We previously showed that infants born with long-gap esophageal atresia (LGEA) demonstrate clinically significant brain MRI findings following repair with the Foker process. The current pilot study sought to identify any pre-existing (PRE-Foker process) signs of brain injury and to characterize brain and corpus callosum (CC) growth. Preterm and full-term infants (n = 3/group) underwent non-sedated brain MRI twice: before (PRE-Foker scan) and after (POST-Foker scan) completion of perioperative care. A neuroradiologist reported on qualitative brain findings. The research team quantified intracranial space, brain, cerebrospinal fluid (CSF), and CC volumes. We report novel qualitative brain findings in preterm and full-term infants born with LGEA before undergoing Foker process. Patients had a unique hospital course, as assessed by secondary clinical end-point measures. Despite increased total body weight and absolute intracranial and brain volumes (cm³) between scans, normalized brain volume was decreased in 5/6 patients, implying delayed brain growth. This was accompanied by both an absolute and relative CSF volume increase. In addition to qualitative findings of CC abnormalities in 3/6 infants, normative CC size (% brain volume) was consistently smaller in all infants, suggesting delayed or abnormal CC maturation. A future larger study group is warranted to determine the impact on the neurodevelopmental outcomes of infants born with LGEA.

Recent findings implicate brain vulnerability following long-gap esophageal atresia (LGEA) repair. We explored the relationship between easily quantifiable clinical measures and previously reported brain findings in a pilot cohort of infants following LGEA repair. MRI measures (number of qualitative brain findings; normalized brain and corpus callosum volumes) were previously reported in term-born and early-to-late premature infants (n = 13/group) <1 year following LGEA repair with the Foker process. The severity of underlying disease was classified by an (1) American Society of Anesthesiologist (ASA) physical status and (2) Pediatric Risk Assessment (PRAm) scores. Additional clinical end-point measures included: anesthesia exposure (number of events; cumulative minimal alveolar concentration (MAC) exposure in hours), length (in days) of postoperative intubated sedation, paralysis, antibiotic, steroid, and total parenteral nutrition (TPN) treatment. Associations between clinical end-point measures and brain MRI data were tested using Spearman rho and multivariable linear regression. Premature infants were more critically ill per ASA scores, which showed a positive association with the number of cranial MRI findings. Clinical end-point measures together significantly predicted the number of cranial MRI findings for both term-born and premature infant groups, but none of the individual clinical measures did on their own. Listed easily quantifiable clinical end-point measures could be used together as indirect markers in assessing the risk of brain abnormalities following LGEA repair.

Tranexamic acid (TXA), a synthetic antifibrinolytic drug, has proven efficacy and is recommended for major pediatric surgery to decrease perioperative blood loss. Accumulating evidence suggests that TXA reduces bleeding and transfusion in a variety of adult neurosurgical settings. However, there is a paucity of research regarding TXA indications for pediatric neurosurgery and thus, there are currently no recommendations for its use with this specific population. The objective of this study is to evaluate the existing practice of TXA administration for pediatric neurosurgery at a U.S. tertiary care pediatric hospital over a five-year period. The authors conclude that TXA administration is feasible and should be considered for pediatric neurosurgical cases where potential blood loss is a concern.