© Springer Nature Singapore Pte Ltd. 2017
Saravana Kumar and Rachel Maria Gomes (eds.)Bariatric Surgical Practice Guide10.1007/978-981-10-2705-5_1212. Gastroesophageal Reflux and Bariatric Surgery
(1)
Bariatric Surgery, Ruby Hall Clinic, Pune, India
(2)
Department of Upper GI Surgery and Minimal Access Surgery, GEM Hospital and Research Centre, Coimbatore, India
12.1 Introduction
Gastroesophageal Reflux Disease (GERD) is a disorder of the upper gastrointestinal tract that is characterized by heartburn and acid regurgitation. According to the evidence-based consensus GERD is defined as ‘a disease that is associated with troublesome symptoms and/or complications on account of reflux of stomach contents into the esophagus’. GERD is a disorder of the upper gastrointestinal tract that is defined by heartburn and acid regurgitation [1, 2].
There are many factors responsible for occurrence of GERD. These include transient lower esophageal sphincter (LES) relaxations, hypotensive LES and/or anatomic disruption of the esophageal hiatus or the phreno-esophageal membrane at the gastroesophageal junction (GEJ) like a hiatus hernia (HH).
The most common symptoms associated with GERD include heartburn, regurgitation, laryngitis, chronic cough, water brash, aspiration, wheezing, night time awakening with choking, belching or burping more than normal, and difficulty in swallowing.
12.2 GERD and Obesity
The prevalence of GERD is estimated to be between 10 and 20 % in the Western world, with a lower frequency in Asia [3]. Obesity is a very important risk factor for development of GERD which has been increasing in prevalence and is strongly associated with adverse metabolic, cardiovascular, chronic inflammatory and malignant health outcomes [4]. It has been shown that increasing weight leads to both increased esophageal reflux of acid and mechanical dysfunction of LES [5]. The other factors that influence the raised gastroesophageal gradient seen in obesity include raised intra-abdominal pressure (IAP), raised intra gastric pressure (IGP), raised negative inspiratory intra-thoracic pressure, oesophageal motor and sensory abnormalities, increase in prevalence of HH, increase in serum female hormonal levels, increase in comorbidities and a mechanical separation between the LES and the extrinsic compression provide by the diaphragmatic crura [6, 7]. Obese patients have also been reported to have higher rates of esophageal motility disorders and bolus transit impairments compared to normal BMI patients with GERD [8, 9].
It has also been shown that people who are obese are six times more likely to develop GERD than normal BMI people, being more common among pre-menopausal women and women on hormone therapy (including birth control pills), suggesting the possibility of estrogen to be a factor in GERD pathogenesis. Morbidly obese men (BMI >35 kg/m2) are 3.3 times more likely to have reflux symptoms than men of normal weight with morbidly obese women being 6.3 times more likely to have these same symptoms compared to normal weighted women. It is being speculated that estrogen stimulates the production of nitrous oxide which relaxes smooth muscle fibers such as in the LES [10]. Brian et al. had observed a relationship between increasing BMI and the frequency of reflux symptoms and noted that for those who had a reduction in BMI of 3.5 or more there was nearly a 40 % reduction in heartburn and other GERD symptoms than for women who did not lose weight [11].
It is also important to understand that the long-term effectiveness of fundoplication in the treatment of GERD in obese individuals (BMI >30) been questioned due to higher failure rates compared to normal weight counterparts [12, 13]. Although there is only limited evidence suggesting that obesity diminishes the efficacy of Nissen fundoplication, several other factors may impede the outcome of the procedure. Firstly, obesity can create several technical difficulties precipitating higher rates of surgical failures. For instance, an enlarged left lobe of the liver can interfere with visualization of the hiatus. Fatty deposition at the esophagogastric junction can impede proper suture placement. Lastly, a thick abdominal wall may hinder manipulation of laparoscopic instruments [4].
12.3 GERD and Laparoscopic Sleeve Gastrectomy (LSG)
Laparoscopic Sleeve Gastrectomy (LSG) has emerged as a popular bariatric procedure worldwide due to its relative operative simplicity, lack of anastomoses, retention of normal gastrointestinal continuity and absence of a malabsorptive component [14–16]. But, it is generally believed that LSG increases the incidence/severity of GERD and is considered a contraindication in patients with pre-existing GERD.
The increasing incidence of de-novo GERD could be related to lack of gastric compliance, increased intraluminal pressure, removal of the gastric fundus, alteration in the angle of His, lower LES pressure, hiatal herniation, narrowing at the junction of the vertical and horizontal parts of the sleeve (incisura), twisting of the sleeve, dilation of the remnant fundus etc [17–20].
Arias et al. in his retrospective review of 130 patients who had undergone LSG noted an 2.1 % incidence of de novo GERD [21]. Carter et al. had reported the results of 176 patients who had undergone LSG with 34.6 % having preoperative GERD. Postoperatively, 49 % complained of immediate (within 30 days) GERD symptoms, 47.2 % had persistent GERD symptoms that lasted >1 month, and 33.8 % of patients were taking medications specifically for GERD. The most common symptoms were heartburn (46 %), followed by heartburn with regurgitation (29.2 %) [22].
