Gastroesophageal Reflux Disease

gastrointestinal tract and abdomen Gastroesophageal Reflux Disease and Hiatal Hernia James A. Rydlewicz, MD, Matthew R. Pittman, MD, and Kyle A. Perry, MD Gastroesophageal reflux disease (GERD) was not identified as a significant clinical problem and the underlying cause of esophagitis until the mid-2th century. Over the intervening decades, GERD has become an increasingly common condition in Western societies, affecting an estimated 18 to 27% of adult Americans. 1 Given the high incidence of reflux in the general population and its impact on patient quality of life, a systematic approach to its diagnosis and treatment is essential. This review outlines the basic pathophysiology, evaluation, and treatment algorithms for patients with GERD and hiatal hernia. Disease Definition According to the Montreal Consensus definition, GERD develops when reflux of gastric contents into the distal esophagus causes troublesome symptoms and/or complications. 2 The definition of troublesome symptoms is somewhat vague but generally includes any that adversely affect an individual s subjective well-being. Complicated GERD is defined by the presence of severe esophagitis, benign esophageal stricture, or Barrett esophagus. The diagnosis of nonerosive reflux disease (NERD) is given to patients with typical acid reflux symptoms in the absence of tissue injury and accounts for up to 7% of GERD patients in primary care settings. 3 Anatomy and Physiology of the Gastroesophageal Junction The components of the antireflux mechanism at the gastroesophageal junction (GEJ) include a mechanically effective lower esophageal sphincter (LES), esophageal clearance, and a functional gastric reservoir. The LES, a zone of high pressure above the GEJ, plays a major role in the prevention of gastric contents refluxing into the esophagus. The LES is composed of the diaphragmatic hiatus and the collar sling musculature and clasp fibers of the distal esophagus and gastric cardia [see Figure 1]. Normally, the LES creates a zone of increased pressure (1 to 3 mmhg) compared with intraluminal gastric pressure (5 mm Hg). By definition, reflux occurs when the pressure in the LES is too low to prevent reflux of gastric contents into the esophagus. 4 Standardized normal ranges of lower esophageal resting and relaxation pressure have been established using esophageal manometry. Diagnosis clinical manifestations GERD presentation can be classified into two distinct syndromes: esophageal and extraesophageal. Symptoms of esophageal syndrome include heartburn, dysphagia, chest pain, and regurgitation, and their presence on the clinical 215 Decker Intellectual Properties Inc Figure 1 Normal gastroesophageal junction anatomy. history is typically sufficient to make the diagnosis of GERD. Although frequently used interchangeably, heartburn is defined as a burning sensation in the retrosternal area, whereas regurgitation is the perception of flow of refluxed gastric contents into the proximal esophagus, mouth, or hypopharynx. 2 Extraesophageal symptoms including cough, hoarseness, asthma, laryngitis, globus pharyngeus, and dental erosions are less specific and usually require further investigation. Worrisome symptoms, including weight loss, progressive dysphagia, gastrointestinal bleeding, and vomiting, suggest a complication of the disease process or malignancy. 5 A complete history should be obtained focusing on typical and atypical symptoms as well as severity. Inquiry into the use of antacids, histamine receptor blockers, or proton pump inhibitors (PPIs) and their effectiveness is an important element of the history. Risk factors for GERD should also be noted [see Table 1]. 5 physical examination Physical examination has limited utility in the diagnosis of GERD. Examination should focus on oropharynx and neck examinations. Patients with proximal reflux can have Table 1 Risk Factors for GERD 5 Obesity Male sex Hiatal hernia Cigarette smoking Alcohol consumption Caffeine intake History of irritable bowel syndrome GERD = gastroesophageal reflux disease. DOI 1.231/78.246

gastro gastroesophageal reflux disease and hiatal hernia 2 signs of poor dentition and mucosal changes in the oropharynx. Cervical and supraclavicular lymph nodes should be palpated. Lymphadenopathy in this area may suggest malignancy of the esophagus or stomach. 4 diagnostic tests Although the initial diagnosis and management of GERD consist of symptomatic assessment and successful management of symptoms through dietary modification and acid suppression therapy, a thorough preoperative workup for objective evidence of acid reflux is required to optimize surgical outcomes in patients with refractory symptoms [see Figure 2]. The goal of testing is to objectively confirm the diagnosis of GERD, define any anatomic abnormalities, and identify underlying functional abnormalities of the esophagus. 6 Testing modalities include upper endoscopy, video esophagography, ph testing, and manometry. Recommendations from the Society of American Gastrointestinal and Endoscopic Surgeons (SAGES) state that the diagnosis of GERD can be made if any of the following conditions exist: positive ph testing, esophageal mucosal breaks on endoscopy in patients with typical symptoms, confirmed Barrett esophagus on biopsy, or peptic stricture in the absence of malignancy. 7 Endoscopy Esophagogastroduodenoscopy (EGD) is an important step in the evaluation of GERD as direct visualization of the esophageal mucosa can provide objective evidence of reflux. The presence of mucosal breaks, defined as an area of erythema or slough clearly demarcated from adjacent mucosa, has a very high specificity for GERD. 8 Mucosal injury can then be classified using either the Los Angeles or the Savary- Miller classification systems. EGD can also aid in the identification of complicated reflux with the presence of stricture, esophagitis, or Barrett esophagus. 6 Barrett esophagus is the replacement of esophageal squamous epithelium with columnar mucosa in the distal esophagus and represents a direct complication of GERD. Endoscopically, it appears as mucosa with a salmon-pink color [see Figure 3]. Barrett esophagus is confirmed with biopsies revealing intestinal metaplasia with characteristic goblet cells on histology. 9 The presence of Barrett esophagus places a patient at an increased risk for developing adenocarcinoma, and four quadrant biopsies at 2 cm intervals should be performed to confirm the diagnosis and assess for the presence of dysplasia. Endoscopic features should be reported according to the Prague C and M criteria, which Typical GERD symptoms Empirical treatment with daily PPI Response? Yes No 3-to 6-month maintenance Increase to b.i.d PPI Response? Yes No Objective reflux testing: 1. Esophagography 2. Upper endoscopy 3. ph study 4. Esophageal manometry Surgical intervention Figure 2 Treatment algorithm for patients with symptomatic gastroesophageal reflux disease (GERD). PPI = proton pump inhibitor.

