Figure 42-15. Representation of the loss of competence of the lower esophageal sphincter with shortening of its length. As a

critical length is reached, there is a precipitous drop in sphincter pressure reflecting loss of competence. (From Pettersson GB,

Bombeck CT, Nyhus LM. The lower esophageal sphincter: mechanisms of opening and closure. Surgery 1980;88:307–314, with

permission.)

The third characteristic of the LES high-pressure zone is its position. A portion of the overall length of

the high-pressure zone is normally exposed to the positive intra-abdominal pressure environment and is

commonly referred to as the abdominal length of the LES.19 During periods of increased intra-abdominal

pressure, the resistance of the LES would easily be overcome if its position were such that abdominal

pressure was unable to be applied equally to the LES and the stomach.20–22 This is analogous to sucking

on a soft soda straw immersed in a bottle of liquid; the positive hydrostatic pressure of the fluid and the

negative pressure inside the straw from sucking cause the straw to collapse instead of allowing the

liquid to flow up the straw in the direction of the negative pressure. When the abdominal length of the

LES is inadequate, increases in intra-abdominal pressure will be applied to the stomach but not the LES

thereby encouraging reflux to occur. Studies have shown that the critical length of abdominal LES is 1

cm, below which almost no LES pressure will be sufficient to maintain competency of the sphincter.15

In the fasting state deficits in LES pressure, overall length, or abdominal length will lead to an

increased likelihood of sphincter incompetence. An LES defective in all three parameters is particularly

likely to be associated with increased reflux of gastric juice into the esophagus. This reflux can result in

inflammatory injury to the mucosa and ultimately to the muscularis propria of the esophageal body,

thereby causing a reduced contraction amplitude of the esophageal body and interrupted or dropped

peristaltic sequences. Continued reflux can lead to progressive loss of effective esophageal clearance,

protracted esophageal exposure to the refluxed material and ultimately further organ injury (Fig. 42-

16).23,24

Causes and Consequences of the Failure of the Gastroesophageal Barrier

Early GERD is initiated by increased transient losses of the barrier as a result of gastric overdistention

from excessive air and food ingestion.11,25 The tension vectors produced by gastric wall distention pull

on the gastroesophageal junction, which results in the terminal esophagus being “taken up” into the

stretched fundus, thereby reducing the length of the LES. With overeating, a critical length is reached

(usually about 1 to 2 cm) at which the sphincter gives way; its pressure drops precipitously, and reflux

occurs (Fig. 42-15). If the swallowed air is vented, gastric distention is reduced, the length of the LES is

restored, and competency returns until subsequent distention again shortens it and further reflux occurs.

Aerophagia is common in patients with GERD because they swallow their saliva more frequently to

neutralize the acidic gastric juice that is refluxed into the esophagus.26 Together, the actions of

overeating and air swallowing result in the common complaint of postprandial bloating, repetitive

belching, and heartburn in patients with early GERD. The high prevalence of the disease in the Western

world is thought to be a result of the eating habits of Western society.27 Gastric distention from

overeating, along with delayed gastric emptying resulting from the increased ingestion of fatty foods,

leads to prolonged periods of postprandial gastric distention with shortening of the LES and repetitive

transient loss of the barrier. Surgical correction with a fundoplication prevents the shortening of the

barrier with progressive degrees of gastric distention by diverting the forces that pull on the

gastroesophageal junction.14

Figure 42-16. Overview of the progressive nature of GERD and the effect of the lower esophageal sphincter and esophageal body

on reflux in the upright and supine positions.

