Surgical Treatment of Benign Esophageal Diseases

Esophageal Wall

The esophagus is lined with stratified, nonkeratinizing squamous epithelium ( Fig. 36-1 ), isolated from the remainder of the esophageal wall by a basement membrane. Immediately beneath the basement membrane is the lamina propria, a thin layer of loose connective tissue with a complex of collagen and elastic fibers. It contains a network of endothelium-lined channels, both capillaries and lymphatics. The muscularis mucosae supports the lamina propria and is composed of a longitudinal layer of smooth muscle. This continuous muscle layer pleats the inner layers of the esophagus into a series of folds that disappear with distention. The epithelium, lamina propria, and muscularis mucosae comprise the esophageal mucosa.

The submucosa is composed of connective tissue that contains a network of blood vessels and lymphatics. Elastic fibers and collagen combine to make this the strongest esophageal layer. Submucosal glands are mixed types, producing a combination of serous and mucous secretions. These submucosal glands are unique to the esophagus and allow differentiation of the esophagus from the stomach in instances of glandular epithelial metaplasia. Ducts from these glands pierce the mucosa to drain into the esophageal lumen.

The muscularis propria is the muscular sleeve that provides the propulsive force necessary for swallowing. There are two layers of muscle: an inner circular layer and an outer longitudinal layer. The proximal 4% to 5% of the esophagus is composed completely of striated muscle and the distal 54% to 62% completely of smooth muscle. Smooth muscle first appears in the anterior circular layer. The transition from striated to smooth muscle in the circular muscle layer is gradual, and the 50/50 point is approximately 5 cm from the cricopharyngeus muscle.

The cricopharyngeus (upper esophageal sphincter [UES]) is a continuous transverse band of muscle originating from the cricoid cartilage ( Fig. 36-2 ). Superiorly, the muscle of the cricopharyngeus blends with the inferior pharyngeal constrictor muscle. A posterior defect, Killian triangle, is an inverted fan-shaped weakness in the inferior constrictor at the superior border of the cricopharyngeus. Inferiorly, the cricopharyngeus merges with the inner, circular layer of the muscularis propria. The longitudinal muscle layer of the muscularis propria originates from the lateral aspect of the cricoesophageal tendon. Posteriorly, these anterior and lateral components converge to meet at the midline. Thus, the proximal 1 to 2 cm of the posterior cervical esophagus is composed only of inner circular muscle, creating a potential for a mirror-image triangular area of weakness called Laimer triangle.

Contraction of the longitudinal muscle fibers of the esophageal body produces esophageal shortening. The inner circular muscle is arranged in incomplete rings producing a helical pattern. Muscle layers are equal and uniform in thickness until the distal 3 to 4 cm of the esophagus. Here, the inner circular layer thickens and divides into incomplete horizontal muscular clasps on the lesser curve aspect of the distal esophagus and oblique fibers on the greater curve aspect. These become gastric sling fibers (see Fig. 36-2 ). Although no complete circular bands exist at the lower esophageal sphincter (LES), this area of rearranged circular fibers corresponds to the high-pressure zone of the LES.

The esophagus lies in a bed of fat, neurovascular, and connective tissue and elastic fibers termed the adventitia. This layer of loose connective tissue surrounding the esophagus contains lymphatics and regional lymph nodes, blood vessels, and nerves. Unlike the stomach, small bowel, and colon, it has no serosa, except in its short abdominal segment.

Lymphatics begin as blind endothelium-lined saccules in the lamina propria just below the epithelium and basement membrane. An immunohistochemical study of the esophageal wall using lymphatic endothelial marker D2-40 has provided insight into the lymphatic anatomy of the esophageal wall (see Fig. 36-1 ). The lamina propria contains a dense longitudinal plexus of lymphatic vessels. Rare perforating lymphatics have been found draining into a sparse circumferential lymphatic network in the outer margin of the submucosa. Perforating lymphatics from the submucosal plexus, usually running with an artery and vein, penetrate the inner circular layer of the muscularis propria. Here, they drain into a circumferential intramuscular plexus that accompanies the artery, vein, and nerves of this space. Afferent lymphatics, usually accompanied by an artery and vein, drain the intramuscular plexus into the lymphatic channels in the adventitia. No direct connection from the lamina propria network and the thoracic duct has been identified. Existence of direct routes from mural lymphatics to the thoracic duct, without a relay through regional lymphatics and lymph nodes, has been documented by many authors; however, the exact patterns and occurrence of these pathways are highly variable.