gastro gastroesophageal reflux disease and hiatal hernia 3 a b Figure 3 Barrett esophagus. (a) Schematic and (b) endoscopic images of long segment Barrett esophagus. include the length of circumferential (C) and maximum (M) extent of the visualized Barrett esophagus. 1 Esophagography One of the most important aspects of the preoperative evaluation is a detailed delineation of gastroesophageal anatomy. A contrast swallow study, typically video esophagography with barium, provides this information [see Figure 4]. The esophagogram can identify esophageal functionality, evidence of reflux, and anatomic abnormalities. Spontaneous reflux on a swallow study, seen in about 4% of patients with GERD symptoms, is a strong indicator of reflux. 6 The anatomic abnormalities most commonly observed are hiatal hernias, strictures, obstructing lesions, and irregularities in the shape of the esophagus. Hiatal hernias are present in 8% of patients with symptomatic GERD. They are best seen with the patient in the prone position as the increased intra-abdominal pressure accentuates the hernia. The study should characterize the size of the hiatal hernia and can differentiate between type I (sliding) hiatal hernias and type II to IV (paraesophageal) hiatal hernias. Identification of luminal narrowing, dilation, or twisting of the lumen is necessary for determining optimal management, and esophageal contour is readily evaluated by esophagography. Contrast radiography can detect obstructing lesions, including strictures, tumors, and diverticula, and video esophagography also allows the surgeon to assess the peristaltic function of the esophagus, which can be used in concert with manometry to identify esophageal motility disorders. 6,11 Ambulatory ph Monitoring Ambulatory ph monitoring is the gold standard test to identify abnormal esophageal acid exposure. It detects the presence of acid reflux, characterizes the reflux episodes, and determines if patient symptoms correlate with acid Figure 4 Normal barium esophagogram. reflux events. A ph study documenting abnormal acid exposure should be obtained prior to consideration for antireflux surgery but may be omitted in the setting of severe erosive esophagitis (Los Angeles class C or D) or biopsy- proven long segment Barrett esophagus as these conditions occur only in the setting of GERD. Traditional catheter-based 24-hour ph monitoring is obtained via a transnasal catheter placed 5 cm proximal to the manometrically identified LES. Although effective for

gastro gastroesophageal reflux disease and hiatal hernia 4 quantifying acid reflux, numerous drawbacks are associated with this technique. It is uncomfortable for the patient and often quite lifestyle limiting, and dysphagia and epistaxis are commonly reported after placement. 12,13 A newer ph testing technology, the wireless 48-hour Bravo capsule (Medtronic, Shoreview, MN), allows a longer period of esophageal monitoring with increased patient comfort. The GEJ is identified using endoscopy or manometry, and the probe is secured to the esophageal mucosa 6 cm proximal to the GEJ. The benefits of this technique include increased patient compliance, tolerability, and less deviation from normal activity and dietary habits. The increased duration of monitoring has been reported to detect 22% more patients with abnormal esophageal acid exposure compared with 24-hour monitoring. 14 Before any ph test, patients should stop all acid-reducing medications. PPIs should be discontinued 2 weeks prior to testing, whereas histamine-blocking medications can be continued until 48 hours previously. The data collected fall into six parameters: (1) total number of reflux episodes; (2) percentage of total time with an esophageal ph less than 4; (3) percentage of upright time with an esophageal ph less than 4; (4) percentage of supine time with an esophageal ph less than 4; (5) the duration of the longest reflux episode; and (6) the number of reflux episodes lasting more than 5 minutes. 6 These parameters are combined and compared with normal ranges and then valued according to the DeMeester score. A DeMeester score greater than 14.7 indicates abnormal esophageal acid exposure [see Figure 5]. An abnormal DeMeester score has been identified as the most important predictor of successful outcome following laparoscopic Nissen fundoplication. 15 Esophageal Manometry Esophageal motility is best assessed by manometry. Esophageal manometry identifies primary motility disorders that may present with symptoms very similar to GERD. Furthermore, the adequacy of esophageal peristalsis should be determined preoperatively to help guide surgical therapy. 6 Overall, approximately 6% of patients with GERD will have manometric findings of an abnormal LES or impaired motility. 11 Manometry is performed using catheters with multiple transducers spaced at equal distances from the end. Specifically, it assesses the LES, the esophageal body, and the cricopharyngeal area (upper esophageal sphincter). The LES and body pressures are assessed by having the patient swallow water and recording the pressures generated in the esophageal lumen. Peristalsis is characterized by tracing the wave amplitude, progression, and morphology [see Figure 6]. Analyzing the coordination of peristalsis and contractile force generated can help guide the type of fundoplication to be performed, because patients with absent peristalsis will have less dysphagia with a partial fundoplication compared with a complete (Nissen) fundoplication. 6,11 However, despite anecdotal evidence, there are no data that support the use of manometry to decide which type of fundoplication to perform in patients with intact peristalsis. 16 Artifact Heartburn Regura Meal Cough Supine Chest pain Ignore ph 8 Esophageal 6 4 2 2: 6: 16: 2: Reflux Table: Acid Reflux Analysis, Day 1 Total Upright Supine PostPr HrtBm Regurg Cough Chest pain Duration of Period (hh: mm) Number of Refluxes Number of Long Refluxes > 5 (min) Duration of longest reflux (min) Time ph < 4 (min) Fraction Time ph < 4 (%) 22:46 1:5 11:56 8:25 :19 :4 :4 1:5 83 68 16 31 8 3 7 14 1 4 3 7 49 7 61 2 2 1 358 219 139 124 8 2 2 26.2 33.7 19.3 24.5 38.3 55.. 3.4 DeMeester Score: Acid Reflux Analysis, Day 1 Total score: 81.4, DeMeester normals less than 14.72 (95th percentile) Figure 5 Test results from day 1 of a 48-hour wireless ph study.

