or in a chair. This symptom is often less well relieved with antacids or antisecretory agents, although it

may change in character from acidic to a more “bland” nature.

Dysphagia is generally manifested by a sensation of food hanging up in the esophagus rather than

difficulty transferring the bolus from the mouth to the esophageal inlet (oropharyngeal dysphagia).

Classically, dysphagia limited to only solid food, with normal passage of liquids, suggests a mechanical

disorder such as a large hernia, stricture, or tumor, whereas difficulty with both solids and liquids

suggests a functional or motor disorder such as achalasia. Dysphagia often develops slowly enough that

the patient may adjust his or her eating habits and not be particularly alarmed or aware of the problem.

Thus, a thorough esophageal history includes an assessment of the patient’s dietary history. Questions

should be asked regarding the consistency of food that is typically eaten and whether the patient

requires liquids with the meal, is the last to finish, has interrupted a social meal, chokes or vomits with

eating, or has been admitted on an emergency basis for food impaction. These assessments, in addition

to the ability to maintain nutrition, help to quantify the dysphagia and are important in determining the

indications for surgical therapy.

Many patients with GERD often manifest “atypical” or extraesophageal symptoms, such as cough,

asthma, hoarseness, and noncardiac chest pain. Atypical symptoms are the primary complaint in 20% to

25% of patients with GERD and are secondarily present in association with heartburn and regurgitation

in many more. It is considerably more difficult to prove a cause-and-effect relationship between atypical

symptoms and GE reflux than it is to do so for the typical symptoms, and the etiology of these

symptoms is often multifactorial. Often a trial of high-dose PPIs is helpful, but it takes several months

to evaluate the full impact of the therapy since if GERD is causing the inflammation that leads to the

symptoms, it takes time for that inflammation to improve or resolve with GERD therapy. Antireflux

surgery can provide excellent symptom relief in these patients, but careful testing to document GERD is

critical particularly in those with little or no response to medical therapy.

The diagnosis of GERD based on symptoms alone is correct in only approximately two-thirds of

patients.78 This is because these symptoms are not specific for GE reflux and can be caused by other

diseases such as achalasia, diffuse spasm, esophageal carcinoma, pyloric stenosis, cholelithiasis, gastritis,

gastric or duodenal ulcer, and coronary artery disease. This fact underscores the need for objective

diagnosis before the decision is made for surgical treatment.

Physiology of the Antireflux Barrier

The common denominator for virtually all episodes of gastroesophageal reflux, whether physiologic or

pathologic, is the loss of the normal gastroesophageal high-pressure zone and the resistance it imposes

to the flow of gastric juice from an environment of higher pressure, the stomach, to an environment of

lower pressure, the esophagus. This barrier, composed of both anatomic (flap valve and diaphragm) and

physiologic (LES) components, acts to prevent reflux during stressed and unstressed conditions. The key

determinates of the barrier include:

1. The frequency of swallow- and non–swallow-induced transient relaxations of the LES

2. The structural integrity of the LES

3. Anatomic alterations of the diaphragmatic crura and gastroesophageal flap valve represented by the

angle of His

The presence or absence of pathologic esophageal acid exposure (i.e., abnormal 24-hour pH studies) is

not only influenced by the degree of barrier loss but also by esophageal and gastric functional

characteristics including esophageal clearance, intra-abdominal pressure, and gastric emptying

abnormalities.

Transient Relaxation of the Lower Esophageal Sphincter

The lower esophageal high-pressure zone is normally present except in two situations: (a) after a

swallow, when it momentarily relaxes to allow passage of food into the stomach, and (b) when the

fundus is distended with gas, and it is reflexly relaxed to allow venting of the gas (a belch). In 1982,

Dodds et al.79 reported that non–swallow-induced transient relaxations of the lower esophageal

sphincter (TLESRs) were a significant mechanism of gastroesophageal reflux in normal individuals and

patients with GERD. These spontaneous relaxations occurred without pharyngeal contraction, were

prolonged (>10 seconds), and, when reflux occurred, were associated with relaxation of the crural

diaphragm. Underscoring the importance of the crural diaphragm to barrier integrity, Mittal et al.80

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later showed that pharmacologic elimination of lower esophageal sphincter pressure to zero did not

result in reflux unless crural diaphragmatic contraction was also absent. Gastric distention, upright

posture, and meals high in fat have all been shown to increase the frequency of TLESRs.80,81 The latter

observations suggest that unfolding of the sphincter may be responsible for the loss of sphincter

pressure.