The arterial supply of the esophagus is parasitic. It is derived from blood vessels supplying other organs in the neck, chest, and abdomen. Generally, these vessels divide at a distance from the esophagus and send small segmental branches to that segment of the esophagus. Esophageal blood supply has three principal sources. The superior and inferior thyroid arteries supply the cervical esophagus. The proximal and middle thoracic esophagus receives blood from branches of the bronchial arteries. The only dedicated esophageal arteries are one or two branches that arise from the anterior aspect of the aorta below the tracheal carina. In one third of autopsy specimens, no esophageal artery could be identified. These esophageal arteries directly supply the lower thoracic esophagus. The lower thoracic esophagus and abdominal esophagus receive arterial branches from the left gastric and, occasionally, the splenic arteries. The combination of a segmented arterial supply derived from multiple sources and a rich intramural vascular plexus ensures an excellent esophageal blood flow and permits extensive esophageal mobilization without esophageal arterial insufficiency or ischemia. Because esophageal arteries branch from larger arteries some distance from the esophagus, stripping of the esophagus from its bed during transhiatal (blunt) esophagectomy is possible without direct ligation of the esophageal arterial supply. Arterial spasm provides adequate hemostasis; thus, significant bleeding does not complicate this procedure.

Subepithelial esophageal venules drain into a substantial submucosal venous plexus that extends the length of the esophagus. There are venous connections between the lower thoracic and abdominal esophagus and the portal venous system. Venules then pierce the muscularis propria to drain into veins on the surface of the esophagus. Regional drainage is directed to the inferior thyroid and brachiocephalic veins in the neck, the azygous and hemiazygos veins in the chest, and the left gastric and splenic veins in the abdomen.

Both parasympathetic and sympathetic nerves innervate the esophagus. Branches of the vagus nerve supply parasympathetic fibers that are motor to the muscle coat and secretomotor to the submucosal glands. The cervical and thoracic sympathetic chain and the celiac plexus provide sympathetic fibers that promote contraction of sphincters and relaxation of the esophageal body muscle, increase peristaltic and glandular activity, and cause vasoconstriction. These fibers enter the esophageal wall with the blood supply and form fibers and ganglia within it. The myenteric (Auerbach) plexus is positioned between the longitudinal and circular layers of the muscularis propria and controls these muscles. The submucosal (Meissner) plexus controls the muscularis mucosa and submucosal glands.

Regional Anatomy

The esophagus spans the lower neck, thoracic cavity, and upper abdomen ( Fig. 36-3 ). The anatomy of the esophagus is best divided into fifths: cervical, upper thoracic, middle thoracic, lower thoracic, and abdominal esophagus. The anterior wall of the cervical esophagus is in intimate contact with the posterior membranous trachea. The recurrent laryngeal nerves course anteriorly and laterally in the tracheoesophageal groove. The carotid sheaths bind the cervical esophagus laterally. The posterior wall of the cervical esophagus lies on the vertebral bodies.

The thoracic esophagus occupies the posterior mediastinum and passes anteriorly to the vertebral bodies. The upper thoracic esophagus lies posteriorly to the trachea and is bound laterally by the mediastinal pleura. In its lower left aspect, it is sandwiched between the azygous vein on the right and the aortic arch on the left. The middle thoracic esophagus lies behind the pulmonary hilum and between the azygous vein and descending aorta. The lower thoracic esophagus has the same lateral and posterior boundaries but lies behind the pericardium. The thoracic duct is situated between the azygous vein and descending thoracic aorta and posteriorly and to the right of the lower and midthoracic esophagus. At approximately the level of the fourth thoracic vertebra, it crosses the midline to become a left-sided structure.

The abdominal esophagus is cradled in the muscular esophageal hiatus. The inferior vena cava is on the right posterolateral aspect; the abdominal aorta is on the left posterolateral aspect. Superiorly, the left lateral segment of the liver overlies the esophagus and esophagogastric junction (EGJ).

History and Physical Examination

The symptoms most commonly associated with esophageal diseases are heartburn, regurgitation, dysphagia, and odynophagia. Other symptoms that may be associated with esophageal disease are sore throat, hoarseness, cough, bad taste, globus, hiccup, aspiration, wheezing, chest pain, nausea, vomiting, choking, hematemesis, and melena. Symptom composition depends on the esophageal disorder and is discussed in various sections of this chapter. Physical examination of the esophagus is indirect and focuses on head and neck, thoracic, and abdominal findings.