gastro gastroesophageal reflux disease and hiatal hernia 5 Treatment medical management Patients with typical symptoms of GERD can be managed initially with a trial of acid suppression therapy and lifestyle modifications. Head of the bed elevation and abstaining from eating meals 2 to 3 hours before sleeping have been shown to improve symptoms. Weight loss for patients with a body mass index (BMI) greater than 25 has also been successful in reducing symptoms. Avoidance of alcohol, caffeine, peppermint, spicy foods, and cigarette smoking has not proven to improve reflux symptoms. 17 PPIs are the strongest medications for gastric acid suppression. They irreversibly bind to H +,K + -ATPase (proton pump) on the parietal cell, blocking the final pathway of acid secretion. 5 PPIs generally take effect after 4 to 5 days of use, and patients should be given an 8-week trial of PPIs to assess symptom relief. Dosing is started at once per day and may increase to twice a day based on the severity of reflux symptoms. With daily PPI use, 2 to 3% of patients will have persistent reflux symptoms requiring additional over-the-counter medication for relief. 18 This population of patients should be considered for surgical management [see Figure 6]. surgical management The SAGES has published guidelines for the surgical treatment of GERD. 19 Patients considered for surgery include those who have failed medical management, have complications of GERD (Barrett esophagus, peptic stricture, severe esophagitis), or have extraesophageal manifestations (cough, hoarseness, aspiration, chest pain, asthma). It is important for the surgeon to evaluate the patient to determine if the symptoms responded to medical therapy, and the diagnosis of reflux must be confirmed through objective testing. The best surgical outcomes are achieved in patients with typical GERD symptoms that are responsive to PPI therapy or who have ambulatory ph studies with good symptom correlation. 2 Special consideration should be undertaken when evaluating the morbidly obese patient with reflux symptoms as the role of Roux-en-Y gastric bypass for reflux control in this population is evolving. In 29, a review assessing the efficacy of bariatric surgical therapies for managing GERD found that Roux-en-Y gastric bypass surgery significantly improved GERD symptoms assessed by postoperative questionnaire. 21 Many surgeons agree that Roux-en-Y gastric bypass should be the preferred operation for morbidly obese patients, particularly those with other obesity-related medical conditions, given the additional health benefits of weight loss and concern of fundoplication durability in these patients. 22 24 Nissen Fundoplication Laparoscopic Nissen fundoplication is the most common antireflux procedure performed in the United States. Key steps in the creation of a 36 wrap have been standardized to obtain reproducible outcomes. Based on a consensus of 4 experienced foregut surgeons, a standardized approach to Nissen fundoplication has been proposed [see Table 2]. 25 patient positioning The patient is placed supine on the operating room table in a split-leg position, but the low lithotomy position can also be used. The arms are tucked, the legs are secured, and a strap is wrapped around the patient s waist to allow for steep reverse Trendelenburg positioning during the procedure. The monitors are placed at the head of the bed to allow for ergonomically neutral visualization by the surgeon and assistants. The surgeon stands between the patient s legs while the assistant stands on the left side of the patient with the camera operator on the patient s right side. Intraluminal pressure (mm Hg) 2 2 8 8 8 5 Pharynx Upper Esophageal Sphincter Upper Esophagus Middle Esophagus Lower Esophagus Lower Esophageal Sphincter Figure 6 Graphs of esophageal intraluminal pressures assessed by esophageal manometry. trocar placement A Veress needle or Hasson technique is used to establish pneumoperitoneum. After insufflation, the costal margins are identified and the GEJ is marked externally. Next, a camera port is placed just to the left of midline, 15 cm caudal to the GEJ. A 1 mm working port is placed in the left upper quadrant, just below the costal margin, and the second working port is placed in the right upper quadrant. Another 5 mm assistant port is placed in the left midabdomen, and a Table 2 Standardized Approach to Nissen Fundoplication 25 1. Opening of the phrenoesophageal ligament in a left-to-right fashion 2. Preservation of the hepatic branch of the anterior vagus nerve 3. Dissection of both crura 4. Transhiatal mobilization to allow approximately 3 cm of intra-abdominal esophagus 5. Short gastric vessel division to ensure a tension-free wrap 6. Crural closure posteriorly with nonabsorbable sutures 7. Bougie placement 8. Creation of a 1.5 2 cm wrap with the most distal suture incorporating the anterior muscular wall of the esophagus

gastro gastroesophageal reflux disease and hiatal hernia 6 Nathanson liver retractor is introduced in the subxiphoid space to retract the left lateral segment of the liver and expose the esophageal hiatus. crural dissection The initial dissection begins with opening the pars flaccida using the energy device and carrying the dissection cephalad to identify the right crus of the diaphragm. Care must be taken to avoid injury to the hepatic branch of the vagus nerve. In about 5% of patients, a replaced left hepatic artery can be encountered during this dissection. The aberrant left hepatic artery should be isolated and preserved throughout the rest of the dissection whenever possible. Blunt dissection is then performed on the medial boarder of the right crus and carried superiorly. The phrenoesophageal ligament is then divided in a transverse direction. Care must be taken to avoid injury to the esophagus and anterior vagus nerve when dividing the phrenoesophageal ligament. Dissection is carried out to the left crus, where blunt dissection is performed inferiorly along the medial border of the crus. The dissection is returned to the right crus and carried inferiorly until the surgeon identifies the confluence of the crura. a fundus mobilization The mobilization of the fundus is initiated at the inferior pole of the spleen. The short gastric vessels are ligated close to the stomach using an energy device. Entry into the lesser sac is achieved, and the division of the short gastric vessels is carried proximally until complete mobilization of the fundus is accomplished. Once completed, the base of the left crus should be clearly visualized. At this point, the retroesophageal window can be dissected safely to circumferentially mobilize the esophagus. A Penrose drain can then be placed in through the retroesophageal window and secured around the esophagus. transhiatal dissection The assistant uses the Penrose drain to retract the esophagus inferiorly. Transhiatal, circumferential mobilization of the esophagus is completed using blunt dissection. Mobilization is continued until at least 2.5 cm of intra-abdominal esophageal length is obtained [see Figure 7a]. Patients with a history of esophagitis may have dense adhesions, and care must be taken during dissection to prevent esophageal injury or hemorrhage. b c d Figure 7 Laparoscopic Nissen fundoplication. (a) Completion of esophageal mobilization with adequate intra-abdominal esophageal length. (b) Completed posterior cruroplasty. (c) Fully mobilized gastric fundus prior to fundoplication. (d) Completed Nissen fundoplication.