As a result of these findings, TLESRs became commonly accepted as the major mechanism of

gastroesophageal reflux regardless of the underlying severity of disease, despite evidence to the

contrary. The facts that in over 80% of patients with symptomatic gastroesophageal reflux a hiatal

hernia could be identified and that most patients with erosive esophagitis and Barrett esophagus had

incompetent lower esophageal sphincter characteristics at rest were largely ignored by many. When

these facts are taken into account, particularly in association with the known characteristics of TLESRs,

it seems likely that transient relaxations are (a) a physiologic response to gastric distention by food or

gas, (b) the mechanism of belching, and (c) responsible for physiologic reflux episodes in individuals

with normal lower esophageal sphincter and hiatal anatomy, but not the primary mechanism of GERD.

Evidence supporting this has been provided via studies of Van Herwaarden et al.,82 in which ambulatory

esophageal manometry and esophageal pH monitoring were performed on patients with and without

hiatal hernia. Patients with hiatal hernia had greater esophageal acid exposure and more reflux

episodes, but the frequency of TLESRs, and the proportion associated with reflux, was similar in both

groups. They concluded that excess reflux in patients with GERD and hiatal hernia is caused by a

combination of low LES pressure, swallow-induced relaxation, and straining.

Structural Integrity of the Lower Esophageal Sphincter

In humans a zone of high pressure can be identified at the junction of the esophagus and stomach. This

lower esophageal “sphincter” provides an important component of the barrier between the esophagus

and stomach that normally prevents gastric contents from entering the esophagus. It has no anatomic

landmarks, but its presence can be identified by a rise in pressure over gastric baseline as a pressure

transducer is pulled from the stomach into the esophagus.

There are three characteristics of the lower esophageal sphincter that maintain its resistance or

barrier function to intragastric and intra-abdominal pressure challenges. They are its pressure, its

overall length, and the length exposed to the positive pressure environment of the abdomen (Table 42-

1). The tonic resistance of the lower esophageal sphincter is a function of both its pressure and the

length over which this pressure is exerted.21 The shorter the overall length of the high-pressure zone,

the higher the pressure must be to maintain sufficient resistance to remain competent (Fig. 42-13).

Consequently, a short overall sphincter length can nullify a normal sphincter pressure.12 Further, as the

stomach fills, the length of the sphincter decreases, rather like the neck of a balloon shortening as the

balloon is inflated. If the overall length of the sphincter is abnormally short when the stomach is empty,

then with minimal gastric distention there will be insufficient sphincter length for the existing pressure

to maintain sphincter competency, and reflux will occur.

The third characteristic of the lower esophageal sphincter is its position, in that a portion of the

overall length of the high-pressure zone should be exposed to positive intra-abdominal pressure. During

periods of increased intra-abdominal pressure, the resistance of the lower esophageal sphincter would

be overcome if the abdominal pressure were not applied equally to the high-pressure zone and stomach.

This is akin to sucking on a soft soda straw immersed in a bottle of Coke; the hydrostatic pressure of the

fluid and the negative pressure inside the straw due to sucking cause the straw to collapse instead of

allowing the liquid to flow up the straw in the direction of the negative pressure. If the abdominal

length is inadequate, the sphincter cannot respond to an increase in applied intra-abdominal pressure by

collapsing, and reflux is more liable to result. If the high-pressure zone has an abnormal low pressure, a

short overall length, or minimal exposure to the abdominal pressure environment in the fasting state,

then there is a permanent loss of lower esophageal sphincter resistance and the unhampered reflux of

gastric contents into the esophagus throughout the circadian cycle. This is referred to as a permanently

defective sphincter and is identified by having one or more of the following characteristics: a highpressure zone with an average pressure of less than 6 mm Hg, an average overall length of 2 cm or less,

and an average length exposed to the positive pressure environment of the abdomen of 1 cm or less.83

Compared with normal subjects, these values are below the 2.5th percentile for each parameter. The

most common cause of a permanently defective sphincter is an inadequate abdominal length, most

likely a consequence of the development of a hiatal hernia. It is important to note that an inadequate

abdominal length or an abnormally short overall length can nullify the efficiency of a sphincter with a

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normal pressure.

