Laparoscopic Revision Roux-en-Y Gastric Bypass Surgery After Previous Anti-rflux Surgery: Intermediate Results

The epidemic of overweight and obesity in the United States of America along with its comorbidities continues to expand. Bariatric surgery has demonstrated to be the most effective and sustained method to control severe obesity and its comorbidities. For instance, type 2 diabetes mellitus was completely resolved in 76.8 percent, systemic arterial hypertension was resolved in 61.7 percent, dyslipidemia improved in 70 percent, and obstructive sleep apnea-hypopnea syndrome was resolved in 85.7 percent. Furthermore, bariatric surgery significantly increases life expectancy (89 percent) and decreases overall mortality (30-40 percent), particularly deaths from diabetes, heart disease, and cancer. Lastly, preliminary evidence about downstream savings associated with bariatric surgery offset the initial costs in 2 to 4 years.

Since 1998, there has been a substantially progressive increase in bariatric surgery. In 2005, the American Society of Metabolic and Bariatric Surgery "ASMBS" reported that 81 percent of bariatric procedures were approached laparoscopically. 205,000 people, in 2007, had bariatric surgery in the United States from which approximately 80 percent of these were Gastric Bypass. Moreover, there is a mismatch between eligibility and receipt of bariatric surgery with just less than 1 percent of the eligible population being treated for morbid obesity through bariatric surgery. Along with the increasing number of elective primary weight loss procedures, up to 20 percent of post RYGB patients cannot sustain their weight loss beyond 2 to 3 years after the primary bariatric procedure. Thus, revisional surgery for poor weight loss and re-operations for technical or mechanical complications will rise in a parallel manner.

Three systematic reviews and meta-analysis have examined the association between obesity (BMI >30kg/m2) and several GERD-related disorders, including 1) GERD symptoms, 2) erosive esophagitis "EE", and 3) esophageal adenocarcinoma "EA". Obesity is associated with a 1.5-to-2-fold increased risk of GERD symptoms and EE and a 2- to 2.5-fold increased risk of EA. In two large case-control studies, abdominal diameter (waist-hip ratio), but not BMI, is an independent risk factor for another GERD-related disorder, Barrett´s esophagus "BE".

Current pathophysiological mechanisms of GERD in the obese encompass the following. 1) Mechanical: I) increased intra-gastric pressure: increased intra-peritoneal and abdominal wall fat mass increases the intra-abdominal and peri-gastric pressures with subsequent increased gastroesophageal pressure gradient "GEPE" with augmented esophageal acid exposure. Each BMI unit increase corresponds to a 10 percent increase in intra-gastric pressure. II) Hiatal Hernia: "HH" disrupts the integrity of the sphincter mechanisms and prolongs esophageal acid clearance. Thin, normal, overweight, and obese subjects have a 1.0, 1.9, 2.5, and 4.2 risk of having HH compared to thin subjects, respectively. 2) Motility: I) Increased Transient LES Relaxation "TLESR" are associated with acid reflux during the postprandial period, especially during inspiration. II) Low LES basal pressure: Increased prevalence of abnormally low LES basal pressure in the overweight and obese in comparison to the normoweight subject. III) Esophageal motility abnormality: Jaffin et al, with esophageal manometry, reported 61 percent of patients with altered esophageal motility from which 59 percent had altered visceral pain perception (asymptomatic). IV) Delayed gastric emptying: mostly associated with one of its major comorbidities, diabetes mellitus. 3) Esophageal sensitivity: Mercer et al., with a Bernstein test, found a significant difference between normoweight and obese subjects without clinical evidence of GERD (0 percent vs. 86 percent, respectively) for esophageal hypersensitivity. 4) Hormonal: mostly mediated by estrogen and adiponectin. 5) Environmental (Diet): high-fat, saturated fatty acids, high-cholesterol, and high caloric density diets have been associated with the highest likelihood of perceiving an acid reflux event; fat may confer its sensory effect by activating pain facilitatory pathways or by deactivating pain inhibitory pathways.

The most recent data is not conclusive on whether increased BMI affects acid-suppressive therapy for GERD. However, MacDougall et al. found that increased BMI was significantly associated with long-term acid suppression therapy. This can be explained based on either a higher prevalence of factors that predispose overweight and obese subjects to severe GERD, such as HH, greater GEPG, increased number of TLESR, or standard doses of PPI´s are suboptimal for patients with increased BMI and GERD.