• Suspect laryngopharyngeal reflux (LPR) in a patient with chronic laryngitis; 50% to 60% of such cases are related to LPR. B
• Refer patients with risk factors for head and neck cancer or whose symptoms persist despite lifestyle modification and medical management to an otolaryngologist. A
• While symptoms of LPR should show improvement after 6 to 8 weeks of proton pump inhibitor therapy, advise patients to continue treatment for 4 to 6 months to ensure that laryngeal lesions and edema resolve. B
Strength of recommendation (SOR)
A Good-quality patient-oriented evidence
B Inconsistent or limited-quality patient-oriented evidence
C Consensus, usual practice, opinion, disease-oriented evidence, case series
Laryngopharyngeal reflux (LPR), the retrograde movement of gastric content into the upper aerodigestive tract, is a common—and commonly underdiagnosed—condition. Characterized by inflammation of the laryngopharynx, LPR can coexist with gastroesophageal reflux disease (GERD), but it is a distinct disorder.1 In GERD, the lower esophageal sphincter malfunctions, whereas LPR involves a dysfunctional upper esophageal sphincter.
Because both conditions involve acid reflux, LPR is sometimes mistaken for GERD. Often, too, patients and physicians alike attribute LPR’s signs and symptoms, which are largely nonspecific, to other causes. The hoarseness and laryngitis that are characteristic of LPR may be blamed on vocal cord abuse or smoking, for instance; the chronic cough and throat clearing associated with LPR thought to be caused by allergies; and the sore throat and postnasal drip that often accompany LPR attributed to infection. Another reason LPR is underdiagnosed: Primary care physicians, who are often the first clinicians from whom symptomatic patients seek treatment, are often unfamiliar with this lesser-known reflux disease.2
The failure to recognize and provide timely treatment for LPR may increase patients’ risk for a number of conditions, including laryngeal ulcers, granulomas, subglottic stenosis, chronic sinusitis, laryngospasm, nasal congestion, and asthma.1 Evidence suggests that LPR increases the risk for esophageal and laryngeal carcinomas,3,4 and for laryngeal injury from intubation, as well.1 To minimize these risks, it is important for primary care physicians to promptly identify this disorder, treat it appropriately, and recognize red flags that warrant referral to a specialist.
How LPR develops, what to look for
There is no gold standard for the diagnosis of LPR. Nonetheless, a review of the pathophysiology and clinical presentation of this reflux disorder and the ways in which it differs from GERD will help you identify cases of LPR. The prevalence of LPR in the general population is uncertain. But reports suggest that as many as 10% of otolaryngology referrals are for patients with a classic presentation of LPR, and that 50% to 60% of cases of chronic laryngitis are related to LPR.1,5,6
The laryngopharynx becomes irritated and inflamed
When the physiological barriers protecting the laryngopharynx from the retrograde flow of gastric content break down, gastric contents can directly irritate the ciliated columnar epithelial cells of the upper respiratory tract, leading to ciliary dysfunction. A lack of mucous clearance leads to mucous stasis and, subsequently, to excessive throat clearing and the sensation of postnasal drip.7 In addition, the laryngopharyngeal epithelium becomes inflamed, and this affects the sensitivity of laryngeal sensory endings and leads to laryngospasm and coughing.8 The inflammatory reaction in turn leads to vocal fold edema, contact ulcers, and granulomas. These changes make patients with LPR particularly prone to developing hoarseness, globus pharyngeus—a sensation of a foreign body in the larynx—and sore throat.5,7 The gastric content can also act indirectly by initiating laryngeal reflexes through irritation of the esophagus, leading to vagally mediated changes such as chronic cough and bronchoconstriction.
Enzyme production declines. Under normal circumstances, carbonic anhydrase isoenzyme III (CAIII) is produced in the posterior aspect of the larynx, catalyzing the production of bicarbonate and neutralizing stomach acid.9-11 In LPR, however, the production of CAIII decreases significantly, thereby exposing the larynx to stomach acid without the enzyme’s protective effect.9,10 At the same time, a marked increase in pepsin levels intensifies laryngeal injury.10,12,13
The larynx is highly vulnerable. The laryngopharynx is much more susceptible to pathology from gastric reflux than the esophagus, for a number of reasons. Damage can occur with much less exposure to acid,1 not only because of the decrease in CAIII, but also because of the absence of peristalsis in the larynx.
What’s more, the esophagus has the ability to clear gastric reflux and minimize damage to the epithelial layer.9,10,14,15 In most patients who develop signs and symptoms of LPR, there has been enough gastric reflux to damage the laryngopharynx but not enough to overcome the protective mechanisms of the esophagus. That’s why most LPR patients have little or none of the heartburn and esophagitis that are classic symptoms of GERD.