Head and Neck Manifestations of Gastroesophageal Reflux Disease

Abstract

Laryngopharyngeal reflux (LPR) occurs when gastric contents pass through the upper esophageal sphincter (UES) into the upper aerodigestive tract (UADT). These relatively brief episodes can have sinister implications, resulting in irritation to the delicate mucosa of the larynx, pharynx, Eustachian tubes, and nasal passages. The subsequent inflammatory changes that take place are responsible for many of the signs and symptoms that have come to define the disease process. The majority of patients with LPR lack the classic gastroesophageal reflux (GER) symptoms of heartburn, and dysphagia, therefore making the diagnosis more challenging (Koufman, Laryngoscope, 101:1–78, 1991). Instead, patients with LPR commonly present with a constellation of symptoms reflective of UADT inflammation including chronic cough, hoarseness, and postnasal drip (Fennerty, Gastroenterol Clin North Am, 28:861–873, 1990; Koufman, Gastroesophageal reflux and voice disorders. In: Rubin J (ed) Diagnosis and treatment of voice disorders. Igaku-Shoin, New York, pp 161–175, 1995). Unfortunately, the relative ubiquity of these nonspecific symptoms makes the diagnosis of LPR difficult to establish based solely on clinical presentation. In turn, further workup is often necessary, requiring a combination of laryngoscopy (Fennerty, Gastroenterol Clin North Am, 28:861–873, 1990; Maronian et al., Laaryngology, 110:606–612, 2001), dualprobe pH monitoring (Muderris et al., Arch Otolaryngol Head Neck Surg, 135:163–167, 2009), and multichannel intraluminal impedance (MCII) testing (Kawamura et al., Am J Gastroenterol, 99:1000–1010, 2004; Hoppo et al., J Gastrointest Surg, 16:16–25, 2012). While each of these tests provides important diagnostic data, they are not without shortcomings. In fact, an accurate diagnostic tool for LPR has yet to be identified, and clearly defined diagnostic criteria have yet to be agreed upon. While the workup of LPR remains controversial, the treatment is more widely accepted and employs a combination of behavioral changes and medical management including PPIs, H2 blockers, mucosal cryoprotectants, and prokinetic agents. Response to therapy is often variable, and many patients require aggressive antiacid intervention to have complete resolution of symptoms (Vaezi, Nat Clin Pract Gastroenterol Hepatol 2:595–603, 2005). Despite these aggressive approaches, there are subsets of patients deemed refractory to medical management. In these cases, surgical intervention may be needed to achieve complete or even partial resolution of symptoms (Oelschlager et al., Gastrointest Surg, 6:189–194, 2002; Brown et al., Surg Endosc, 25:3852–3858, 2011).