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Gastroesophageal reflux disease (GERD) is one of the most common disorders seen in the general population. Approximately 10% of the population experiences heartburn daily, 15% in any given week, and about half of all people experience it any given year.1 The spectrum of disease may vary from occasional postprandial substernal discomfort, to development of peptic stricture or even development of carcinoma in the setting of Barrett esophagus. Physicians should identify and select for treatment those patients at risk of developing complications. This chapter covers the etiology, diagnosis, complications, and treatment of GERD.
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NORMAL ANATOMY AND PHYSIOLOGY
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The esophagus is lined by layers of stratified nonkeratinizing squamous epithelium. The squamous epithelium is divided into three layers, superficial, intermediate, and basal. The basal cell layer comprises 15% of the epithelium thickness and is the only layer that normally contains mitotic figures. The lamina propria is deep to these layers and contains glandular structures similar to those found in the gastric cardia. Superficial to the epithelium is a layer of mucus with surface bicarbonate. Glands that produce mucus exist in the proximal esophagus and near the gastroesophageal (GE) junction. The mucus reaches the intervening layers of the esophagus through peristalsis. Unlike the stomach, this layer is rudimentary and provides little protection against prolonged acid exposure.
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The sensation of “heartburn” or discomfort from reflux is transmitted via spinal splanchnic afferent nerves. These sensations may be modulated by vagal afferent nerves. Peristalsis in association with a series of high-pressure zones allows for the forward movement of contents into the stomach and retards the return of contents into the esophagus. The intrinsic lower esophageal sphincter (LES) and its extrinsic components are mainly responsible for preventing the reflux of gastric contents into the esophagus (Fig. 37-1). The LES can be identified by intraluminal manometry as a zone of high pressure 2 to 4 cm in length at the GE junction. A ringed circular muscle is present at this junction. The vessel density and amount of connective tissue is greater in LES muscle than in the remainder of the esophagus. Mitochondria and smooth endoplasmic reticulum also exist in greater density in this area.
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The LES exerts a resting basal pressure in normal individuals. Contributing to this resting tone is the tonic muscular contraction that is the hallmark of the LES and distinguishes it from the esophageal body. Inhibition of LES contraction is mediated largely through nitric oxide, while excitation is mediated through acetylcholine. Ablation of all neural input still leaves the LES with its intrinsic basal smooth muscle tone. This muscular tone is not distributed evenly throughout the LES. The pressure is greatest in the lowest 2 cm of the LES and is greater on the left side where ...