Achalasia After Bariatric Surgery.

[BACKGROUND] Obesity is an epidemic on the rise. Increasing body mass index (BMI) has been associated with a number of comorbid diseases, including rarely reported motility disorders such as achalasia. Motility disorders are prevalent in obese patients, possibly more prevalent when compared to the nonobese population. Identification of motility disorders is important before bariatric surgery and may alter the planned type of procedure performed. Limited data exist regarding the development or existence of esophageal motility disorders after bariatric surgery. This study aims to characterize patients who have undergone bariatric surgery and subsequently developed or were diagnosed with achalasia.

[METHODS] Patients with a diagnosis of achalasia who previously underwent bariatric surgery were identified. Data collected included baseline demographics, perioperative parameters, and postoperative outcomes. Descriptive statistics were computed for all variables.

[RESULTS] Ten patients met the inclusion criteria. All patients had endoscopy and manometry confirming diagnosis of achalasia after previous bariatric surgery. Eight patients had undergone Roux-en-Y gastric bypass (RYGB), and two patients had vertical banded gastroplasty (VBG). Median length of time from bariatric surgery to diagnosis was 6 years. Two patients had undergone Botox(®) treatment, and five had gone through the scope esophageal dilations. All patients had a surgical intervention for achalasia, specifically Heller myotomy (HM) (n = 4 open, n = 4 laparoscopic) was performed in the eight RYGB patients, whereas near total gastrectomy and esophagectomy (n = 1), and transhiatal esophagectomy with a partial gastrectomy (n = 1), were performed in each of the patients who previously underwent VBG. These patients were considered to have end-stage achalasia. All patients showed significant decrease in BMI after bariatric surgery (11.1 ± 1.5 kg/m(2)). Six of the eight patients who underwent HM achieved resolution of achalasia symptoms at a mean time of 1.6 months and remained asymptomatic for the total follow-up of 36 months. One patient developed recurrent achalasia 2 years after HM and subsequently underwent a peroral endoscopic myotomy. One HM patient was lost to follow-up. The two patients who underwent esophagectomies were symptom free at 36 months.

[CONCLUSION] Although the incidence of achalasia in the bariatric population is unknown, it does coexist and should be treated when identified. Dysmotility is not uncommon and rarely is the workup completed to identify achalasia before bariatric surgery. Increasing our attention to identify motility diseases preoperatively and specifically raising awareness that achalasia can occur after bariatric surgery will result in better care for patients. Our results suggest achalasia can be effectively treated with surgical therapy after previous bariatric surgery.