Chapter 16. Perspective on Benign Esophageal Disease

The preceding two chapters address benign diseases of the esophagus, including the diagnosis, evaluation, and management of hiatal hernia, motility disorders, and gastroesophageal reflux disease (GERD). In commenting on these entities, we follow the structure of these chapters.

Hiatal hernia (HH), as common as it is, is truly idiopathic. While HH is rare in Asian and African populations, exact predisposing features are difficult to pin down. In a North American population, GERD is more common among middle-aged males,1 and giant hiatal hernias (often called paraesophageal hernias) are more common among elderly women.2 The predisposing conditions for development of these large hernias in elderly women include diaphragmatic stress during pregnancy (years earlier), loss of abdominal domain, kyphosis (as a result of degenerative spine disease),3,4 and greater longevity than their male counterparts. There may also be collagen ultrastructural defects responsible for hiatal hernia development, but there is insufficient evidence yet to confirm this hypothesis.5–8

The natural history of hiatal hernia may explain the changing symptoms seen in these patients. Early, small “sliding” hiatal hernias (type 1) predispose to GERD by separating the lower esophageal sphincter (LES) from the crural diaphragm, effacing the angle of His, and placing the LES in the thorax where negative intrathoracic pressure contributes to a reduced resting pressure relative to intra-abdominal pressure.9 Over the years, and as the hernia defect grows larger, type 1 hiatal hernia may evolve into type 3 (aka mixed paraesophageal hernia) where the gastric fundus again resumes a position cephalad to the GE junction. This progression will often re-create a GE junction flap valve, and the patients will notice that GERD markedly improves. Replacing the GERD symptoms are symptoms of early satiety, postprandial chest pain, and iron deficiency anemia (in 30%) as a result of visible or occult gastric bleeding by erosions or ulcers at the level of the diaphragm, known as Cameron's ulcers or erosions.10,11 Because of this natural progression, it is understandable why type 2 HH, in which the GE junction remains below the diaphragm, is distinctly rare and probably only occurs when the GE junction is so tightly anchored to the preaortic fascia that the development of a hiatal hernia only results in an attenuation of the phrenoesophageal ligament and cephalad displacement of the gastric fundus. An even rarer event is the parahiatal hernia, where a diaphragmatic defect adjacent to the hiatus allows cephalad migration of the fundus. This is so rare that a true incidence has not been determined, but it presents as a type 2 HH and may be encountered once or twice in an esophageal surgeon's career.

Despite evolving support for the strategy of “watchful waiting” for the asymptomatic hiatal hernia, the incidental detection of a giant HH will warrant questioning about upper GI symptoms. Close questioning reveals that most patients with this defect are either symptomatic or anemic. In either situation, repair is warranted. Far and away the most common approach to repair in the 21st century is laparoscopic hiatal hernia repair. There are no known advantages to open repair.12 Esophageal lengthening is as easily performed with laparoscopic access, the wedge Collis gastroplasty,13 as it is with thoracic access. As well, the recurrence rate of open and laparoscopic repair appears similar, despite the lack of randomized trials.

The “Achilles heel” of giant hiatal hernia repair (usually type 3, mixed paraesophageal hernia) is hiatal hernia recurrence. It was a bit of a shock to most laparoscopic surgeons when they began to see frequent hiatal hernia recurrences with simple sutured repair (20–50%). The most common strategy to prevent recurrent HH is the placement of a large piece of bioprosthetic mesh in a U-shaped configuration, posterior to the esophagus. While early data suggested this technique to be much superior to sutured repair, late follow-up of a randomized controlled trial (RCT) demonstrated a disappointing greater than 50% recurrence rate with and without bioprosthesis.14 Rather than abandoning the use of mesh, many surgeons are searching for a better bioprosthesis. New trials will better tell us which bioprosthesis to use. Another strategy that appears to be of value is esophageal lengthening. When used selectively, in 20–40% of patients with giant hernias, HH recurrence rates seem to have decreased. Additionally, the symptomatic consequence of a small hiatal hernia recurrence is generally minimal, suggesting that it is a rare recurrence that will lead to reoperation.