gastro gastroesophageal reflux disease and hiatal hernia 7 If adequate esophageal length cannot be achieved with extensive mediastinal dissection, an esophageal lengthening procedure may be required. Our preferred technique is a wedge gastroplasty, in which a wedge resection of the fundus creates a segment of neoesophagus. Following esophageal mobilization, a 48 French Maloney dilator is placed into the esophagus beyond the GEJ, and a point on the greater curvature 2.5 cm from the angle of His is identified. A transverse staple line that abuts the dilator is created first, and a longitudinal staple line along the dilator toward the angle of His creates the neoesophagus. The fundoplication is then created as described below, with care taken to place the top stitch into the native esophagus to avoid leaving gastric mucosa above the high-pressure zone created by the fundoplication. crural closure The hiatus is closed by reapproximating the crura. We recommend a posterior cruroplasty with interrupted, nonabsorbable, braided suture. Pledgets may be used to strengthen the crural closure, although nonpledgeted sutures are also acceptable [see Figure 7b]. creation of fundoplication When performing the fundoplication, the fundus of the stomach is brought posterior to the esophagus. A so called shoeshine maneuver is performed to ensure that there is no twist in the fundus and adequate gastric mobilization has been achieved [see Figure 7c]. This is done by grasping the fundus on both sides of the esophagus and rocking it back and forth to confirm that both sides are freely mobile and oriented correctly. A 54 to 6 French Maloney dilator is then placed under direct visualization. Good communication between the surgeon and the anesthesiologist is imperative to prevent iatrogenic injury to the esophagus. A so called floppy fundoplication is performed by placing a nonabsorbable suture through the fundus on the left side of the fundus, then through the esophagus, and finally through the fundus on the right. Three sutures are placed to create a short, 2 to 3 cm wrap [see Figure 7d]. A fixation suture is then placed between the superior portion of the fundoplication and the esophagus or right crus to prevent slipped fundoplication. Although Nissen fundoplication represents the most commonly performed antireflux procedure performed, partial fundoplications may also be performed. Indications for partial fundoplication include severe esophageal dysmotility, antireflux procedure in the setting of Heller myotomy for achalasia, patients who have developed severe dysphagia following a Nissen fundoplication, or patients with significant aerophagia. Many types of partial fundoplication have been described, including the Belsey Mark IV (27 anterolateral wrap), Dor (18 anterior wrap), Toupet (27 posterior wrap), Thal (9 anterior wrap), and Hill gastropexy (9 anterior wrap and posterior esophagogastropexy). The most commonly used partial fundoplication in the setting of significant esophageal dysmotility is the Toupet fundoplication, which provides adequate reflux control with a lower incidence of postoperative dysphagia in this patient population. postoperative care Patients are admitted to the hospital for one night and receive a clear liquid diet postoperatively with avoidance of carbonated beverages to prevent gastric distention. Pain is treated with a combination of intravenous and oral medications, and scheduled antiemetic medications are provided for the first 24 hours. Postoperative contrast studies are reserved for patients who demonstrate unusual symptoms, including severe abdominal pain, unexplained tachycardia, or excessive vomiting/retching. Patients are discharged with a thick liquid diet for 1 week followed by a soft diet until perioperative dysphagia resolves, typically between 3 and 6 weeks after surgery. complications Most early complications of fundoplication are minor and transient in nature. Dysphagia is the most common postoperative symptom, occurring in about 5% of patients. Patients typically report a temporary difficulty in swallowing solid food that resolves within weeks of the operation. The proposed mechanism is swelling of the wrap leading to a narrowing at the distal esophagus. Postoperative vomiting and retching are a serious problem and occur in up to 6% of patients. Retching can cause the fundoplication to break down. Aggressive use of antiemetic medications is encouraged to prevent this. 26 28 Patients with persistent dysphagia, however, need to be evaluated for anatomic abnormalities. Typical modalities include EGD and pill esophagography with a 13 mm tablet. 29 If the fundoplication is too tight, endoscopic dilations either with solid-core or pneumatic dilators will relieve symptoms in 5 to 75% of the cases. 3 Gas bloat syndrome is another common postoperative complication seen in roughly 15 to 8% of patients. This ill-defined syndrome results from the inability to vent gas from the stomach after fundoplication. The condition is temporary, with a vast majority of patients becoming symptom free after 2 months. The mechanism appears to be multifactorial. One cause is the inability of the surgically altered GEJ to relax in response to gastric distention. Second, aerophagia, or swallowing of air, is common in GERD patients. Finally, injury to the vagus nerve during dissection can cause delayed gastric emptying. Treatment is nonsurgical and includes eating slowly, simethicone, prokinetic agents, and smoking cessation. 29 Intraoperative complications include gastric and esophageal perforation, with rates of to 4% reported in the literature. The highest incidence of perforation is seen in redo fundoplication, with rates around 4%. Pneumothorax is another potential complication secondary to mediastinal dissection. Documented incidence rates are to 1.5%. When a pneumothorax does occur, it is typically due to pleural disruption and rarely requires intervention. 7 Splenic and hepatic injuries occur in to 2.2% of patients undergoing Nissen fundoplication. Morbidity from splenic injuries has decreased with laparoscopy as the short gastric vessels are more easily identified for safe ligation. Conversion rates of approximately 2% are seen in tertiary care centers when a standardized technique is employed. 25 Thirty-day mortality is low, with a reported incidence of.3%. 26

