerebral Resistivity As a clinical illustration of the capability of resistivity maps to give easily readable clinical information on the resistivity of the vascular network, serial examinations have been performed on a full-term infant subjected to therapeutic hypothermia after neonatal hypoxo ischemic encephalopathy. 27,28 The patient was maintained under mild whole-body hypothermia (33.51C) from 6 hours of life and for 72 hours. When the period of cooling concluded, rewarming was cautiously conducted and the servocontrolled rectal temperature was allowed to rise by no more than 0.51C per hour, to a maximum of 36.5±0.21C.…”