Dysphagia in the high-risk infant: potential factors and mechanisms

Abstract

Neonatal dysphagia, or abnormalities of swallowing, represent a major global problem, and consequences of dysfunctional feeding patterns carry over into infancy and toddler age groups. Growth, development, and independent feeding skills are all delayed among high-risk infants. Such a group comprises premature birth, low-birth-weight, congenital anomalies, perinatal asphyxia, postsurgical, and sepsis categories. The conflict between pathophysiologic and pragmatic feeding strategies remains a major conundrum and is largely due to a lack of validated diagnostic approaches amid heterogeneity of the patient phenotype. Thus, well-tested feeding management strategies that can be generalizable are lacking. Furthermore, the aerodigestive symptoms and signs, potential risk factors, and contributory etiologies remain nonspecific. This article presents mechanistic evidence related to the pathophysiologic basis of neonatal dysphagia as well as potential opportunities to improve feeding abilities and long-term development.

Keywords: aerodigestive reflexes; dysphagia; feeding disorders; gastroesophageal reflux; neonate.

FIGURE 1

Risk factors for neonatal feeding difficulties. There are numerous risk factors for neonatal feeding difficulties that are present throughout the continuum of an infant’s hospital course. GER, gastroesophageal reflux; GERD, gastroesophageal reflux disease.

FIGURE 2

Symptoms, signs, and associations with neonatal dysphagia. GERD, gastroesophageal reflux disease.

FIGURE 3

Schematic representation of aerodigestive reflexes evoked on esophageal provocation. An esophageal bolus activates proximal aerodigestive reflexes (e.g., UES contraction or UES relaxation, obstructive apnea, or glottal closure). Similarly, downstream responses or UES relaxation and peristaltic reflex responses are also operational. LES, lower esophageal sphincter; UES, upper esophageal sphincter.

FIGURE 4

Schematic representation of aerodigestive reflexes evoked on pharyngeal stimulation. A pharyngeal bolus activates pharyngeal reflexive swallow, PUCR or PURR, deglutition apnea, and pharyngo-glottal closure reflexes. Downstream responses include LES relaxation. LES, lower esophageal sphincter; PUCR, pharyngo-UES contractile reflex; PURR, pharyngo-UES relaxation reflex; UES, upper esophageal sphincter.

FIGURE 5

Contributory factors and potential central and regional mechanisms associated with neonatal dysphagia. BPD, bronchopulmonary dysplasia; CPG, central pattern generator; CNS, central nervous system; ENS, enteric nervous system; GERD, gastroesophageal reflux disease; GI, gastrointestinal; NEC, necrotizing enterocolitis.