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Tuesday, February 2, 2021

CAMERON LESIONS AND DISORDERS OF THE CARDIA

CAMERON LESIONS AND DISORDERS OF THE CARDIA

Cameron lesions are either gastric erosions or linear ulcerations that occur at the level of the diaphragm in patients with a hiatal hernia sac. Cameron lesions were first described in 1986 by Cameron and Higgins, who discovered them in a series of patients. They occur in approximately 5% of patients who undergo upper endoscopy and are found to have a hiatal hernia. They are more common in elderly patients and in those with large sliding hiatal hernias. The cause of these lesions is either mechanical trauma or ischemia secondary to sliding of the hiatal hernia. Medication effects from NSAIDs as well as acid peptic disease also play a part in their formation. Most patients with Cameron lesions present with iron deficiency anemia, although overt upper gastrointestinal bleeding can be seen. Treatment of a Cameron ulcer varies; the use anti secretory agents should be the first line of therapy. In addition, stopping any caustic medications should be advised. For those patients with persistent symptoms or findings, a surgical procedure should be recommended which mainly focuses on reducing the hiatal hernia and preventing its recurrence.

Ulcers within the stomach are classified based on their location and their association with duodenal ulcers. Ulcers within the cardia are considered type 4 ulcers and have low basal acid output and no relation- ship to duodenal ulcers. In this respect they are very similar to type 1 ulcers, which are located in the gastric body. Type 2 ulcers located in the antrum and type 3 ulcers located within 3 cm of the pylorus are more likely to have higher basal acid output and to be related to duodenal ulcers. Type 4 cardia ulcers form from abnormally low defensive mechanisms of the stomach as a result of reduced production of bicarbonate or mucus or an increase in prostaglandin secretion. Atrophic gastritis caused by H. pylori which migrates proximally from the antrum also plays a role. These factors can increase the mucosal disruption that NSAIDs cause in the stomach.

CAMERON LESIONS AND DISORDERS OF THE CARDIA
Plate 4-46


Intestinal metaplasia in the cardia is mainly a result of H. pylori infection. In this case, the entire stomach generally is infected with this organism and the pathologic consequences of atrophic gastritis and intestinal metaplasia are seen. In these individuals, the stomach is generally pale or patchy white, with a reduction in gastric folds. Biopsies throughout the stomach typically reveal atrophy, and pH testing often reveals a high pH of 6.0 to 7.0. Histologic examination may not reveal H. pylori infection, so it is important to test for the microbe with alternative tests, such as stool antigen or breath tests. This is unlike intestinal metaplasia of the distal esophagus, or Barrett esophagus, in which the underlying mechanism is pathologic acidic, nonacidic, or bilious reflux that leads to the change. One distinguishing characteristic is that in true intestinal metaplasia of the distal esophagus, the goblet cells stain with alcian blue, whereas in intestinal metaplasia of the cardia, this is not the case.

The prevalence of cancer of the gastric cardia is increasing, but the prevalence of distal gastric cancers is decreasing. Distinguishing gastric cardia cancers from distal esophageal cancers can be extremely challenging. The true cardia arises from the gastroesophageal junction with a small 1- to 4-cm extension into the proximal stomach. In some instances, the cardia mucosa extends into the distal 1 to 2 cm of the esophagus, making anatomic distinctions between the cardia and esophagus difficult. Gastric cardia cancers are generally a result of H. pylori infection (type A cancers). In these cases, examination of the stomach reveals diffuse atrophy and examination of the esophagus reveals an absence of Barrett esophagus. In a second subset of cancers, type B cardia cancers, the cause is related to Barrett esophagus, with extension into the cardia. These cancers are often indistinguishable from true distal esophageal cancers, which arise from the gastroesophageal junction; endoscopic examination of the esophagus reveals Barrett esophagus, but examination of the remaining stomach is often macroscopically and microscopically normal. Autoimmune gastritis can also lead to cancer, although it is a rare occurrence.


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