The technique of repair described is little different from our approach, with a few exceptions. A split leg table is superior to low lithotomy stirrups, as the setup is simpler and the risk of lower extremity nerve compression and deep vein thrombosis (DVT) is decreased by the elimination of stirrup-related pressure points and knee flexion. We also use a mechanical scope holder, which increases operative efficiency and decreases surgeon fatigue, by maintaining a steady image. The pneumatic camera holder is attached to the right side of the bed, near the right hip.

Early in a surgeon's experience with laparoscopic giant HH repair, it was customary to recognize three problems: failure to identify the esophagus (leading to lighted dilator use), disorientation in the epiphrenic and lesser curvature fat, and bleeding from the lesser curvature vessels, including the left gastric artery. All of these problems may be solved by keeping the dissection focused on the diaphragmatic crura, detaching the hernia sac from the crura circumferentially and stripping the peritoneal sac from the lower posterior mediastinum. With this strategy, the esophagus becomes readily visible without the need for a lighted bougie, the fat is reduced by the reduction of the hernia sac, and the lesser curvature vessels are caudal to the field of dissection.

While the closure of a large defect may seem daunting, two strategies seem to allow closure of nearly all large hernias: (1) start posteriorly, as is described in this chapter, and (2) reduce the intra-abdominal pneumoperitoneum pressure to 5–8 mm Hg. With these steps it is almost never necessary to place anterior sutures, which are prone to tearing out because the diaphragm is often quite attenuated anteriorly, and the transverse orientation of the anterior crural arch makes closure technically difficult. Excessive anterior angulation of the distal esophagus is only a problem if the esophagus is not adequately mobilized off the aorta in the lower mediastinum.

The most common (albeit quite rare) esophageal motility disorder of surgical concern is achalasia. The etiology of achalasia outside of the tropics is unknown, but the disease is remarkably democratic, affecting young and old, male and female, and all ethnicities nearly equally.15,16 Such a pattern strongly suggests the current hypothesis that an immunologic response to viral exposure is responsible for the observed myenteric neural degeneration.17,18 While herpes virus has been implicated as the most likely “culprit” by some, the evidence is far from convincing.

The treatment of achalasia with laparoscopic Heller myotomy and partial fundoplication has become the predominant primary therapy over the last 15 years. A recent randomized trial demonstrating equivalence of balloon dilation and Heller myotomy is unlikely to change our approach, as the balloon dilation strategy required intensive surveillance and frequent retreatment, as compared to laparoscopic Heller myotomy.19 The only real “debate” in this field has been whether to fashion an anterior (Dor) or posterior (Toupet) fundoplication after dividing the LES. A recent randomized trial, closed due to lack of accrual, shows a slight, but not significant, advantage in diminished post-op reflux with the posterior fundoplication.20 Nonetheless, worldwide, the anterior fundoplication is preferred as it requires less posterior dissection and it does not angle the GE junction anteriorly as the posterior fundoplication may do. The only “trap” of the Heller myotomy is carrying the myotomy too far above the diaphragm and inadequately on the stomach. If there is any esophageal outflow obstruction (from reflux stricture, angulation, or incomplete myotomy), the supradiaphragmatic myotomy site, lacking muscular support, may create an epiphrenic diverticulum, a result of the pressurized esophagus. Intraoperative endoscopy, immediately after the creation of the myotomy will identify easily if the myotomy extends to the dilated esophagus and onto the proximal stomach. A completely divided LES will open with air insufflations such that the endoscope “perched” in the distal esophagus can visualize the stomach through the previously spastic high-pressure zone, which will still appear as a waist.

