The Effect of Preterm Birth and RLN Damage on Airway Protection and Maturation

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Coordination among the functional components of the aerodigestive system, particularly between swallowing and respiration, is critical for successful airway protection in infants. Disruption of this coordination can produce failure of airway protection, manifest as pulmonary aspiration. Preterm birth is one cause of this disruption and subsequent aspiration. These problems may be compounded with damage to the recurrent laryngeal nerve (RLN) resulting from cardiovascular repairs necessitated by prematurity. Because the current understanding of the pathologies in these fragile patients is based largely on non-invasive technologies, the causal relationship between disordered coordination and airway protection, including how development impacts this system, is unknown. In particular, we do not know the biomechanical alterations that cause aspiration nor what, if any, longitudinal changes occur in biomechanics that may promote airway protection. We propose to investigate the longitudinal course of maturation of airway protection in preterm/term infants, with and without RLN damage. The use of a validated preterm animal model will permit the collection of detailed data, using invasive methods, including high-speed, biplanar videofluoroscopy, that are not appropriate for human patients. The work proposed here will determine how preterm birth effects the sensorimotor interactions that underlie successful airway protection as well as how RLN damage impacts those interactions through three specific aims: (SA1) Determine the longitudinal development of coordination between respiration and swallowing in control infant pigs born at term from birth through weaning; (SA2) Determine the longitudinal development of the coordination between respiration and swallowing after preterm birth using pigs delivered at the equivalent of human gestational age of 30-32 weeks; (SA3) Determine the interaction between the maturation of airway protection and RLN injury in both (SA3a) control term infants and (SA3b) preterm infants. By working with a proven and validated animal model of translational importance, the study proposed here will provide data on the underlying normal and pathophysiologic mechanisms that cause failure of airway protection in preterm infants. These data, collected longitudinally and in sufficient quantity to assess within individual variation and ontogenetic changes within individuals, will provide insight not possible from human patients. Such data will change our understanding of the potential for recovery and treatment recommendations. Furthermore these data can be the basis for designing intervention strategies based on understanding of the mechanisms underlying the pathophysiology.