gastro gastroesophageal reflux disease and hiatal hernia 8 outcomes Given its high success and low complication rates, laparoscopic Nissen fundoplication is the gold standard for operative intervention for refractory and complicated GERD. A large literature review of patients undergoing laparoscopic Nissen fundoplication showed that 93% of patients are symptom free at 1 year postoperatively, 3% require some medications to control their symptoms, and 97% report satisfaction with their results. 26 Long-term outcomes are also quite good. One institutional review of 239 patients who had undergone laparoscopic Nissen fundoplication at least 1 years previously found that 85% of the patients reported complete or greatly improved GERD symptoms and 85% would undergo the operation again. 31 Two major trials have compared medical therapy with surgical therapy for control of GERD. Lundell and colleagues reported that patients who underwent surgical management had a higher rate of successful management (66.7%) than patients who underwent medical therapy alone (46.7%) after 7 years of treatment. 32 The Long-Term Usage of Esomeprazole vs Surgery for Treatment of Chronic GERD (LOTUS) trial evaluated 554 patients who were initially responsive to medical therapy and were then randomized to either laparoscopic Nissen fundoplication or medical therapy with esomeprazole. Relief of GERD symptoms at 5 years was higher in the esomeprazole group (92%) than in the surgical cohort (85%), although the difference did not reach statistical significance. Surgery was found to better control regurgitation (2% versus 13%) but did come with a higher incidence of dysphagia (11% versus 5%), bloating (4% versus 28%), and flatulence (57% versus 4%) when compared with medical therapy. Of note, nearly a quarter (23%) of patients in the medical arm required dose escalation of PPI therapy to maintain symptom relief. 33,34 Both medical and surgical management of GERD have been shown to provide excellent long-term results in patients with symptomatic GERD. Medical management represents the optimal therapy in patients with heartburn and regurgitation symptoms that are completely controlled with medical therapy and those who are hesitant about the potential side effects of reflux surgery. Antireflux surgery has been shown to provide superior symptom relief in patients with significant regurgitation and should also be considered for patients with refractory heartburn in the setting of a positive ambulatory ph study and for patients with concerns about the long-term side effects of daily PPI use. fundoplication failure The majority of fundoplication failures occur within 2 years of the initial operation. 7 Common presenting complaints include recurrent heartburn and dysphagia. Hunter and colleagues described four patterns of fundoplication failure. 35 Type 1A (3 to 8%) is herniation of the fundoplication into the chest, which results from breakdown of the crural repair or failure to achieve a tension-free segment of intra-abdominal esophagus. Type 1B (15 to 3%) is a slipped Nissen fundoplication where part of the gastric cardia lies above the fundoplication. Type II (23%) is a posterior paraesophageal hernia caused by inadequate hiatal closure and redundant retroesophageal fundus following fundoplication. Type III (1%) occurs as a result of misplacement of the wrap at the initial operation. 36 Finally, complete disruption of the fundoplication is less common and occurs in 3 to 14% of failed operations. 35 Laparoscopic Magnetic GEJ Reinforcement Although laparoscopic Nissen fundoplication is very effective for resolving symptoms of GERD, new minimally invasive and endoscopic procedures have emerged in recent years. Magnetic gastroesophageal junction reinforcement (MGJR) using the LINX Reflux Management System (Torax Medical, St. Paul, MN) is a novel laparoscopic procedure that attempts to prevent reflux by reinforcing the LES [see Figure 8]. The device is composed of titanium beads with magnetic cores that are placed around the GEJ as a ring to strengthen the sphincter. A recently published clinical trial reported 1 patients undergoing MGJR in 13 centers. 37 In this series, 64% of patients had either normalization or a 5% reduction in esophageal acid exposure after device implantation, and 93% reported at least 5% reduction in the average daily PPI dose. At the 1-year follow-up, 92% of patients achieved at least a 5% improvement in Gastroesophageal Reflux Disease Health Related Quality of Life (GERD-HRQL) score. At the 3-year follow-up, improvements in GERD-HRQL remained stable. 38 MGJR has proven efficacious for reducing esophageal acid exposure and improving GERD symptoms and quality of life in the short term. Potential benefits include that it is placed in a standard fashion, it is removable, and it expands, allowing food and gas to pass through easily. 37 Although the early results appear promising, studies assessing long-term outcomes and direct comparisons with other treatment modalities are required before the true effectiveness of the device can be determined. Endoluminal GERD Therapies Over the past few decades, several endoscopic approaches for the treatment of GERD have been developed to serve as a bridge between lifelong medical therapy and invasive surgical procedures. Endoluminal techniques, including radiofrequency energy, injectable polymers, and suturing devices, have shown promise, but inadequate efficacy and durability or safety concerns have limited the available treatment options. Currently, two endoluminal GERD treatments, transoral fundoplication (TF) and radiofrequency ablation (Stretta procedure), are commercially available in the United States and may be considered for reflux management in patients with symptoms refractory to acid suppression and a hiatal hernia smaller than 2 cm. 39 transoral fundoplication TF using the EsophyX device (Endogastric Solution Inc., Redmond, WA) creates a 27 to 32 endoscopic fundoplication. TF is performed under general anesthesia in the operating room with the patient placed in the left lateral decubitus position. The device consists of the fastener cartridge and polypropylene H fasteners. It is placed over the endoscope and delivered into the stomach, where a helical retractor is used to pull the GEJ into the device. The full-thickness H fasteners are then deployed through the stomach and esophagus to create an esophagogastric fundoplication. 39

