11 - MRI Imaging Findings in a Population of Infants with Neonatal Encephalopathy but No Metabolic Acidosis

Publication Number: 1009.11

Yi Li, Department of Radiology, University of California, San Francisco, San Francisco, CA, United States; Yvonne Wu, University of California, San Francisco, School of Medicine, San Francisco, CA, United States; Aditi Lahiri, Kaiser Permanente Division of Research, Berkeley, CA, United States; Michael W. Kuzniewicz, Kaiser Permanente Northern California, Los Gatos, CA, United States; Marie-Coralie Cornet, UCSF Benioff Children's Hospital San Francisco, San Francisco, CA, United States

Background: Hypoxic-ischemic encephalopathy (HIE) is the most common cause of neonatal encephalopathy (NE) and typically presents with perinatal acidosis. Among infants who have undergone MRI for NE but who lack acidosis, the range of imaging abnormalities is not well described.

Objective: To describe the MRI findings in infants with NE but no perinatal acidosis.

Design/Methods: A pediatric neuroradiologist reviewed the clinical brain MRIs of all singleton infants ≥ 35 weeks born at 15 Kaiser Permanente Northern California hospitals between 2012 and 2019 who met the following criteria: 1) NE documented by Sarnat examination between 1-6 hours of age that persisted beyond 6 hours of age, was accompanied by seizures, or was treated by therapeutic hypothermia (TH), and 2) absence of perinatal acidosis defined as cord blood pH < 7 and/or base deficit>10 on cord or first infant gas in the first 2 hours after birth. Infants with a major congenital anomaly or genetic syndrome were excluded. Brain findings were categorized by injury type (i.e., HIE pattern, punctate white matter injury, hemorrhage, arterial ischemic stroke, other). Severity of HIE pattern injury (Figure 1) was graded by the Barkovich scoring system. Perinatal clinical and laboratory information was obtained by chart review. This study was approved by KPNC IRB.

Results: Among 281,992 infants in this cohort, 596 (2.1 per 1000 births) had NE, of whom 104 (17%) had no evidence of perinatal acidosis. Of the 104 infants with NE but no perinatal acidosis, 48 (46%) underwent brain MRI (Table 1), and 17 (35%) had normal imaging. The most common abnormality was HIE pattern injury, identified in 14 infants (29%). Among those with HIE pattern injury, 10 (71%) had watershed, 2 (14%) had basal ganglia/thalamic, and 4 (28%) had both patterns of injury (Table 2). Additional findings included intracranial hemorrhage (N=13, 28%), punctate white matter injury (N=6, 12.5%), arterial ischemic stroke (N=1, 2%), and other patterns (N=10, 21%). Notably, 23 (48%) underwent TH despite the absence of perinatal acidosis. A third of infants who received TH and 58% of infants who did not had evidence of HIE pattern of injury on MRI.

Conclusion(s): In this large birth cohort, HIE pattern of injury was the most common finding among infants with NE but no evidence of perinatal acidosis. These results underscore the diagnostic challenges of early HIE recognition, as over 1/4 of infants without acidosis demonstrated HIE-type brain injury on imaging. Improved tools to identify infants with HIE and remote HIE are needed to guide timely neuroprotective interventions in the early postnatal period.

Demographics and clinical characteristics of infants with NE and no acidosis with and without HI pattern of injury.
Data is presented as N(%) or median (IQR). P values obtained by chi-squared, Fisher's exact test, t-test, and Wilcoxon Rank-Sum Test as appropriate.
1. The Neighborhood Deprivation Index reflects the concentration of poverty, resource scarcity, and social disadvantage within a neighborhood. It includes measures of economic, social, and housing-related deprivation. It was divided into tertiles for this analysis.

Table 2. MRI brain abnormalities encountered in cohort of infants with NE without acidosis. Several infants had more than one abnormal MRI finding.


Figure 1. Example of acute and subacute watershed HIE-pattern of injury in a infant with NE but no acidosis, imaged at 7 days.
A) Right frontal cortical and subcortical reduced diffusion (large white arrow) compatible with acute ischemia, and associated network injury in the brain. Additional scattered parasagittal watershed distribution cortical and subcortical B) T1 hyperintensity (thin black arrows) and C) T2 hyperintensity (thin white arrows) without corresponding reduced diffusion compatible with subacute injury.