Several factors must work in concert to produce clinical effects of esophageal reflux. Normal subjects may have a few short-duration reflux episodes postprandially and in the upright position. Those in whom reflux has produced symptoms or pathologic changes will demonstrate more frequent and prolonged episodes of reflux, which also tend to occur at night. The factor or factors that cause this difference are not entirely known. However, important differences between persons with and without reflux might help explain these findings.
The LES is a specialized bundle of circular muscle at the lower end of the esophagus with different physical and pharmacologic characteristics when compared with the circular muscle above and below it. Although mean LES pressure is significantly lower in subjects with GERD than in normal persons, much overlap occurs between the groups; LES pressure is not very useful in predicting whether reflux is present in an individual patient unless the pressure is very low. The most common event associated with reflux appears to be a transient relaxation of the LES unassociated with either swallowing or the distention of the esophageal body by refluxed fluid. Thus, two abnormalities of LES may be associated with reflux: a sphincter with very low tone, as measured by LES pressure, or inappropriate relaxation of a normally competent sphincter.
Several factors are important in removing refluxed material from the esophagus. The upright position facilitates esophageal emptying by gravity. Peristaltic waves initiated by swallowing or by esophageal distention help remove the refluxed material. Acid placed within the esophagus is cleared less well by patients with GERD than by normal subjects, although the manometric tracings seen in both groups seem identical. Clearing of acid regurgitation occurs in two phases: the bulk of the fluid is returned to the stomach by a peristaltic contraction, and the remaining acid film clinging to the esophageal wall is neutralized by swallowed saliva.
The composition and perhaps the quantity of the refluxed material also play a role in the production of GERD. Gastric acid and pepsin seem clearly important in the pathogenesis of GERD. Bile salts, and possibly pancreatic enzymes, may be responsible in patients in whom acid is absent. The combination of bile salts plus acid is more injurious to the esophagus than either agent alone. Other less well-studied factors, such as altered or abnormal esophageal mucus, swallowed saliva of high bicarbonate content, and diminished resistance of the esophageal mucosa to digestion, may be important in determining the amount of mucosal damage in GERD.
Esophageal squamous epithelium reacts to reflux by an increase in the basal cell or germinative layer. The dermal pegs are increased in height and may become more vascular. If the process becomes more severe, the epithelial layer is destroyed, with the appearance of micro-ulcers and classic signs of inflammation in the lamina propria, such as infiltration with polymorphonuclear leukocytes and edema. Even deeper lesions cause first submucosal and then muscular inflammation and fibrosis, resulting in an esophageal stricture. Why reflux is so common, yet inflammation and stricture formation are relatively uncommon, is not known.
Reflux during pregnancy, once thought to be due to the increased abdominal pressure from the fetus, may be due mainly to diminished LES strength caused by increased estrogen and progesterone. Weight gain also tends to aggravate reflux through an unknown mechanism. Resection of the lower esophageal area for cancer or myotomy for achalasia can lead to severe postoperative reflux. Gastroesophageal reflux with stricture formation is especially severe in patients with progressive systemic sclerosis.
The crural diaphragm usually wraps around the gastroesophageal junction to augment the intrinsic LES. In a hiatal hernia, an anatomic displacement of the LES and crural diaphragm is seen. Although hiatal hernias may be associated with reflux, the presence of a hiatal hernia is now considered to be much less of a factor in GERD than previously thought, because it is present in a large percentage of normal subjects. It is not appropriate to spend time trying to define whether a hiatal hernia is present or absent in dealing with most patients with GERD; rather, the focus should be on the symptoms of reflux.
Labels: Acid Reflux Causes