Magnetic Sphincter Augmentation and Postoperative Dysphagia: Characterization, Clinical Risk Factors, and Management

Gastroesophageal reflux disease (GERD) is the most prevalent foregut disease in the Western population.^1‐3 This disease is often a chronic condition and affects approximately 25% of the adult population in the USA and is the most common gastrointestinal indication for seeking medical attention worldwide. The two main treatment options for patients with GERD are long-term acid suppression therapy with proton-pump inhibitors (PPI) and laparoscopic fundoplication. Medical acid suppression therapy is an effective first-line therapy in most patients. However, nearly 40% of patients experience breakthrough symptoms.^4,5 In addition, long-term use of PPI can lead to adverse events such as susceptibility to infectious diarrhea, osteoporosis, and drug interactions. Laparoscopic Nissen fundoplication is the surgical treatment option offered to patients whose condition has failed to respond to medical therapy or who desire to be free from dependence on medical therapy. However, this operation is underused due to the fears of long-term side effects such as gas bloat, inability to belch or vomit, and anatomic failure of the repair. The limitations of pharmacologic therapy and fundoplication leave many patients and clinicians in the difficult position to either tolerate a lifetime of drug dependence with incomplete symptom relief or to undergo a complex surgical procedure that is has been difficult to disseminate on a large scale and may have considerable side effects.

In 2012, the US Food and Drug Administration approved the use of magnetic sphincter augmentation (MSA) as a surgical intervention for the patients diagnosed with GERD. Since then, studies have shown that MSA is a safe and effective treatment resulting in freedom from PPI and pH normalization rates comparable with those reported for laparoscopic Nissen fundoplication.^5‐8 Magnetic sphincter augmentation has become an increasingly common procedure for patients with GERD and is currently offered to patients in more than 300 centers in the USA and approximately 30000 LINX devices (Ethicon, Johnson & Johnson, Shoreview, MN) have been implanted worldwide.

Although studies suggest that the side effect profile of MSA is superior to LNF as evidenced by less gas bloating and a preserved ability to belch and vomit,⁹ postoperative dysphagia remains the most common complaint of patients after MSA. Early postoperative dysphagia has been reported in 43–83% of the patients.^10‐12 Although dysphagia resolves in the majority of these patients after 8 weeks, this symptom persists in some patients and may require endoscopic dilation or device removal. Despite the higher prevalence of dysphagia after MSA, there is a paucity of data pertaining to the characterization and management of persistent dysphagia. More specifically, the factors that predict dysphagia after surgery have not been characterized. This study was designed to characterize dysphagia after MSA, review the management of this complaint, and identify the preoperative factors that predict persistent dysphagia after MSA.

A total of 380 patients underwent magnetic sphincter augmentation (MSA) during the study period. Demographic and baseline clinical characteristics of this cohort are shown in Table 1. At a mean (SD) follow up of 11.5 (8.7) months, 88.5% were satisfied with the outcome of surgery, 93.3% were free of PPI use, and 76.2% had normalization of their distal esophageal acid exposure. GERD-HRQL total score was improved from preoperative value of 33.7 (18.9) to 7.9 (9.8), p < 0.001.

Magnetic sphincter augmentation (MSA) was developed to address the need for an alternative treatment option in the management of patients with GERD through an outpatient laparoscopic procedure that does not alter gastric anatomy, augments the physiologic barrier to reflux, and can be reversed if necessary. MSA has gained popularity as a highly standardized technique for the treatment of reflux disease resulting in successful outcomes that are reproducible. This procedure is now offered in 300 centers in the USA and approximately 30,000 implants have performed worldwide.

Reflux disease and its complications are most often the consequence of an incompetent anatomical mechanical barrier. An ideal surgical option should restore this barrier with minimal to no side effects. The results of the feasibility, pivotal, and FDA post-approval studies have shown that magnetic sphincter augmentation is highly effective in reducing typical GERD symptoms, reducing daily PPI dependence, improving patients’ quality of life, and decreasing esophageal acid exposure.^12,20 The results of the present study demonstrate a similarly high degree of symptom control, improvement in quality of life, and liberation from antisecretory medication use. MSA is comparable with LNF in the control of GERD symptoms while limiting procedure-related side effects,¹² and therefore may provide a solution to the deficits experienced with the established medical and surgical GERD therapies.

Despite these advantages, persistent dysphagia in post-MSA patients ranges from 3 to 19% of cases, which is higher in contrast to post-fundoplication cases.²¹ In the present study, dysphagia was the most common procedure-related side effect seen in 15.5%. In the 2010 feasibility study of 44 patients who underwent MSA, early dysphagia was the most common complaint and occurred in 43% of the patients and in majority of patients resolved by 90 days, and in only one patient (2.3%), the device was explanted for persistent dysphagia.²² In the 2013 pivotal study of 100 patients who had MSA, dysphagia was again found to be the most frequent complaint, present in 68% of patients in the immediate postoperative period and reducing to 11% at 1 year and 4% at 3 years follow up.²³ In the FDA post-approval study, the most common procedure-related symptom was dysphagia, present in 82.7% of the 67 patients but resolved in 79% of these patients at a median time of 8 weeks. A review of the FDA’s Manufacturer and User Facility Device Experience (MAUDE) data repository performed in 2016 revealed that 133 events deemed serious enough for report. In this report, dysphagia remained the most common complication with 60 cases submitted.²⁴

