Overview
The pathophysiology of GERD is complex. The antireflux barrier is created by a combination of the normal anatomical configuration of the esophagogastric junction (EG) and the strength and function of the lower esophageal sphincter (LES).
 | | Figure 4. Mechanism of gastroesophageal reflux disease. |
A weak antireflux barrier causes reflux in the majority of patients (Figure 4). Gastroesophageal reflux disease most often occurs when LES pressure (measured manometrically) is low or the normal angulation of the EG junction is lost (as occurs when a hiatus hernia is present) (Figure 5). Studies in which esophageal acidity is monitored over extended periods (continuous pH monitoring) have demonstrated that most normal individuals experience reflux on a daily basis (Figure 6).
 | | Figure 6. Continuous esophageal pH monitoring demonstrating physiological reflux. |
Physiologic reflux (reflux in normal individuals) is generally brief in duration, relatively infrequent, and occurs almost exclusively after meals and is caused by a sudden relaxation of the LES that is not induced by swallowing. This type of relaxation, called transient spontaneous LES relaxation, is also the predominant mechanism of reflux in patients with GERD. However, whereas transient spontaneous relaxation is responsible for 98% of reflux events in normal individuals, it accounts for only about 60% of reflux events in patients with reflux. Most other reflux events in patients with GERD occur when resting LES pressure is inadequate to resist the pressure within the stomach. Other factors contribute to the severity of reflux. Weak or uncoordinated esophageal contractions (perhaps occurring in response to esophageal irritation from reflux disease itself) delay esophageal clearance of refluxed material. This prolongs the duration of esophageal contact with refluxed digestive gastric contents. Saliva is an effective natural antacid. Reflux often stimulates salivation, a potentially beneficial response that enhances dilution and neutralization of refluxed gastric contents. If the rate of salivation is low, or if an individual is unable to swallow his own saliva, refluxed material remains in the esophagus for prolonged periods of time. This increases the severity of esophageal irritation and the probability of esophageal damage. Most symptoms of GERD occur because of the irritating nature of gastric contents. The severity of esophageal damage correlates fairly well with the amount of time the esophagus is bathed in refluxed acid. Patients with higher gastric acid secretion and those who reflux bile (which has entered the stomach from the duodenum), are more likely to have severe esophageal damage than those with lower gastric acid secretion and no bile in the gastric contents. An additional factor in determining reflux severity is the amount of pressure placed on the antireflux barrier. Reflux is more likely to occur after eating, while lying down, and when there is delayed gastric emptying. Occasionally, impaired gastric emptying alone can cause severe gastroesophageal reflux disease.
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