gastro gastroesophageal reflux disease and hiatal hernia 9 a b Closed Position Closed Position Open Position Bolus of food Being Swallowed Open Position Figure 8 Laparoscopic gastroesophageal junction reinforcement. (a) Linx device. (b) Correct position of device around the gastroesophageal junction. A recent meta-analysis of published clinical studies demonstrated that TF improves heartburn and disease- specific quality of life scores and allows the elimination of daily PPIs in approximately two thirds of patients. 4 Although esophageal acid exposure improves in most cases, TF does not consistently normalize esophageal acid exposure. The clinical data evaluating this therapy continue to emerge, and controlled trials and long-term outcome studies are required to assess its efficacy, durability, and role in reflux management. the stretta procedure The Stretta procedure (Mederi Therapeutics Inc, Greenwich, CT) uses radiofrequency ablation to decrease the compliance of the LES and create a physiologic antireflux barrier. This procedure can be performed as an outpatient procedure under conscious sedation in the endoscopy suite. The procedure consists of four treatment levels above the LES and two treatment levels in the gastric cardia. The radiofrequency ablation causes scarring and collagen deposition at the GEJ, effectively leading to a reduction in compliance of the LES and decreased relaxation. 39 Similar to TF, the Stretta procedure produces significant improvement in GERD symptoms, patient satisfaction, and disease-specific quality of life, and the initial efficacy has been demonstrated in two controlled trials. 41,42 This procedure also improves esophageal acid exposure but does not normalize it on a consistent basis. Small cohort studies have demonstrated improved acid control for up to 48 months, but larger studies with long-term follow-up are needed. 43 Hiatal Hernia Hiatal hernia occurs in approximately 1% of the population; however, paraesophageal hiatal hernias are a relatively rare condition consisting of approximately 15% of hiatal hernias. Since first identified in 193, the importance of paraesophageal hernias has been recognized because of the resulting symptoms and complications, including chest pain, early satiety, gastrointestinal hemorrhage, chronic a nemia, and acute gastric volvulus. The management of hiatal hernias has evolved following the introduction of laparoscopy, and several areas of controversy remain as surgical technique continues to evolve. Anatomy The esophageal hiatus is the opening in the crural diaphragm through which the esophagus passes from the mediastinum into the abdominal cavity. The crura originate from the anterior lumbar vertebral bodies and pass upward as they curve around the esophagus and connect with the diaphragm. The hiatus most often arises from the limbs of the right crus, although some contribution from the left crus is often present. 44 The esophagus is tethered to the diaphragm by the phrenoesophageal ligament, which is formed from the fascia transversalis on the undersurface of the diaphragm. 45 This membrane serves to tether the distal esophagus within the abdomen. 46 classification Hiatal hernias are classified as one of four types according to the position of the GEJ relative to the diaphragm [see Figure 9]. A type I (sliding) hiatal hernia occurs when the gastric cardia herniates into the mediastinum through the esophageal hiatus, with the GEJ located above the diaphragm. This is the most common type of hiatal hernia, accounting for 85% of cases. Type II to IV hiatal hernias represent paraesophageal hernias. A type II (rolling) hiatal hernia is a true paraesophageal hernia in which the GEJ remains in the normal anatomic position and the fundus of the stomach herniates through the hiatus. These account for.5 to 5%

gastro gastroesophageal reflux disease and hiatal hernia 1 a b Type I Phrenoesophageal Ligament Type II GEJ Diaphragm GEJ c d Type III GEJ Type IV Figure 9 Classification of paraesophageal hernia: (a) type I (sliding); (b) type II (rolling); (c) type III (mixed); (d) type IV. GEJ = gastroesophageal junction. of all hiatal hernias and warrant surgical repair due to the risk of acute gastric volvulus. The most common type of paraesophageal hernia encountered in surgical practice is a type III (mixed) hiatal hernia in which both the fundus and the GEJ herniate into the posterior mediastinum. Finally, a type IV hiatal hernia contains viscera other than the stomach, most commonly colon, spleen, or small bowel. 46,47 Diagnosis clinical manifestations Many patients with hiatal hernias are asymptomatic. When symptoms do occur, they are related to the type of hiatal hernia. Symptoms of heartburn and regurgitation are most commonly associated with type I hiatal hernias. The location of the GEJ above the diaphragm and loss of the anatomic angle of His contribute to GERD. Paraesophageal hernias most often present with chest pain, dysphagia, epigastric pain, vomiting, postprandial fullness, and anemia. This is secondary to compression of the stomach by the crural diaphragm and resulting partial obstruction or stress ulceration. 46 Acute gastric volvulus can occur and presents with severe epigastric pain and retching with an inability to vomit. Iron deficiency anemia can be caused by Cameron ulcers, which are linear gastric erosions and ulcers on the mucosal folds of the stomach at the neck of the hiatal hernia [see Figure 1]. They are found in 5% of upper endoscopies in which hiatal hernias are present. 48 diagnostic tests Chest X-ray Diagnostic imaging for hiatal hernias is very similar to the imaging for the workup of GERD. An upright chest x-ray

