Achalasia 5 years following Roux-en-y gastric bypass.

Oesophageal achalasia is a rare, but serious condition in which the motility of the lower oesophageal sphincter (LES) is inhibited. This disorder of idiopathic aetiology complicates the peristaltic function and relaxation of the LES that may cause symptoms such as dysphagia, epigastric pain, and regurgitation of an obstructed food. The following case describes achalasia in a patient 5 years following a laparoscopic Roux-en-Y gastric bypass (RYGB). The patient underwent a laparoscopic Heller myotomy without a fundoplication. Although achalasia seems to be a rare occurrence in obese patients, this is the third case documented in a patient who previously had an RYGB. The role of performing a fundoplication in these patients remains to be elucidated.

INTRODUCTION

Oesophageal myotomy is the most commonly performed procedure to treat achalasia by disrupting the smooth muscles in the distal oesophagus. However, gastroesophageal reflux disease (GERD) may develop following the myotomy given the laxity of the lower oesophageal sphincter (LES). Therefore, an anti-reflux procedure is necessary to mitigate GERD. Partial fundoplication is the most attractive procedure to relieve acid reflux post-oesophageal myotomy. However, in morbidly obese patients who have previously undergone Roux-en-y gastric bypass (RYGB), the anatomy has been altered. Thus, the approach toward rectifying achalasia in this subset of patients needs to be modified. To the best of our knowledge, this is only the third case of achalasia following RYGB.[12] Herein, we report a case of achalasia in a patient who had previously undergone an RYGB.

CASE REPORT

A 48-year-old Caucasian female with a previous history of a laparoscopic RYGB 5 years earlier (pre-operative body mass index [BMI] 44.57 kg/m2, current BMI 29.7 kg/m2) presented with dysphagia to solid foods, regurgitation, and atypical chest pain for weeks. An upper gastrointestinal series (UGI) demonstrated a dilated oesophagus and stricture at the LES. Endoscopy revealed a tortuous oesophagus with retained food products and Candida plaques. The stricture was balloon dilated. Oesophageal manometry documented elevated resting LES pressure, aperistalsis, and failure of LES relaxation.

The patient was scheduled for laparoscopic oesophageal myotomy. The distal oesophagus was carefully dissected into the chest. Adhesions to the gastric pouch were released. A myotomy beginning 1 cm distal to the gastroesophageal junction (GEJ) on the gastric pouch was performed, extending 7 cm cephalad onto the distal oesophagus using electrocautery. Intra-operative endoscopy was performed to ensure complete disruption of the circular muscle layer without evidence of narrowing. An anti-reflux procedure was not performed. Routine UGI was performed on post-operative day 1 [Figure 1] illustrating free passage of contrast into the gastric pouch without evidence of the leak or delayed transit. Four months later, the patient continued to tolerate solids without difficulty or regurgitation. Moreover, the patient had no symptoms of GERD at that time and remained medication-free.

Figure 1

The upper gastrointestinal series at post-operative day 1 illustrates free passage of contrast into the gastric pouch

She was seen 43 months again post-operatively, presenting with symptoms of dysphagia and reflux. A UGI illustrated oesophageal dilatation, narrowing at the GEJ, and delayed oesophageal emptying into the stomach [Figure 2]. At present, she is scheduled to undergo oesophageal manometry and pH testing to assess for the recurrent achalasia.

Figure 2

The upper gastrointestinal series at 43 months post-operatively illustrates recurrent narrowing of the distal oesophagus and distal dilatation suspicious for recurrent achalasia

MANAGEMENT AND DISCUSSION

The curious nature of this case revolves around the rare occurrence of achalasia in the obese population following bariatric surgery. The possible manifestation of the disease in this population can be misdiagnosed due to their misinterpreted symptoms. Almogy et al. postulated that typical achalasia symptoms in the obese can manifest as respiratory complaints such as atypical cough and aspiration.[3] This same set of respiratory symptoms in obese patients typically correlates with obstructive sleep apnoea (OSA). Thus, achalasia may be misdiagnosed as a primary respiratory issue. Our patient had respiratory complaints pre-RYGB which was diagnosed as moderate OSA.

Fundoplication during an oesophageal myotomy in an RYGB patient remains a topic of debate. Fundoplication can be a difficult task to undertake given the anatomical rearrangements of the gastric anatomy. Robert et al. revealed that in non-RYGB patients, a Heller myotomy was sufficient to inhibit reflux in 90% of patients with achalasia provided the anatomical fixation of GEJ is respected.[4] In our case, the patient most likely developed recurrent achalasia and then symptoms of GERD followed. Thus, the role of redo oesophageal myotomy should be entertained to address both issues.

Roux-en-Y gastric bypass combined with an oesophageal myotomy may be sufficient to combat GERD without an anti-reflux procedure as acid production is dramatically lower following RYGB.[5] Furthermore, medical management of symptoms may be sufficient to combat GERD. If the patient continues to have excess weight loss, acid production may also continue to decrease. Our patient's reflux symptoms dissipated following Heller myotomy, hence at the time of redo myotomy, a fundoplication may not be necessary.

Achalasia following RYGB has been reported less than a handful of times in the literature.[12] Further studies would be necessary to elucidate any causal relationship. Any patient with suspected oesophageal dysmotility prior to undergoing bariatric surgery should have oesophageal manometry performed.