Postoperative Problems 2011: Fundoplication and Obesity Surgery




The population of the Western world is abundantly exposed to food. Together with the introduction of fast food, this situation has contributed to an exponential increase in morbid obesity. Similarly, the prevalence of gastroesophageal reflux disease (GERD) has increased significantly in the past decades, representing one of the most common gastrointestinal (GI) disorders in the Western world. The fact that morbid obesity is a significant risk factor for GERD certainly contributes to this tendency.


Neurogastroenterologists are mainly confronted with GERD patients presenting at the outpatient clinic or in the endoscopy room, often referred by the primary care physician with symptoms resistant to proton pump inhibitors (PPIs). With the introduction of laparoscopic surgery, however, more patients, especially younger patients or patients unwilling to take lifelong PPIs, are treated surgically. Although laparoscopic antireflux surgery is very effective in controlling reflux, the neurogastroenterologist is increasingly confronted with postsurgery complications; a similar situation now exists for obese patients who have undergone bariatric surgery. Weight reduction and GERD are, for the most part, effectively treated by the relevant surgical techniques used, but patients with symptoms resulting from abnormal motility secondary to altered anatomy or stenosis as a consequence of these procedures are increasingly presenting at our motility unit. In the current review, we will focus on the postoperative complications of obesity surgery and fundoplication most commonly observed in the outpatient clinic.


Obesity Surgery


Obesity is a major medical problem that has seen such a dramatic increase in prevalence in the United States that it now exceeds 30% in both genders and in most age groups. As obesity is a major risk factor for several serious medical conditions, such as arterial hypertension, cancer, diabetes, and cardiovascular diseases, this disorder should be rigorously treated. Although different treatment modalities have been introduced, the best long-term results are currently obtained with obesity surgery. For the most part, 1 of 3 different techniques is used to reduce food intake: laparoscopic adjustable gastric banding (LAGB), Roux-en-Y gastric bypass (RYGBP), and sleeve gastrectomy.


LAGB, introduced in 1993, is one of the most frequently performed surgical procedures to treat obesity worldwide, as it is a relatively simple to perform, minimal invasive and reversible. An inflatable device is positioned around the proximal stomach and then connected to a port reservoir, which is implanted 4 to 6 cm cranial to the xiphoid process and fixed to the periosteum of the sternum. Approximately 4 weeks after surgery the band is filled with 2 to 4 ml of saline, thereby creating a small reservoir above the band, ensuring early satiation and reduced food intake. The volume is adjusted during follow-up so that, while solid food intolerance is avoided, food intake is reduced to approximately one-third to one-half of the volume ingested prior to surgery. In the Roux-en-Y gastric bypass, the stomach is largely bypassed with only a small proximal gastric pouch remaining, while the stomach is drastically reduced in size by a sleeve gastrectomy.


In the early postsurgical period, complications such as leakage, infection, and bleeding can occur with all 3 procedures, but these are managed by the surgical team. Here, we will focus more on the long-term impact of these procedures on GI motility/physiology and the associated symptoms/complications, which will largely depend on the type of surgery to which the patient was exposed. Esophageal dysmotility disorders (dysphagia, esophageal dilatation, and heartburn [esophagitis]) are the main complications following LAGB, whereas dumping is the major complication of the 2 other techniques. These are the problems that the gastroenterologist is most likely to encounter.


Esophageal Dysmotility Disorders


In patients referred with dysphagia or heartburn following LAGB, displacement of the gastric band or an overinflated band should be excluded by imaging or endoscopy. A recent detailed analysis of a large series of patients (N = 167) treated with LAGB reported, indeed, that band deflation had to be carried out in approximately 30% (47 patients). These patients presented with symptoms of solid food intolerance, nightly aspiration, and vomiting more than twice per week. On imaging, 7 patients had a hypercontractile esophagus, 34 had significant dilatation with anterior/posterior pouch slipping, and, most importantly, 6 patients presented with a major achalasia-like dilatation. The latter patients had to be reoperated on for band removal. Thus, radiographic evaluation of the position of the band and an estimation of transit through the esophagus are crucial. Data on esophageal motility assessed by esophageal manometry or impedance recordings, in this situation, are not available yet and are eagerly awaited.


The radiographic features described (ie, esophageal dilatation, hypercontractility [nutcracker-like esophagus], and, in the most advanced stage, an achalasia-like picture) most likely result from the chronically increased resistance that has to be overcome by the esophagus and are very similar to the situation created by a too-tight fundoplication (see later). Initially, the esophagus will try to overcome the resistance, resulting in a hypercontractile state, which will gradually “exhaust” the esophagus with resultant dilatation and, ultimately, an achalasia-like picture. Interestingly, following deflation or removal of the gastric band, esophageal dilatation has completely reversed.


After gastric bypass, dysphagia can develop due to a stricture at the stoma in up to 19% of patients. Usually, it is advised to perform balloon dilation only up to 15 mm in diameter, in order to preserve the restrictive function of the RYGBP. In most patients, resolution of symptoms can be obtained with endoscopic treatment.


