Achalasia presenting as acute airway obstruction is an uncommon complication. We report the case of an elderly woman with previously undiagnosed achalasia who presented with acute respiratory distress due to megaesophagus. Emergency endotracheal intubation and insertion of a catheter into the esophagus, with continuous aspiration was required. Upon introduction of the esophageal catheter an abruptand audible air decompression occurred, with marked improvement of the clinical picture. Endoscopic injection of botulinum toxin was chosen as the definitive treatment with good clinical result. The pathophysiology of the phenomenon of esophageal blowing in achalasia is unclear, but different hypothetical mechanisms have been suggested. One postulated mechanism is an increase in upper esophageal sphincter (UES) residual pressure or abnormal UES relaxation with swallowing in achalasia patients. We reviewed the UES manometric findings in 50 achalasia patients and compared it with measurement performed in 45 healthy controls. We did not find any abnormalities in UES function in any of our achalasia patients group, or in the case under study. An alternative hypothesis postulates that airway compromise in patients with achalasia results from the loss UES belch reflex (abnormal UES relaxation during esophageal air distension), and in fact, an abnormal UES belch reflex was evidenced in our case.

Gastric relaxation invariably precedes nausea and emesis and is of the same magnitude whether induced by apomorphine (central stimulus) or intragastric lipid infusion (peripheral stimulus). Nevertheless, in some instances and depending on the nature of the stimulus, fundic relaxation is a physiological event unassociated with nausea.