Gastroesophageal (GE) reflux is a normal physiologic process whereby gastric and pancreaticobiliary secretions reflux into the esophagus. This process becomes pathologic when the normal response to reflux fails and symptoms ensue. Gastroesophageal reflux disease (GERD) is one of the most frequently encountered problems seen in clinical practice today. The American College of Gastroenterology estimates that roughly 60 million adults report suffering from reflux symptoms at least once a month.¹ Almost 24 percent of the population report heartburn daily and 43 percent have weekly episodes.² The reported incidence of GERD has nearly doubled in the last 3 decades,³ with current annual expenditure on proton pump inhibitors (PPIs) in excess of US$ 14 billion.⁴

Lower Esophageal Sphincter

GERD develops when the normal protective barriers employed by the esophagus are overcome, exposing it to repeated and chronic insult. A crucial role in the pathogenesis of GERD is mediated by contact of the esophageal mucosa with refluxate that can be composed of acid, bile, and pancreaticobiliary secretions. The mechanisms involved in the pathogenesis of GERD are multiple and include anatomic factors, motor abnormalities, impaired esophageal clearance, and altered mucosal resistance.

Anatomic Barrier

The lower esophageal sphincter (LES) is a 3- to 4-cm segment of distal esophagus.⁵ This high-pressure zone remains under tonic contraction, with resting pressures maintained at 10 to 30 mm Hg. Although large fluctuations are seen during a 24-hour period, resting pressure does not directly correlate with the severity of reflux.⁶

The LES mechanism has three distinct characteristics: sphincter length, pressure, and location.⁷ The overall intra-abdominal length of the LES is of crucial importance to the esophageal surgeon. A decrease in overall length or intra-abdominal LES correlates directly with the degree of LES incompetence (Fig. 14-1).⁸ In addition, the location of the LES is also important in maintaining competence. The LES is subject to elevated pressures, but due to its intra-abdominal position, the sphincter collapses and prevents reflux.⁶

Acid Clearance and Bile Exposure

Normal acid clearance is dependent on esophageal motility. Esophageal dysmotility is found in 40 to 50 percent of the GERD population.⁹ In these patients, decreased clearance leads to increased acid and bile exposure, resulting in esophagitis, stricture, and initiation of malignant degeneration.⁹

Hiatal Hernias

Hiatal hernias are frequently found in patients with GERD and are present in 70 to 90 percent of patients with severe reflux. In the presence of a sliding hiatal hernia, the compression of the crus and the angle of His are disrupted. Hiatal hernias change the acute angle produced by the angle of His and disrupt the flap valve mechanism that prevents reflux.⁶ In addition, a hiatal hernia results in dilation of the diaphragmatic crus and loss of the extrinsic compression provided by the diaphragm on the GE junction.¹⁰ Migration of the stomach into the chest results in the disassociation of the LES from the crural diaphragm, resulting in failure of the antireflux barrier. The disruption of the GE junction lowers the threshold for LES relaxation, worsens positional reflux, diminishes esophageal clearance, and acts as a reservoir for gastric and duodenal secretions.¹¹

Causes of GERD and Progression

In a normal individual, lower esophageal relaxation occurs after a swallow. The swallow decreases LES tone to allow entry of food or fluids into the stomach. In GERD, transient LES relaxation or TLESRs are found to be the underlying cause of pathologic reflux.¹² TLESRs are defined as brief episodes of LES relaxation that are unrelated to swallowing or peristalsis. Neurophysiology studies indicate that TLESRs are visceral reflexes with vagal afferent and efferent pathways that transmit information to and from the dorsal nucleus of the vagus.¹⁰ Gastric distension, by stimulation of proximal gastric tension and stretch receptors, has been recognized as a major factor inducing TLESRs.⁵ TLESRs are found in both normal individuals without symptomatic reflux and those with GERD.

With increasing frequency of these episodes, mucosal inflammation follows. Inflammation and injury lead to shortening of the esophagus. This critical point is termed as the permanently defective LES.⁷ Characteristics include an average pressure less than 6 mm Hg, length less than 2 cm, and an intra-abdominal length less than 1 cm.⁷ As the cycle continues, advanced GERD becomes a more difficult disease process to manage medically; while symptoms may be controlled by acid suppression, reflux is still present (Fig. 14-2). This continued exposure can lead to the Barrett’s metaplasia, stricture, and cancer.