Box 36-1 lists systemic diseases with esophageal manifestations. Some are discussed later in this chapter. These potential underlying disorders should be considered during the history and physical examination.

Investigations

Patients with suspected esophageal disease will typically undergo barium esophagram and/or esophagoscopy as their initial diagnostic tests.

Barium Esophagram

A three-phase study assessing mucosa, contour, and function of the esophagus is optimal. In the double-contrast phase, conducted with the patient ingesting high-density barium and CO ₂ tablets in the upright position, the mucosa is examined ( Fig. 36-4 ). Next, esophageal function is assessed in the right anterior oblique (RAO) position with the ingestion of low-density barium in single swallows at 20- to 30-second intervals ( Fig. 36-5 ). The examination is videotaped. The value of attempting to elicit reflux in this phase is questionable because 20% of normal individuals have radiologic reflux. Barium tablets or barium-coated marshmallows or solids may demonstrate abnormalities not visualized by liquid barium studies. The final phase, the full-column technique, is performed with the patient in a semiprone RAO position and low-density barium. Multiple quick swallows produce a column of barium that fully distends the esophagus. This optimizes imaging of the distal esophagus and can demonstrate small hiatal hernias, subtle strictures, or distal rings ( Fig. 36-6 ). The esophagus is allowed to empty, and the remaining barium coating the esophageal wall provides a mucosal relief study, now rarely performed.

The timed barium esophagogram is a simple test of esophageal emptying ( Fig. 36-7 ). After the patient ingests a premeasured amount of barium, usually 250 mL, spot films are taken at 1-, 2- and 5-minute intervals and, if necessary, at 10 minutes and 20 minutes after barium ingestion. This allows simple quantification of esophageal emptying and is useful for evaluations of both motility disorders and the results of therapy.

Esophageal Manometry

Esophageal manometry is indicated (1) to establish the diagnosis of dysphagia when obstruction and eosinophilic esophagitis have been excluded, (2) for placement of intraluminal devices such as a pH probe, and (3) before antireflux surgery. It is possibly indicated for dysphagia after antireflux surgery or therapy for achalasia. High-resolution manometry (HRM) is a major advance over traditional low-resolution manometry in that it has increased the number of pressure sensors from 5 to 36, has decreased the distance between sensors from 5 to 1 cm, and includes sensors in the pharynx and proximal stomach ( Fig. 36-8 ). Sophisticated computer algorithms extrapolate between these sensors, permitting a continuous, seamless assessment of intraluminal esophageal pressure from pharynx to stomach. The display of intraluminal pressure as a color spectrum on a plot of esophageal position ( y axis) against time ( x axis) produces a pressure topography of swallowing ( Fig. 36-9 ). Catheter placement is easier, and study duration is markedly shorter by eliminating the LES pull-through. As a result of these features, this technology has had widespread adoption into clinical practice.

HRM accurately measures LES relaxation by compensating for LES movement with swallows. HRM also determines latency until esophageal contraction after a swallow stimulus to assess for premature contractions, as well as multiple smooth muscle contraction parameters (antegrade peristalsis, amplitude, intrabolus pressure). These and other topographic metrics are shown in Figure 36-9 . Table 36-1 lists the Chicago Classification Criteria of Esophageal Motility Disorders based on these topographic metrics and agreed on by an international panel of experts. More extensive discussion of HRM (e.g., detailed assessment of EG junction morphology allowing separation of LES and diaphragm [for detecting hiatal hernia, etc.]), other metrics, and use in lap band surgery is available elsewhere. Continued experience with HRM and especially outcome data should allow refinements in the classification scheme in the future.

TABLE 36-1

Chicago Classification Criteria of Esophageal Motility Disorders

Modified from Bredenoord A, Fox M, et al: Chicago classification criteria of esophageal motility disorders defined in HRM esophageal pressure topography. Neurogastroenterol Motil 24(Suppl 1):57–65, 2012.

