Surgery for Gastroesophageal Reflux Disease in the Morbidly Obese Patient

Abstract

The prevalence of gastroesophageal reflux disease (GERD) has mirrored the increase in obesity, and GERD is now recognized as an obesity-related comorbidity. There is growing evidence that obesity, specifically central obesity, is associated with the complications of chronic reflux, including erosive esophagitis, Barrett's esophagus, and esophageal adenocarcinoma. While fundoplication is effective in creating a competent gastroesophageal junction and controlling reflux in most patients, it is less effective in morbidly obese patients. In these patients a bariatric operation has the ability to correct both the obesity and the abnormal reflux. The Roux-en-Y gastric bypass is the preferred procedure.

Introduction

Obesity was first recognized as a growing public health concern in the 1970s and 1980s as measured by the National Health and Nutrition Examination Survey (NHANES). This study showed a dramatic increase in the prevalence of obesity, defined as a body mass index (BMI) ≥30 kg/m², from 20% of the US population in 1990 to 35% in 2010.¹ Despite some predictions that estimated the prevalence of obesity in 2030 as 50%, the numbers appear to have reached a plateau.² The prevalence of GERD has mirrored this increase, and GERD is now recognized as an obesity-related comorbidity. The prevalence of GERD, defined by heartburn and or regurgitation at least once a week, is estimated at 18%–27%, but the incidence of GERD in the obese population has been reported to be as high as 72%.^3–4 Obesity carries a significantly increased risk of GERD, and GERD is directly related to the degree of obesity. For increasing BMI categories of <25, 25–30, and >30 kg/m², the prevalence of GERD is 23%, 27%, and 50%, respectively. At least half of the patients who qualify for bariatric surgery may have GERD.⁵

There is growing evidence that obesity, specifically central obesity, is associated with the complications of chronic reflux, including erosive esophagitis, Barrett's esophagus, and esophageal adenocarcinoma. In a large endoscopic study, El-Serag reported that participants with erosive esophagitis were more likely to be overweight or obese compared to those with no erosions.⁴ A similar association was reported by Lee et al. in another large endoscopy study with 3000 participants and showed more than a threefold increase in erosive esophagitis in obese individuals.⁶ Studies looking to find associations between Barrett's esophagus and obesity have reported similar findings. Using data from the Kaiser Permanente database, Corley et al. found that, independent of BMI, a larger abdominal circumference was associated with Barrett's esophagus.⁷ Many studies have shown an increase in recent years in the incidence of esophageal adenocarcinoma. A Swedish study found that obesity had an odds ratio of 16.2 for development of esophageal adenocarcinoma compared with the lowest BMI category (BMI <22 kg/m²).⁸ The combined increase in the complications of GERD would suggest that the severity of GERD is increasing in addition to the prevalence. Despite the parallel increase in GERD and obesity, GERD is not ubiquitous in the obese population; therefore, it is not independently responsible for GERD.

Normal Antireflux Mechanisms

Normal protective anatomic structures and mechanisms that prevent reflux include the lower esophageal sphincter (LES), angle of His, esophageal clearance, gastric emptying, and the diaphragm. Effective reflux control is a complex multifactorial process, and no single abnormality has been implicated as the common pathway that causes reflux. The LES is a constricting muscle that creates a high-pressure zone just proximal to the esophagogastric junction. The LES pressure created overcomes the intrathoracic pressure gradient. Its effectiveness is a function of LES tone, length, intra-abdominal position, and the normal frequency and duration of transient lower esophageal sphincter relaxations (TLESRs).⁹ The angle of His creates a mechanical partition that serves to physically separate the fundus and its food contents from the esophagus. It also helps to prevent retrograde flow during gastric distention.¹⁰ Refluxed gastric contents are cleared in an antegrade manner by esophageal peristalsis assisted by the lubricating effects of saliva. Normal gastric emptying helps to limit the availability of gastric contents to reflux into the esophagus. The diaphragm provides external compression proximal to the esophagogastric junction and helps to overcome the transgastric pressure gradient.

