Esophageal stenosis may be congenital or more commonly acquired. When acquired the narrowing generally is caused by fibrous thickening of the submucosa and atrophy of the muscularis propria. Stenosis due to inflammation and scarring may be caused by chronic gastroesophageal reflux, irradiation, ingestion of caustic agents, or other forms of severe injury. Stenosis-associated dysphagia usually is progressive; difficulty eating solids typically occurs long before problems with liquids.
http://ebooksmedicine.net
Efficient delivery of food and fluids to the stomach requires coordinated waves of peristaltic contractions. Esophageal dysmotility interferes with this process and can take several forms, all of which are characterized by discoordinated contraction or spasm of the muscularis. Because it increases esophageal wall stress, spasm also can cause small diverticula to form. Esophageal dysmotility can be separated into several forms depending on the character of the contractile abnormalities.
Achalasia is characterized by the triad of incomplete lower esophageal sphincter (LES) relaxation, increased LES tone, and esophageal aperistalsis. Primary achalasia is caused by failure of distal esophageal inhibitory neurons and is, by definition, idiopathic. Degenerative changes in neural innervation, either intrinsic to the esophagus or within the extraesophageal vagus nerve or the dorsal motor nucleus of the vagus, may lead to secondary achalasia. This occurs in Chagas disease, in which Trypanosoma cruzi infection causes destruction of the myenteric plexus, failure of LES relaxation, and esophageal dilatation. Duodenal, colonic, and ureteric myenteric plexuses also can be affected in Chagas disease. Achalasia-like disease may be caused by diabetic autonomic neuropathy, infiltrative disorders such as malignancy, amyloidosis, or sarcoidosis, and lesions of dorsal motor nuclei, which may be produced by polio or surgical ablation.
Ectopic tissues (developmental rests) are common in the gastrointestinal tract. The most frequent site of ectopic gastric mucosa is the upper third of the esophagus, where it is referred to as an inlet patch. Although the presence of such tissue generally is asymptomatic, acid released by gastric mucosa within the esophagus can result in dysphagia, esophagitis, Barrett esophagus, or, rarely, adenocarcinoma. Gastric heterotopia, small patches of ectopic gastric mucosa in the small bowel, particularly within a Meckel diverticulum, or colon, may present with occult blood loss due to local injury caused by acid secretion.
Instead of returning directly to the heart, venous blood from the gastrointestinal tract is delivered to the liver via the portal vein before reaching the inferior vena cava. This circulatory pattern is responsible for the first-pass effect, in which drugs and other materials absorbed in the intestines are processed by the liver before entering the systemic circulation. Diseases that impede portal blood flow cause portal hypertension, which can lead to the development of esophageal varices, an important cause of massive and frequently life-threatening bleeding.
One of the few sites where the splanchnic and systemic venous circulations can communicate is the esophagus. Portal hypertension induces development of collateral channels that allow portal blood to shunt into the caval system. However, these collateral veins enlarge the subepithelial and submucosal venous plexi within the distal esophagus. These vessels, termed varices, develop in 50% of cirrhotic patients, most commonly in association with alcoholic liver disease. Worldwide, hepatic schistosomiasis is the second most common cause of varices. A more detailed consideration of portal hypertension is given in Chapter 16.
MORPHOLOGYVaricescanbedetectedbyangiography,butaremostcommonlydetectedduringendoscopy(