Dumping Syndrome


The dumping syndrome is a well-described complication of both gastric bypass and sleeve gastrectomy and has also been documented, albeit less frequently, following esophageal surgery. This condition results from too rapid passage of food from the stomach into the small bowel. Under normal conditions gastric emptying is tightly controlled through intimate coordination of motility of the proximal stomach, acting as a reservoir, and the distal stomach, where mixing and grinding result in the reduction of the ingested food into particles small enough to leave the stomach. The accommodation-reflex of the proximal stomach is a vagovagally mediated motor pattern that inhibits the tone of the proximal stomach, thereby creating a reservoir to temporarily store food. Impaired relaxation of the proximal stomach results in early satiation and has been identified as an important pathophysiological mechanism in functional dyspepsia. The main task of the distal stomach, on the other hand, is to gradually brake down food particles to a diameter of 1 to 2 mm, the critical size for passage through the pylorus and thus exiting the stomach. Finally, the pylorus, by acting as a gatekeeper controlling the outflow of the stomach, also significantly contributes to gastric emptying.


After upper GI surgery, such as a sleeve or partial gastrectomy, vagotomy, or even esophageal surgery, the absence of the vagovagal accommodation reflex and/or anatomical reduction of the size of the proximal stomach leads to an impaired reservoir function of the stomach and accelerated gastric emptying. In the case of either a Roux-en-Y gastric bypass surgery or a resection of the distal stomach (Billroth I and II), the grinding activity of the antrum and the sifting function of the pylorus are eliminated resulting in the rapid arrival of large food particles in the small intestine. The increased exposure of the duodenum to these large, less easily digested, particles is considered to be the main pathophysiologic mechanism responsible for the development of the dumping syndrome after esophageal and, more frequently, gastric surgery.


Typically, dumping symptoms can be divided into early (within 30 minutes) and late (1 to 3 hours after meal ingestion). Early symptoms are divided into GI complaints, such as abdominal pain, diarrhea, borborygmi, bloating, and nausea and the more specific vasomotor complaints such as flushing, palpitation, perspiration, tachycardia, hypotension, and even syncope. Early symptoms are probably a result of a fluid shift to the hyperosmolar duodenal lumen, resulting in a decrease of circulating volume and, thereby, to postprandial tachycardia, hypotension and, eventually, although rarely, syncope. Additionally, the carbohydrate overload leads to a rapid release of GI peptide hormones that alter GI motility and can, in itself, also lead to the observed hemodynamic effects. Late symptoms occur up to 3 hours postprandially and include hypoglycemia, perspiration, hunger, fatigue, and syncope. The excessive presentation of carbohydrates to the jejunum is thought to generate a rapid increase in insulin release via glucagon-like peptide (GLP-1), which eventually leads to hypoglycemia and related symptoms.


The diagnosis of dumping syndrome is mainly based on clinical assessment and a modified oral glucose tolerance test. From 50 to 75 g of glucose solution is ingested after an overnight fast. Immediately before and up to 180 minutes after ingestion, blood glucose concentration, hematocrit, pulse rate, and blood pressure are recorded every 30 minutes. This provocative test is considered positive if late hypoglycemia (120 to 180 minutes) occurs or an early (30 minutes) rise in hematocrit (>3%) occurs. The best predictor of dumping, however, seems to be an increase in pulse rate (>10 bpm) after 30 minutes. Assessment of accelerated gastric emptying can be helpful, but this test does not have good sensitivity and specificity.


With the increased use of bariatric surgery, the incidence of dumping syndrome is rising; implying that clinicians should be familiar with the presentation and management of this syndrome. The first steps in the treatment of dumping syndrome are dietary measures. Patients are advised to eat more and smaller portions more frequently and to avoid drinking during the meal. Furthermore, the intake of fast-uptake carbohydrates should be limited. Most patients respond well to dietary measures, but for those who do not, acarbose is the next treatment step. Acarbose is an alpha-glycosidase hydrolase inhibitor that hinders the uptake of carbohydrates in the jejunum. Small studies have indeed shown a reduction in hypoglycemia and an improvement in symptoms ( Table 1 ). However, because of its mechanism of action, acarbose is only helpful in patients with late dumping symptoms, as gastric emptying is unaffected. Furthermore, the frequent occurrence of side effects, such as bloating, flatulence, and diarrhea, hinder patient compliance. If patients fail to respond to acarbose, the next step is subcutaneous injection of somatostatin analogs, of which short-acting (octreotide) and long-acting (lanreotide, LAR) variants exist. Somatostatin analogs delay gastric emptying and small bowel transit and inhibit the release of GI hormones and insulin, and thus act on several pathophysiologic mechanisms involved in both the early and late phases of dumping. As a consequence, these agents have proven successful in the treatment of the postoperative dumping syndrome ( Table 2 ). As the long-acting variant has a confirmed effect on quality of life and is preferred by patients, monthly administration with LAR is indicated in patients with proven dietary-refractory dumping syndrome and impaired quality of life. Known side effects, such as gallstone formation and steatorrhea, have to be considered in the decision on treatment. If patients do not tolerate or do not respond to somatostatin analogues, surgery or continuous enteral feeding might be necessary but the results of these treatments are unpredictable.


Sep 7, 2017 | Posted by in GASTROENTEROLOGY | Comments Off on Postoperative Problems 2011: Fundoplication and Obesity Surgery

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