RESPIRATORY COMPLICATIONS OF GASTROESOPHAGEAL REFLUX DISEASE

Paul D. Siegel; Julian Katz

doi:10.1016/S0095-4543(05)70339-0

More than a century ago, Osle 28 noted a relationship between the upper gastrointestinal tract and symptoms of asthma. He observed that “severe paroxysms may be induced by overloading the stomach” and that “ asthmatic patients learn to take the heavy meals in the early part of the day.” Articles more recently have appeared in the medical literature concerning a relationship between gastroesophageal reflux disease (GERD) and respiratory symptoms. These fall largely into two categories: (1) the relationship of chronic pulmonary fibrosis, chest radiographic abnormalities, and laryngeal symptoms to GERD and (2) the relationship of GERD to asthma and chronic cough. The aspiration of significant quantities of gastric acid into the tracheobronchial tree long has been recognized as causing an acute chemical pneumonitis, often complicated by secondary bacterial pneumonia or adult respiratory distress syndrome. 3 The relationship between chronic bibasilar interstitial fibrosis, pleural thickening with adhesions, and gastroesophageal reflux with aspiration of small quantities of gastric content is less clear, however. Recurrent or chronic aspiration pneumonitis has been reported in 10% to 20% of patients with GERD, and pulmonary fibrosis can occur following acute severe aspiration pneumonitis. 36 Thickened pleura and bilateral parenchymal scarring have been associated with an increased duration of reflux, as measured by esophageal pH monitoring. 32 Restrictive defects in pulmonary function also have been noted with prolonged episodes of reflux in the elderly. 31 It appears that gastroesophageal reflux alone is not sufficient to cause repeated aspiration of large enough quantities of gastric content to cause pulmonary fibrosis because laryngeal and cough reflexes protect the airway and lungs from damage. If these airway protective reflexes are impaired by advanced age, CNS disease, neuromuscular disease, or laryngeal disease or injury, recurrent aspiration of the gastric content that has refluxed into the esophagus can occur. These patients tend to be middle-aged or older and have frequent mild episodes of bronchitis and basilar pneumonitis and persistent or recurring episodes of slightly productive cough, often related to sleep or the supine position. Physical examination may show bibasilar crackles, and the chest radiograph may reveal reticular or linear densities at the lung bases. Although this condition is associated with gastroesophageal reflux, it is the impairment of airway protective reflexes that is the important factor, and treatment usually is directed toward that aspect of the problem. Reflux also should be treated when it is present in such a patient to decrease the quantity of gastric content presented to the upper airway. There is a group of respiratory symptoms related to GERD collectively known as acid laryngitis. 7,9,14 These symptoms are hoarseness (especially in the morning), repeated need to clear the throat, a sensation of pressure or foreign body deep in the throat, and nocturnal or early-morning wheezing. They may be present singly or in varying combinations and usually are believed to be caused by irritation of the larynx and hypopharynx by gastric contents. The mechanism responsible for the sensation of fullness or choking known as globus pharyngeus is unknown but may relate to cricopharyngeus muscle spasm or acid inflammation of the hypopharynx or be referred from the distal esophagus. Laryngeal granulomas and subglottic stenosis also have been reported in association with GERD. Erythema of laryngeal structures, especially the posterior larynx, has been considered a clue to acid laryngitis. Laryngeal cancer even has been associated with reflux. These laryngeal signs and symptoms may be the presenting complaint in the absence of the classic symptoms of GERD, and because reflux may be intermittent, even esophageal pH monitoring may not be sensitive enough to establish the diagnosis. Because medical therapy of GERD is typically successful in relieving the symptoms, a trial of therapy may be worthwhile. The relationship of asthma and chronic cough to GERD has been the subject of many studies 13,22,25,27,30 in the medical literature for more than several decades. GERD is considered the third most common cause of chronic cough in patients with a normal chest radiograph, behind sinus disease and variant asthma. Up to 75% of asthmatics have reflux symptoms, and about 40% are estimated to have reflux esophagitis. In the 1970s surgeons noted unexplained improvement in respiratory symptoms in some patients who had been operated on to correct GERD. This was followed by studies 5,8 in pediatric populations in which smoking was not a confounding variable. These showed a high prevalence of reflux in infants who had unexplained respiratory symptoms, with improvement in respiratory symptoms when reflux was treated with postural and dietary therapy. More recent studies have identified GERD in about three-fourths of 139 asthmatic children studied 1 and more than one half of asthmatic adults. 