GERD and Obesity

Abnormal pH and manometric measurements provide the link between obesity and GERD.^11,12 A number of different anatomic and physiologic derangements have been postulated as causes of increased esophageal acid exposure in the general population, and most of these proposed variables are accentuated in the obese population. Murray et al. reported an adjusted odds ratio of 1.82 (95% CI, 1.33–2.5) for overweight patients with weekly heartburn symptoms compared with 1.5 (95% CI, 1.13–1.99) for individuals of average weight.¹³ Ruhl et al. showed that for every increment of BMI of 5, the risk of GERD increased by 1.2.¹⁴ The proposed mechanisms include hiatal hernias, esophageal dysmotility, hypotensive LES, inappropriate TLESRs, and higher transdiaphragmatic pressure gradients.

The prevalence of hiatal hernias in the general population is disputed, with a wide range that spans from 13% to 59%.^15–17 The prevalence in the obese population appears to be increased, with a range somewhere between 40% and 50%.^18,19 A number of studies show that obesity is a risk factor for hiatal hernia formation. Pandolfino et al. found that the elevated esophagogastric pressure gradient in obese patients supports the development of a hiatal hernia.¹⁹ Wilson et al. showed that elevated BMI is an independent risk factor for development of hiatal hernias and that the probability increases with each successive level of BMI.²⁰ Hiatal hernias disrupt the normal anatomic barriers to reflux.^16,17 The crura of the diaphragm no longer correlate with the esophagogastric junction. The angle of His is stretched and obtuse and makes this anatomic structure ineffective at diverting gastric flow away from the esophagus.

The prevalence of esophageal dysmotility is increased in obese patients. Interestingly, this has been identified in mostly asymptomatic patients, with common abnormal findings, including nutcracker esophagus, hypotensive LES, and other nonspecific motility disorders.^21–23 TLESRs are more frequent in obese patients, and there is an incremental increase with higher BMI and waist circumference.^24,25 The primary stimulus for TLESR is fundic distension.^26,27 Obesity causes increased intra-abdominal pressure, confirmed by intragastric manometry, which can contribute to increased TLESRs.^28–31 Obesity increases the output of bile and pancreatic enzymes, although the direct effect of this variable on GERD is not completely understood.³²

Effectiveness of Nissen Fundoplication

Fundoplication procedures, which serve to increase the cardioesophageal competence, are effective treatment options for GERD patients of normal weight. Multiple studies and meta-analyses with 10-year follow-up have shown that 90% of patients achieve symptom control with surgical intervention.^33–37 Despite the effectiveness of symptom control, 15%–20% of postoperative patients restart proton-pump inhibitor (PPI) therapy. However, objective testing using pH monitoring shows that only one-third of patients who restart PPIs after surgery actually have recurrent reflux.³⁸

Positive response to surgery can be well predicted with appropriate patient selection. The strongest predictors of a successful fundoplication include the presence of typical symptoms, a positive pH test, and/or a good response to PPI therapy.^39,40

Impact of Obesity on Fundoplication Failure

As patterns of fundoplication failure have been characterized, obesity has emerged as a risk factor for GERD recurrence. Obese patients having antireflux surgery have higher rates of reoperation, lack of satisfaction, or severe symptoms.

Perez et al.⁴¹ found obese patients having either a laparoscopic Nissen fundoplication or Belsey Mark IV procedure had a 31% recurrence rate versus a 4.5% rate if patients had a normal weight at 37-month follow-up. In another study, Morgenthal et al.⁴² reported that BMI less than 35 kg/m² was one of the few variables that were associated with successful outcomes at 10-year follow-up. Pandolfino et al.¹⁹ showed that BMI and waist circumference correlated with intragastric pressure and gastroesophageal pressure gradient and suggested that these two factors may be the underlying etiology for the higher failure rate. Likewise, Akimoto et al. found that, among 124 patients having reoperation for failed fundoplication, morbidly obese patients (16.7%) were more likely than controls to have disrupted or herniated fundoplications.⁴³

A number of other studies document conflicting results, but they are limited by the general applicability in severely obese patients, short follow-up, and lack of objective physiologic outcomes.^44–47 While the data regarding obesity as a risk factor for failed fundoplication are conflicting, obesity is associated with recurrent herniation after incisional hernia repair,^48,49 implying that a similar etiology may exist at the diaphragmatic hiatus. Although antireflux surgery reestablishes phrenoesophageal competence, this strategy does nothing to address the patient's obesity and the associated comorbid conditions.

