Gastroesophageal Reflux Disease (GERD) (cont.)
Charles Patrick Davis, MD, PhD
Charles Patrick Davis, MD, PhD
Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.
In this Article
What causes GERD?
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The cause of GERD is complex. There probably are multiple causes, and different causes may be operative in different individuals or even in the same individual at different times. A small number of patients with GERD produce abnormally large amounts of acid, but this is uncommon and not a contributing factor in the vast majority of patients. The factors that contribute to GERD are lower esophageal sphincter abnormalities, hiatal hernias, abnormal esophageal contractions, and slow or prolonged emptying of the stomach.
Lower esophageal sphincter
The action of the lower esophageal sphincter (LES) is perhaps the most important factor (mechanism) for preventing reflux. The esophagus is a muscular tube that extends from the lower throat to the stomach. The LES is a specialized ring of muscle that surrounds the lower-most end of the esophagus where it joins the stomach. The muscle that makes up the LES is active most of the time. This means that it is contracting and closing off the passage from the esophagus into the stomach. This closing of the passage prevents reflux. When food or saliva is swallowed, the LES relaxes for a few seconds to allow the food or saliva to pass from the esophagus into the stomach, and then it closes again.
Several different abnormalities of the LES have been found in patients with GERD. Two of them involve the function of the LES. The first is abnormally weak contraction of the LES, which reduces its ability to prevent reflux. The second is abnormal relaxations of the LES, called transient LES relaxations. They are abnormal in that they do not accompany swallows and they last for a long time, up to several minutes. These prolonged relaxations allow reflux to occur more easily. The transient LES relaxations occur in patients with GERD most commonly after meals when the stomach is distended with food. Transient LES relaxations also occur in individuals without GERD, but they are infrequent.
The most recently-described abnormality in patients with GERD is laxity of the LES. Specifically, similar distending pressures open the LES more in patients with GERD than in individuals without GERD. At least theoretically, this would allow easier opening of the LES and/or greater backward flow of acid into the esophagus when the LES is open.
Hiatal hernias contribute to reflux, although the way in which they contribute is not clear. A majority of patients with GERD have hiatal hernias, but many do not. Therefore, it is not necessary to have a hiatal hernia in order to have GERD. Moreover, many people have hiatal hernias but do not have GERD. It is not known for certain how or why hiatal hernias develop.
Normally, the LES is located at the same level where the esophagus passes from the chest through the diaphragm and into the abdomen. (The diaphragm is a muscular, horizontal partition that separates the chest from the abdomen.) When there is a hiatal hernia, a small part of the upper stomach that attaches to the esophagus pushes up through the diaphragm. As a result, a small part of the stomach and the LES come to lie in the chest, and the LES is no longer at the level of the diaphragm.
It appears that the diaphragm that surrounds the LES is important in preventing reflux. That is, in individuals without hiatal hernias, the diaphragm surrounding the esophagus is continuously contracted, but then relaxes with swallows, just like the LES. Note that the effects of the LES and diaphragm occur at the same location in patients without hiatal hernias. Therefore, the barrier to reflux is equal to the sum of the pressures generated by the LES and the diaphragm. When the LES moves into the chest with a hiatal hernia, the diaphragm and the LES continue to exert their pressures and barrier effect. However, they now do so at different locations. Consequently, the pressures are no longer additive. Instead, a single, high-pressure barrier to reflux is replaced by two barriers of lower pressure, and reflux thus occurs more easily. So, decreasing the pressure barrier is one way that a hiatal hernia can contribute to reflux.
There is a second way in which hiatal hernias might contribute to reflux. When a hiatal hernia is present, there is a hernial sac, which is a small pouch of stomach above the diaphragm. The sac is pinched off from the esophagus above by the LES and from the stomach below by the diaphragm. What's important about this situation is that the sac can trap acid that comes from the stomach. This trap keeps the acid close to the esophagus. As a result, it is easier for the acid to reflux when the LES relaxes with a swallow or a transient relaxation.
Finally, there is a third way in which hiatal hernias might contribute to reflux. The esophagus normally joins the stomach obliquely, which means not straight on or at a 90-degree angle. Due to this oblique angle of entry, a flap of tissue is formed between the stomach and esophagus. This flap of tissue is believed to act like a valve, shutting off the esophagus from the stomach and preventing reflux. When there is a hiatal hernia, the entry of the esophagus into the stomach is pulled up into the chest. Therefore, the valve-like flap is distorted or disappears and it no longer can help prevent reflux.
As previously mentioned, swallows are important in eliminating acid in the esophagus. Swallowing causes a ring-like wave of contraction of the esophageal muscles, which narrows the lumen (inner cavity) of the esophagus. The contraction, referred to as peristalsis, begins in the upper esophagus and travels to the lower esophagus. It pushes food, saliva, and whatever else is in the esophagus into the stomach.
When the wave of contraction is defective, refluxed acid is not pushed back into the stomach. In patients with GERD, several abnormalities of contraction have been described. For example, waves of contraction may not begin after each swallow or the waves of contraction may die out before they reach the stomach. Also, the pressure generated by the contractions may be too weak to push the acid back into the stomach. Such abnormalities of contraction, which reduce the clearance of acid from the esophagus, are found frequently in patients with GERD. In fact, they are found most frequently in those patients with the most severe GERD. The effects of abnormal esophageal contractions would be expected to be worse at night when gravity is not helping to return refluxed acid to the stomach. Note that smoking also substantially reduces the clearance of acid from the esophagus. This effect continues for at least 6 hours after the last cigarette.
Emptying of the stomach
Most reflux during the day occurs after meals. This reflux probably is due to transient LES relaxations that are caused by distention of the stomach with food. A minority of patients with GERD, about 20%, has been found to have stomachs that empty abnormally slowly after a meal. The slower emptying of the stomach prolongs the distention of the stomach with food after meals. Therefore, the slower emptying prolongs the period of time during which reflux is more likely to occur.
In addition to the above, some medications may cause or worsen GERD. Some common medications that may have this effect include anticholinergics, antihypertensives such as beta blockers or calcium channel blockers, bronchodilators, dopamine-active drugs, progestin, sedatives, and tricyclic antidepressants. Individuals should not stop taking these or any drugs that are prescribed until the prescribing doctor has discussed the potential GERD situation with the them.
Reviewed by Charles Patrick Davis, MD, PhD on 12/23/2011
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