The presence of a permanently defective sphincter has several implications. First, it is commonly

associated with esophageal mucosal injury and predicts that the patient’s symptoms may be difficult to

control with medical therapy.23,34 It is now accepted that when the sphincter is permanently defective,

it is irreversible, even when the associated esophagitis is healed. The presence of a permanently

defective sphincter is commonly associated with reduced esophageal body function,84 and if the disease

is not brought under control, the progressive loss of effective esophageal clearance can lead to severe

mucosal injury, repetitive regurgitation, aspiration, and pulmonary failure.

Anatomic Alterations

With the advent of clinical roentgenology, it became evident that a hiatal hernia was a relatively

common abnormality although not always accompanied by symptoms. Philip Allison, in his classic

treatise published in 1951, suggested that the manifestations of GERD were caused by the presence of a

hiatal hernia. For most of the next two decades, hiatal hernia was considered the primary

pathophysiologic abnormality leading to GERD. Indeed, the Allison repair, among the first surgical

attempts to treat GERD, consisted of a hernia repair only. As techniques of esophageal manometry were

developed in the late 1950s and 1960s, allowing identification and study of the lower esophageal

sphincter, attention was slowly diverted away from the hernia as the main pathophysiologic

abnormality of GERD. In 1971, Cohen and Harris

85 published a study of the contributions of hiatal

hernia to lower esophageal sphincter competence in 75 patients, concluding that hiatal hernia had no

effect on GE junction competence. This paper, published in the New England Journal of Medicine, and the

growing use of esophageal manometry shifted the emphasis away from the hernia almost exclusively

toward features of the lower esophageal sphincter as the primary abnormality in symptomatic GERD.

Perhaps serendipitously, studies of the phenomenon of TLESRs identified the diaphragmatic crura as

an important factor in preventing reflux during periods of loss of LES pressure.86 In normal subjects,

even with absent LES pressure, reflux does not occur without relaxation of the crural diaphragm.

Coincidentally, Hill et al.87 stressed the importance of the physiologic flap valve created by the angle of

His as a barrier to gastroesophageal reflux. The endoscopic appearance of the flap valve can be

correlated with abnormal esophageal acid exposure, emphasizing that the geometry of the

gastroesophageal region is also important to barrier competence.47 If mechanical forces set in play by

gastric distention are important in pulling on the terminal esophagus and shortening the length of the

high-pressure zone or “sphincter,” then the geometry of the cardia, that is, the presence of a normal

acute angle of His or the abnormal dome architecture of a sliding hiatus hernia, should influence the

ease with which the sphincter is pulled open. Evidence that this occurs was provided by Ismail et al.,16

who showed a close relationship between the degree of gastric distention necessary to overcome the

high-pressure zone (yield pressure) and the morphology of the cardia (Fig. 42-25). No relationship

between the yield pressure and lower esophageal sphincter resting pressure and length was found. A

higher intragastric pressure was needed to open the sphincter in patients with an intact angle of His

when compared to patients with a hiatal hernia. The presence of a hiatal hernia also disturbs esophageal

clearance mechanisms likely due to loss of anchorage of the esophagus in the abdomen. Kahrilas et al.

have shown that complete esophageal emptying was achieved in 86% of swallows in control subjects

without a hiatal hernia, 66% in patients with a reducing hiatal hernia, and only 32% of patients with a

nonreducing hiatal hernia.88 Impaired clearance in patients with nonreducing hiatal hernias further

supports the contribution of hiatal hernia to the pathogenesis of GERD. Thus, present evidence is

overwhelming that hiatal hernia does indeed play a significant, if not primary, role in the

pathophysiology of GERD.

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