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Although extraesophageal gastric reflux has been implicated as a cause of many pediatric airway and respiratory diseases, its prevalence in these conditions remains unknown due to the relative lack of sensitivity and/or specificity of traditional reflux testing methods. A prospective study of 222 children (ages 1 day to 16 years) was performed with 24-hour double-probe (simultaneous esophageal and pharyngeal) pH monitoring. Seventy-six percent (168/222) of the study population had abnormal findings in either one or both of the pH probes. Of those, 46% (78/168) had pharyngeal reflux (extraesophageal gastric acid documented by the pharyngeal probe), despite having normal esophageal acid exposure times according to the esophageal probe. Thus, had the pharyngeal probe not been used, 46% of the children with documented extraesophageal (pharyngeal) reflux would have been falsely presumed to have normal reflux parameters. Patients with laryngeal abnormalities, pulmonary abnormalities, and emesis had significantly more pharyngeal acid reflux (p.001) than patients with nonrespiratory symptoms. These data suggest that extraesophageal reflux may be underestimated by single-probe intraesophageal monitoring alone, and that laryngopharyngeal reflux may play a role in the pathogenesis of the conditions studied.

A canine model was used to investigate the efferent laryngeal responses to stimulation by topically applied acid and pepsin. Five adult mongrel dogs were studied. Electromyographic recordings from the thyroarytenoid muscle were measured with hooked-wire electrodes as an acid solution (normal saline/hydrochloric acid at pH 6.0, 5.0, 4.0, 3.0, 2.5, 2.0, 1.5, and 1.0) was sequentially instilled into the larynx. Laryngospasm (tonic, sustained contraction of the thyroarytenoid muscle) occurred in all animals at pH 2.5 to 2.0 or less. Control substances such as neutral pH isotonic saline, hypotonic saline, hypertonic saline, water, and pepsin alone failed to produce laryngospasm. Next, solutions containing both acid (in the same pH range) and pepsin were tested. The laryngeal responses were similar to those of acid alone. The superior laryngeal nerves were sectioned bilaterally and the above experiments repeated. None of the test solutions produced laryngospasm; however, when capsaicin (1%) was instilled into the subglottis, laryngospasm occurred. Thus, chemoreceptors in the subglottis (supplied by the recurrent laryngeal nerves) appear to be responsive to capsaicin stimulation but not to acid stimulation. The data suggest that pH-sensitive chemoreceptors in the canine larynx cause laryngospasm (when the pH of the test solution is 2.5 or less) and that these acid receptors are supplied by the superior laryngeal nerves.