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In advanced GERD, permanent loss of sphincter length occurs from inflammatory injury that extends

from the mucosa into the muscular layers of the LES. Fletcher et al.28 showed that in the fasting state,

there is a persistent region of high acidity in the area of the gastroesophageal junction and that this

region of acidity migrates 2 cm proximally after meals.29 This migration occurs from distention of the

stomach with eating and pulling apart of the distal high-pressure zone or LES, thus allowing the area of

high acidity to move proximal to the squamocolumnar junction. This proximal movement exposes the

distal esophageal squamous mucosa to acid and results in the formation of cardiac mucosa. Cardiac

mucosa is an acquired mucosa that replaces chronically injured squamous mucosa in the terminal

esophagus.30 The inflammatory process can extend into the muscular layer of the LES, thereby resulting

in muscle cell injury with permanent shortening of the high-pressure zone or LES and a concomitant

reduction in the amplitude of the high-pressure zone or barrier pressure.30–32 A defective barrier is

recognized when the length or pressure of the LES measured during the fasting state is below the 2.5

percentile of normal.33

For clinicians, the finding of a permanently defective LES has several implications. First, symptoms in

patients with a defective LES can be difficult to manage, and mucosal damage may persist with medical

therapy.34 Surgery is usually required to achieve consistent long-term symptom relief in these patients

to restore a gastroesophageal barrier and interrupt the natural history of the disease. It has been shown

repeatedly that a laparoscopic Nissen fundoplication can consistently restore the length and pressure of

the LES to normal parameters.35 Newer techniques of sphincter augmentation such as with a magnetic

bracelet is an alternative means of restoring the LES that is gaining in popularity.36 Second, a

permanently defective LES is commonly associated with reduced contractility and abnormal wave

progression of the esophageal body.37 For this reason, careful evaluation of the esophageal body is

critical in the evaluation for antireflux surgery for potential tailoring of the operation with a partial

fundoplication. Third, a permanently defective LES and the loss of effective esophageal clearance can

lead to mucosal injury such as erosive esophagitis or Barrett metaplasia, repetitive regurgitation and

aspiration events and ultimately pulmonary fibrosis. Without reestablishing a barrier, chronic use of

acid suppression therapy may simply mask the symptoms due to modification of the pH; however, in

the setting of a structurally defective LES, reflux will continue unabated.38

EVALUATION OF ESOPHAGEAL FUNCTION

A thorough understanding of the patient’s underlying anatomic and functional deficits is fundamental to

the successful treatment of esophageal disease. The diagnostic tests that are employed to evaluate the

esophagus are those used to visualize structural abnormalities, to detect functional abnormalities, and to

measure esophageal exposure to gastric juice. At the authors’ center a panel of four diagnostic tests are

used routinely in the evaluation of known or suspected reflux disease: barium esophagram, upper

endoscopy, high-resolution esophageal manometry, and ambulatory pH monitoring.

Radiographic Evaluation

Radiographic assessment of the anatomy and function of the esophagus and stomach is one of the most

important aspects of the esophageal evaluation, provided the surgeon has a working knowledge of

esophageal physiology. Classically, the barium esophagram has been described as a road map for the

esophagus. The first diagnostic test in patients with suspected esophageal disease should be a barium

swallow that includes a full assessment of the stomach and the duodenum.39 Video recording of the

study greatly aids in the evaluation by providing the surgeon with a real-time visualization of bolus

transport and the size and reducibility of the hiatal hernia. The study also provides anatomic

information, such as the presence of obstructing lesions and structural abnormalities of the foregut.

The pharynx and the UES are evaluated in the upright position, allowing assessment of the timing and

coordination of the events of pharyngeal transit.40 This includes oropharyngeal bolus transport,

pharyngeal contraction, opening of the pharyngoesophageal segment, and degree of airway protection

during swallowing. It readily identifies a diverticulum, stasis of the contrast medium in the valleculae,

cricopharyngeal bar, or narrowing of the pharyngoesophageal segment. These are anatomic

manifestations of neuromuscular disease and result from the loss of muscle compliance from the

deinnervation of the skeletal muscle of the pharynx and the cervical esophagus.41

The assessment of bolus transport on video esophagography often adds to or complements the

information obtained by esophageal manometry. Esophageal clearance is optimally assessed by

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observing several individual swallows of barium with the patient in both the upright and supine

positions; the study can be performed with both liquid and solid bolus material. During normal

swallowing, a primary peristaltic wave is generated that completely strips the bolus out of the

esophagus and into the stomach. Residual material rarely stimulates a secondary peristaltic wave;

rather, an additional pharyngeal swallow is usually required.

