The pathologic hallmark of GERD is the development of reflux-related esophageal injury. The symptoms of heartburn, painful swallowing, and atypical chest pain commonly relate to the presence of this esophageal mucosal irritation. Inadequate function of the lower esophageal sphincter mechanism leading to an excessive amount of gastric acid reflux into the esophagus is the most common pathologic component causing esophageal mucosal injury (esophagitis); however, other abnormalities of esophagogastric function can also contribute to pathologic esophageal acid exposure. Possible abnormality in any of the several components of the normal esophageal mucosal defense system must be considered when evaluating the patient with reflux-induced esophagitis. (Figure 1) We will briefly describe other components of this "defense" system and the possible aberrations that can contribute to the esophageal injury pattern associated with GERD. (Table 1)

Table 1 - Physiologic alterations contributing to GERD

Salivary volume and bicarbonate concentration Esophageal body acid clearance (esophageal peristalis) Integrity of the physiologic lower esophageal sphincter Gastric acid secretion Duodenal gastric reflux of biliary contents Gastric outlet obstruction from peptic ulcer disease

Salivary volume and bicarbonate is increased during the cephalic phase of the gastric acid stimulation. This salivary response reduces the temporal acid exposure to the esophagus during the initial phase of mastication and the normal relaxation response of the lower esophageal sphincter to swallowing. Patients with reduced salivary output (e.g., Sjogren's syndrome, patient undergoing major head and neck surgery or cervical radiation treatment) can have a greater susceptibility to acid-peptic reflux esophagitis.

A second component to the esophageal mucosal defense system is the peristaltic stripping wave of the esophageal body. Impaired esophageal peristalsis often seen with scleroderma, other connective tissue disorder syndromes, and acha-lasia of the esophagus can lead to prolonged acid reflux exposure. In these circumstances of impaired esophageal motility, the ineffective clearance of even small amounts of gastric acid refluxed into the esophagus can lead to esophageal mucosal injury.

Figure 1 - Illustration of the various components to pathologic esophageal injury from GERD

A third potential etiologic factor leading to esophageal irritation is an excessive volume and concentration of acid secreted by the stomach. A minority of patients suffering from GERD are "acid hypersecretors." This increased acid secretion can also overwhelm the defense system and lead to peptic ulceration of the stomach, duodenum and esophagus. Gastric outlet obstruction related to peptic ulceration and/or impaired gastric emptying from other causes (idiopathic or diabetes-related gastroparesis) must also be ruled out in patients identified with significant esophagitis. Mechanical aspects of poor gastric emptying leads to an increased propensity for esophageal reflux. Gastric distention associated with these problems stimulates increased gastric acid production. Thus a variety of pathologic mechanisms may be at play in precipitating the esophageal mucosal injury associated with GERD.

Physicians and surgeons attending to patients with reflux esophagitis must look into all of the potential components that may lead to the esophageal mucosal injury. Along these lines, it is important to recognize that anti-reflux surgery only addresses correction of the impairment in the lower esophageal sphincter mechanism. The presence of any of the other components to the esophagitis algorithm mandates careful independent management. In some instances, correction of these other associated problems can obviate the need to consider anti-reflux surgery for the patient's GERD.

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