Our performance of myotomy varies a bit from the technique described. Without a dilator in the esophagus (which may be hard to pass in the dilated esophagus), the anterior esophagus and upper 3 cm of stomach is cleared of all fat and neurovascular tissue such that the longitudinal muscle is clearly visible on the anterior wall of the esophagus (12 o'clock). We divide the epiphrenic fat pad with ultrasonic shears anteriorly, but we do not remove it as it makes a good handle for the first assistant. It is usually necessary to create a passage behind the anterior vagus nerve to remain on the anterior surface of the esophagus. When the esophagus and stomach are cleared off prior to myotomy, bleeding during the performance of myotomy is dramatically reduced. The submucosal plane is achieved just superior to the GE junction with Metzenbaum-type laparoscopic scissors. Firm lateral traction and countertraction by the surgeon's left hand pulling toward the liver and first assistant grasping a divided epiphrenic fat pad and pulling in the opposite direction will frequently disrupt the circular muscle with minimal sharp dissection. Once the submucosal plane is achieved, a blunt closed grasper can be run several centimeters up the esophagus in the submucosal plane, making subsequent division of the circular muscle quite easy with a pair of scissors. It is not necessary to use any thermal instruments (electrosurgery or ultrasonic dissector) near the mucosa. “Blanching” of the mucosa should be treated as a perforation in situ and should be oversewn as described in the text. The best strategy for dividing the proximal gastric portion of the LES is teasing distraction of the muscle fibers with two Hunter-type or Maryland-type graspers. It is critical that the mucosa be cleared of all circular smooth muscle, and blunt undermining of the myotomy allows the cut edges of the muscle to retract out of sight behind the esophagus (frequently) just above the angle of His. Endoscopy is then performed as mentioned previously, and a “leak test” with air insufflation is then performed. Finally, a large (56–60F) Maloney dilator is passed by the surgeon or assistant to ensure that all circular muscle has been divided and undermining is adequate. Then, partial anterior (our favorite) or posterior fundoplication, as elegantly described in the previous chapter, is performed.

Failures of Heller myotomy are thankfully few, and the appropriate approach to failure has not been entirely defined. Some prefer balloon dilation, with a 3- to 3.5-cm balloon, but the same risk of perforation as with primary balloon dilation drives most surgeons to consider remyotomy. Esophagogastroduodenoscopy (EGD), to rule out cancer, ulcer, or stricture, should be complemented by video esophagram and high-resolution esophageal motility study. The appearance of a diverticulum at the supradiaphragmatic myotomy site should be addressed by an attempt at relieving the esophageal outflow obstruction. Rarely is diverticulectomy indicated and it will be ineffective at relieving recurrent dysphagia if the primary problem is not addressed. After complete LES myotomy, LES resting pressure should be less than 10 mm Hg. If the LES resting pressure is above 12–15, we usually recommend redo Heller myotomy. If the sphincter is already completely ablated (LES resting pressure <10), redo myotomy is unlikely to be successful. Under these circumstances, and especially with a mega or sigmoid esophagus, esophagectomy may be the best next step. The end-stage achalasic esophagus is amenable to minimally invasive surgery (MIS) esophagectomy techniques, but should not be treated with transhiatal esophagectomy or esophageal stripping, as the mediastinal blood vessels supplying a mega esophagus are much larger than normal and stripping may result in uncontrolled mediastinal bleeding.

The approach to other “named” esophageal motor disorders is a bit more controversial. As a general principle, nutcracker esophagus should not be treated with a long myotomy, (it won't help), and the dysphagia associated with diffuse esophageal spasm is best alleviated when the LES is divided. It may be unnecessary to take the myotomy as high as the top of the corkscrew appearance on contrast esophagram to achieve a successful outcome. In other words, the laparoscopic Heller myotomy and partial fundoplication may be the best operation for this condition. This is indeed a relief, as it may be difficult to tell vigorous achalasia from diffuse esophageal spam (DES) in many patients. The treatment of esophageal diverticula is well described in the prior chapter. Because of the propensity of distal esophageal diverticulectomy staple lines to leak (up to 30% in some early studies), we have taken the following three steps that seem to have solved the problem: (1) perform a Heller myotomy to decrease intraesophageal pressure, even in the absence of demonstrable LES hypertension, (2) sew the esophageal smooth muscle over the site of the staple line if possible and perform the myotomy 90 degrees away from the staple line and at least as far proximal as the proximal border of the diverticulum, and (3) leave the patient on a liquid diet for 7 days postoperatively to allow staple line healing before introducing solid foods. Occasionally, safe and complete diverticulectomy can only be performed with thoracoscopic access when laparoscopic access cannot safely expose the proximal extent of the diverticulum.

The diagnosis, evaluation, and management of gastroesophageal reflux disease (GERD) is extremely well covered in the text. I focus, in this commentary, on only four things: indications for surgery, proper use of the many tests available to assess the anatomy and pathophysiology of the esophagus and stomach, choice of an operation, and long-term effectiveness of laparoscopic antireflux surgery, especially as compared to treatment with proton pump inhibitor (PPI).

