Reversible Pseudoachalasia in a Patient with Laparoscopic Adjustable Gastric Banding

The incidence of obesity in the United States has increased dramatically along with its associated comorbidities (eg, heart disease, hypertension, and type 2 diabetes) and mortality risk.¹ Bariatric surgery has surfaced as one effective method to counteract morbid obesity. Compared with complete gastric bypass surgery, laparoscopic adjustable gastric banding (LAGB) has become more popular because of its reversibility and association with a shortened hospital course and fewer complications.² Complications from LAGB are typically device-related; however, recent reports of pseudoachalasia have surfaced.

Case Report

A 55-year-old woman presented with nocturnal cough and acid reflux. Her medical history included gastroesophageal reflux disease, iron deficiency, and laparoscopic adjustable gastric band placement that had been performed for treatment of obesity 3 years before presentation. She denied smoking cigarettes or use of alcohol or drugs. Her family history was only significant for hypertension in her mother. She had undergone an esophagogastroduodenos-copy 4 years prior without significant findings.

Her reflux symptoms, which had persisted for the past year, were unrelieved despite use of a proton pump inhibitor and over-the-counter antacids. She coughed nightly, regurgitated food, and had occasional nonbloody vomiting. Her physical examination findings were unremarkable other than the palpable laparoscopic band. Her metabolic panel and complete blood count were unremarkable.

A barium esophogram revealed a dilated esophagus beginning at 5 cm in the upper thoracic esophagus and channeling through to the gastric region with absent peristalsis (Figures 1 and 2). A gastric emptying study revealed esophagogastric junction (EGJ) obstruction with retention of the radiotracer. An endoscopy demonstrated a corrugated distal esophageal mucosa with pooling of secretions and a properly placed gastric band of the gastric cardia. A biopsy of the esophageal area showed mild none-osinophilic chronic inflammation.

Figure 1.

A dilated esophagus channeling through to the gastric region, with absent peristalsis, is shown. The arrow indicates the gastric band.

Figure 2.

A view of the dilated esophagus and gastric band (arrow).

Esophageal manometry revealed high lower esopha-geal sphincter pressure (LES) and aperistalsis findings consistent with achalasia. Subsequent band reduction resulted in a complete resolution of the patient’s symptoms.

Discussion

Pseudoachalasia, or secondary achalasia, is a motility disorder that may be indistinguishable from achalasia. The danger of missing the diagnosis is that the condition can advance to an inoperable malignancy or result in an unneeded procedure, such as a myomectomy or pneumatic dilation. Pseudoachalasia was first described in 1947 by Ogilvie in a case that included submucosal infiltration of the lower esophagus by a carcinoma mimicking achalasia.³ Approximately 3—4% of the cases diagnosed as achalasia are in fact pseudoachalasia.⁴ The majority of cases of pseudoachalasia are caused by mechanical obstruction; however, infiltration of the myenteric plexus by underlying disease also has been described. Reversal of the underlying process, as in our case, leads to remission of pseudoachalasia.⁵ Gockel and colleagues reviewed 264 cases between 1968 and 2002 in which the majority of cases were explained by malignant disease (53.9% primary and 14.9% secondary malignancy), followed by benign lesions (12.6%) or a complication of surgical procedures at the distal esophagus or proximal stomach (11.9%).⁴ The symptoms of pseudoachalasia commonly include dysphagia, dyspepsia, regurgitation, retrosternal pain, and weight loss.

Pseudoachalasia is often indistinguishable from achalasia on barium studies and esophageal manometry. In pseudoachalasia, a clinician may find a rigid cardia or fail to pass the endoscope into the stomach. Failure to respond to calcium channel blockers, pneumatic dilation, or surgery is common. As in this case, the ability to distinguish between achalasia and pseudoachalasia often occurs after removal of a laparoscopic band.^6,7

With the prevalence rate of obesity in the United States at 35.5% in men and 35.8% in women,⁸ LAGB has become a frequent procedure for the management of obesity. LAGB is an independent risk factor for pseuodoachalasia.⁶ In a study of 121 patients followed after LAGB, esophageal dilation greater than 3.5 cm developed in 14% of patients in association with the development of an achalasia-like syndrome of dysphagia and vomiting.⁹ However, pseudoachalasia evoked from LAGB appears to be reversible in most cases, as shown by Khan and colleagues who followed 6 patients with LAGB who had symptoms of achalasia.⁶ These patients showed absent peristalsis on manometry and esophageal dilation on barium swallow consistent with pseuodo-achalasia.⁶ After either partial liquid removal or complete removal of the laparoscopic band, symptoms resolved in all patients. Esophageal dilation improved in all patients, but manometric findings were variable: 2 patients had persistent aperistalsis, 2 patients had partial peristalsis, and 1 patient had complete return of normal peristalsis.

The mechanism of esophageal dilation and dysmotil-ity postgastric banding is unknown. LES pressure and LES residual pressure are increased after LAGB.¹⁰ A proposed mechanism is the high outflow resistance caused by the gastric band at the LES that creates a high-pressure area leading to a progressive weakening of the esophageal musculature. The inflammation around the laparoscopic band, with fibrosis or neuromuscular damage, may account for the variability of manometric studies.

One hypothesis for reversibility of manometry when the band is removed is that a chronic inflammatory process is prevented from becoming irreversible. Altered esophageal peristalsis after LAGB in patients with insufficient LES pressure may permit reflux secondary to the obstruction created by the gastric band.¹¹ Gastroesophageal reflux damage to the esophageal muscular layers induces low-amplitude peristalsis in the esophagus combined with high pressure created by the band.^12,13 Esophageal manometry cannot determine whether the high-pressure area is secondary to a hypertensive LES or from LAGB.⁶

High-resolution manometry (HRM) with esophageal pressure topography (EPT) may increase the sensitivity of detecting the exact metrics.⁷ In a study of 22 patients who had undergone LAGB and had esophageal symptoms (dysphagia, vomiting, and regurgitation), esophageal dys-motility was prevalent. Three patients received a diagnosis of achalasia, 15 received a diagnosis of functional EGJ obstruction, and 2 received a diagnosis of hypotensive peristalsis.¹⁴ Only 2 patients had normal results, and 2 patients continued to be symptomatic despite removal of the band (1 had functional EGJ obstruction, and 1 had achalasia). Even with HRM with EPT, the proximity of the band to the LES made it very difficult to separate the contributions that each makes to intraluminal pressure.⁶

Conclusion

Although the exact mechanism of pseudoachalasia in patients with LAGB is undefined, complete resolution of symptoms is seen in most cases with release of the band. Dysphagia in patients with LAGB should prompt a search for pseudoacha-lasia to prevent long-term sequelae.