GERD Asthma

Two mechanisms have been proposed as the pathogenesis of GERD asthma. The first, the so-called reflux theory, maintains that asthma is the result of the aspiration of gastric contents. The second or reflex theory maintains that vagally mediated bronchoconstriction follows acidification of the lower esophagus. The evidence supporting a reflux mechanism is fivefold. First, clinical studies have documented a strong correlation between idiopathic pulmonary fibrosis and hiatal hernia. The presence of GERD was shown to be highly associated with several pulmonary diseases, not only asthma, in recent studies. Second, pathologic acid exposure in the proximal esophagus is often identified in patients with asthma and reflux disease. Third, scintigraphic studies have shown aspiration of ingested radioisotope in some patients with reflux and respiratory symptoms. Fourth, simultaneous tracheal and esophageal pH monitoring in patients with reflux disease has documented tracheal acidification in concert with esophageal acidification. Finally, animal studies have shown that tracheal instillation of hydrochloric acid profoundly increases airways resistance.
A reflex mechanism is primarily supported by the fact that bronchoconstriction occurs following the infusion of acid into the lower esophagus. This can be explained by the common embryologic origin of the tracheoesophageal tract and its shared vagal innervation. Second, patients with asthma and pathologic distal esophageal acid exposure but normal proximal esophageal acid exposure may experience an improvement in their asthma after antireflux therapy.
The primary challenge in implementing treatment for reflux-associated asthma lies in establishing the diagnosis. In patients with predominantly typical reflux symptoms and secondary respiratory complaints, the diagnosis may be straightforward. However, in a substantial number of patients with GERD asthma, the respiratory symptoms dominate the clinical scenario. GE reflux in these patients is often silent and is uncovered only when investigation is initiated. A high index of suspicion is required, notably in patients with poorly controlled asthma despite appropriate bronchodilator therapy. Supportive evidence for the diagnosis can be gleaned from endoscopy and stationary esophageal manometry. Endoscopy may show erosive esophagitis or Barrett's esophagus. Manometry may indicate a hypotensive LES or ineffective body motility, defined by 30% or more contractions in the distal esophagus of less than 30 mm Hg in amplitude.
The gold standard for the diagnosis of GERD asthma is ambulatory dual-probe pH monitoring. One probe is positioned in the distal esophagus and the other at a more proximal location. Sites for proximal probe placement have included the trachea, pharynx, and proximal esophagus. Most authorities would agree that the proximal esophagus is the preferred site for proximal probe placement. Although ambulatory esophageal pH monitoring allows a direct correlation between esophageal acidification and respiratory symptoms, the chronologic relationship between reflux events and bronchoconstriction is complex.