Otolaryngology: Open Access
Open Access

Chronic laryngitis; Gastroesophageal reflux disease (GERD); Voice disorders; Hoarseness; Vocal cord edema

Introduction

Chronic laryngitis is a common condition characterized by persistent hoarseness, throat clearing, and dysphagia. It often leads to significant morbidity, affecting quality of life, and can result from various etiologies, including smoking, voice abuse, infections, and gastroesophageal reflux disease (GERD). Among these, laryngopharyngeal reflux (LPR) has emerged as a major cause of chronic laryngitis. LPR occurs when stomach acid or other gastric contents rise up into the laryngopharyngeal area, irritating the mucosal lining. Unlike GERD, LPR can occur without typical symptoms of heartburn, making its diagnosis more challenging. Chronic laryngitis is a common and often debilitating condition that results in persistent inflammation of the vocal cords and the surrounding laryngeal structures. This condition is typically characterized by symptoms such as hoarseness, throat clearing, voice fatigue, dysphagia (difficulty swallowing), and a sensation of a lump in the throat (globus sensation) [1]. While the majority of cases of chronic laryngitis are linked to lifestyle factors such as smoking, excessive voice use, or viral infections, increasing evidence suggests that laryngopharyngeal reflux (LPR) is a major contributor to its pathogenesis. LPR, often described as a more subtle manifestation of gastroesophageal reflux disease (GERD), occurs when gastric contents, including acid, bile, and pepsin, reflux into the laryngopharynx, irritating and inflaming the mucosal lining of the larynx. This refluxate, although chemically potent, often goes unnoticed by patients because it does not always produce the classic symptoms of heartburn or regurgitation that are typically associated with GERD. The relationship between LPR and chronic laryngitis is complex and multifactorial. While both GERD and LPR involve the reflux of stomach contents, LPR is thought to specifically affect the upper airway, including the larynx, pharynx, and the vocal cords, leading to distinct clinical manifestations. In contrast to GERD, where heartburn is the hallmark symptom, LPR may present with a variety of atypical symptoms such as chronic cough, hoarseness, globus sensation, chronic throat clearing, and the sensation of postnasal drip. These symptoms often overlap with those of other conditions, making the diagnosis of LPR challenging [2]. The precise pathophysiology of LPR remains an area of active research. However, it is believed that LPR is primarily caused by the dysfunction of the lower esophageal sphincter (LES) and the upper esophageal sphincter (UES), which leads to the backward flow of gastric contents into the laryngopharynx. Unlike GERD, which typically involves acid reflux into the esophagus, LPR can occur in the absence of overt acid reflux into the esophagus. This phenomenon is known as "silent reflux," which is particularly insidious because it often goes undiagnosed or misdiagnosed for extended periods, allowing the condition to worsen and lead to chronic laryngitis. The gastric contents involved in LPR may consist not only of stomach acid but also pepsin, an enzyme that remains active at a neutral pH, thus prolonging the inflammatory response in the larynx and other upper respiratory structures. The symptoms of chronic laryngitis due to LPR can significantly impact the quality of life of affected individuals, as they often experience chronic discomfort and difficulty speaking, swallowing, or even breathing. These symptoms are particularly troublesome for individuals who rely on their voice for professional purposes, such as singers, teachers, and public speakers. Furthermore, the ongoing inflammation of the laryngeal structures can lead to complications such as vocal cord edema, scarring, and the development of contact ulcers or granulomas. If left untreated, LPR may also contribute to the development of more severe outcomes, including laryngeal cancer. Diagnosis of LPR as a cause of chronic laryngitis is fraught with difficulties due to the absence of specific symptoms and the overlap with other common laryngeal conditions, such as allergies, viral infections, or even structural abnormalities [3]. As such, diagnosing LPR requires a high degree of clinical suspicion and often involves a combination of patient history, endoscopic examination, and specialized tests such as 24-hour pH monitoring, multichannel intraluminal impedance (MII), and pepsin detection in saliva. Among these, flexible laryngoscopy is a crucial diagnostic tool, allowing clinicians to visualize signs of inflammation and other characteristic findings of LPR, such as vocal cord edema, erythema, and contact ulcers. Treatment of chronic laryngitis due to LPR is similarly multifaceted. It typically involves lifestyle modifications, such as dietary changes, smoking cessation, and weight management, as well as pharmacologic therapies aimed at reducing gastric acid production and promoting esophageal motility. Proton pump inhibitors (PPIs) are considered the mainstay of treatment for reducing gastric acidity and controlling reflux episodes. In addition to PPIs, H2-receptor antagonists, antacids, and prokinetic agents may also be used in conjunction with other therapeutic strategies. In cases where medical therapy fails to provide adequate relief, surgical interventions, such as fundoplication, may be considered to improve esophageal sphincter function [4]. Despite the availability of effective treatments, the outcomes for individuals with chronic laryngitis caused by LPR can vary significantly. Early diagnosis and intervention are critical for reducing symptom severity, preventing long-term complications, and improving the overall quality of life. However, because LPR is often a chronic and recurring condition, long-term management may be necessary. Continued research into the pathophysiology of LPR and the development of more effective diagnostic and therapeutic approaches will be essential in improving patient outcomes and reducing the impact of LPR on those suffering from chronic laryngitis [5].

