Transmigration of the lower esophageal mucosa.

Abstract

From the earliest days of roentgenology the esophagogastric segment has intrigued the observer, and the anatomical landmarks have been variously interpreted by a multitude of workers. As pointed out by Cimmino (1), over a thousand papers dealing with this very small area appeared between 1930 and 1946. A variety of terms has been used to describe an appearance seen both at fluoroscopy with barium swallow and on roentgenograms, suggesting prolapse of the lower esophagus into a gastric hiatal hernia or into the gastric fundus below the diaphragm. A paper published in France in 1934 made the first mention of “invagination of the esophagus” (5). Since its appearance there have been sporadic references to the subject, almost all in the European literature. In 1951, Feldman described retrograde extrusion or prolapse of the gastric mucosa into the esophagus in 2 cases, and referred to the only other known example, reported by Wells in 1947 (11). Feldman considered the condition completely separated from hiatal hernia but noted that it might present a picture which could easily be confused with hernia (2). In the illustration of his second case, the lower esophagus presents an appearance which would now be called invagination, but no mention of this entity was made in the paper. In 1955 an Australian surgeon, K. W. Starr, reported a case in which there was incompetence of the cardioesophageal sphincter, with no hiatal hernia. At operation, cardioesophageal intussusception could easily be produced and reduced. The condition was thought to be very rare (10). Klinefelter, in 1956, added 3 cases of his own to the 11 then recorded in the world literature in which invagination occurred in hiatal hernia. In his opinion there was a greatly increased incidence of dysphagia in patients with invagination. He also believed it was usually necessary to bring the patient from the Trendelenburg to the erect position to demonstrate the invagination, a view not shared by other workers (4). After careful review, the present author feels that in the 3 cases illustrated in Klinefelter's paper no true hiatal hernia was demonstrated; in each instance esophagoscopy was negative and no surgical exploration was made. It seems likely, therefore, that invagination occurred in a normal phrenic ampulla, although the fact may not have been recognized. In June 1959, Haakon Ödegaard reported a further 8 cases of invagination of the esophagus into gastric hiatal hernia (6). The incidence in sliding hernia was found to be about 26 per cent, but no mention was made of the condition apart from hernia. This worker found no specific symptoms related to the invagination. Again, careful review of the cases illustrated suggests that invagination had frequently occurred into a prominent phrenic ampulla rather than into a hernia. Undoubtedly many cases reported by radiologists as small sliding hiatal hernias are not in fact true herniations.