How Bariatric Operations Impact GERD

For most patients, bariatric surgery is the best treatment for morbid obesity by reducing body weight and metabolic comorbidities, including diabetes, hypertension, and hypercholesterolemia. Bariatric surgery reduces GERD symptoms and the use of antireflux medications.^5,50,51 This is not surprising, since gastric bypass is utilized in lean patients with failed fundoplications to divert refluxate from the esophagus when fundoplication is not possible.^52,53

Different bariatric procedures may variably affect the derangements that contribute to GERD in the first place, but also may have later effects. LES tone or distensibility may be impacted by adjustable gastric banding,⁵⁴ vertical sleeve gastrectomy (VSG^55,56), and gastric bypass.⁵⁷ Hiatal hernias may be corrected at the time of bariatric operation. Gastric emptying may be accelerated or delayed by the degree of restriction, the occurrence of strictures, or through redirection of the alimentary channel around the pylorus.

Weight loss alone is a recommended medical treatment modality for GERD in obese patients and reduces GERD symptoms in a dose-dependent pattern.⁵⁸ Fraser-Moodie et al. showed a significant correlation between weight loss and esophageal pH in an uncontrolled study of 34 obese patients with GERD.⁵⁹ Mathus-Vliegen et al. demonstrated a similar correlation with a decreased upright esophageal pH <4 (8.0% versus 5.5%) and postprandial reflux episodes (49.0 versus 32.1) in patients with a mean weight loss of 12.4 kg in 13 weeks.^60,61 Loss of visceral fat has also been shown to improve reflux parameters.⁶¹ Sing et al. performed a prospective interventional trial of 332 patients with 6-month follow-up that showed that a structured weight-loss program caused complete resolution of GERD symptoms in the majority of subjects.⁶² Some weight-loss programs have been able to achieve an initial weight loss of 10%, but a meta-analysis of 22 behavioral weight loss studies showed an average weight loss of 4% compared with 1% for the control groups; the maximal effect was seen in the first 6 months of treatment initiation.^63–65

Given the mounting evidence for the benefits of bariatric surgery to morbidly obese patients, coupled with the emerging association of obesity with fundoplication failure, bariatric surgery is now considered the appropriate surgical GERD therapy despite the fact that objective postoperative measures of GERD are comparable between fundoplication and gastric bypass.³ Initial concerns regarding the higher risk of bariatric interventions versus fundoplication are now tempered by recent data showing comparable morbidity and mortality rates.⁶⁶ Now, the major academic discussion centers around the rate of GERD associated with various bariatric operations.

Gastric Bypass and Duodenal Switch—Effect on GERD

Gastric bypass has now emerged as the preferred operation for patients with GERD and severe obesity.^67,68 Gastric bypass addresses symptomatic reflux in several ways. With 50%–70% of excess body weight loss expected, gastric bypass addresses the reflux attributable to obesity and increased intra-abdominal pressure.⁶⁹ By construction of a small, isolated proximal stomach pouch with a Roux-en-Y reconstruction (with at least a 100-cm alimentary limb), gastric bypass limits acid and bile reflux into the esophagus.^70–72 The small pouch also serves to decrease access to the parietal cell mass and in turn acid production near the gastroesophageal junction.⁷³ The Roux-en-Y reconstruction diverts bile from the gastroesophageal junction and decreases alkaline reflux.⁷⁴ The classic description of gastric bypass does not alter the LES anatomy, but the diaphragmatic hiatus is readily accessible. Repair of hiatal hernias 2 cm or greater is recommended, thereby restoring the gastroesophageal junction to an intra-abdominal location.

