Laryngopharyngeal reflux ( LPR ), also known as extraesophageal reflux disease ( EERD ), silent reflux , and supra-esophageal reflux , is a retrograde flow of gastric contents into the larynx, oropharynx and/or nasopharynx. LPR causes respiratory symptoms such as coughing and wheezing and is often associated with head and neck complaints such as dysphonia, globus pharyngis, and dysphagia. LPR can play a role in other diseases, such as sinusitis, otitis media, and rhinitis, and may be an asthma comorbidity. While LPR is commonly used interchangeably with gastroesophageal reflux disease (GERD), it presents with a different pathophysiology.
LPR is reported to affect about 30% of the US population. However, LPR occurs in as many as 50% of individuals with sound disorders.
Video Laryngopharyngeal reflux
Signs and symptoms
The symptoms of an extraesophage are derived from exposure to the aerodigestive tract over the contents of the stomach. This causes various symptoms, including hoarseness, postnasal droplets, sore throat, difficulty swallowing, indigestion, chronic cough, wheezing, globus pharyngeus, and chronic clearing of the throat. Some people with LPR experience heartburn, while others have little to no heartburn because the refluxed stomach does not settle in the esophagus long enough to irritate the surrounding tissue. Individuals with a more severe form of LPR may have tooth enamel abrasion due to gastric contents in the intermittent oral cavity.
In addition, LPR can cause inflammation of the vocal tract that causes symptoms of dysphonia or hoarseness. Hoarseness is regarded as one of the main symptoms of LPR and is associated with complaints such as tension, vocal fatigue, musculoskeletal tension, and severe glottic attack, all of which can reduce a person's ability to communicate effectively. In addition, LPR patients may try to compensate for their hoarseness by increasing muscle tension in their vocal tract. This hyper-functional technique is adopted in response to the inflammation caused by LPR can cause a condition called muscle tension dysfonia and can persist even after hoarseness and inflammation have disappeared. A speech pathologist will often need to be involved to help solve this maladaptive, compensatory pattern through the application of sound therapy.
LPR appears as a chronic and intermittent disease in children. LPR in children and infants tends to manifest with a series of unique symptoms. Symptoms seen in children with LPR include cough, hoarseness, stridor, sore throat, asthma, vomiting, globus sensation, wheezing, aspiration and recurrent pneumonia. Common symptoms of LPR in infants include wheezing, stridor, persistent or recurrent cough, apnea, difficulty eating, aspiration, regurgitation, and failure to thrive. In addition, LPR in children generally coincides with laryngeal disorders such as laringomalacia, subglottic stenosis, and laryngeal papillomatosis.
Maps Laryngopharyngeal reflux
Relationship with GERD
LPR is often regarded as a GERD subtype that occurs when the stomach contents flows upward through the esophagus and reaches the level of the larynx and pharynx. However, LPR is associated with presentation of different symptoms. LPR and GERD often differ in the prevalence of relative heartburn and throat clearance. While heartburn is present in more than 80% of GERD cases, it only occurs in 20% of cases of LPR. Clearance of the throat shows an opposite prevalence pattern, occurring in about 87% of LPR cases and less than 5% of GERD cases. Unlike GERD, LPR also poses a risk of bronchitis or pneumonitis because reflux of stomach acid to the level of the larynx can lead to aspiration. LPR is also often associated with erythema, or redness, and edema of the laryngeal tissue affected by the contents of the stomach. In contrast, most cases of GERD are nonerosive, with no apparent injury to the mucosal lining of the esophageal tissue exposed to refluxed material.
The difference in the molecular structure of the epithelial tissue lining the laryngopharyngeal region may be responsible for the different manifestations of LPR symptoms compared with GERD. In contrast to the stratified epithelial stratification that is resistant to the esophageal lining, the larynx is surrounded by ciliated breathing epithelia, which is more fragile and prone to damage. While the epithelium lining the esophagus survives as much as 50 times the daily exposure of gastric contents, which is the highest estimate considered to be within the range of normal physiological function, injury to the laryngeal epithelium may occur after exposure to only a small amount of acidic gastric contents.
Diagnosis
LPR comes with symptoms and non-specific signs that make differential diagnosis difficult to achieve. Furthermore, the symptoms of the disorder strongly overlap with other symptoms of the disorder. Therefore, LPR is less diagnosed and less treatment. Because there are several potential etiologies for respiratory symptoms and laryngeal LPR, diagnosing LPR based on symptoms alone is unreliable. Laryngoscope findings such as erythema, edema, laryngeal granuloma, and interarytenoid hypertrophy have been used to confirm the diagnosis; However, these findings are not specific and have been described in most asymptomatic subjects undergoing laryngoscopy. Response to acid suppression therapy has been suggested as a diagnostic tool to confirm the diagnosis of LPR, but studies have shown that response to empirical trials of such therapy (such as with proton pump inhibitors) in these patients is often disappointing. Several studies have emphasized the importance of measuring proximal esophagus, or ideal pharyngeal exposure, in patients with clinical symptoms of LPR to document reflux as the cause of symptoms.
