editorial Gastroesophageal Reflux Disease after Bariatric Surgery: A New Problem of an Old Disease
Zvi Perry*
Surgical
Ward A, Soroka University Medical Center, Israel
*Corresponding author: Zvi Perry, Surgical Ward A, Soroka University Medical Center Beer-Sheva, Israel. Tel: +97286400610; Fax: +97286477633; Email: zperry@bgu.ac.il
Received Date: 30 August, 2018; Accepted Date: 04 September, 2018; Published Date: 10 September, 2018
Citation: Perry Z (2018) Gastroesophageal Reflux Disease after Bariatric Surgery: A New Problem of an Old Disease. Ar Med Surg Pathol: AMSP-101. DOI: 10.29011/AMSP-101/100001
Editorial
Morbid Obesity is a worldwide epidemic [1]. The usage of diet, eating habit modifications or pharmacotherapy has been found to be inefficient, while surgical treatment is considered the only proven treatment to reduce and maintain the weight loss [2,3] in short and long term, as well as giving a valid medical monitoring over time [4,5]. Surgical weight reduction has been correlated with reduced morality over time. Bariatric surgery is the only effective and durable treatment for morbid obesity (BMI ≥ 40 kg/m2) [3,6]. Close to 200,000 patients in the US underwent bariatric procedures in 2015 according to the American Society for Metabolic and Bariatric Surgery (ASMBS). Current common bariatric procedures include Laparoscopic Sleeve Gastrectomy (LSG), Laparoscopic Roux-en-Y Gastric Bypass (LRYGB), and Laparoscopic Adjustable Gastric Banding (LAGB) [7,8]. Indications for a bariatric procedure currently include a BMI ≥ 40 kg/m2 without coexisting medical problems, or a BMI ≥ 35 kg/m2 with one or more severe obesity- related comorbidities [2,9]. Choosing the appropriate bariatric procedure for each patient is challenging. For example, several studies have attempted, based on patient characteristics, to select the optimal patient for LAGB [3,5]. This is even more problematic when considering the presence or new formation of Gastro Esophageal Reflux Disease (GERD). The likelihood of developing Gastro-Esophageal Reflux Disease (GERD) after these procedures is greatly increased and if it is present, the disease is aggravated. After bariatric surgery (mainly in restrictive procedures such as LSG or LAGB) GERD symptoms occur in 30-50% of patients [10]. In these cases, the mechanisms of GERD have not yet been well understood. This pattern is harmful for the quality of life of our patients. In these operations, the weakening of the esophageal peristalsis results in a reduction of esophageal clearance.
It reduces the contractile ability of the esophagus wall, weakening the pressure in the lower esophageal sphincter (LES). This leads to the de-structuring anti-reflux function of the LES, and slowing of gastric emptying [11]. These effects are the result of dissection of ligaments, viscera, the parietal peritoneum, and the lower esophageal-diaphragmatic membrane (continuing as a separate structure in the posterior mediastinum). As a result of these manipulations the angle of His is destroyed [12]. A partial destruction of the muscle mechanisms reduces LES tone. The most persistent change is accompanied by partial damage to the muscle tissue at the time of the LES manipulation. It normally runs along a fold of mucous membrane (plica cardiac) - inner bottom border, and ends at the cardia of the diaphragm, from the left surface of the abdominal part of the esophagus. This leads to the relaxation of LES, and a pressure reduction. This forms a single space between the stump of the stomach and esophagus. In addition, after LSG and LGB, the fundus of the stomach stump is missing (after LGB isolated), and the place where the air bubble is usually localized is missing. Normally, the intra-abdominal pressure of the air bubble should help make a tight fit of the mucous membrane of the valve to the right wall of the abdominal part of the esophagus. In the absence of a gas bubble, the gas content of the gastric stump falls freely into the esophagus. Also, as a result of the operation, the residual stomach develops gastric paresis. The resulting days after surgery show peristalsis that is asynchronous, which leads to disruption of motor function. Aggressive substances are not cleared from the esophagus properly, which in turn leads to the development (or worsening) of inflammatory changes in the mucous. This further stimulates existing disorders of contractile ability which develop into a "vicious cycle". It creates the conditions that lead to the development of GERD, manifestations of which arise from the first days after the operation.
Thus, we as physician and surgeons alike need to be aware, and aggressively treat GERD in bariatric patients, due to the high risk of short (mainly decreased healing of the manipulated stomach) and long-term untreated reflux disease (the risk of Barret's esophagus).
In conclusion - the current article has tried to shed some light upon the formation and mechanisms of a reflux disease in the bariatric patient, as well as to encourage health professionals to take actions and treat this persistent and potentially life-threatening disease