Gastroesophageal reflux disease pathophysiology is multifactorial and linked to a misbalance between the aggressiveness of the refluxate into the esophagus or adjacent organs and the failure of protective mechanisms associate or not to a defective valvular mechanism at the level of the esophagogastric junction incapable of dealing with a transdiaphragmatic pressure gradient. Antireflux mechanisms include the lower esophageal sphincter and abdominal esophagus, the diaphragm, the angle of His, the Gubaroff valve, and the phrenoesophageal membrane. Protective mechanisms include esophageal motility, saliva production, and epithelial protection. Disruption of this balance occurs most commonly due to the presence of a hiatal hernia, esophageal dysmotility, a rise in abdominal pressure (obesity), and decrease in thoracic pressure (chronic lung diseases).
The motility of the pharynx and upper esophageal sphincter (UES) is still poorly understood. It is also unclear if the motility of this area may be compromised in patients with achalasia. This study aims to evaluate the motility of the pharynx, UES, and proximal esophagus in patients with esophageal achalasia. Sixty patients with achalasia underwent high-resolution manometry (HRM) (52 % females, mean age 54 years). Esophageal dilatation was classified according to the radiologic diameter in Type I (<4 cm): 6 %; Type II (4-7 cm): 36 %; Type III (7-10 cm): 34 %; and Type IV (>10 cm): 24 %. HRM classified 43 % of the patients as Chicago Type I and 57 % as Type II. Manometric parameters were compared to normal values obtained from a previous study in volunteers. The motility of the velopharynx showed short, premature, and hypertonic contraction. The epiglottis also showed hypertonic contraction. The UES had increased residual pressure. Chicago classification Type II patients had higher UES residual pressure (p = 0.03). The degree of esophageal dilatation did not correlate with manometric parameters. Achalasia may affect the motility of the pharyngo-upper esophageal area. The changes observed may represent functional alterations to prevent aspiration, especially in patients with Chicago classification Type II achalasia.
Achalasia may present in a non-advanced or an advanced (end stage) stage based on the degree of esophageal dilatation. Manometric parameters and esophageal caliber may be prognostic for the outcome of treatment. The correlation between manometry and disease stage has not been yet fully studied. This study aims to describe high-resolution manometry findings in patients with achalasia and massive dilated megaesophagus. Eighteen patients (mean age 61 years, 55% females) with achalasia and massive dilated megaesophagus, as defined by a maximum esophageal dilatation >10 cm at the barium esophagram, were studied. Achalasia was considered secondary to Chagas' disease in 14 (78%) of the patients and idiopathic in the remaining. All patients underwent high-resolution manometry. Upper esophageal sphincter was hypotonic and had impaired relaxation in the majority of patients. Aperistalsis was seen in all patients with an equal distribution of Chicago type I and type II. No type III was noticed. Lower esophageal sphincter did not have a characteristic manometric pattern. In 50% of the cases, the manometry catheter was not able to reach the stomach. Our results did not show a manometric pattern in patients with achalasia and massive dilated esophagus.
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