In addition, some potential LPR biomarkers have been investigated. These include inflammatory cytokines, carbonic allhydrases, E-cadherin and mucin; However, their direct implications in LPR are still being developed. The presence of pepsin, an enzyme produced in the stomach, in the hypopharynx also becomes an increasingly studied biomarker for LPR. Research shows that pepsin stomach enzyme plays an important role in the complex mechanism behind LPR.
Before the diagnosis can be made, the doctor should record the patient's medical history and ask for details about the symptoms that appear. Questions such as the Reflux Symptom Index (RSI), Life Quality Index (QLI) for LPR, Glottal Closure/Function Index (GCI) and Voice Handicap Index (VHI) can be provided to obtain information about the patient's health history as well as their symptomatology. Physical examination should then be performed with a certain concentration around the head and neck. The scope with a special camera lens made of fiber-optic strands is gently inserted into the throat and returns the image to the monitor. It gives a clear picture of the throat and larynx. LPR signs include redness, swelling, and obvious irritation. Other more invasive tests, such as optical fiber transnasal laryngoscopy, 24 hour ambulatory dual probe pHmetri, pharyngeal pHmetry, transnasal esophagoscopy (TNE) and biopsy may be used. A noninvasive test for LPR diagnosis is a collection of reflux in which the refluxed material is collected and analyzed. Another noninvasive diagnostic test that can be used is an empirical test of proton pump inhibitor therapy; However, this test is mostly successful in diagnosing GERD.
There is no agreed assessment technique for identifying LPR in children. From a debatable diagnostic tool, multichannel intraluminal impedance with pH monitoring (MII-pH) is used because it recognizes acid reflux and non-acidic. A more common technique used is the monitoring of a 24 hour dual pH probe. Both devices are expensive and therefore not widely used.
Treatment
Symptomatic management for patients in this GERD spectrum subgroup is difficult. Once the patient is identified, changes in behavior and diet are suggested. Food modification can include limiting the intake of chocolate, caffeine, food and acidic liquids, gas drinks and high-fat foods. Behavioral changes may include weight loss, smoking cessation, limiting alcohol consumption and avoiding food consumption just before bedtime. Lifestyle changes in children diagnosed with LPR include dietary modification to avoid foods that will worsen reflux (eg, chocolate or acidic and spicy foods), change position (eg, sleep on your side), modify food textures (eg, feed thickening to increase passing bolus consciousness), and eliminate food intake before bed.
Proton pump inhibitors (PPIs) are the leading pharmaceutical interventions selected to eliminate and reduce LPR and are usually recommended for continuous use twice daily for a period of 3-6 months. PPI has proven to be ineffective in very young children and uncertain efficacy in older children, for whom its use has been discouraged. While PPIs may provide limited clinical benefit to some adults, there is sufficient evidence to support routine use. Many studies show that PPIs are no more effective than placebo in treating LPR.
When medical management fails, Nissen fundoplication can be offered. However, patients should be informed that surgery may not result in complete elimination of LPR symptoms and even with immediate success, later symptom relapse is still possible.
There are also more promising but more recent surgical interventions including Stretta and LINX.
One way to assess treatment outcomes for LPR is through the use of sound quality measures. Measurements of objective and objective sound quality can be used to assess treatment outcomes. Subjective measures include scales such as Grade, Roughness, Breathiness, Asthenia, Strain Scale (GRBAS); Index of Reflux Symptoms; Sound Handicap Index (VHI); and the scale of sound symptoms. Objective measurements often depend on acoustic parameters such as jitter, shimmer, signal-to-noise ratio, and fundamental frequency, among others. Aerodynamic measures such as vital capacity and maximum phonation time (MPT) have also been used as objective measures. However, there is no consensus on how best to use these measures or which measures are best for assessing treatment outcomes for LPR.
History
LPR was not discussed as a separate condition from GERD until the 1970s and 1980s. However, at about the same time that GERD was first recognized as a clinical entity in the mid-1930s, a connection between intestinal symptoms and airway disease was suggested. Later, acid-associated laryngeal ulceration and granuloma were reported in 1968. Subsequent studies have shown that acid reflux may be a contributory factor in other larynx and respiratory conditions. In 1979, the relationship between respiratory symptoms and gastric reflux was first documented. At the same time, treatment of reflux disease proved to relieve the symptoms of the airway.
References
External links
- Refluxgate
- Live with Reflux
- Stretta
- LINX
Source of the article : Wikipedia
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