Laryngopharyngeal reflux (LPR), also known as extraesophageal reflux disease (EERD), atypical reflux, silent reflux, and supra-esophageal reflux, is the build-up of reflux into the larynx, oropharynx and/or the nasopharynx . LPR causes symptoms such as cough, wheezing and hoarseness and is often associated with head and neck complaints such as dysphonia, globus pharyngeus and dysphagia. LPR may play a role in other diseases such as sinusitis, otitis media and rhinitis and can be a relevant comorbidity of asthma . LPR is commonly used interchangeably with Gastroesophageal Reflux Disease (GERD), however, LPR presents with a different pathophysiology than GERD .
LPR reportedly affects approximately 30% of the U.S. population. However, as many as 50% of individuals with voice disorders experience LPR to some degree..
Video Laryngopharyngeal reflux
Background
LPR was not discussed as a separate clinical entity from gastroesophageal reflux disease (GERD) until the 1970s and 1980s. 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. 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.
People who suffer from GERD usually have symptoms such as esophageal damage that result from the stomach acid shooting up into the esophagus. The acid can irritate the tissues of the esophagus resulting in a sore throat and persistent coughing. Patients who suffer from laryngopharyngeal reflux, or LPR, are more likely to experience symptoms as a result of stomach acid refluxing into the larynx.
In recent years, it became apparent that stomach acid is only a part of the equation. Research suggests that the stomach enzyme pepsin plays a crucial role in the complex mechanism behind LPR. The body produces pepsin in the stomach to digest proteins. During reflux episodes, pepsin is delivered into the airways where they are destroying proteins inside of mucosa cells and therefore creating damage. The activity of pepsin correlates with the acidity of the environment. Each time something acid is consumed or acid is refluxed, pepsins are activated and the symptoms worsen.
Maps Laryngopharyngeal reflux
Signs and symptoms
Extraesophageal symptoms are the result of exposure of the upper aerodigestive tract to the gastric juice. This causes a variety of symptoms, including hoarseness, postnasal drip, sore throat, difficulty swallowing, indigestion, wheezing, chronic cough, globus pharyngis and chronic throat-clearing. Some people with LPR have heartburn, while others have little or none of these symptoms. This is because the material that refluxes does not stay in the esophagus for very long. In other words, the acid does not have enough time to irritate the esophagus. Individuals with more severe forms of LPR may experience abrasion of tooth enamel due to intermittent presence of gastric contents in the oral cavity.
Adults who are afflicted with LPR often experience the acrid taste of bile emanating from the back of their throat. This is also likely to be accompanied by a lump-like sensation in the throat, making it difficult to swallow. The throat may also seem to burn and breathing can be difficult. These symptoms are most often prevalent just after waking.
LPR may also result in sinusitis and difficulty breathing.
LPR is a chronic and intermittent disease in children. LPR in children and infants tends to manifest with a unique set of symptoms. Common symptoms of LPR in infants include wheezing, stridor, persistent or recurrent cough, apnea, feeding difficulties, aspiration, regurgitation, and failure to thrive. Symptoms seen in children with LPR include a cough, hoarseness, stridor, sore throat, asthma, vomiting, globus sensation, wheezing, aspiration and recurrent pneumonia. LPR in children is commonly concomitant with laryngeal disorders such as laryngomalacia, subglottic stenosis and laryngeal papillomatosis .
Relationship to GERD
LPR is often regarded as a subtype of gastroesophageal reflux disease (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. 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. 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. 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. In contrast, most cases of GERD are nonerosive, with no apparent injury to the mucosal lining of the esophagus.
Differences in the molecular structure of the epithelial tissue lining the laryngopharyngeal region may be partly responsible for the different symptomatic manifestations of LPR in comparison to GERD. In contrast to the resistant stratified squamous epithelium lining the esophagus, the larynx is lined by ciliated respiratory epithelium, which is more fragile and susceptible to damage. While the epithelium lining the esophagus is capable of withstanding as many as 50 instances of exposure to gastric contents each day, which is the uppermost estimate considered to be within the range of normal physiologic functioning, injury to laryngeal epithelium can occur following exposure to only minute amounts of acidic gastric contents.