The protocol developed and utilized at the authors’ institution has previously been reported.42 Normal

subjects in the prone position should be able to clear at least three of five 10-mL liquid barium boluses

with one swallow and have only one episode of proximal escape or distal retention of a barium bolus

with the five swallows. Normal subjects can also clear a solid barium bolus with four or fewer swallows

in the upright position. Motility disorders with disorganized or simultaneous esophageal contraction

give a segmented appearance to the barium column. This can often give a beading or corkscrew

appearance to the barium within the esophagus. In patients with dysphagia, the use of a bariumimpregnated marshmallow, piece of bread, or hamburger can identify an esophageal transport

disturbance that is not evident on the liquid barium study. A 13-mm barium tablet is another useful

adjunct that can be used to determine how well solid material can clear the esophagus, and identify

areas of clinically significant narrowing since solid food dysphagia typically is present with luminal

narrowing below 13 mm.

A hiatal hernia is present in a high percentage of patients with gastroesophageal reflux.43 These are

best demonstrated with the patient in the prone position; the increased intra-abdominal pressure

produced in this position promotes displacement of the hernia above the diaphragm. The hiatal hernia is

an important component of the underlying pathophysiology of reflux. A large (>5 cm) or irreducible

hiatal hernia may be associated with chronic reflux and esophageal foreshortening. The diagnosis of

reflux disease is not accurately made on video esophagram. Spontaneous reflux to the level of the

thoracic inlet seems to correlate with a positive pH test, but evoked reflux and spontaneous reflux into

the distal esophagus are not. Moreover, failure to observe reflux during a video esophagram does not

indicate the absence of disease.

A full-column technique with distention of the esophageal wall can discern extrinsic compression of

the esophagus, and a fully distended esophagogastric region is necessary to identify narrowing from a

Schatzki ring, stricture, or obstructing lesion. Mucosal relief or double-contrast films can be obtained to

enhance the detection of small neoplasms, esophagitis, and varices. Assessment of the stomach and

duodenum during the barium study is helpful for the evaluation of the patient with esophageal

symptoms (ESs). A gastric or duodenal ulcer, a neoplasm, or poor gastroduodenal transit can mimic

many of the symptoms that are suggestive of an esophageal disorder.

Endoscopic Examination

Endoscopic evaluation of the esophagus is essentially the physical examination of the foregut. It is a

critical part of the assessment of a patient with esophageal disease and is indicated in essentially every

patient who is being evaluated for GERD. A barium study obtained before esophagoscopy is helpful to

the endoscopist by directing attention to locations of subtle change and alerting the examiner to such

potential danger spots as a cervical vertebral osteophyte, an esophageal diverticulum, a deeply

penetrating ulcer, or a carcinoma. Regardless of the radiologist’s interpretation of an abnormal finding,

each structural abnormality of the esophagus should be examined visually with an endoscope.

During every endoscopic examination, the locations of three specific landmarks are routinely obtained

relative to the front incisors: the squamocolumnar junction, gastroesophageal junction, and the

diaphragmatic crura. The crura are usually evident by having the patient sniff. The gastroesophageal

junction is the location at which the gastric rugal folds meet the tubular esophagus; it is normally

aligned with the squamocolumnar junction. The squamocolumnar junction is the location at which the

velvet and darker rose-colored columnar epithelium changes to the lighter squamous epithelium. When

this junction is not clear, narrow band imaging (NBI), a feature that is standard on all modern

endoscopic systems, is extremely helpful in distinguishing columnar from squamous mucosa. Particular

effort should be made to detect any tongues, islands, or a circumferential segment of columnar-lined

esophagus (CLE) in the distal esophagus.

When erosive esophagitis is found, an objective grading system should be utilized to communicate the

severity of the findings. Currently, the Los Angeles classification is the most commonly utilized

system.44 Grade A is defined as one or more mucosal break ≤5 mm that does not extend between the

tops of mucosal folds. Grade B is defined as one or more mucosal break >5 mm that does not extend

between the tops of the mucosal folds. Grade C is defined as one or more mucosal break that is

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