Discussion

Laryngopharyngeal reflux (LPR) has emerged as a critical factor in the pathogenesis of chronic laryngitis, an often debilitating condition that impacts voice quality and overall quality of life. As LPR presents with a range of nonspecific symptoms, its role in chronic laryngitis remains underdiagnosed or misdiagnosed, making it a challenging clinical entity. The growing recognition of LPR’s contribution to chronic laryngitis underscores the need for a comprehensive approach to diagnosis, treatment, and management. This discussion explores key issues related to the pathophysiology, diagnostic challenges, treatment options, and long-term outcomes for patients affected by both LPR and chronic laryngitis [6]. The pathophysiology of LPR in chronic laryngitis involves the reflux of gastric contents, primarily acidic fluid, pepsin, and bile, into the larynx and pharynx, where it causes mucosal injury. The direct contact of these gastric secretions with the delicate laryngeal tissue leads to inflammation, edema, and in some cases, permanent damage. Unlike GERD, where the refluxate is confined to the esophagus and often manifests as heartburn, LPR can occur with or without heartburn, making it more challenging to diagnose [7]. Additionally, the stomach's proteolytic enzyme pepsin, which is activated at a low pH, remains active even in a neutral pH environment such as the laryngeal mucosa. This ability of pepsin to remain biologically active at a neutral pH has significant implications for sustained mucosal injury and the chronic nature of LPR. In chronic laryngitis, LPR contributes to vocal cord edema, erythema, and, in severe cases, scarring or the formation of contact ulcers. These changes not only impair vocal function but also make the laryngeal mucosa more vulnerable to further injury, creating a vicious cycle. Over time, this inflammation can lead to irreversible structural changes, such as fibrosis and vocal cord deformities, which may necessitate long-term vocal rehabilitation or, in extreme cases, surgical intervention. The diagnosis of LPR in patients with chronic laryngitis remains challenging due to the overlap in symptoms with other common conditions, including allergies, viral or bacterial infections, and even psychological disorders like anxiety or depression. Symptoms like chronic cough, hoarseness, throat clearing, and globus sensation are not exclusive to LPR and can often be seen in other upper airway conditions. This diagnostic ambiguity leads to delays in appropriate treatment, worsening patient outcomes. Endoscopic evaluation through flexible laryngoscopy is a critical diagnostic tool, as it allows clinicians to visualize signs of laryngeal inflammation, vocal cord edema, and contact ulcers, which are indicative of LPR. However, the presence of these findings is not specific to LPR, as other causes of laryngitis can result in similar visual findings [8]. Therefore, clinicians must combine laryngoscopy with additional diagnostic tests to confirm LPR. These may include 24-hour pH monitoring, which remains the gold standard for detecting acid reflux into the larynx, and multichannel intraluminal impedance (MII), which allows for the detection of both acidic and non-acidic reflux episodes. Although these tests can provide valuable insights, they are not always accessible or feasible for all patients due to their high cost and invasive nature. Recently, the detection of pepsin in the saliva or throat washings has emerged as a promising non-invasive diagnostic marker for LPR. Pepsin is a key component of gastric juices and its presence in the upper airway can indicate reflux of gastric contents [9]. Although this test shows promise, more research is needed to establish its reliability and clinical utility across different patient populations. The treatment of LPR-induced chronic laryngitis is multifaceted and should focus on both lifestyle modification and pharmacologic intervention. Lifestyle changes are crucial in managing LPR and include dietary adjustments such as avoiding trigger foods (spicy, acidic, and fatty foods), weight loss, and elevating the head of the bed during sleep. Smoking cessation is also essential, as tobacco smoke exacerbates both reflux and laryngeal inflammation. Pharmacological management, primarily involving proton pump inhibitors (PPIs) such as omeprazole and lansoprazole, is considered the cornerstone of treatment. PPIs reduce gastric acid production, thus decreasing the acidity of the refluxate. However, evidence suggests that PPIs may not be entirely effective in controlling LPR symptoms, particularly in patients who experience non-acidic reflux, which may occur in some cases of LPR. In such instances, prokinetic agents like metoclopramide or alginate-based formulations (e.g., Gaviscon) may help reduce reflux episodes and protect the esophagus and larynx from further injury. Despite the availability of pharmacological therapies, many patients with LPR-induced chronic laryngitis do not experience complete symptom resolution, especially when treatment is initiated late or when non-adherence to lifestyle changes persists. In these cases, long-term therapy may be required, and voice therapy may become necessary to rehabilitate vocal cord function and reduce discomfort [10].

Conclusion

In conclusion, laryngopharyngeal reflux (LPR) plays a significant role in the development and persistence of chronic laryngitis, serving as a key factor in many cases that do not respond to conventional treatments. The diagnosis of LPR requires a combination of clinical assessment, patient history, and advanced diagnostic techniques such as pH monitoring and laryngoscopy. Early recognition and appropriate management of LPR are crucial for improving patient outcomes. Treatment strategies include lifestyle modifications, pharmacologic interventions such as proton pump inhibitors and H2 blockers, and, in some cases, surgical interventions for refractory cases. With proper diagnosis and tailored treatment, the symptoms of chronic laryngitis associated with LPR can be effectively managed, leading to better quality of life and reduced recurrence of laryngeal inflammation. However, ongoing research into the mechanisms of LPR and its long-term impact on laryngeal health is essential for refining treatment strategies and improving patient outcomes in the future.

Acknowledgment

None

Conflict of Interest

None

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