As has been pointed out, GERD is a very common condition, and a very small proportion of GERD patients elect to have antireflux surgery. While it is clear that the majority of patients are effectively managed with daily PPI, it is now recognized that as many as 40% of individuals will have persistent troublesome symptoms despite PPI treatment. Troublesome reflux is defined as mild GERD symptoms daily, or moderate to severe symptoms two to three times per week. Of all reflux symptoms, PPI therapy is most likely to control chest pain and heartburn. Only 17% of GERD patients will have regurgitation symptoms adequately controlled with PPI.21 Therefore, we can define two populations poorly served with PPI for typical (esophageal) GERD symptoms, those with troublesome heartburn and chest pain despite adequately dosed PPI, and those with troublesome regurgitation that is unlikely to benefit from PPI. Both of these groups are ideally suited for laparoscopic antireflux surgery, as long as the diagnosis of GERD is secure, based on a standard evaluation.

The use of laparoscopic antireflux surgery for laryngopharyngeal reflux (LPR) may be equally effective, if used in the right patient. Because supraesophageal and/or laryngopharyngeal symptoms may be caused by so many common problems (eg, allergies, environmental factors, cigarette smoking, postnasal drip, infections), it is more difficult than it might appear to determine who truly has symptomatic LPR that would be improved by the elimination of all gastroesophageal reflux. While many technologies have been developed over the years to detect LPR, including dual-channel pH recording and nasopharyngeal pH recording, both these methods have proven difficult to validate. Two new promising methodologies, sputum pepsin measurement22 and esophageal/nasopharyngeal impedance measurement, appear to be much more accurate for determining the presence of LPR and will probably become the test of choice in the near future to establish this diagnosis.

The preoperative evaluation of the patient with GERD is well described in the chapter outlined previously. Several years ago, we observed that all patients with heartburn responsive to PPI and erosive esophagitis, stricture, or Barrett's esophagus had an abnormal 24-hour pH study. Thus, we dropped routine pH testing in these patients as the diagnosis of GERD was secure without pH testing in this population. Currently, we reserve pH testing for patients with no esophagitis, Barrett's esophagus or stricture, and for those with atypical symptoms. As mentioned previously, a pH study is not really needed prior to repair of the giant hiatal hernia, unless the patient's only symptom is heartburn and the EGD shows a pristine esophagus. This is rare indeed.

Operation choice for GERD is still a matter of some debate focused on the comparative long-term effectiveness of partial posterior (Toupet) fundoplication and total (Nissen) fundoplication. For many years the partial fundoplication was used in North America only for patients with ineffective or absent esophageal motility, as reflux control was less when a partial fundoplication was performed. When ineffective peristalsis is detected, it now appears that total and partial fundoplication create equivalent low levels of postoperative dysphagia. When peristalsis is completely absent (eg, achalasia or scleroderma), one should consider a partial fundoplication. Having said this, randomized data from Europe23 suggest that the partial fundoplication provides equivalent reflux control in most GERD patients, regardless of motility pattern, while decreasing gas-related symptoms. Bottom line: either type of laparoscopic fundoplication may be performed. East of the Atlantic Ocean, perform a posterior partial fundoplication. On the west “bank” of the Atlantic Ocean, perform a total fundoplication.

Finally, there is great debate over the long-term effectiveness of laparoscopic Nissen fundoplication as compared to chronic PPI use. If one solely relies on the resumption of PPI as the indicator of fundoplication failure, the surgical failure rate may approach 30–40%, but physiologic assessment of these patients demonstrates that only 30% of this group will truly be refluxing, bringing the true failure rate (at 10 years) to about 10%.24 Most patients who have had a good result from a first fundoplication will desire a redo fundoplication when the valve truly fails. The most common failure pattern is the recurrent HH, often a result of intra-abdominal stressors such as retching, straining, coughing, obesity, trauma, and excessive heavy lifting. The rate of reoperation following laparoscopic fundoplication performed by an expert is approximately 1%/year.

The comparative effectiveness of fundoplication to medical therapy has been tested in several randomized trials. When study entrance is restricted to those rendered asymptomatic on standard doses of PPI, surgery and medical therapy perform equivalently.25 When the entrance criteria are broadened to include those with a partial response to PPI, fundoplication usually emerges as the most reliable and durable method for elimination of GERD symptoms.