The presentation of GERD is highly variable and symptoms are divided into two broad categories: esophageal and extraesophageal symptoms. Heartburn and regurgitation are the most common complaints. The classic presentation is retrosternal pain occurring 30 to 60 minutes after a meal, particularly in the recumbent position. The combination of both heartburn and regurgitation is 90 percent accurate in the diagnosis of GERD. Odynophagia and dysphagia are other common esophageal symptoms. Alarm symptoms include unintended weight loss, hematemesis, black or bloody stool, and recurrent vomiting. They are present in about 10 percent of patients presenting to primary care and require urgent endoscopy.¹³

Extraesophageal symptoms are increasingly being linked to reflux disease.¹⁴ In most cases, the symptoms are not recognized. Pulmonary complications due to aspiration of gastric contents into the pulmonary system lead to pneumonia, airway inflammation, and chronic cough. Reflux that reaches the oral cavity can result in water brash, sour taste in the mouth, and dental erosions. Finally, reflux to the vocal cords can result in laryngitis and hoarseness.¹⁴

A patient with typical symptoms, such as heartburn and regurgitation, can be diagnosed with GERD, and a trial of acid-reducing medications is indicated.¹⁵ Although not a truly diagnostic technique, response to empiric therapy with PPIs is strongly suggestive of GERD and is also a predictor of patients who benefit from antireflux surgery. A recent American Gastroenterological Association position statement supports the use of diagnostic testing for esophageal reflux to (1) avoid misdiagnosis, (2) identify complications of reflux disease, and (3) evaluate empirical treatment failures.¹¹ Patients with atypical symptoms or who have failed medical therapy require additional testing.

Flexible endoscopy is essential in the evaluation of GERD. Endoscopic findings of a “mucosal break” or areas of slough or erythema demarcated from adjacent normal-appearing mucosa are confirmatory findings of esophagitis. Furthermore, it is mandatory to obtain mucosal biopsies to exclude malignancy. Endoscopy can also be used to grade the degree of disruption of the flap valve mechanism.¹⁶ This is done on a retroflexed view of the GE junction. The flap valve is graded according to the Hill classification (Hill grade 1–4; 1 = normal closed valve, 4 = open valve, associated hiatus hernia).¹⁶

Twenty-four-hour pH monitoring is the gold standard test to evaluate reflux esophagitis. A pH probe is placed 5 cm above the manometrically determined LES. The probe records the total number of acid exposures with a pH less than 4, total acid-exposure time, upright and supine episodes, number of reflux episodes, number of episodes lasting greater than 5 minutes, and the duration of the longest episode. An overall composite score is calculated and can be used to quantify the severity of GERD. Simpler methods to determine abnormal reflux can be used and can be calculated by finding the percent time the pH is less than 4; in normal individuals, this should be less than 4 percent.¹⁷

Finally, manometric testing is required particularly in patients who are being considered for surgical intervention. Esophageal manometry is performed by inserting a water-perfused catheter into the esophagus and then withdrawing the catheter as the patient swallows. Manometry gives information regarding the location, pressure, and length of the LES. Manometry also helps to assess the esophageal body and the effectiveness of peristalsis. Normally, a patient should have 80 percent successful swallows but when that number drops to 60 percent, the diagnosis of ineffective esophageal dysmotility is given.¹⁸

Newer techniques for esophageal functional testing such as wireless pH capsule monitoring, duodenogastroesophageal reflux (formerly referred to as alkaline or bile reflux) detection, and esophageal impedance testing have been introduced over the past decade. These techniques have been shown to have superior sensitivity and recording accuracy and provide more information to predict patients most at risk for future complications.¹⁹

Medical management of GERD is severity based. Most patients with mild symptoms can be treated with lifestyle modification including smoking cessation or weight loss, while others may be treated with over-the-counter antacids or H₂-blockers for the prevention of occasional symptoms of reflux.¹⁵ Patients with moderate-to-severe symptoms require scheduled pharmacotherapy. Antisecretory drugs are strongly recommended for both symptomatic relief and healing of erosive esophagitis. PPIs have been shown to be superior to H₂-receptor antagonists and are normally 90 percent effective in treating erosive esophagitis. There is good evidence that twice-daily PPI therapy may be an effective treatment in patients who fail daily therapy. Most patients are treated for 8 to 10 weeks, and although they will heal, many will relapse in 6 to 9 months if taken off therapy (Fig. 14-3). Debate still surrounds the optimal management of the patient who suffers from GERD, but it is now well accepted that surgical intervention is an alternative and possibly a superior option for many patients with reflux disease.²⁰

An indication for antireflux surgery is often a failure to respond to or inability to tolerate PPI therapy. The best evidence for efficacy of surgery exists for patients with severe esophagitis and/or excessive distal esophageal acid exposure when PPI therapy is held.¹¹ Patients who are symptomatic after 3 months of medical therapy with stricture, aspiration, or bleeding, or those who have a large hiatal hernia are candidates for an antireflux procedure. It is important to document the correct diagnosis and demonstrate the presence or absence of esophageal dysmotility. All surgical candidates should undergo manometry and pH testing.

The goals of antireflux surgery are to reestablish the LES pressure, relocate the LES within the abdomen, and finally close any hiatal defect. The laparoscopic Nissen fundoplication has emerged as the procedure of choice in antireflux surgery. When done either open or laparoscopically, the key elements of the Nissen fundoplication include the following:

1. 
   

   Complete dissection of the esophageal hiatus and both crura

   
   
2. 
   

   Mobilization of the gastric fundus by division of the short gastric vessels

   
   
3. 
   