Diagnosis
As there are multiple potential etiologies for the respiratory and laryngeal symptoms, establishing LPR as the cause based on symptoms alone is unreliable. Laryngoscopic findings such as erythema, edema, laryngeal granulomas, and interarytenoid hypertrophy have been used to establish the diagnosis; but these findings are very nonspecific, and have been described in the majority of asymptomatic subjects undergoing laryngoscopy. LPR presents with non-specific symptoms and signs that make differential diagnosis difficult to achieve. Furthermore, symptoms of the disorder overlap greatly with symptoms of other disorders. Therefore, LPR is under-diagnosed and under-treated. Response to acid-suppression therapy has been suggested as a diagnostic tool for confirming diagnosis of LPR, but studies have shown that the response to empirical trials of such therapy (as with proton-pump inhibitors) in these patients is often disappointing. Several studies have emphasized the importance of measuring proximal esophageal, or, ideally, pharyngeal acid exposure in patients with clinical symptoms of LPR, to document reflux as the cause of the symptoms.
Additionally, several potential biomarkers of LPR have been investigated. These include inflammatory cytokines, carbonic anyhydrase, E-cadherin and mucins, however their direct implications in LPR are still being established. The presence of Pepsin (enzyme produced in the stomach) in the hypopharynx has also become an increasingly researched biomarker for LPR.
Before a diagnosis can be made, the doctor will need to record the patient's medical history and may ask for details about the symptoms that the patient is experiencing. Questionnaires can be administered to receive information about the patient's medical history as well as their symptomatology. The following questionnaires may be used: Reflux Symptom Index (RSI), Quality-of-Life Index (QLI) for LPR, Glottal Closure/Function Index (GCI) and Voice Handicap Index (VHI).The doctor will then need to perform a physical examination with particular concentration around the head and neck. The doctor may need to use a specialized camera lens made of fiber optic strands. This is gently fed down the patient's throat which then feeds back images to a monitor. This enables the doctor to get a clearer look at the throat, particularly the larynx. Tell-tale signs include redness, swelling, and obvious irritation. Other diagnostic tests can be used. Some invasive tests include: Fibre-optic transnasal laryngoscopy and 24-h ambulatory dual probe pHmetry and pharyngeal pHmetry . Some noninvasive tests include: empirical trial of PPI therapy and noninvasive collection of refluxate . Once a diagnosis is made, the doctor will propose a treatment method.
There is no agreed-upon assessment technique to identify LPR in children . Of these debated diagnostic tools, multichannel intraluminal impedance with pH monitoring (MII-pH) is used as it recognizes both acid and non-acid reflux . A more common technique that is used is 24-h dual probe pH monitoring. Both of these tools are expensive and are therefore not widely used .
Treatment
Management of symptoms for patients within this subgroup of the GERD spectrum is difficult. Once these patients are identified, behavioural and dietary changes are advised. Dietary modifications may include limiting the intake of chocolate, caffeine, acidic food and liquids, gaseous beverages and foods high in fat. Behavioral changes may include weight loss, cessation of smoking, limiting alcohol consumption and avoiding the ingestion of food shortly before bed. Lifestyle changes in children diagnosed with LPR include dietary modifications to avoid foods that will aggravate reflux (including chocolate, acidic and spicy food, etc), altering positioning (e.g. sleeping on your side), modifying the textures of foods (e.g. thickening feeds to heighten awareness of the passing bolus) and eliminating the intake of food before bed.
Proton Pump inhibitor's (PPIs) are the leading pharmaceutical intervention chosen for the relief and reduction of laryngopharyngeal reflux and they are typically recommended for ongoing use twice a day for a period of 3-6 months. 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. While PPIs may provide limited clinical benefits in some adults, there is insufficient evidence to support routine use. Many studies show that PPIs are not more effective than Placebo in treating LPR. Some studies have pointed to a larger role of pepsin in causing damage to tissue, and of patients having had success with combination of higher dose PPIs and Sodium Alginate preparations (Gaviscon Advanced).
A study published in the medical journal JAMA in September 2017, A Comparison of Alkaline Water and Mediterranean Diet vs Proton Pump Inhibition for Treatment of Laryngopharyngeal Reflux, showed that dietary changes alone can produce symptom improvements that are comparable to proton-pump inhibitor drugs with none of the side effects. Craig Zalvan MD, the lead investigator for the study, stated that "...medication couldn't be the only method to treat reflux. And recent studies reporting increased rates of stroke and heart attack, dementia and kidney damage from prolonged PPI use made me more certain." The study outlines the role of the digestive enzyme pepsin in damaging the laryngopharynx and confirms that eating foods which are less acidic will reduce pepsin-related symptoms.
When medical management fails, Nissen fundoplication can be offered. 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.
References
External links
- Refluxgate
- Living with Reflux
Source of article : Wikipedia
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