Atypical or extraesophageal symptoms of GERD arise from the respiratory tract and are most commonly thought to be caused by microaspiration of gastric contents. They can be divided into laryngeal symptoms such as hoarseness, throat pain and Globus sensation; and pulmonary symptoms including cough, shortness of breath and asthma (either with or without associated chronic lung injury). Although aspiration is the most likely route of injury, distal esophageal acid exposure may activate the vagus nerve. Due to common innervation of the trachea and esophagus, this may result in bronchospasm and cough. Atypical symptoms are much more difficult to elicit an etiology for as they can also occur from respiratory or pulmonary causes. Furthermore, extraesophageal GERD symptoms less commonly resolve with proton pump inhibitor (PPI) therapy. This is attributed to persistent microaspiration causing ongoing injury, even when acid production is suppressed by medical therapy [2]. When patients present with extraesophageal symptoms and GER, it is our practice to refer patients for evaluation by a laryngologist or pulmonologist. If a nongastrointestinal cause cannot be identified it is appropriate to proceed with LARS.

Patients referred for surgical evaluation will occasionally experience dysphagia related to their GERD. In this patient population, the most common cause is esophageal mucosal inflammation and damage. The inflammatory changes can manifest as diffuse esophageal inflammation, a Schatzki ring or a peptic stricture. Although the incidence of peptic strictures has significantly decreased in the age of PPI therapy, they are considered pathognomonic for long-standing reflux. If found on upper endoscopy, peptic strictures should always be biopsied to rule out intestinal metaplasia, dysplasia or malignancy. Similarly to peptic strictures, Schatzki rings also arise in the distal esophagus. They can be differentiated on endoscopy by the appearance of submucosal fibrotic bands as opposed to the mucosal scarring seen in peptic stricture disease. Both should be dilated to relieve obstruction but Schatzki rings do not need to be biopsied unless there is a visible mucosal abnormality. Some patients with dysphagia in the setting of GERD have no identifiable anatomic etiology. In these cases the dysphagia usually resolves with control of reflux. Patients who present with sudden dysphagia to solids and liquids without anatomic abnormalities should be evaluated for neuromuscular or autoimmune disorders.

Many patients present for surgical evaluation with a longstanding diagnosis of GERD based on typical symptoms and response to PPI therapy. However, there are four key diagnostic tests to help establish a diagnosis of GERD as well as evaluate gastroesophageal anatomy and function. These tests can help guide surgeon decision making and predict the success of an antireflux operation.

Surgical therapy should be considered in patients who have an objective diagnosis of GERD based on preoperative testing and inadequate symptom and disease control despite maximal medical therapy. Other indications include patients with extra-esophageal manifestations or complications of GERD such as peptic stricture, esophageal ulcerations, or recurrent aspiration [38–42]. Occasionally patients will have adequate symptoms control with medical management but request surgery to avoid prescriptions or medication side effects.

We routinely administer preoperative antibiotics to reduce the risk of surgical site infection and preoperative subcutaneous heparin to reduce risk of venous thromboembolic events. Sequential compression devices are placed prior to induction. After initiation of general anesthesia, a Foley is inserted and the patient is placed in a modified low lithotomy position with all extremities well padded. The surgeon stands between the patient legs to obtain optimal ergonomics and the assistant stands at the patient’s left. Steep reverse Trendelenburg is utilized to facilitate exposure of the hiatus and displace the abdominal viscera inferiorly. An 11 mm incision is made at the left costal margin lateral to the mid-clavicular line. A Veress needle is inserted and used to establish pneumoperitoneum. The abdomen is entered under visualization with a bladed optical access port. Three additional 5 mm ports are then placed (Fig. 5.4). The camera port is placed 2 cm to the left of the midline and 10 cm below the costal margin. The assistant drives camera and operates through the left inferior port. The primary surgeon operates through the left upper quadrant and left subcostal port. A Nathanson liver retractor is placed through a small subxyphoid incision.

Our dissection is first begun at the left crus by dividing the phrenogastric membrane. The lesser sac is entered at the inferior edge of the spleen and the short gastric vessels are ligated and divided to mobilize the gastric fundus. This is carried superiorly until the previously dissected left crus is encountered. After the fundus is mobilized to expose the left crus, the phrenoesophageal membrane is incised. The mediastinum is carefully entered through the phrenoesophageal membrane between the left crus and esophagus. The dissection is continued superiorly as well as anteriorly by dividing the peritoneum overlying the anterior crus. The gastrohepatic ligament is then divided to the level of the right crus. The right phrenoesophageal membrane is divided and right crural dissection is performed in a similar fashion to the left side (Fig. 5.5). A retroesophageal window is created and a penrose drain is placed around the esophagus. This is used to safely retract the esophagus during the mediastinal dissection and creation of the fundoplication. The esophagus is mobilized until at least 3 cm of intra-abdominal esophagus is achieved. During this dissection, care must be taken to preserve the anterior and posterior vagal nerves. The hiatus is closed posteriorly using permanent interrupted sutures and approximated to allow a 52-French bougie (Fig. 5.6). The crural fascia is incorporated into the closure rather than the muscle fibers alone. Closure begins posteriorly where the left and right crura join and then proceeds anteriorly. The esophagus should maintain straight orientation without excessive angulation and the bougie should pass easily. The repaired hiatus should allow passage of a closed laparoscopic instrument between the esophagus and crura.