gastro gastroesophageal reflux disease and hiatal hernia 11 resuscitation, electrolyte replacement, and nasogastric tube placement should all be performed preoperatively. 52 Figure 1 Endoscopic view of Cameron ulcers at the level of the diaphragm in the setting of a type III paraesophageal hernia. may reveal an air-fluid level in the mediastinum if a large portion of the stomach is located in the chest. Esophagography Barium contrast study is excellent at assessing the position of the GEJ and the length of the esophagus. It also allows one to measure the size of the hernia. Video esophagography can give insight into the motility of the esophagus and identify reflux. Endoscopy Upper endoscopy should be performed to rule out erosions, lesions, or malignancies. Careful inspection of the gastric mucosa is imperative when performing endoscopy for anemia in patients with a hiatal hernia as Cameron lesions are missed in up to 21% of EGDs. 48 Esophageal Manometry Although difficult to perform in patients with a large paraesophageal hernia, esophageal manometry can be useful to evaluate the esophageal body peristalsis prior to planned fundoplication. If the patient has poor peristalsis or significant preoperative dysphagia, the surgeon may consider a partial fundoplication rather than a complete fundoplication to reduce the incidence of postoperative dysphagia. 49 Surgical Management The indications for surgical repair of hiatal hernias relate to the hernia classification. Type I hiatal hernias should be evaluated and repaired based on the treatment algorithm for GERD. It has been generally accepted that reasonable surgical candidates with paraesophageal hernias should undergo surgical repair regardless of symptoms. This recommendation is based on early data that showed high morbidity and mortality following emergent surgical repair of incarcerated paraesophageal hernias. More recent studies suggest that conservative management is an acceptable alternative for asymptomatic paraesophageal hernia due to relatively low rates of gastric volvulus and hernia incarceration. 5,51 Symptoms of GERD, gastric outlet obstruction, early satiety, and refractory iron deficiency anemia are all indications for surgery. 49 Patients who present with acute incarceration of paraesophageal hernia require expedient surgical intervention to prevent necrosis or perforation. Intravenous fluid Laparoscopic Paraesophageal Hernia Repair Laparoscopic paraesophageal hernia repair is performed in a similar fashion to Nissen fundoplication, described earlier. The principles of paraesophageal hernia repair include (1) reduction of the stomach and complete excision of the hernia sac; (2) adequate mediastinal esophageal mobilization; (3) repair of the diaphragmatic hiatus; and (4) fundoplication. 53 The patient positioning and trocar placement are identical to those described for laparoscopic Nissen fundoplication. The stomach is gently reduced from the hernia sac, and the left crus is identified. The dissection is begun along the left crus between the endothoracic fascia and carried to the right, and the phrenoesophageal membrane is divided. The pars flaccida of the lesser omentum is divided, and the dissection proceeds similarly along the right crus until the hernia sac can be reduced in its entirety. Following reduction of the hernia sac, mediastinal mobilization of the esophagus is carried out to provide 2.5 cm of tension-free intra-abdominal esophagus. In cases of shortened esophagus, an esophageal lengthening procedure may be required. When adequate esophageal length is available, a posterior crural repair is performed using interrupted, pledgeted, nonabsorbable sutures. In cases of large hiatal defects, reducing the pneumoperitoneum pressure may reduce tension and facilitate crural closure. A complete or partial fundoplication is then performed to prevent postoperative reflux as the anatomic angle of His has been compromised. 51 The reinforcement of hiatal closures using synthetic or bioprosthetic mesh has gained popularity due to the high rate of recurrence following laparoscopic paraesophageal hernia repair. Two randomized trials have assessed the use of synthetic mesh in this setting. 54,55 These demonstrated a reduction in hiatal hernia recurrence, but complications, including mesh erosion, ulceration, stricture, and infection, are also well documented. 52,56 Hiatal reinforcement with bioprosthetic meshes has been shown to reduce recurrence rates in the first 6 months without the severe complications associated with synthetic mesh. 57 Long-term studies, however, have failed to demonstrate a reduction in hiatal hernia recurrence, and the indications for mesh reinforcement of crural repairs remain controversial. 58 Summary GERD and hiatal hernia represent a common surgical problem in the United States that requires lifelong medical management in a significant proportion of patients. Of these, up to 3% will experience troublesome breakthrough symptoms while taking at least daily acid-suppressing medications and should be considered for antireflux procedures. Laparoscopic Nissen fundoplication remains the gold standard procedural GERD therapy and can achieve excellent reflux control and high levels of patient satisfaction in appropriately selected patients. Surgical repair should be considered for patients with paraesophageal hernias, although watchful waiting may be considered in asymptomatic high-risk surgical patients.

