Clinical manifestations of laryngopharyngeal reflux.
Laryngopharyngeal reflux (LPR) is ubiquitous and associated with many head and neck symptoms and diagnoses. In some cases, the symptom is the diagnosis--for example, LPR can cause sore throat, chronic cough, globus pharyngeus, and laryngospasm. Alternately, LPR can be associated with specific histopathologic lesions--for example, vocal process granulomas. LPR can be the sole cause or an etiologic cofactor in the development of many disorders of the aerodigestive tract.
This article provides an overview of the protean manifestations of laryngopharyngeal reflux (LPR) (table (1-106)), and it includes a comprehensive list of references. We have intentionally not included all reflux-related conditions. For example, many conditions related to gastroesophageal reflux disease (GERD)--such as reflex bradycardia, noncardiac chest pain, esophageal dysmotility, and stricture--are adequately covered in the GERD literature and are not discussed in this article. We have focused primarily on the otolaryngologic manifestations of LPR.
The most common symptom of LPR is hoarseness/dysphonia (92%). (6) Koufman reported that patients with intermittent hoarseness often complained of several episodes a year of "laryngitis" that lasted for a period of days or weeks. (6) Additional symptoms experienced by most patients included chronic throat clearing (50%), chronic cough (44%), globus pharyngeus (33%), and dysphagia (27%). More than half of these patients denied having any heartburn whatsoever; among the rest, 13% had two or fewer episodes per week, and only 10% complained of more frequent heartburn.
Although many patients with LPR experience mild to moderate dysphonia as their primary symptom, some experience more serious conditions. Less common laryngeal manifestations of LPR include laryngospasm, arytenoid fixation, laryngeal stenosis, and carcinoma. (1,3,6,13-38,47-51) LPR is also associated with the development of polypoid degeneration (Reinke's edema), (1,56) vocal fold nodules (figure 1), (1,22,55) and functional voice disorders. (1,52-54)
Certain reflux-related conditions are worthy of specific mention and discussion. These conditions include granulomas, paroxysmal laryngospasm, polypoid degeneration, laryngeal stenosis, carcinoma of the larynx, and reflux and functional voice disorders.
The etiology of laryngeal granulomas is multifactorial, but LPR should always be suspected as possibly playing a role. Granulomas can occur as a result of the combination of acute mucosal ulceration of the vocal process, LPR, and chronic vocal trauma caused by throat clearing and/or a hard glottal attack. (1,7,39-47) By itself, chronic vocal trauma can lead to vocal fold ulcers and granulomas, but LPR is a cofactor in most cases. The clinician should consider each of the possible contributing etiologic factors and correct each if therapy is to be effective. In the case of granulomas, effective antireflux therapy is sufficient to allow for healing in most patients, as long as vocally abusive behaviors also are corrected. (40,41)
Laryngospasm is an uncommon complaint, but patients who experience this frightening symptom are usually able to describe events in vivid detail. (6,49-51) If the clinician mimics the characteristics of severe inspiratory stridor, the patient will confirm that his or her breathing during an attack does sound similar. Laryngospasm is often paroxysmal, and it usually occurs without warning. An attack wakes some patients from their sleep. In other cases, attacks occur during the day. In some cases, the attacks have a predictable pattern--for example, during exercise. Some patients are aware of a relationship between LPR and their laryngospasm attacks, while others are not. (49) In our experience, most patients with paroxysmal laryngospasm respond well to antireflux therapy; antireflux surgery (fundoplication) is sometimes necessary for patients who fail medical treatment. (7,49,50)
In a canine model, Loughlin et al showed that chemoreceptors on the epiglottis responded to acid stimulation at a pH level of 2.5 or less by triggering reflex laryngospasm. (50) The afferent limb of this reflex is supplied by the superior laryngeal nerve; nerve interruption abolished the laryngospasm reflex. (50)
LPR-induced laryngospasm can also be associated with paradoxical vocal fold movement and even with sudden infant death syndrome. (86-92) These areas clearly deserve further research.
Polypoid degeneration (Reinke's edema) occurs as a result of chronic laryngeal irritation over a period of many years. It is usually bilateral and occurs most often in elderly women who smoke. It is also seen in nonsmoking patients with LPR and/or hypothyroidism.
Polypoid degeneration can improve with antireflux therapy and smoking cessation, but most patients with these lesions require surgical treatment. It is interesting to note that this group of patients has been reported to have a very high incidence (41%) of prolonged (>4 wk) postoperative dysphonia. (5) This, in part, might have to do with continued (or inadequately treated) LPR after surgery.