De Groot et al. performed a systematic review on bariatric surgery and its effects on GERD. All but one of the eleven studies identified showed improvements in GERD symptoms after gastric bypass. Objective measurements, including endoscopy and 24-hour pH monitoring, were utilized in four of the studies; the remaining measuring tools included GERD questionnaires.⁷⁵ Frezza et al. found an immediate improvement in GERD symptoms, which suggest that the anatomic manipulation is the initial mechanism decreasing GERD following gastric bypass.⁶⁸ Naik et al.⁷⁴ provided a more recent review that further characterizes the impact of weight-loss surgery on esophageal symptoms and physiology and provides higher level evidence.^{67–70,73–77} For example, Madalosso et al.⁶⁷ utilized a standardized definition and classification system for GERD (Montreal consensus) and a prospective study design and found reductions in GERD prevalence from 64% to 33%, with reduced esophageal acid exposure and medication requirements after gastric bypass.

Like gastric bypass, biliopancreatic diversion-duodenal switch (BPD-DS) is another restrictive and malabsorptive operation for morbid obesity that is often reserved for the largest patients. The procedure also improves GERD by reducing esophageal acid exposure, preventing bile reflux, and inducing substantial weight loss. Sugerman and Baltasar reported 76% and 100% resolution of GERD in patients following BPD-DS.^78–81 However, a comparative study found that GERD symptoms and medications were not reduced as much by BPD-DS versus a gastric bypass,⁸² despite the greater weight loss with the BPD-DS.

Vertical Sleeve Gastrectomy—Effect on GERD

VSG emerged as the first stage of a two-stage approach to duodenal switch. The procedure involves resection of 80%–85% of the gastric volume leaving a lesser-curvature based tubular stomach above a functioning pylorus. This resection is believed to have potential as an antireflux operation because it removes a substantial portion of the parietal cell mass, causes significant weight loss, and may increase gastric emptying. However, the relatively long and narrow anatomical configuration of a vertical gastric sleeve may also have the potential to increase GERD through increased resistance to esophageal and gastric emptying.

Rebecchi et al.⁸³ assessed pH profiles in 65 patients before and 2 years after VSG and found that those with preoperative GERD had significant reduction in esophageal acid exposure, whereas those without preoperative GERD only developed symptoms in 5.4% of cases. However, Gorodner et al. reported esophageal manometry and pH profiles before and 1 year after VSG in 14 patients and found reduced LES pressures (17.1–12.4 mmHg) and increased DeMeester score (12.6–28.4).⁸⁴

In 2011, a systematic review on the topic of GERD after VSG was performed by Chiu et al. The authors found too much variance in the literature to draw a conclusion on the effect of VSG on GERD symptoms.⁸⁵ A more recent systematic review by Oor et al.⁸⁶ found 33 studies on the same topic. Of these, 16 reported an increase and 12 a decrease in the prevalence of GERD symptoms after VSG. Eight studies used esophageal function tests, including those mentioned above, and again there were paradoxical results. When data were pooled for meta-analysis, the heterogeneity was high and no strong conclusions were possible. The authors postulate that variations in technique and management of concomitant hiatal hernias may explain the differences that still exist in the literature.

Therefore, at the present time, the exact effect of laparoscopic VSG on the prevalence of GERD remains unanswered. Surgeons should carefully evaluate preoperative GERD symptoms and should counsel patients carefully when helping patients determine their choice between bariatric options.

