Antireflux Procedure – Laparoscopic

Pathophysiology

The lower esophageal sphincter (LES) has the primary role of preventing reflux of the gastric contents into the esophagus. The sphincter is not a distinct anatomic structure but is a unique physiologic entity, located just cephalad to the gastroesophageal junction (GEJ). It is clearly identifiable as a zone of high pressure during manometric evaluation as the sensing device passes from the stomach into the esophagus.

Several factors contribute to the generation of this high-pressure zone. The first is the intrinsic musculature of the distal esophagus. These muscle fibers differ from those in other areas of the esophagus in that they are in a state of tonic contraction. They normally relax with initiation of a swallow and then return to a state of tonic contraction. The second contributing factor to LES pressure is the sling fibers of the cardia. These fibers are at the same anatomic depth as the circular muscle fibers of the esophagus but are oriented in a different direction. They run diagonally from the cardia-fundus junction to the lesser curve ( Figure 15-1-1 ). These fibers are responsible for a significant percentage of the lower esophageal high-pressure zone. The third contributing factor to the maintenance of the high-pressure zone in the distal esophagus is the diaphragm. As the esophagus passes from the chest to the abdomen, it is surrounded by the crura of the diaphragm. During inspiration, the anteroposterior diameter of the crural opening is decreased, compressing the esophagus and increasing the measured pressure at the LES. This concept is particularly important for the interpretation of esophageal mano­metry tracings. By convention, the LES pressure is assessed at mid or end expiration, thereby providing reliable, reproducible pressure measurements. The last component of the pressure generated at the lower esophageal high-pressure zone is the transmitted pressure of the abdominal cavity. The abdominal compartment has a relatively higher pressure than the thoracic cavity. A GEJ that is firmly anchored in the abdominal cavity will be exposed to a greater transmural pressure than one that is in the posterior mediastinum.

Gastroesophageal reflux may occur when the pressure of the high-pressure zone in the distal esophagus is too low to prevent gastric contents from entering the esophagus or when a sphincter with normal pressure undergoes spontaneous relaxation, not associated with a peristaltic wave in the body of the esophagus. Other changes in the high-pressure zone, such as shortening, which occurs as part of cephalad displacement or as gastric distention from food or air, may also eliminate the barrier and result in reflux. Because even small changes in the high-pressure zone compromise its effectiveness, reflux episodes occur in normal people. The distinction between gastroesophageal reflux disease (GERD) and gastroesophageal reflux is a fine and important one and requires knowledge of associated symptoms, mucosal damage of the esophagus, total amount of acid exposure, and other factors.

GERD is often associated with a hiatal hernia. Although any type of hiatal hernia may give rise to an incompetent cardia, the most common is the type I hernia ( Figure 15-1-2A ), also called a sliding hiatal hernia. A type I hernia is present when the GEJ is not maintained in the abdominal cavity by the phrenoesophageal ligament (membrane). Thus, the cardia migrates back and forth between the posterior mediastinum and peritoneal cavity. The phrenoesophageal ligament is a continuation of the endoabdominal fascia, which reflects onto the esophagus at the hiatus. It lies just superficial to the peritoneal reflection at the hiatus and continues into the mediastinum ( Figure 15-1-3 ). Although the presence of a small sliding hernia does not necessarily imply an incompetent cardia, the larger its size, the greater the risk for abnormal gastroesophageal reflux.

Hiatal hernias are classified by their anatomy into three types (I to III). Types II and III hiatal hernias are often referred to as paraesophageal hernias and, although they may be associated with GERD, are also larger, more difficult hernias to treat and may be associated with acute or chronic obstructive symptoms. A type II hernia (see Figure 15-1-2B ), also called a rolling or paraesophageal hernia, occurs when the GEJ is anchored in the abdomen but the hiatal defect, which is usually large, provides space for viscera to migrate into the mediastinum. The relatively negative pressure in the thorax facilitates visceral migration. Usually, the fundus of the stomach migrates into the mediastinum; however, the colon and spleen are also occasionally identified. A type III hernia (see Figure 15-1-2C ) is a combination of the first two, in which the GEJ and fundus (or other viscera) are free to move into the mediastinum.

A hiatal hernia is neither necessary nor sufficient to make the diagnosis of GERD, and the presence of such a hernia does not constitute an indication for operative correction. The theoretical implications of a type I or III hiatal hernia being present is that the cardia and distal esophagus have the potential to be exposed to the negative pressure of the thoracic cavity. This would lower the pressure at the LES, thereby allowing reflux to occur more readily. Many patients with hiatal hernias do not have symptoms and do not require treatment.

Clinical Presentation

The most common presentation of patients with GERD includes a long-standing history of heartburn and a shorter history of regurgitation. Heartburn, when typical, is a reliable symptom. Heartburn is confined to the epigastric and retrosternal areas. It is identified as a caustic or stinging sensation. It does not radiate to the back and is not characteristically described as a pressure sensation. It is best to ask the patient to describe in detail the sensation that he or she is experiencing. Sometimes, the symptoms will be more characteristic of peptic ulcer disease, cholelithiasis, or coronary artery disease.

The presence of regurgitation indicates progression of the disease. Some patients will be unable to bend over without experiencing the unpleasant event. A distinction between regurgitation of undigested and digested food needs to be made. Undigested food in the regurgitant is indicative of a different pathologic process, such as an esophageal diverticulum or achalasia.

In addition to heartburn and regurgitation, some patients suffer from dysphagia. Usually, dysphagia represents a mechanical obstruction and is more pronounced with solid food ingestion than with liquids. If dysphagia for liquids and solids occurs at the same time and is present with the same intensity, a neuromuscular disorder is suspected. When a patient is found to have dysphagia, peptic stricture of the distal esophagus is most likely to be the cause. However, tumor, diverticula, and motor disorders need to be excluded because this determination will affect the operative approach.

Other symptoms may be present in patients with gastroesophageal reflux. Most arise from the gastrointestinal tract; however, many patients will have symptoms involving the respiratory tract as well, called extraesophageal symptoms. The frequency of symptoms in more than 1000 patients evaluated at the gastrointestinal function laboratory of the University of Washington is shown in Table 15-1-1 . Although many patients with gastrointestinal symptoms will also complain of extraesophageal symptoms, it is less common for a patient to present with only respiratory symptoms.

Physical Examination

The physical examination of patients with GERD rarely contributes to confirmation of the diagnosis. In patients with advanced disease, several observations may help identify the source of the patient's discomfort. A patient who constantly drinks water during the interview is facilitating esophageal clearance, which may be indicative of continual reflux or distal obstruction. Other patients with advanced disease will sit leaning forward and carry out the interview with their lungs inflated to almost vital capacity. This is an attempt to keep the diaphragm flattened, the anteroposterior diameter of the hiatus narrowed, and thus the LES pressure elevated. Patients who have severe proximal reflux with regurgitation of gastric contents into their mouth may have erosion of their dentition (revealing yellow teeth caused by the loss of dentin), injected oropharyngeal mucosa, or signs of chronic sinusitis.

The physical examination may be helpful in determining the presence of other pathologic entities. The presence of abnormal supraclavicular lymph nodes in a patient with heartburn and dysphagia may suggest esophageal or gastric cancer. If the patient's retrosternal pain is reproducible with palpation, a somatic cause is likely. Short of these extreme presentations, the physical examination is generally not helpful in confirming or excluding gastroesophageal reflux as a pathologic entity.