Hiatal Hernia and Gastroesophageal Reflux Disease

Chapter 44 Hiatal Hernia and Gastroesophageal Reflux Disease

The role of operative treatment for gastroesophageal reflux and hiatal hernias changed dramatically during the 1990s. Once a relatively uncommon procedure, many antireflux operations and hiatal hernia repairs (mostly for paraesophageal hernias) are now performed in many centers around the world. The driving force behind increased surgical referral for treatment was the development of minimally invasive surgery. Although the techniques of antireflux operations have not changed, the approach to the operation has become more acceptable to the patient and referring physician because of the small incisions, relatively short hospital stay, and lack of associated perioperative pain when compared with open approaches. Thus, the surgeon must be familiar with all aspects of evaluating and treating both entities because he or she is ultimately responsible for the successful outcome of the patient.

Gastroesophageal Reflux Disease


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 (Fig. 44-1). 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, assess the LES pressure 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.1 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 (Fig. 44-2A), 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 (Fig. 44-3). 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 Fig. 44-2B), 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. This is discussed in more detail later in this chapter (“Paraesophageal Hernias”). A type III hernia (see Fig. 44-2C) 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 44-1. 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. This is discussed in detail at the end of this section.2

Table 44-1 Prevalence of Symptoms in Gastroesophageal Reflux Disease*

Heartburn 80
Regurgitation 54
Abdominal pain 29
Cough 27
Dysphagia for solids 23
Hoarseness 21
Belching 15
Bloating 15
Aspiration 14
Wheezing 7
Globus 4

* In more than 1000 patients evaluated. Symptoms reported occurred more frequently than once a week.

Preoperative Evaluation

The preoperative workup in a patient being considered for operative treatment will help confirm the diagnosis, exclude other pathologic entities, and direct the operative intervention.


A significant amount of information about the function of the esophageal body and LES may be obtained from stationary esophageal manometry. This test will allow the surgeon to rule out primary motility disorders such as achalasia, which may mimic the symptoms of reflux and, in patients with GERD, will allow the surgeon to plan the operative procedure better by providing data about the ability of the esophagus to clear itself of ingested food. The manometry catheter is a flexible tube with pressure-sensing devices (water, perfused, or solid state) arranged at 5-cm intervals (Fig. 44-4). The upper esophageal sphincter (UES) is notoriously difficult to analyze because it migrates during the cervical phase of swallowing. Fortunately, the characteristics of the UES are infrequently relevant to clinical practice. The pertinent information to be gained from the manometry tracings concerns the function of the LES and the esophageal body.

The LES is analyzed for mean resting pressure. This may be determined in two ways, a station pull-through and a rapid pull-through. Most laboratories report the values recorded from the station pull-through. With this method, pressures are measured while the catheter is stagnant, with the radial ports at the high-pressure zone of the LES. Rapid pull-through measurements are obtained while the catheter is being pulled across the high-pressure zone at a rate of 1 cm/second. The latter measurements are usually higher than the station pull-through measurements because of the artifact of catheter movement. Normal pressures for a station pull-through at the LES range from 12 to 30 mm Hg. The sphincter generally relaxes to the pressure of the gastric baseline for several seconds when a swallow is initiated. Other information to be gained from the LES is the total length, intra-abdominal length, and location of the sphincter relative to the nares. The longer the high-pressure zone and the longer the intra-abdominal component, the greater is the barrier to reflux of gastric contents.

The esophageal body is assessed to determine the effectiveness of peristalsis. With the four channels located at 3, 8, 13, and 18 cm above the LES, the patient is given a series (at least 10) of 5-mL aliquots of water to swallow. Peristaltic activity is reported as the percentage of initiated swallows that are transmitted to each channel successfully. Normally, a patient has more than 80% peristalsis. The second characteristic of clinical importance is the amplitude of the peristaltic wave. The amplitude is simply the average of the pressures generated in the distal esophagus during effectively transmitted peristaltic waves. Ineffective esophageal motility is defined as less than 70% peristalsis or distal esophageal amplitudes lower than 30 mm Hg and is often associated with significant GERD.