Adjustable Gastric Band—Effect on GERD

Laparoscopic adjustable gastric banding (LAGB) achieved widespread popularity following FDA approval in the United States in 2001 due to low mortality, reversibility, and ease of placement.⁸⁷ As long-term results accrued, some series showed that up to 60% of patients required reoperation.⁸⁸ There is a growing body of literature evaluating safety of revisional surgery for LAGB patients experiencing weight-loss failure with or without other complications, whether by a single procedure or a staged approach.^89,90 Potential complications of LAGB include dysphagia or pseudoachalasia, infection, band slippage, esophageal dilatation, band erosion, and band leakage.⁹¹

The impact of adjustable gastric bands on GERD is not clear. Some studies report improvement in GERD symptoms, medications, and pH-metric data.^54,92,93 Others show increased esophageal acid exposure, symptoms, and esophageal dysmotility.^94–96 Merrouche et al.⁹⁷ reported increases in DeMeester scores after adjustable gastric banding (11.5 ± 5.1 before to 51.7 ± 70.7 after implant).

LAGB has lost popularity as a primary treatment for obesity, and for these reasons, most bariatric surgeons do not recommend LAGB to severely obese patients with significant GERD, particularly in the setting of hiatal hernia.

Comparing Different Bariatric Operation Effects on GERD

Treating GERD with bariatric surgery is a reasonable approach in that much of GERD is related to obesity and its effects on antireflux mechanics. Weight loss alone is an effective adjunct or treatment for obese patients suffering from GERD. Bariatric procedures have different mechanisms by which weight loss is induced, and this variety also contributes to the differential effects on GERD symptomatology and pathology.

Pallati et al.⁹⁸ reviewed the Bariatric Outcomes Longitudinal Database (BOLD) in 2014 and found 22,870 patients with GERD (but no hiatal hernia) before bariatric surgery. At 6-month follow-up, gastric bypass showed a 56% reduction in GERD scores, which was better than the 46% reduction after an adjustable gastric band and the 41% reduction after a VSG. Peterli et al.⁹⁹ reported 1-year data from the Swiss Multicentre Bypass or Sleeve Study (SM-BOSS), a prospective randomized trial comparing laparoscopic gastric bypass and sleeve gastrectomy, and found that gastric bypass patients had a 75% rate of GERD improvement versus 50% after a VSG. Of note, the sleeve gastrectomy showed a 12.5% rate of new GERD symptoms in asymptomatic patients. Oor et al. reviewed 33 articles assessing sleeve gastrectomy and the effect on GERD. The results were highly heterogeneous with paradoxical outcomes despite objective esophageal function tests.⁸⁶

Neither fundoplications nor any of the bariatric procedures discussed are associated with a 100% resolution rate of GERD. Gastric bypass reports the most beneficial effects on GERD in morbidly obese patients. Sleeve gastrectomy has unpredictable success rates in treating GERD, with significant chance of de novo GERD developing, or existing GERD worsening. For these reasons, GERD in the setting of morbid obesity should be a relative contraindication to sleeve gastrectomy, and gastric bypass should be the procedure of choice in these patients.

Recommendations

GERD is a common disease that is often well treated with medications and lifestyle changes. For patients who fail these measures, surgical treatment is a proven method of treatment. Fundoplication is efficacious for well-selected patients, namely those with normal weight, typical symptoms, objective evidence of acid reflux, and symptom improvement or resolution with PPI usage.

The prevalence of GERD is increasing in association with the worldwide obesity epidemic. Fundoplication in obese patients has a higher failure rate, and it fails to address obesity as a contributing cause of GERD. Therefore, reflux in the setting of obesity requires careful consideration regarding the optimal treatment.

Each respective bariatric procedure controls reflux through various anatomic changes and subsequent weight loss. These procedures now have morbidity and mortality profiles similar to laparoscopic fundoplication procedures, negating the argument that fundoplications are safer. Bariatric procedures also improve or resolve obesity-related comorbidities, including diabetes, hypertension, sleep apnea, and others.

Presently, all bariatric procedures carry the potential to treat or improve GERD. Between the most commonly performed operations today, VSG and gastric bypass, the effect of GERD following sleeve gastrectomy is the least predictable. Historically, gastric bypass is a reliable antireflux operation. Until more is learned about outcomes after sleeve gastrectomy and its physiologic mechanisms, Roux-en-Y gastric bypass should be the preferred procedure for morbidly obese patients with significant GERD.

Footnotes

Disclosure Statement

No competing financial interests exist.

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