This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on Web of Science (26)  • Contact me when this article is cited  Related Content  • Similar articles in this journal  Social Bookmarking   What's this?

GORDON M. CARVER, Jr., M.D.; W. C. SEALY, M.D.

AMA Arch Surg. 1954;68(3):286-295.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

THE PATIENT with peptic esophagitis has long been neglected, allowing progression of the disease to chronic ulceration, fibrosis, and stricture. This neglect has been due to a failure of appreciation of the pathogenesis and clinical course of the disease and an ineffective therapeutic program.

Peptic esophagitis is an inflammatory process of the esophagus which occurs when there is a persistent association of gastric or intestinal secretions with the nonresistant squamous mucosa of the esophagus.¹ The reflux of these secretions into the esophagus is due to nonfunction or failure of the cardiac sphincter mechanism. This is usually caused by an associated sliding hiatus hernia, persistent vomiting, or the surgical excision or disruption of the cardiac sphincter (Table 1).

The major factors involved in the prevention of regurgitation into the esophagus by the cardiac sphincter can be identified. The inferior constrictor muscle of the esophagus and the oblique gastric muscles about . . . [Full Text PDF of this Article]

Author Affiliations
DURHAM, N. C.

From the Division of Thoracic Surgery, Duke University School of Medicine.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?