High-resolution manometry is now being used to characterize esophageal function more accurately as compared with standard manometry. The specific advantage of high-resolution manometry is that it allows for effective continuous recording of motor activity along the entire length of the esophagus and yields a more complete and detailed picture of esophageal motility. A color-contour plot with time as the x-axis and esophageal length as the y-axis is produced by the recording device. Pressure is represented by a color scale (Fig. 44-5). This method also provides a more detailed analysis of the LES and is less likely to show a decrease in LES pressure with deglutition, sometimes referred to as pseudorelaxation.

pH Monitoring

The gold standard for diagnosing and quantifying acid reflux is the 24-hour pH test. This study is performed by placing a thin catheter containing one or more solid-state electrodes in the esophagus. The electrodes are spaced 5 to 10 cm apart and are capable of sensing fluctuations in the pH between 2 and 7. The electrodes are connected to a data recorder that the patient wears for the period of observation. There is a digital clock displayed on the recorder. When the patient has an event (e.g., heartburn, chest pain, eructation), he or she records the event in a diary, noting the time on the recorder (Fig. 44-6).

A large amount of information may be gleaned from the study—total number of reflux episodes (pH < 4), longest episode of reflux, number of episodes lasting longer than 5 minutes, extent of reflux in the upright position, and extent of reflux in the supine position. An overall score is obtained with the use of a formula that assigns a weight to each item according to its capacity to cause esophageal injury. This value, known as the DeMeester score, needs to be less than 14.7. A simpler way to determine whether abnormal reflux is occurring is to estimate the total percentage of time that the pH is below 4 in the proximal and distal channels. This is calculated by dividing how long the pH was lower than 4 by the total duration of the study and multiplying by 100. In the proximal esophagus (15 cm above the LES), acid exposure normally occurs less than 1% of the time; in the distal esophagus (5 cm above the LES), it normally occurs less than 4% of the time.

The patient’s symptom diary needs to be correlated with episodes of reflux. The correlation of heartburn or chest pain with a decrease in the pH has significant clinical value because it helps confirm a cause and effect relationship. When interpreting these studies, it should be remembered that patients often do not maintain their normal activities and eating patterns when they have the catheter in place. Thus, their symptoms may not be as prevalent during the study period. If there is symptom correlation with low pH measurements, the suspicion of reflux-induced disease may be confirmed, even if the total acid exposure is normal.

Impedance pH testing is now being performed at specialized centers; this allows for further characterization of the refluxate as being acidic or nonacidic. Impedance monitoring detects reflux events based on the change in resistance to flow of an electrical current between electrodes, regardless of whether the refluxate is gas, liquid, or mixed. The intraluminal impedance increases with air and decreases with a liquid bolus. As compared with standard pH monitoring, impedance pH testing can distinguish between a true reflux event and ingestion of an acidic beverage by characterizing retrograde movement, as opposed to antegrade (normal swallow) along the esophagus. Also, another advantage is the ability of impedance pH testing to determine the proximal extent of reflux, which may be particularly useful for patients with extraesophageal symptoms such as cough, hoarseness, wheezing, or aspiration. One disadvantage, however, is that the automated analytic software tends to overestimate the number of reflux episodes, making it mandatory for all studies to be personally reviewed and edited manually, which can be time-consuming. Several studies have revealed that 30% to 40% of patients with persistent symptoms, despite maximal proton pump inhibitor (PPI) therapy with normal distal acid exposure as assessed by standard pH monitoring, have non–acid reflux events, with a high symptom correlation.4,5 These persistent complaints tend to be regurgitation, chest pain, cough and, much less frequently heartburn. Currently, it remains unclear how impedance pH testing should be implemented in the clinical management of GERD. Until more research has been carried out, it should only be performed at specialized esophageal centers and in select patients. It tends to have the highest yield in patients with atypical symptoms of GERD or in patients with pulmonary symptoms thought to be related to or exacerbated by proximal esophageal reflux events.6


The esophagogram provides valuable information in the evaluation of patients with symptoms of GERD when an operation is contemplated or when the symptoms do not respond as expected. Often, spontaneous reflux during the examination will be demonstrated. Although reflux may be induced in patients who do not have the disease, the occurrence of spontaneous reflux lends support to the diagnosis of abnormal gastroesophageal reflux. The true value of the study is to determine the external anatomy of the esophagus and proximal stomach. The presence and size of a hiatal hernia may be characterized (Fig. 44-7). Although this neither confirms nor refutes the presence of disease, it is extremely beneficial in planning the operation. A mediastinal GEJ that does not reduce into the peritoneal cavity during the study is a predictor of a more difficult operation that may require an esophageal lengthening procedure. Peptic esophageal strictures may also be found on an esophageal contrast study. The presence of a stricture will taint the interpretation of the 24-hour pH study, especially if it is tight enough to prevent reflux. Other anatomic abnormalities, such as diverticula, tumors, and unexpected paraesophageal hernias, will be discovered during esophagography. Esophagograms are being replaced by CT scans, which, when reconstructed, provide all the information of the esophagogram but have the benefit of providing information about the other adjacent organs.