Although studies indicate that dysphagia is the most common complaint after MSA, there is paucity of data in regard to characterization of the dysphagia, management of this complaint, and the factors that predict dysphagia after MSA. In this study, normal preoperative hiatal anatomy and dysphagia were found to be independent risk factors for persistent postoperative dysphagia. These findings likely reflect the complex nature of GERD from both anatomic and patient perception perspectives coupled with device sizing and the healing response at the GEJ after MSA; these factors are variable and unique to each patient. There is a higher degree of preoperative outflow resistance at the gastroesophageal junction in patients with hiatal hernia and surgical repair of hernia reduces this resistance, whereas those with normal preoperative hiatal anatomy may not have outlet obstruction from hiatal hernia and they may develop an amplified perception of postoperative dysphagia in the face of the relative obstruction caused with MSA. Preoperative dysphagia may result from an esophageal motility disorder, GERD-related inflammation, outlet obstruction from hiatal hernia, or a combination therein. The development of persistent postoperative dysphagia in this setting may represent a pre-existing predisposition to enhanced afferent neural input, combined with these preoperative clinical factors, which is then subsequently worsened by MSA. Despite having a lower mean postoperative DeMeester score, patients with persistent postoperative dysphagia had less improvement in the symptoms of GERD compared with those without dysphagia and were more often placed back onto antisecretory therapy. Postoperative esophageal distention from air swallowing driven by an increase in GEJ resistance after MSA is the probable culprit.

Currently, there are no established manometric criteria to guide patient selection for MSA. We showed that having less than 80% peristaltic contractions in the distal esophagus is a predictor of persistent postoperative dysphagia. This finding emphasizes the importance of consistent and organized peristalsis in the movement of a food bolus across the GEJ after the relative obstruction of MSA is imposed. This risk factor may serve as a harbinger for further degradation of effective peristalsis when the esophagus is subsequently challenged with MSA. Magnetic augmentation of the LES increases the outflow resistance of the GEJ. Therefore, the focus of the clinicians has been to not offer MSA in patients with weak esophageal motor function. However, less attention has been paid to those in whom an elevated DCI is indicative of vigorous esophageal contractility. Among patients with hypercontractile esophagus (DCI > 40000 mmHg cm sec), we observed a stepwise increase in the rate of persistent dysphagia with increasing DCI (Fig. 2) and these patients should be counseled that they may be at increased risk for persistent postoperative dysphagia.

The incidence of immediate postoperative dysphagia is 63% in our patients. This rate is consistent with the values reported in the literature and is higher than those reported for LNF. One partial explanation for this observation is that LNF patients remain on a liquid or soft diet for the first 7–10 days after surgery, whereas MSA patients are instructed to start solid food immediately after surgery. With improvement in our comprehensive preoperative counseling and management of patients’ expectations and detailed direction in postoperative diet, we observed a decline in the rate of immediate postoperative dysphagia. This decline, however, became more pronounced when we changed our protocol to increase device sizing (Fig. 4).

The host response to the titanium magnetic ring is highly variable and may result in a spectrum of response pertaining to inflammation and healing; this variability most certainly impacts the dysphagia rates after MSA and will require further delineation and investigation. Our reoperative experience showed that within the first 6–8 weeks after MSA, we typically witness a loose network of tissues around the LINX (Fig. 5a), whereas later on, there is a robust capsule around the implant (Fig. 5b, c). While forming a robust fibrinous response around, the implant will have theoretical benefit of further augmentation of the reflux barrier and minimizing the chance of re-herniation, if there is exaggerated host inflammatory reaction, it may increase postoperative dysphagia. Anecdotally, we have observed such a response more often in those with underlying autoimmune or connective tissue disorders.

An increase in the outflow resistance caused by a tight crural closure or an undersized device that is evidenced by an increase in intrabolus pressure on HRM (Fig. 6a, b) or fluid retention and stasis esophagitis (Fig. 7) will only be remedied by addressing the anatomical problem. These findings emphasize the importance of detailed evaluation of the patients with persistent dysphagia after MSA with radiologic, endoscopic, or esophageal physiology testing.

As we gained experience with the management of postoperative dysphagia, we noticed the importance of three principles in decreasing the need for dilation after MSA:

A solid diet is started on the day of surgery and patients are instructed to have frequent small meals and try to eat one tablespoon of yogurt or pudding or a cracker every hour while awake for 8 weeks after surgery. These dietary instructions facilitate device actuation and prevent scarring in the closed position. We have experienced a decrease in the rate of postoperative dysphagia and need for dilation after establishing these dietary recommendations.

Dilation within 8 weeks of surgery was not successful in alleviating dysphagia. In fact, many patients reported worsening of their dysphagia when the procedure was done in the early postoperative period. Early dilation can increase the acute inflammatory response around the device that can potentially worsen the dysphagia. If dysphagia persists beyond 8 weeks despite following dietary exercise, we then consider endoscopic dilation under fluoroscopic guidance followed by a 7-day course of steroid and 2 weeks of hourly eating.

In our practice, we prescribe 20 mg prednisone twice a day for 7 days with no tapering. We chose this regimen based on the review of literature and our clinical experience. This steroid course is not strong enough to suppress the hypothalamic–pituitary–adrenal (HPA) axis that would necessitate the need for steroid tapering, but it is enough to minimize the inflammatory response surrounding the implant. It is important to emphasize that there is currently no data to support the use of steroid after dilation in the relief of postoperative dysphagia. The current recommendations are based on expert opinion and high-volume center anecdotal experience.

There is reduction in the efficacy of dilation with each subsequent procedure, and after the third dilation, there is minimal benefit. We will consider device explant in patients with persistent dysphagia after three dilations. Our proposed algorithm in management of dysphagia after MSA is shown in Fig. 8.