gastro gastroesophageal reflux disease and hiatal hernia 12 Financial Disclosures: James A. Rydlewicz, MD, Matthew R. Pittman, MD, and Kyle A. Perry, MD, have no relevant financial relationships to disclose. Annotated Key References El-Serag HB, Sweet S, Winchester CC, Dent J. Update on the epidemiology of gastro-oesophageal reflux disease: a systematic review. Gut 214;63:871 8. This systematic review study provides an excellent overview of the changing epidemiology of GERD worldwide over the past several decades and demonstrates the increasing disease burden in Western societies. Galmiche JP, Hatlebakk J, Attwood S, et al. Laparoscopic antireflux surgery vs esomeprazole treatment for chronic GERD: the LOTUS randomized clinical trial. JAMA 211;35:1969 77. This European randomized controlled trial examined the outcomes of medical and surgical therapy for GERD with longterm follow-up. It demonstrated that both methods provide excellent long-term results but that surgical therapy may be more efficacious for patients with significant regurgitation. Oelschlager BK, Pellegrini CA, Hunter JG, et al. Biologic prosthesis to prevent recurrence after laparoscopic paraesophageal hernia repair: long-term follow-up from a multicenter, prospective, randomized trial. J Am Coll Surg 211;213:461 8. This study presents the long-term follow-up of a randomized controlled trial evaluating the use of biologic mesh reinforcement of the crural repair in patients with paraesophageal hernia. This study showed that the use of mesh decreased the early recurrence rate at the 6-month follow-up but did not improve the long-term outcomes (5-year follow-up) compared with primary cruroplasty. References 1. El-Serag HB, Sweet S, Winchester CC, Dent J. Update on the epidemiology of gastro-oesophageal reflux disease: a systematic review. Gut 214;63:871 8. 2. Vakil N, Veldhuyzen van Zanten S, Kahrilas P, et al. The Montreal definition and classification of gastroesophageal reflux disease (GERD): a global evidence-based consensus. Am J Gastroenterol 26;11:19 2. 3. Patel D, Vaezi M. Normal esophageal physiology and laryngopharyngeal reflux. Otolaryngol Clin North Am 213;46: 123 41. 4. Peterson R, Pellegrini C, Oelschlager B. Hiatal hernia and gastroesophageal reflux disease. In: Townsend C, Beauchamp R, Evers B, Mattox K, editors. Sabiston textbook of surgery. 19th ed. Philadelphia: Elsevier-Saunders; 212. p. 167 86. 5. Nwokediuko SC. Current trends in the management of gastroesophageal reflux disease: a review. ISRN Gastroenterol 212;212:391361. 6. Watson TJ, Peters JH. Evaluation of esophageal function for antireflux surgery. Gastrointest Endosc Clin N Am 25; 15:347 6. 7. Stefanidis D, Hope WW, Kohn GP, et al. Guidelines for surgical treatment of gastroesophageal reflux disease. Surg Endosc 21;24:2647 9. 8. Lundell LR, Dent J, Bennett JR, et al. Endoscopic assessment of oesophagitis: clinical and functional correlates and further validation of the Los Angeles classification. Gut 1999; 45:172 8. 9. Spechler SJ. Barrett esophagus and risk of esophageal cancer: a clinical review. JAMA 213;31:627 36. 1. Sharma P, Dent J, Armstrong D, et al. The development and validation of an endoscopic grading system for Barrett s esophagus: the Prague C & M criteria. Gastroenterology 26;131:1392 9. 11. Jobe BA, Richter JE, Hoppo T, et al. Preoperative diagnostic workup before antireflux surgery: an evidence and experience-based consensus of the esophageal diagnostic advisory panel. J Am Coll Surg 213;217:586 97. 12. Lacy BE, O Shana T, Hynes M, et al. Safety and tolerability of transoral Bravo capsule placement after transnasal manometry using a validated conversion factor. Am J Gastroenterol 27;12:24 32. 13. Patti MG, Diener U, Tamburini A, et al. Role of esophageal function tests in diagnosis of gastroesophageal reflux disease. Dig Dis Sci 21;46:597 62. 14. Tseng D, Rizvi AZ, Fennerty MB, et al. Forty-eight-hour ph monitoring increases sensitivity in detecting abnormal esophageal acid exposure. J Gastrointest Surg 25;9:143 52. 15. Campos GM, Peters JH, DeMeester TR, et al. Multivariate analysis of factors predicting outcome after laparoscopic Nissen fundoplication. J Gastrointest Surg 1999;3:292 3. 16. Broeders JA, Sportel IG, Jamieson GC, et al. Impact of ineffective oesophageal motility and wrap type on dysphagia after laparoscopic fundoplication. Br J Surg 211;98:1414 21. 17. Katz P, Gerson LB, Vela MF. Guidelines for the diagnosis and management of gastroesophageal reflux disease. Am J Gastroenterol 213;18:38 28. 18. Fass R. Proton-pump inhibitor therapy in patients with gastro-oesophageal reflux disease: putative mechanisms of failure. Drugs 27;67:1521 3. 19. Stefanidis, Hope WW, Kohn GP, et al. Guidelines for surgical treatment of gastroesophageal reflux disease. Surg Endosc 21;24:2647 69. 2. Oelschlager BK, Quiroga E, Para JD, et al. Long-term outcomes after laparoscopic antireflux surgery. Am J Gastroenterol 28;13:28 7. 21. De Groot NL, Burgerhart JS, Van De Meeberg PC, et al. Systematic review: the effects of conservative and surgical treatment for obesity on gastroesophageal reflux disease. Aliment Pharmacol Ther 29;3:191 2. 22. Prachand VN, Alverdy JC. Gastroesophageal reflux disease and severe obesity: fundoplication or bariatric surgery? World J Gastroenterol 21;16:3757 61. 23. Madalosso CA, Gurski RR, Callegari-Jacques SM, et al. The impact of gastric bypass on gastroesophageal reflux disease in patients with morbid obesity: a prospective study based on the Montreal consensus. Ann Surg 21; 251:244 8. 24. Nelson LG, Gonzalez R, Haines K, et al. Amelioration of gastroesophageal reflux symptoms following Roux-en-Y gastric bypass for clinically significant obesity. Am Surg 25; 71:95 3. 25. Attwood SE, Lundell L, Ell C, et al. Standardization of surgical technique in antireflux surgery: the LOTUS Trial experience. World J Surg 28;32:995 8. 26. Smith CD. Surgical therapy for gastroesophageal reflux disease: indications, evaluations, and procedures. Gastrointest Endosc Clin N Am 29;19:35 48. 27. Niebisch S, Peters JH. Update on fundoplication for the treatment of GERD. Curr Gastroenterol Rep 212;14:189 96.