In the past, a Heller myotomy was considered to be ineffective in patients with achalasia and a markedly dilated or sigmoid-shaped esophagus. Esophagectomy was the standard treatment. The aims of this study were (a) to evaluate the results of laparoscopic Heller myotomy and Dor fundoplication in patients with achalasia and various degrees of esophageal dilatation; and (b) to assess the role of endoscopic dilatation in patients with postoperative dysphagia. One hundred and thirteen patients with esophageal achalasia were separated into four groups based on the maximal diameter of the esophageal lumen and the shape of the esophagus: group A, diameter<4.0 cm, 46 patients; group B, esophageal diameter 4.0-6.0 cm, 32 patients; group C, diameter>6.0 cm and straight axis, 23 patients; and group D, diameter>6.0 cm and sigmoid-shaped esophagus, 12 patients. All had a laparoscopic Heller myotomy and Dor fundoplication. The median length of follow-up was 45 months (range 7 months to 12.5 years). The postoperative recovery was similar among the four groups. Twenty-three patients (20%) had postoperative dilatations for dysphagia, and five patients (4%) required a second myotomy. Excellent or good results were obtained in 89% of group A and 91% of groups B, C, and D. None required an esophagectomy to maintain clinically adequate swallowing. These data show that (a) a laparoscopic Heller myotomy relieved dysphagia in most patients with achalasia, even when the esophagus was dilated; (b) about 20% of patients required additional treatment; (c) in the end, swallowing was good in 90%.

Laparoscopic fundoplication increased LES pressure and the strength of esophageal peristalsis in patients with abnormal preoperative esophageal motility. A total fundoplication resulted in normalization of peristalsis in the majority of patients.

Although the etiology of gastroesophageal reflux disease (GERD) is multifactorial, the pathophysiology of the disease in morbidly obese patients remains incompletely understood. The aims of this study were to compare in morbidly obese (body mass index (BMI) > or =35) and nonmorbidly patients (BMI <35) with GERD: (a) lower esophageal sphincter (LES) profile; (b) esophageal body function; and (c) esophageal acid exposure. We reviewed esophageal manometry and ambulatory 24-hour pH monitoring studies of 599 consecutive patients with GERD (DeMeester score >14.7). Patients were divided into two groups according to the BMI: (1) 520 patients (86.8%) with BMI <35 and (2) 79 patients (13.2%) with BMI > or =35. While the DeMeester score was not different between the two groups, morbidly obese patients had higher LES pressure and higher amplitude of peristalsis in the distal esophagus (DEA). Among these patients, LES and DEA pressures were often hypertensive. A linear regression model showed that BMI, LES pressure, LES abdominal length, and DEA were independently associated with the DeMeester score. These data showed that: (a) BMI was independently associated to the severity of GERD; and (b) in most morbidly obese patients with GERD, reflux occurred despite normal or hypertensive esophageal motility. These findings show that the pathophysiology of GERD in morbidly obese patients might differ from that of nonobese patients, suggesting the need for a different therapeutic approach.

Ambulatory pH monitoring is essential in patients with a manometric pattern of either diffuse esophageal spasm (DES) or nutcracker esophagus (NE), since these diseases can be considered a primary esophageal motility disorder (PEMD) only in the absence of gastroesophageal reflux disease (GERD). If GERD is present, the motility abnormality is considered secondary, and treatment is directed toward reflux. The aims of this study were to determine in patients with a manometric picture of DES and NE (1) if symptoms alone can distinguish PEMD from GERD and (2) the value of ambulatory pH monitoring. A total of 180 patients fulfilled the manometric criteria for NE, and 124 (69%) of them had GERD detected by ambulatory pH monitoring. Among the 56 patients with PEMD, 31 (55%) were taking proton pump inhibitors on the assumption that GERD was present. Chest pain prevalence was similar when the two groups were compared; however, the symptom was more severe in the PEMD patients. Heartburn prevalence and severity was higher in the GERD group. A total of 121 patients fulfilled the manometric criteria for DES, and 73 (60%) of them had GERD detected by ambulatory pH monitoring. Among the 48 patients with PEMD, 39 (81%) were taking proton pump inhibitors. Dysphagia was more prevalent in the PEMD group. These data show that (1) 2 of 3 of patients with a manometric picture of NE or DES have GERD and (2) symptoms did not distinguish PEMD from GERD. Esophageal manometry and pH monitoring are essential to distinguish PEMD from GERD and to guide appropriate therapy.