Laryngopharyngeal sensory deficits in patients with laryngopharyngeal reflux and dysphagia

There are no reliable means of quantifying the edema that results from acid exposure to the posterior larynx in patients with laryngopharyngeal reflux (LPR). However, it is possible to quantify laryngopharyngeal sensitivity i n these patients by endoscopic administration of air pulses to the laryngea l mucosa in order to elicit the laryngeal adductor reflex. The purpose of t his study was to determine whether patients with LPR have sensory deficits in the laryngopharynx, and whether treatment of these patients with a proto n pump inhibitor (PPI) results in resolution of sensory deficits. Flexible endoscopic evaluation of swallowing with sensory testing was prospectively performed in 54 patients with dysphagia without neurologic disease and in 2 5 healthy controls. The laryngopharyngeal sensory level, posterior laryngea l edema, and LPR were assessed. We defined LPR as passage of food material from the esophageal inlet retrograde into the hypopharynx. Patients with LP R were placed on 3 months of omeprazole or lansoprazole and then retested. Patients without LPR were placed on Hz blockers for 3 months and then retes ted. In the dysphagia group, 48 of 54 patients (89%) had edema of the poste rior larynx, and 42 of 54 (78%) had laryngopharyngeal sensory deficits. We noted LPR in 38 of 54 (70%). In the control group, 1 of 25 subjects (4%) ha d edema, sensory deficits, and LPR. The differences in incidence of edema, sensory deficits, and LPR between the dysphagia group and the control group were significant (p < .001, <chi>(2) test). Twenty-three patients with LPR placed on a PPI returned for follow-up, with improvement in laryngeal edem a in 14 of the 21 (67%) who had pretreatment edema and resolution of sensor y deficits in 15 of the 19 (79%) who had pretreatment deficits. In the non- LPR, non-PPI group, 11 of 16 patients returned for follow-up, with improvem ent in laryngeal edema in none of the 11 and improvement in sensory deficit s in 1 of the 11 (9.1%). The differences in improvement in laryngeal edema and sensory deficits between the LPR, PPI group, and the non-LPR, non-PPI g roup were significant (p < .01, Fisher's exact test). We conclude that pati ents with dysphagia and edema of the posterior larynx as a result of LPR ha ve sensory deficits in the laryngopharynx. Treatment of these patients with a PPI appears to result in resolution of laryngopharyngeal edema and impro vement of sensory deficits, both subjectively and objectively.