Esophageal motility disorders in the morbidly obese population.

BACKGROUND: Most studies investigating esophageal motility among the morbidly obese have focused on the relationship between lower esophageal sphincter (LES) pressure and gastroesophageal reflux disease (GERD). Very few studies in the literature have examined motility disorders among the morbidly obese population in general outside the context of GERD. This study aimed to determine the prevalence of esophageal motility disorders in obese patients selected for bariatric surgery. METHODS: A total of 116 obese patients (81 women and 35 men) selected for laparoscopic gastric banding underwent manometric evaluation of their esophagus from January to March 2003. Tracings were retrospectively reviewed for the end points of LES resting pressure, LES relaxation, and esophageal peristalsis. RESULTS: The study patients had a body mass index (BMI) of 42.9 kg/m2, and a mean age of 48.6 years. The following abnormal manometric findings were demonstrated in 41% of the patients: nonspecific esophageal motility disorders (23%), nutcracker esophagus (peristaltic amplitude >180 mmHg) (11%), isolated hypertensive LES pressure (>35 mmHg) (3%), isolated hypotensive LES pressure (<12 mmHg) (3%), diffuse esophageal spasm (1%), and achalasia (1%). Only one patient with abnormal esophageal motility reported noncardiac chest pain. CONCLUSIONS: Despite a high prevalence of esophageal dysmotility in our morbidly obese study population, there was a conspicuous absence of symptoms. Although the patients in this study were not directly questioned with regard to esophageal symptoms, several studies in the literature support our conclusion.

Iatrogenic achalasia. A case series.

Between 1984 and 1992, 14 cases of "secondary" achalasia were diagnosed at our institution, five due to malignancy and nine as a result of esophageal or paraesophageal surgery. Preoperative manometry had excluded preexistent achalasia in eight of nine of the latter patients. Dysphagia developed immediately postoperatively in all. Esophagram and subsequent manometry were consistent with achalasia. All failed conventional dilation sessions and eight of nine underwent pneumatic dilation: Five were cured by this alone, two required surgery (one for iatrogenic perforation), and one was lost to follow-up. This achalasia-like picture appears to be the result of a tight antireflux repair that impairs the ability of the lower esophageal sphincter to completely relax, creating a functional obstruction with proximal dilation and stasis. Such secondary achalasia appears to be a distinct clinical entity and was more common than that associated with neoplasia in our institution. Therapeutically, pneumatic dilation was required and probably causes partial disruption of a tight surgical repair.