Laryngopharyngeal reflux
Laryngopharyngeal reflux | |
---|---|
Other names | Extraesophageal reflux disease (EERD),[1] Silent reflux,[2] and Supra-esophageal reflux[3] |
Sagittal illustration of the anterior portion of the human head and neck. In LPR, the pharynx (1), oropharynx (2) and larynx (3) are exposed to gastric contents that flow upward through the esophagus (4). | |
Specialty | Gastroenterology |
Laryngopharyngeal reflux (LPR) or laryngopharyngeal reflux disease (LPRD) is the retrograde flow of gastric contents into the
LPR reportedly affects approximately 10% of the U.S. population. However, LPR occurs in as many as 50% of individuals with voice disorders.[9]
Signs and symptoms
Extraesophageal symptoms result from exposure of the upper aerodigestive tract to gastric contents. This causes a variety of symptoms, including hoarseness,
Additionally, LPR can cause inflammation in the vocal tract which results in the symptom of dysphonia or hoarseness. Hoarseness is considered to be one of the primary symptoms of LPR and is associated with complaints such as strain, vocal fatigue, musculoskeletal tension, and hard glottal attacks,[12] all of which can reduce a person's ability to communicate effectively.[13] Moreover, LPR patients may try to compensate for their hoarseness by increasing muscular tension in their vocal tract. This hyper-functional technique adopted in response to the inflammation caused by LPR can lead to a condition called muscle tension dysphonia and may persist even after the hoarseness and inflammation has disappeared. A speech–language pathologist will often need to be involved to help resolve this maladaptive, compensatory pattern through the implementation of voice therapy.[14]
LPR presents as a chronic and intermittent disease in children.[4] LPR in children and infants tends to manifest with a unique set of symptoms.[15] Symptoms seen in children with LPR include a cough, hoarseness, stridor, sore throat, asthma, vomiting, globus sensation, wheezing, aspiration and recurrent pneumonia.[15] Common symptoms of LPR in infants include wheezing, stridor, persistent or recurrent cough, apnea, feeding difficulties, aspiration, regurgitation, and failure to thrive.[15] Moreover, LPR in children is commonly concomitant with laryngeal disorders such as laryngomalacia, subglottic stenosis, and laryngeal papillomatosis.[4]
Relationship to GERD
LPR is often regarded as a subtype of GERD that occurs when stomach contents flow upward through the esophagus and reach the level of the larynx and pharynx. However, LPR is associated with a distinct presentation of symptoms.[11] LPR and GERD frequently differ in the relative prevalence of heartburn and throat clearing. While heartburn is present in over 80% of GERD cases, it occurs in only 20% of LPR cases. Throat clearing shows the opposite prevalence pattern, occurring in approximately 87% of LPR cases and in fewer than 5% of GERD cases.[9] Unlike GERD, LPR also poses a risk for bronchitis or pneumonitis as reflux of stomach acid to the level of the larynx can result in aspiration.[16] LPR is also commonly associated with erythema, or redness, as well as edema in the tissues of the larynx that are exposed to gastric contents.[11] In contrast, most cases of GERD are nonerosive, with no apparent injury to the mucosal lining of the esophageal tissue exposed to the refluxed material.[17]
Differences in the molecular structure of the
Diagnosis
LPR presents with
Additionally, several potential biomarkers of LPR have been investigated. These include inflammatory
Before a diagnosis can be made, a physician will need to record the patient's medical history and ask for details about the presenting symptoms. Questionnaires such as the Reflux Symptom Index (RSI), Quality-of-Life Index (QLI) for LPR, Glottal Closure/Function Index (GCI) and Voice Handicap Index (VHI) can be administered to gain information about the patient's medical history as well as their symptomatology.
There is no agreed-upon assessment technique to identify LPR in children.[4] Of the debated diagnostic tools, multichannel intraluminal impedance with pH monitoring (MII-pH) is used as it recognizes both acid and non-acid reflux.[4] A more common technique that is used is 24-hour dual probe pH monitoring. Both of these tools are expensive and are therefore not widely used.[4]
Treatment
Management of symptoms for patients within this subgroup of the
Proton-pump inhibitors (PPIs) are the leading pharmaceutical intervention chosen for the relief and reduction of LPR and are typically recommended for ongoing use twice a day for a period of 3–6 months.[23][29] PPIs have been shown to be ineffective in very young children and are of uncertain efficacy in older children, for whom their use has been discouraged.[30] [dubious ] While PPIs may provide limited clinical benefits in some adults, there is insufficient evidence to support routine use.[30][31][dubious ] Many studies show that PPIs are not more effective than placebos in treating LPR.[32][33] Alginate products show great promise, as they can form a temporary foam barrier at the LES to block acid and pepsin from refluxing.[34]
When medical management fails, Nissen fundoplication can be offered.[35] However, patients should be advised that surgery may not result in complete elimination of LPR symptoms and even with immediate success, recurrence of symptoms later on is still possible.[28]
One way to assess treatment outcomes for LPR is through the use of voice quality measures.[12] Both subjective and objective measures of voice quality can be used to assess treatment outcomes. Subjective measures include scales such as the Grade, Roughness, Breathiness, Asthenia, Strain Scale (GRBAS); the Reflux Symptom Index; the Voice Handicap Index (VHI); and a voice symptom scale. Objective measures often rely on acoustic parameters such as jitter, shimmer, signal-to-noise ratio, and fundamental frequency, among others.[12] Aerodynamic measures such as vital capacity and maximum phonation time (MPT) have also been used as an objective measure.[12] However, there is not yet a consensus on how best to use the measures or which measures are best to assess treatment outcomes for LPR.[34]
Procedures
There is tentative evidence from non-controlled trials that oral neuromuscular training may improve symptoms.[36] This has been approved by the UK National Health Service (NHS) for supply on prescription from 1 May 2022.[37]
Cancer risk
Although tobacco smoking is the most recognized risk factor for hypopharyngeal cancer, biliary reflux has recently been implicated in hypopharyngeal squamous cell carcinoma.[38][39] Weakly acidic bile may increase the risk for hypopharyngeal carcinogenesis by inducing DNA damage.[40] DNA damage, such as DNA strand breaks, can be induced by the bile acid glycochenodeoxycholic acid present in reflux.[41]
History
LPR was not discussed as a separate condition from GERD until the 1970s and 1980s.[11] However, at around the same time that GERD was first recognized as a clinical entity in the mid-1930s, a link between gut symptoms and airway disease was suggested. Later, acid-related laryngeal ulcerations and granulomas were reported in 1968.[42] Subsequent studies suggested that acid reflux might be a contributory factor in other laryngeal and respiratory conditions. In 1979, the link between these airway symptoms and reflux of gastric contents was first documented. At the same time, treatment of reflux disease results was shown to eliminate these airway symptoms.[43]
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- ^ Vageli DP, Doukas PG, Doukas SG, Tsatsakis A, Judson BL. Noxious Combination of Tobacco Smoke Nitrosamines with Bile, Deoxycholic Acid, Promotes Hypopharyngeal Squamous Cell Carcinoma, via NFκB, In Vivo. Cancer Prev Res (Phila). 2022 May 3;15(5):297-308. doi: 10.1158/1940-6207.CAPR-21-0529. PMID 35502554
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