Mark K. Ferguson
Humans have no doubt suffered from the symptoms and complications of gastroesophageal reflux disease (GERD) for millennia. However, recognition of a relationship between acid-pepsin and foregut disorders is relatively recent. The powerful digestive and corrosive capability of gastric juices in humans was first extensively described in 1833 by Beaumont1 as a result of experiments performed on Alexis St. Martin. That reflux of these juices into the esophagus could cause symptoms and result in tissue injury was suspected as early as 1839 by Albers, who, as reported by Tileston,2 described a peptic ulcer of the esophagus that was similar to a peptic ulcer of the stomach. Periodic reports of peptic esophageal ulcer subsequently appeared, although the existence of this phenomenon was still in doubt in the second half of the 19th century. Quincke's3 report of three well-documented cases of peptic esophageal ulceration in 1879 put all doubt to rest. Tileston2 summarized reports of 40 cases of peptic esophageal ulceration extant in the literature before 1906.
One complication of peptic ulceration, esophageal stricture, was described as early as the 15th century, and dilation for stricture was reported in the early 19th century. Endoscopy was in its infancy in the second half of the 19th century, precluding any useful direct viewing of the type or level of a stricture. The determination of the site of a stricture was based on either auscultation as fluid was swallowed, listening for a gurgling or trickling noise at the point of obstruction, or by the passage of bougies.4
Possible causes of obstructions included caustic ingestion, malignancy, webs, and, in retrospect, peptic esophagitis, although the latter etiology was rarely, if ever, suspected. In the absence of an antecedent event such as caustic ingestion, the premortem diagnosis of the etiology of esophageal obstruction was rare. By the time a patient expired from obstructive effects of a peptic stricture, the process was so advanced that detection of a relationship between stricture formation and peptic-acid injury was impossible.
The development of upper gastrointestinal endoscopy led to the premortem diagnosis of esophagitis and esophageal ulceration with some frequency. In 1929 Jackson5 described 88 cases of acute or healed esophageal ulceration identified among 4000 patients with esophageal symptoms. He correctly ascribed the pain of peptic esophageal ulcer to the effects of gastric juices bathing the ulcerated area, and discounted the prevalent notion that peristalsis was the source of esophageal pain.5 Although Jackson suggested that some of these ulcers may have been caused by gastric reflux, that claim was made strongly in the mid-1930s by Lyall,6 who described superficial esophagitis in the presence of reflux and deep esophageal ulcers associated with heterotopic mucosa, now known as Barrett's ulcers. More than 100 years after the initial description of peptic esophageal ulceration, the destructive effects of acid-pepsin on the esophagus were clearly documented.7
Anatomic problems were not generally recognized in the 19th century as being associated with GERD. In a review of case reports of 88 diaphragmatic hernias published before 1847, Bowditch8 identified esophageal hiatal hernias as being among the most common. However, all hernias within this subgroup likely were large paraesophageal hernias that had either strangulated or perforated, and none was documented as being associated with symptoms of gastroe-sophageal reflux.8 At the beginning of the 20th century, only a few of the hundreds of diaphragmatic hernias that had been reported in the literature had been diagnosed premortem.9 The discovery of X-rays in 1895 led to the rapid development of their use as a diagnostic tool, and by 1908 contrast radiography was a reliable technique for the diagnosis of hiatal hernia.10 However, the anatomic deformity and obstructive complications, not symptoms of heartburn, were the primary indication for hiatal hernia repair in the first half of the 20th century.10,11
Chronic peptic ulcer of the esophagus was first related to hiatal hernia in the early 1940s and only dietary therapy was recommended.12 The pathophysiologic mechanism of an ineffective anti-reflux mechanism resulting from hiatal hernia was suggested by Allison13,14 in 1948, who noted improvement after surgical correction of the hernia in seven patients. The relationship between hiatal hernia-associated dysfunction of the esophagogastric junction and symptoms of heartburn was then conclusively made by Allison15 in 1951 when he described the syndrome of heartburn, gastric flatulence, and postural regurgitation, and attributed it to reflux esophagitis. The understanding of this relationship ushered in the era of physiologic therapy for GERD.
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Gastroesophageal reflux disease is the medical term for what we know as acid reflux. Acid reflux occurs when the stomach releases its liquid back into the esophagus, causing inflammation and damage to the esophageal lining. The regurgitated acid most often consists of a few compoundsbr acid, bile, and pepsin.