1803 Pseudoachalasia Following Nissen Fundoplication: A Progression Documented With High Resolution Manometry

Abstract

INTRODUCTION: Pseudoachalasia, indistinct from achalasia in symptoms and high-resolution manometry (HRM) findings, varies by a secondary etiology. Over half of the occurrences arise from malignancy and seldom following surgeries involving the esophagus. This case presents a rare development of pseudoachalasia following Nissen fundoplication, further unique by documenting complete progression on HRM. CASE DESCRIPTION/METHODS: A 68-year-old male with continued dysphagia and gastroesophageal reflux disease underwent repeat EGD showing progression to LA grade B (from grade A) esophagitis and a 5cm (from 3cm) hiatal hernia. Initial HRM had normal findings (Figure 1A). Laparoscopic Nissen fundoplication was performed. Recurrence of symptoms led to two stricture dilations in one year. Repeat HRM showed intact peristalsis and normal LES relaxation, but six of ten swallows had decreased distal latency < 4.5 seconds consistent with esophageal spasm (Figure 1B). He was referred to an esophageal disease clinic and reported dysphagia, poor pill swallow and 15lb unintentional weight loss. Timed barium esophagram revealed a high-grade obstruction in the distal esophagus (Figure 2). EGD had significant resistance to gastric intubation of the scope concerning for an extrinsic compression or achalasia. A CT chest, abdomen and pelvis showed no extrinsic masses or alternative malignancy. HRM had 100% incomplete liquid bolus transit, elevated LES basal (56.7mmHg) and median integrated relaxation (22.4 mmHg) pressures with complete aperistalsis validating Type I Achalasia by Chicago Classifications (Figure 1C). Diagnosis was mechanical esophagogastric junction outflow obstruction with pseudoachalasia secondary to a tight Nissen fundoplication. After Nissen fundoplication takedown, dysphagia resolved and results were maintained at follow up. DISCUSSION: The etiology of pseudoachalasia in this case was theorized as myenteric plexus injury during wrap construction or degeneration from sustained distal obstruction. Intermediary esophageal spasms on HRM may forewarn of developing pseudoachalasia. One should understand the risk, albeit rare, of post-Nissen fundoplication dysmotility. Being cognizant of a possible HRM progression, as identified in this patient, may spur earlier clinical follow up, repeat testing or intervention. Finally, those with rapid onset of achalasia symptoms over age 50 should raise concern and be evaluated with barium esophagram, EGD with biopsies, CT scan and HRM to decipher a secondary etiology.