Treatment and Outcome

Medical Management

When a patient is first seen, a lengthy workup is not necessary if the history and examination are consistent with GERD. It would be prudent to check for chronic anemia in such a patient and to prescribe a 6-week course of acid suppression therapy. Most authors agree that a double dose of a PPI is the initial approach to medical management. Given in this manner, the use of medical therapy becomes in itself a diagnostic tool. If the symptoms persist after a trial of medical therapy, a more extensive evaluation, as described earlier, would be indicated. The medications available to treat acid reflux include antacids, motility agents, histamine 2 (H2) blockers, and PPIs. Although lifestyle modification has been advocated before or as an adjunct to medical therapy, the efficacy of such changes in the treatment of esophagitis has not been proved.8

Pharmacologic treatment of GERD has been revolutionized by the advent of PPIs. This class of drugs is one of the most widely prescribed drugs worldwide and, in 2006, the expenditure on these drugs was approximately $24 billion.9 These drugs act by irreversibly binding the proton pump in the parietal cells of the stomach, thus effectively stopping gastric acid production. The maximal effect occurs after approximately 4 days of therapy and the effects linger for the life of the parietal cell. Thus, the acid suppression will persist for 4 to 5 days after therapy has ended so the patient needs to be off therapy for 1 week before being evaluated with pH monitoring.

Compared with H2 blockers, PPIs are more effective at healing esophageal ulceration secondary to acid exposure.10 These medications are relatively expensive but are well tolerated. Side effects may include headache, abdominal pain, flatulence, constipation, and diarrhea. Recently, long-term side effects of PPI therapy have gained significant attention. Several studies have revealed an association between long-term PPI use and increased risk of nutritional deficiencies and infectious complications.9 The results of these studies, however, need to be interpreted with caution, given that most were limited by small sample size and retrospective design. Larger studies have linked long-term use of PPIs to gastric polyp formation, usually occurring with more than 1 year of treatment. Most of these polyps are hyperplastic and do not appear to be malignant.


The indications for surgical therapy have changed since the advent of PPIs. Certainly, patients with evidence of severe esophageal injury (e.g., ulcer, stricture, Barrett’s mucosa) and incomplete resolution of symptoms or relapses while on medical therapy are appropriate to consider for surgery. Other patients with a long duration of symptoms or those in whom symptoms persist at a young age are initially considered for surgery. In these patients, surgery is considered an alternative to medical therapy rather than a treatment of last resort.

Some patients have absolutely no response of their symptoms to the use of PPIs. They need to be scrutinized further before being offered surgical treatment, as opposed to being considered medical failures who would benefit from surgery. Because PPIs are so effective at decreasing the acid production of the stomach, the diagnosis of GERD in such patients is questionable and must be demonstrated with objective testing.

Since the application of minimally invasive techniques to the treatment of GERD, the cost of surgery has decreased. This has changed how surgical treatment is viewed. Considering the cost of PPI use and the cost of operative treatment with its accepted success rate, the length of time required for medical therapy to become more expensive than surgery is approximately 8 to 10 years.11 This assumes that the patient uses the lowest dose of the medication. Therefore, in patients who have more than 8 years of life expectancy and are in need of lifelong therapy because of a mechanically defective sphincter, surgical therapy may be considered the treatment of choice.

360-Degree Wrap (Left Crus Approach)

The technique described here is the left crus approach to a 360-degree wrap (Nissen fundoplication), which is the procedure of choice for most patients. The left crus approach provides the advantage of a direct and early view of the short gastric vessels and spleen. After this obstacle is negotiated, there is little chance of injuring the spleen during the rest of the procedure.

The patient is placed in a low lithotomy position. The surgeon stands between the patient’s legs, with the assistant on the left side of the patient. The four trocars and liver retractor are placed so that two equilateral triangles sharing a common medial angle are created. The surgeon operates through the two most cephalad ports. The assistant operates through the two closest caudad ports. The liver retractor is placed just left of the midline, in the subxiphoid region (Fig. 44-8).

With the assistant first retracting the greater curve and then the omentum, the left crus and greater curve are dissected by the surgeon. The short gastric vessels are taken early to mobilize the fundus (Fig. 44-9). With the fundus mobilized, the phrenoesophageal membrane over the left crus may be dissected until the crural fibers are identified. The entire length of the left crus is mobilized at this time (Fig. 44-10).

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Aug 1, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Hiatal Hernia and Gastroesophageal Reflux Disease

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