   Closure of the hiatal defect by nonabsorbable sutures

   
   
4. 
   

   Creation of a tensionless 360-degree gastric wrap at the distal esophagus around a 50-to-60-F bougie

   
   
5. 
   

   Creation of a 1.5- to 2-cm wrap with the distal suture incorporating the anterior position of the stomach.²¹

With multiple modern trials that have now been published, there are data that show laparoscopic antireflux surgery (LARS) is more cost-effective and results in better overall symptom control than medical management.^20,22,23 Long-term data continue to accrue and suggest that laparoscopic Nissen fundoplication has become the standard for surgical treatment of GERD, with improved morbidity, length of stay, and return to work.²⁴ Every attempt should be made preoperatively to determine the degree of abdominal esophageal length to allow for a tension-free fundoplication. If sufficient intra-abdominal length is not available, an esophageal-lengthening procedure should be performed. Concern about esophageal motility could also influence operative strategy. Studies have shown that preoperative evidence of motility problems may or may not be associated with higher rates of dysphagia.²¹ This has prompted some surgeons to choose a 270-degree fundoplication (Toupet) that other studies have validated as having a decreased incidence of reoperation for failure (usually due to dysphagia).²⁴

Laparoscopic Nissen Fundoplication

After intubation and decompression of the stomach with a nasal or orogastric tube, the patient is laid in a supine position. Pneumoperitoneum of 15 mm Hg is established and five trocars are placed. Exposure of the hiatus starts with deploying a fan retractor to retract the left lobe of the liver. The gastrohepatic ligament is incised, and the right crus of the diaphragm is identified. The esophagus is dissected away from the right crus of the diaphragm. The phrenoesophageal ligament is incised with care to protect the anterior vagus nerve. The dissection is carried to the left crus. We then carry the dissection into the mediastinum. Once complete, the crural and mediastinal dissection should allow for 2 to 3 cm of tension-free intra-abdominal esophagus. If the length of intra-abdominal esophagus is inadequate, an esophageal-lengthening procedure should be performed.²¹ Attention is then turned to the division of the short gastric vessels and mobilization of the fundus of the stomach. The lesser sac is entered and the short gastrics are divided by a harmonic scalpel. A window is then created posterior to the esophagus while avoiding injury to the posterior vagus nerve. The fat pad is dissected off the GE junction. A 50- to 56-F bougie is then passed to allow for appropriate sizing of the fundoplication. A grasper is then passed through the posterior window, and the fundus is pulled through the window. Care should be taken to ensure that the mobilized fundus is under no tension. Both edges of the wrap can be grasped and gently “shoeshined” back and forth to check adequate length and tension. The fundus is then approximated anterior to the esophagus using full-thickness bites of nonabsorbable suture. The fundoplication length should be 1.5 to 2 cm.²⁵ Each stitch should incorporate partial thickness of the distal esophagus. The bougie is then removed and the crural defect is closed with heavy nonabsorbable sutures (Fig. 14-4).

Laparoscopic Partial Fundoplication

This is generally performed for patients with concomitant GERD and esophageal motility disorders. The approach to the partial 270-degree fundoplication is essentially the same as the laparoscopic Nissen except for the extent of the posterior wrap. The wrap is secured to the left and right crura.

Transient dysphagia, due to edema, is the most common complication; it occurs in almost half of the population and resolves within 3 weeks of the operation. Wrap failure is another early complication and is attributed to a malpositioned wrap at the time of initial operation. In addition, postoperative retching and nausea has been implicated in wrap migration and should be aggressively managed during the postoperative period.²¹ Additional early complications include pneumothorax and esophageal perforation. Reported rates of perforation range from 0 to 4 percent in most series.

Laparoscopic Nissen fundoplication has largely supplanted open fundoplication for surgical management of GERD. The laparoscopic approach has shown equal efficacy with the open approach with respect to long-term management of GERD and is associated with shorter hospitalization, less postoperative pain, faster recovery and return to work, and lower total costs. The overall complication rate is between 5 and 10 percent and includes ileus, pneumothorax, dysphagia, gas bloat, and splenic injury. Multiple studies have reported superiority of LARS over medical management with regard to control of GERD symptoms.^20,22,23 Lundell and colleagues reported a significant rate of sustained remission in surgically treated patients compared with those treated medically. There were significantly more reflux symptoms with medical treatment; however, dysphagia was much more common after surgery.²⁰ Multiple studies consistently report about a 6-percent rate of severe dysphagia, and other complications include early satiety, abdominal bloating, inability to vomit, and diarrhea. Rates of reoperation reported in US studies were 2.3 to 7 percent.²⁶ Ultimately, between 10 and 11 percent of patients with either therapy will have recurrent esophagitis,²⁰ and 30 to 60 percent of patients who have undergone ARS will continue to use antisecretory medication.²⁷ Most importantly, all available trials to date show relative equivalence between the two therapies with regard to development of Barrett’s esophagus or esophageal adenocarcinoma.²⁶