Himpens et al. in 2006 did the only prospective study comparing LSG with gastric band and concluded that at the end of 1 year 21.8 % of patients developed de-novo GERD which decreased to 3.1 % at end of 3 years possibly due to restoration of Angle of His [19]. DuPree et al. in 2014 in their retrospective review of the Bariatric Outcomes Longitudinal Database (BOLD), a total of 4832 patients underwent LSG and 33,867 underwent laparoscopic roux-en-Y gastric bypass (LRYGB), with preexisting GERD present in 44.5 % of the LSG cohort and 50.4 % of the LRYGB cohort. Most LSG patients (84.1 %) continued to have GERD symptoms postoperatively, with only 15.9 % demonstrating GERD resolution. Of LSG patients who did not demonstrate preoperative GERD, 8.6 % developed GERD postoperatively [23].
It has also been reported by a few authors that LSG leads to improvement in GERD. The possible explanation could be reduced intra-abdominal pressure after weight reduction, reduced acid production, accelerated gastric emptying and reduced gastric volume [17]. It has been noted that during LSG if the anatomy of the esophago-gastric junction (EGJ) flap valve is maintained without axial separation of the crura and LES, an elevation of IGP would be transmitted to the intra-abdominal LES thus closing the EGJ. However, if the EGJ flap valve is obliterated, elevations in IGP may increase the volume of refluxate once the EGJ is forced open. Daes et al., in their prospective evaluation of 382 patients, showed a 94 % resolution of symptoms and emphasized the need for careful attention to surgical technique, such as avoiding relative narrowing at the level of incisura, and the importance of placing the anterior stomach wall and posterior stomach wall in an equal and flat position when firing the stapler, in order to prevent the sleeve from rotating [24]. A prospective database from Pallati et al., which included 585 patients, showed a 41 % improvement in GERD symptoms, thus indicating that LSG may be performed in obese patients suffering from GERD [25]. Chiu et al. in a systematic review on GERD and its effects following LSG showed that four studies demonstrated an increase in prevalence with seven studies showing a reduced prevalence of GERD following LSG [26].
Interestingly, there are some studies demonstrating positive outcomes after concomitant LSG and hiatal hernia (HH) repair. Soricelli et al. reported significant improvement of GERD symptoms after a LSG with concomitant HH repair [27]. They described repair of a posterior crural defect with two interrupted non-absorbable sutures, approximating the right and left diaphragmatic pillars. HH repair was shown to be feasible and safe with no postoperative complications related to this procedure. The exposure of the hiatal area in the presence of a HH implies complete freeing of the posterior stomach wall and facilitates complete resection of the gastric fundus. This in turn is of great importance for the success of a LSG in terms of weight loss but also avoids de novo GERD caused by acid secretion and regurgitation of the persistent gastric fundus content into the esophagus. In addition, the postoperative development of de novo reflux symptoms was significantly greater in patients who underwent a LSG without an HH repair compared to those with an HH repair. Similar results have also been shown by Daes et al. and Soliman et al. who had favorable outcomes in the improvements of GERD by combining LSG with HH repair [24, 28]. Gibson et al. had also shown favorable outcomes even with an anterior crural closure [29].
Cheung et al. reported the results from revisional surgery after a LSG (Re-LSG and LRYGB) and found that both procedures were effective in achieving weight loss following a failed LSG. As weight loss may influence GERD symptoms, a Re-SG may also work as an effective tool to reduce GERD [30].
Silecchia et al. reported on the safety and efficacy of Re-LSG (also referred to as laparoscopic fundectomy) in cases where a residual fundus or neofundus is responsible for GERD symptoms. A Re-LSG was done in 19 patients when a residual fundus or neofundus was found in patients with severe GERD symptoms. Of note is that cruroplasty was concomitantly done when a HH was found in this series. All patients had improved GERD symptoms and discontinued proton pump inhibitors (PPIs) [31]. HH is not only responsible for GERD but contributes to the incomplete removal of the gastric fundus, which is often missed at the time of a LSG. The latter is responsible for acid secretion, which is then regurgitated back into the esophagus, especially if there are other factors such as a HH or an impaired LES, and if increased transient relaxation is present. Thus, Re-LSG may be an option for patients with a persistent gastric fundus and or a HH responsible for GERD that is non-responsive to PPIs. However, this procedure should remain limited to patients in whom a relationship between GERD and a persistent gastric fundus is clear, and should be conducted by a specialized bariatric surgeon. If a HH is present, it should be fixed during the same procedure [17].
12.4 GERD and LRYGB
The LRYGB is considered to be the most effective treatment option for GERD in the morbidly obese patient, since it treats GERD effectively and provides the additional benefit of weight loss and improvement in comorbidities [32]. Its efficacy in treating GERD is possibly related to the relatively low acid production of the small-volume (15–30 mL) gastric pouch, reduction of esophageal biliopancreatic refluxate by use of a roux limb measuring at least 100 cm in length and weight loss. The physiological effects of the anatomic configuration of LRYGB, and specifically, the configuration of the gastric pouch, might in fact be a more important contributor to reflux improvement than reducing alkaline bile reflux or weight loss. The cardia region of the stomach, where the pouch is created, has also been shown to relatively lack parietal cells [33].
Frezza et al. conducted a study on a total of 152 patients with pre-existing GERD, on changes in GERD symptoms, quality of life, and patient satisfaction after LRYGB. There was a significant decrease in GERD-related symptoms, including heartburn (from 87 to 22 %), water brash (from 18 to 7 %), wheezing (from 40 to 5 %), laryngitis (from 17 to 7 %) and aspiration (from 14 to 2 %) following LRYGB and the overall patient satisfaction was 97 % [33].