What is the correlation of hiatal hernia and gastroesophageal reflux disease as shown by pH monitoring?
M.Y.M. Chen, D.J. Ott (Winston-Salem), F.H. Miller (Chicago)
A sliding hiatal hernia is a protrusion of the stomach located below the squamocolumnar junction through the esophageal hiatus into the chest. A hiatal hernia may change the function of crural diaphragm and phrenoesophageal ligament, which are anatomic structures that, along with the lower esophageal sphincter (LES), prevent gastroesophageal reflux. The precise relationship of hiatal hernia to gastroesophageal reflux disease (GERD) remains controversial. The presence of a hiatal hernia may affect the antireflux barrier and reduce the efficacy of esophageal acid clearance; therefore, hiatal hernia may be a causative factor promoting gastroesophageal reflux or its sequelae [1-3].
The pathogenesis of GERD is multifactorial and may involve an inadequate antireflux mechanism, volume and potency of the reflux material, esophageal mucosal resistance, and efficiency of esophageal clearance and gastric emptying [1, 4]. Hiatal hernia does not appear to be the primary cause of abnormal gastroesophageal reflux; its existence may result from functional or anatomic factors that promote excessive reflux. Hiatal hernia may increase the likelihood of LES dysfunction or may affect esophageal clearance and thus permit development or exacerbation of GERD. Further investigations are needed to clarify this potential relationship [1].
Evaluation of gastroesophageal reflux
Gastroesophageal reflux is often a normal physiologic phenomenon commonly seen when the patient is in supine position. Spencer [5] first described an esophageal probe used for prolonged pH monitoring in the esophagus in 1969. In 1974, Johnson and DeMeester [6] established 24-hour monitoring as a standard measurement for evaluating gastroesophageal reflux. Total percentage of reflux time at pH less than 4, recorded by an ambulatory recorder through a probe placed in the lower esophagus, is accepted as the most reliable criterion to evaluate abnormal reflux. Johnson et al. [7] suggested that a recorded pH of 4 or lower for more than 3.4% of the total monitoring time indicated abnormal gastroesophageal reflux. At our institution, we define 6% or more of the total monitoring time with a pH less than 4 as the transition point for abnormal gastroesophageal reflux. Reflux episodes occurring at a pH above 4, regardless of their frequency and duration, are categorized as normal. Total reflux time with a pH equal to or lower than 4 for less than 6% of the total monitoring time is considered normal.
All of above pH measurements are recorded from a probe placed 5 cm above the LES. Many investigators use two probes, one in the lower esophagus and the other in the pharynx. Any reflux episode with a pH lower than 4 from the pharyngeal probe is counted as abnormal, regardless of the length of the reflux event. However, pharyngeal reflux is not the subject of this question. The following description of the percentage of reflux time and the pH level refers to episodes that occur and were recorded from the probe placed in the lower esophagus.
Correlation of hiatal hernia and gastroesophageal reflux
The correlation between the presence of hiatal hernia and that of gastroesophageal reflux is controversial. Hiatal hernia is a common radiographic finding. Many patients with hiatal hernia do not have abnormal gastroesophageal reflux, but most patients with reflux disease do have hernias (Figures 1 and 2) [1, 8]. The presence of a hiatal hernia is a poor predictor of abnormal gastroesophageal reflux or reflux esophagitis. Conversely, hiatal hernia is present in about 90% of patients who have reflux esophagitis diagnosed by endoscopic examination [9].
Figure 1. An upper gastrointestinal study shows the barium reflux from the stomach to the mid-esophagus (reflux) and a hiatal hernia (hh).
Figure 2. Double-contrast esophagram shows a hiatal hernia (hh).
More recent studies further support an association of hiatal hernia and abnormal gastroesophageal reflux by observations that the presence of hernia delays esophageal acid clearance [2, 3]. Therefore, a higher prevalence of abnormal gastroesophageal reflux might be expected in patients with a hiatal hernia [10]. In a study of 32 patients with hiatal hernia [11], 26 patients had abnormal gastroesophageal reflux and six did not. The average reflux time at a pH lower than 4 was 23% in patients with reflux and the reflux time was 2% in patients without reflux. Reflux episodes longer than 5 minutes occurred 8 times in patients with reflux and 1.3 time in patients without reflux.
Hiatal hernia is common in patients with abnormal pH testing results. In one of our studies, the prevalence of hiatal hernia was 80% in patients with abnormal pH testing and 60% in patients with normal pH testing (p < .05) [8]. In another investigation, the mean percentage of total esophageal exposure to acid was 3.7% in patients without hiatal hernia and 5.7% in those with hiatal hernia (p < .01) [12]. In patients with no hiatal hernia, 83% of patients had normal 24-hour pH testing, whereas 69% of patients with hiatal hernia, regardless of its size, had normal pH study results (p < .05) [12].
When hiatal hernia is present, the prevalence of reflux esophagitis may be higher. In an earlier study [9], 94% of patients with reflux esophagitis had hiatal hernia, in a population with a 51% prevalence of the disease. In another study [13], 32 (50%) of a total of 64 patients with a hiatal hernia had reflux esophagitis diagnosed endoscopically, and the majority (84%) of patients (32 of 38) with reflux esophagitis had a concomitant hiatal hernia.
Figure 3. Size of hiatal hernia as determined radiographically. A. Minimal hiatal hernia (h). Radiograph shows esophagogastric junction (connected arrows) 12 mm above the esophageal hiatus (arrowheads). Esophageal vestibule (v) is located at the tubulovestibular junction or A level (curved arrow) and esophagogastric junction at the B level. B. Large hiatal hernia. Radiograph shows a mucosal ring at the esophagogastric junction (connected arrows) 3 cm above the level of esophageal hiatus (arrowheads).
Correlation of size of hiatal hernia and gastroesophageal reflux
Since the presence of hiatal hernia may affect gastroesophageal reflux, the size of hiatal hernia may also influence the prevalence of reflux. In one study [12], hiatal hernias were classified as small or large (Figure 3). Small hiatal hernia was defined as having an axial length, measured between the esophagogastric junction and the diaphragmatic hiatal impression of less than 2 cm; larger hiatal hernias were defined as 2 cm or more. The total esophageal exposure to acid was 4.8% in patients with small hiatal hernia and 6.6% in those with larger hiatal hernias. Larger hiatal hernias were associated with a higher prevalence of reflux esophagitis, but the association was not statistically significant. However, the difference in acid exposure between patients with no hiatal hernia and those with a larger hiatal hernia was significant. In the same study, 27% patients with a minimal hernia had abnormal pH monitoring, and 35% patients with a larger hernia had abnormal pH testing [12].
Correlation between the size of the hiatal hernia and the severity of reflux esophagitis has also been done [13]. There was no statistical significance between the size of the hiatal hernia and the severity of esophagitis endoscopically [13].
In summary, the presence of hiatal hernia has been postulated as one of the functional and anatomic factors that may affect LES function and esophageal clearance or promote excessive gastroesophageal reflux. However, hiatal hernia is not the main cause of abnormal gastroesophageal reflux. Hiatal hernia is a poor predictor of the presence of abnormal gastroesophageal reflux; however, most patients with GERD have an associated hiatal hernia. Further investigation is needed to clarify this potential relationship.
References
1. Ott DJ. Gastroesophageal reflux disease. Radiol Clin North Am 1994;32:1147-1166.
4. Dodds WJ. The pathogenesis of gastroesophageal reflux disease. AJR 1988;151:49-56.