Differentiating esophageal sensitivity phenotypes using pH-impedance in intensive care unit infants referred for gastroesophageal reflux symptoms.

Abstract

OBJECTIVE:To identify esophageal sensitivity phenotypes relative to acid (SAcid), bolus (SBolus), acid and bolus (SAcid+Bolus), and none (SNone) exposures in infants suspected with gastroesophageal reflux disease (GERD).METHODS:Symptomatic infants (N=279) were evaluated for GERD at 42(40–45) weeks postmenstrual age using 24-hour pH-impedance. Symptom associated probability (SAP) for acid and bolus components defined esophageal sensitivity: 1) SAcid as SAP≥95% for acid (pH<4), 2) SBolus as SAP≥95% for bolus, 3) SAcid+Bolus as SAP≥95% for acid and bolus, or 4) SNone as SAP<95% for acid and bolus.RESULTS:Esophageal sensitivity prevalence (SAcid, SBolus, SAcid+Bolus, SNone) was 28(10%), 94(34%), 65(23%), and 92(33%) respectively. Emesis occured more in SBolus and SAcid+Bolus vs SNone (p<0.05). Magnitude (#/day) of cough and emesis events increased with SBolus and SAcid+Bolus vs SNone (p<0.05). SAcid+Bolus had increased acid exposure vs SNone (p<0.05). Distributions of feeding and breathing methods were distinct in infants with SBolus vs SNone (both, p<0.05). Multivariate analysis revealed that arching and irritability events/day were lesser at higher PMAs (p<0.001), greater for infants on NCPAP (p<0.01), with SBolus and SAcid+Bolus (p<0.05). Coughs/day was greater at higher PMAs (p<0.001), for infants with gavage and transitional feeding methods (p<0.02), with SBolus and SAcid+Bolus (p<0.05) but lesser with Trach (p<0.001). Number of emesis events/day were greater with SBolus and SAcid+Bolus (p<0.001). Sneezes/day decreased for infants on Trach (p=0.02).CONCLUSIONS:Feeding and breathing methods can influence the frequency and type of aerodigestive symptoms. We differentiated esophageal sensitivity phenotypes in NICU infants referred for GERD symptoms using pH-Impedance. Acid sensitivity alone was rare, which may explain poor response to acid suppressives; aerodigestive symptoms were predominantly linked with bolus spread. Magnitude of esophageal acid exposure and esophageal sensitivity to bolus spread may explain the pathophysiological basis for symptoms.