Diagnosis Criteria

Achalasia

Type I achalasia—Mean IRP > 15 mm Hg, 100% failed peristalsis Type II achalasia—Mean IRP ≥ 15 mm Hg, aperistalsis, panesophageal pressurization ≥ 20% Type III achalasia—Mean IRP ≥ 15 mm Hg, aperistalsis, spastic contractions ≥ 20% swallows EGJ outflow obstruction—Mean IRP ≥ 15 mm Hg, some normal or weak peristalsis

Motility Disorders (Defined as Pattern not Seen in Normal Individuals)

Distal esophageal spasm—Normal mean IRP, ≧20% premature contractions (DL < 4.5 sec) Jackhammer esophagus—At least one swallow DCI > 8000 with single or multipeaked contraction Absent peristalsis—Normal mean IRP, 100% swallows with failed peristalsis

Peristaltic Abnormalities (Defined by Exceeding Statistical Limits of Normal)

Weak peristalsis: Large peristaltic defects—Mean IRP < 15 mm Hg and >20% swallows with >5-cm breaks in 20-mm isobar Small peristaltic defects—Mean IRP < 15 mm Hg and >30% swallows with 2- to 5-cm breaks in 20-mm isobar Frequent failed peristalsis—>30%, but <100% of swallows with failed peristalsis Rapid contractions with normal latency—Rapid contractions > 20% swallows, DL > 4.5 sec Hypertensive peristalsis—Mean DCI > 5000, but lacks hypercontractile (jackhammer) criteria (also termed nutcracker )

Normal (Not Achieving any of the above Diagnostic Criteria)

DCI, Distal contractile integral; DL, distal latency; EGJ, esophagogastric junction; IRP, integrated relaxation pressure; LES, lower esophageal sphincter.

IRP: Lowest average pressure of 4 seconds within the LES window.

Impedance Manometry

The traditional impedance manometry catheter adds an impedance pair at each of the four esophageal pressure sites of the low-resolution manometry catheter (see Fig. 36-8 ). This catheter allows bolus transit to be compared with simultaneous esophageal peristalsis and contraction amplitude and is termed the esophageal function test ( Fig. 36-10 ). In 350 patients studied at a single center, all with achalasia and scleroderma had abnormal bolus transit and more than 95% of those with normal manometry, nutcracker esophagus, and LES dysfunction (high or low) had normal bolus transit. Recently, a catheter with both high-resolution manometry (36 sites, 1 cm apart) and high-resolution impedance (18 impedance pairs) capability was developed to improve on the low resolution of the esophageal function test catheter. A classification of weak peristalsis has been proposed based on this newly developed catheter's ability to correlate abnormalities in peristaltic integrity with failed bolus clearing.

Ambulatory Conventional and Wireless pH Monitoring

Ambulatory pH monitoring detects and quantifies acid gastroesophageal reflux. Because this test is typically performed without acid suppression medication, proton pump inhibitors (PPIs) should be discontinued for 1 week, H ₂ blockers for 24 hours and antacids for 8 hours. Conventional transnasal monitoring is done for 24 hours with the thin pH catheter placed 5 cm above the LES, located by manometry. Patients are instructed to have a “typical day” regarding activity and eating. Because symptom correlation is an important component of this test, the patient presses a symptom button when symptoms occur.

A pH less than 4 has arbitrarily been chosen to define an acid reflux episode. The normal parameters for 24-hour pH monitoring have been defined ( Table 36-2 ). Total acid exposure time, expressed as a percentage of study time, is the best discriminator between normal and abnormal values. Composite scores, such as the DeMeester score and frequency-duration index, are no better than simple measured parameters in identifying abnormal reflux. The symptom index relates symptoms to reflux events and is calculated by dividing symptom episodes with reflux by the total number of symptom episodes multiplied by 100%; 50% is the optimum threshold.

TABLE 36-2

Normal Distal Values for 24-hour pH Monitoring

Parameter	Johnson 95th Percentile	Richter 95th Percentile	Jamieson
			Mean	Percentile
Total time (%)	4.45	5.78	4.5	95
Upright time (%)	8.42	8.15	7.1	93
Supine time (%)	3.45	3.45	1.5	86
No. of episodes	47	46	56	98
No. >5 min	3	4	3	94
Longest episode (min)	19.8	18.5	12	84
Composite score	14.7	—	16.7	96

Wireless pH monitoring is a recent technological advance. The Bravo delivery system “pins” a capsule measuring 6 × 5.5 × 25 mm to the esophagus 6 cm above the squamocolumnar junction, identified by endoscopy. Manometry is not required. Improved patient tolerance allows increased activities and improved food intake; moreover, monitoring is traditionally extended to 48 hours ( Fig. 36-11 ). Wireless pH monitoring has an increased diagnostic yield compared with transnasal monitoring because of higher sensitivity for both abnormal acid exposure and positive symptom-reflux association. Drawbacks are cost, occasional premature detachment, and severe pain requiring endoscopic removal in less than 2% of cases. Similar to nasal pH monitoring, wireless pH monitoring is unable to detect nonacid reflux.