A zone of high pressure can be identified at the junction of the esophagus and stomach. This lower esophageal sphincter provides 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 pressure as a pressure transducer is pulled from the stomach into the esophagus. This 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, it is eliminated to allow venting of the gas (a belch). The common denominator for virtually all episodes of GE reflux, whether physiologic or pathologic, is the loss of the normal 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. In severe disease, this is usually due to the permanent nonexistent or a reduced high pressure zone. In early disease or normal subjects, loss of the high-pressure zone is transient.
Three characteristics of the LES maintain its resistance or barrier function to intragastric and intraabdominal pressure challenges. These are its pressure, its overall length, and the length exposed to the positive-pressure environment of the abdomen. The tonic resistance of the LES is a function of both its pressure and the length over which this pressure is exerted. The shorter the overall length of the high-pressure zone, the higher the pressure must be to maintain sufficient resistance to remain competent. Consequently, a normal sphincter pressure can be nullified by a short overall sphincter length. 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 LES is its position, in that a portion of the overall length of the high-pressure zone should be exposed to positive intraabdominal pressure. During periods of increased intraabdominal pressure, the resistance of the LES would be overcome if the abdominal pressure were not applied equally to the high-pressure zone and stomach. Think of sucking on a soft soda straw immersed in a bottle of carbonated beverage; 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 intraabdominal pressure by collapsing and reflux is more likely to result.
If the pressure in the high-pressure zone is abnormally low, the overall length is short, or the zone is minimally exposed to the abdominal pressure environment in the fasting state, then the LES resistance is permanently lost, and the reflux of gastric contents into the esophagus is unhampered throughout the circadian cycle. A permanently defective sphincter is thus identified by one or more of the following characteristics: a high-pressure 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. In comparison with values in normal subjects, these values are below the percentile for each parameter. The most common cause of a permanently defective sphincter is an inadequate abdominal length, likely secondary to the near ubiquitous presence of a hiatal hernia in patients with GERD.
For the clinician, the finding of a permanently defective sphincter has several implications. Foremost, it is almost always associated with esophageal mucosal injury and predicts that the patient symptoms will be difficult to control with medical therapy. It is a signal that surgical therapy is likely to be needed for consistent and long-term control of the patient's symptoms. 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, 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.
A transient loss of the high-pressure zone can also occur and usually results from a functional problem of the gastric reservoir. Excessive air swallowing or food can result in gastric dilatation, and if the active relaxation reflex has been lost, an increased intragastric pressure. When the stomach is distended, the vectors produced by gastric wall tension pull on the GE junction with a force that varies according to the geometry of the cardia; that is, the forces are applied more directly when a hiatal hernia exists than when a proper angle of His is present. The forces pull on the terminal esophagus, causing it to be taken up into the stretched fundus and thereby reducing the length of the high-pressure zone or sphincter. This process continues until a critical length is reached, usually about 1 to 2 cm, when the pressure drops precipitously and reflux occurs. The mechanism by which gastric distention contributes to shortening of the length of the high-pressure zone, so that its pressure drops and reflux occurs, provides a mechanical explanation for transient relaxations of the LES without invoking a neuromuscular reflex. Rather than a spontaneous muscular relaxation, there is a mechanical shortening of the high-pressure zone, secondary to progressive gastric distention, to the point where it becomes incompetent. These transient sphincter shortenings occur in the initial stages of GERD and are the mechanism for the early complaint of excessive postprandial reflux. After gastric venting, the length of the high-pressure zone is restored and competence returns until distention again shortens it and encourages further venting and reflux. This sequence results in the common complaints of repetitive belching and bloating in patients with GERD. The increased swallowing frequency seen in patients with GERD contributes to gastric distention and is due to their repetitive ingestion of saliva in an effort to neutralize the acid refluxed into their esophagus. Thus, GERD may begin in the stomach, secondary to gastric distention resulting from overeating and the increased ingestion of fried foods, which delay gastric emptying. Both characteristics are common in Western society and may explain the high prevalence of the disease in the Western world.