Most patients with polypoid degeneration have abnormal findings on pH monitoring (pH-metry). (1) Consequently, LPR should be considered in the differential diagnosis. At the very least, patients who undergo vocal fold surgery for this condition should receive intense antireflux treatment prior to surgery and during the perioperative period.
LPR is the primary cause of subglottic (figure 2) and posterior glottic stenosis. (1,3,6,13-32) Chronic, intermittent, or chronic-intermittent LPR can cause, or indefinitely perpetuate, laryngeal inflammation. It has been shown in a canine model that intermittent (three times per week only) applications of acid and pepsin to the subglottic region following mucosal injury results in nonhealing ulceration of the cricoid and in subglottic stenosis. (24) LPR documented by pH-metry has been found in 92% of stenosis cases. (6) In our experience, aggressive antireflux treatment coupled with gentle precision surgical intervention is highly effective in the care of these patients.
Carcinoma of the larynx
The most important risk factors for the development of laryngeal carcinoma are tobacco and alcohol use, but LPR also appears to be an important cofactor, especially in nonsmokers. (1,6,33-38) Koufman reported 31 consecutive cases of laryngeal carcinoma; LPR was documented in 84%, but only 58% overall were active smokers. (6) The exact relationship between LPR and malignant degeneration remains to be proved, but the available [blank.sub.p.H]-metry data suggest that most patients who develop laryngeal malignancy both smoke and have LPR. (33) In addition, leukoplakia and other premalignant-appearing lesions can resolve or partially regress with antireflux therapy. (6)
Tobacco and alcohol adversely influence almost all of the body's antireflux mechanisms. They delay gastric emptying, they decrease both upper and lower esophageal sphincter pressures and esophageal motility, they decrease mucosal resistance, and they increase gastric acid secretion. As a result, smokers and frequent drinkers are strongly predisposed to reflux. The use of [blank.sub.p.H]-metry, followed by antireflux treatment, is recommended for all patients who have laryngeal neoplasia, regardless of the presence or absence of other risk factors. (6,33).
Reflux and functional (nonorganic) voice disorders
The term functional voice disorder applies to a variety of vocal abuse, misuse, and overuse syndromes. These conditions are also called muscle tension dysphonias, because abnormal patterns of laryngeal biomechanics are seen on fiberoptic laryngoscopy. The most common pattern is supraglottic contraction--either anteroposterior contraction (foreshortening of the vocal folds), false vocal fold approximation/compression (plica ventricularis), or both. (52-44)
Functional voice disorders are often associated with the secondary development of histopathologic changes in the vocal folds--including hematomas, nodules, ulcers, granulomas, and Reinke's edema. Some [blank.sub.p.H]-metry data suggest that 70% of patients with these functional lesions have LPR in addition to abnormal laryngeal biomechanics. (1,52) In our experience, antireflux treatment will resolve vocal fold nodules in many patients who have LPR.
Table. Clinical manifestations reported to be related to LPR Type of mainfestation Reference Laryngeal Reflux laryngitis 1-12 Subglottic and tracheal stenosis 1,3,6,13-32 Carcinoma of the larynx 1,6,33-38 Endotracheal intubation injury 6,28 Contact ulcers and granulomas 1,7,39-47 Posterior glottic stenosis 6,24 Arytenoid fixation 47,48 Paroxysmal laryngospasm 6,49-51 Paradoxical vocal fold movement 52-54 Vocal fold nodules 1,22,55 Polypoid degeneration 1,56 Laryngomalacia 57-61 Recurrent respiratory papillomas 1,62 Pachydermia laryngis 2,6,11 Recurrent leukoplakia 6 Pharyngeal Globus pharyngeus 4,6,47,63-66 Chronic sore throat 6,47,66 Dysphagia 6,47,66 Zenker's diverticulum 67 Pulmonary Chronic cough 68-71 Exacerbation of asthma/COPD * 68,69,72-82 Bronchiectasis 68,69 Aspiration pneumonia 83-85 Miscellaneous Sudden infant death syndrome 86-92 Sinusitis 93-97 Otitis media 98-101 Obstructive sleep apnea syndrome 102,103 Dental erosions 104-106 * Chronic obstructive pulmonary disease.
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|Author:||Koufman, James A.|
|Publication:||Ear, Nose and Throat Journal|
|Date:||Sep 1, 2002|
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