11 Asthmatics have shown significantly more frequent reflux and greater esophageal acid exposure times than controls, even without selection based on reflux symptoms and without regard for bronchodilator therapy. 37 Intraesophageal acid infusion also has resulted in a decreased peak expiratory flow rate in asthmatic or nonasthmatic subjects with or without GERD. Measurement or pH probes in the proximal esophagus did not show reflux of acid into the respiratory tract, and asthmatics did not improve their peak flow rates after neutralization of acid as much as the nonasthmatic group. 34 The relationship between asthma and GERD also has been the subject of intense investigation. Bronchodilator medications such as theophylline compounds and beta agonists long have been thought to reduce lower esophageal sphincter tone. Studies 12,17 attempting to show this have shown variable results, however. The mechanisms by which GERD triggers or worsens asthma include reflex bronchoconstriction, alteration of the baseline state of bronchial reactivity, and aspiration of refluxed material. 35 Because the esophagus and bronchial tree share innervation by the vagus nerve, reflex bronchoconstriction in response to vagal stimulation by esophageal acid exposure has been considered. The demonstration of airflow reduction in response to esophageal acidification has not been consistent, however. If there is reflux of acid into the tracheobronchial tree (as shown by a fall in tracheal pH), reduction in peak expiratory airflow has been shown, mostly in asthmatic patients. 18 It appears that esophageal acid reflux into the tracheobronchial tree causes an immediate bronchospastic response in asthmatic patients. Exposure of the distal esophagus to acid without aspiration has not been shown to do this consistently. 15 The presence of gastric acid in the distal esophagus may potentiate the bronchial response to other triggers of asthma. This includes increased sensitivity to hyperventilation while maintaining the arterial Pco 2 at a constant level and to methacholine inhalation challenge. 16 In children with atopic asthma, intraesophageal acid alone had no effect on peak expiratory flow but resulted in significant reduction of inhaled methacholine required to produce a 20% reduction in volume of air able to be expired in 1 second with forced exhalation. 41 Although the exact mechanism of the response is not clear, it appears that exposure to esophageal acid may result in bronchoconstriction through a vagally mediated reflex in many asthmatics and perhaps other selected patients. It also may potentiate the bronchial response on exposure to other triggers of asthma. The aspiration of gastric contents or a combination of aspiration and neural mechanisms may be involved in some patients. The evaluation of patients with respiratory symptoms should include questions regarding the symptoms of GERD. These include heartburn, water brash, regurgitation, and dysphagia. The onset of GERD symptoms before the onset of pulmonary symptoms should suggest the possibility of a causal relationship. Even when GERD symptoms are absent, certain clinical features should arouse the suspicion of GERD as a trigger or cause of respiratory symptoms. These are Signs of laryngeal irritation Choking Neck pain Ear pain Sore throat Frequent throat clearing Sensation of pressure in the throat Hoarseness Stridor Subglottic stenosis Vocal cord ulcers or granulomas Laryngostenosis Chronic cough Aspiration pneumonitis Recurrent pneumonia Bronchiectasis Worsening of asthma with Sleep Recumbency Alcohol ingestion Meals Use of oral bronchodilators Onset of wheezing at a late age Negative family history of asthma Negative elements of chronic bronchitis Normal blood and sputum eosinophil counts Normal IGE level Negative allergen skin tests Positive response to empiric medical therapy for GERD When a patient with asthma or chronic cough meets any of these criteria and does not have an identifiable cause of his or her symptoms, GERD must be considered. The periods of reflux symptoms may not correlate with exacerbations of pulmonary symptoms and may be absent.

RESPIRATORY COMPLICATIONS OF GASTROESOPHAGEAL REFLUX DISEASE

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RESPIRATORY COMPLICATIONS OF GASTROESOPHAGEAL REFLUX DISEASE

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Abstract

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