Diagnosis

The diagnosis of achalasia is strongly suggested by the findings on a barium esophagram. A dilated esophagus, a column of barium with an air-fluid level, and a tapered narrowing at the EG junction, are highly suggestive of acha-lasia. The major diagnostic alternatives for this radiograph appearance are a benign or malignant stricture. However, unlike a stricture, the EG junction usually opens intermittently to a few millimeters allowing small spurts of barium to pass into the stomach. Also with a stricture, dysphagia for liquids and solids usually develops only after a long period of dysphagia for solids only, and esophageal dilatation rarely progresses to the extent typically seen in acha-lasia. In long-standing achalasia, the esophageal lumen may distend to dramatic proportions and take on a tortuous configuration referred to as a "sigmoid esophagus."

Esophageal manometry typically demonstrates complete absence of progressive peristalsis, a high-normal or high resting lower esophageal pressure, and failure of LES relaxation after swallowing. Although LES relaxation is usually < 50% to the intragastric baseline, in a minority of patients, relaxation to the intragastric baseline has been described. However the appearance of this apparently complete relaxation is unusual, demonstrating a much more rapid fall and rise than that seen in normal individuals. This finding corresponds to the minimal distension of the EG junction commonly seen during videoradiographic studies.

In classic achalasia, there is also an absence of contractions in the esophageal body. Although small simultaneous elevations of pressure may follow each swallow, these pressure changes tend to occur earlier than in normal individuals and are of very low amplitude (usually < 30 mm Hg). They represent the effect of pharyngeal contraction— the "pharyngeal squirt"—increasing pressure in the dilatated esophagus, rather than intrinsic esophageal muscular activity. In a variant of achalasia, referred to as "vigorous achalasia," swallowing generates more substantial, but nonetheless simultaneous and, occasionally, multi-phasic increases of esophageal pressure that do represent intrinsic esophageal motor activity. Whether vigorous achalasia is an early phase in the evolution of classic achalasia or is a separate condition with a different pathogen-esis is unknown.

Patients with radiographic studies compatible with achalasia who are subsequently found to have a malignancy involving the EG junction may meet the manometric criteria for achalasia (referred to as "pseudoachalasia" or "secondary achalasia"). Therefore, manometry cannot be relied on to distinguish between true achalasia and a malignant stricture. Because some patients with achalasia develop carcinoma of the esophagus, this can be an important differential diagnosis.

Endoscopy is sometimes used by gastroenterologists as the first test in the evaluation of dysphagia, on the grounds that the procedure will ultimately be required in the examination of patients presenting with this symptom. This may be a tactical mistake. Although it is true that endoscopy in patients with dysphagia may make radiographic examination unnecessary, barium studies are more helpful, providing information on both motor function and structural disease. The endoscopic findings of achalasia, especially before distension of the esophageal lumen becomes pronounced, may be subtle and easily misinterpreted as normal or a stricture. Nonetheless, it is true that in the face of a barium esophagram compatible with achalasia, endoscopic examination is required to rule out a benign or malignant stricture.

The diagnosis is confirmed when a tight EG junction that does not distend with air insufflation is covered by normal-looking overlying mucosa and allows the endoscope to pass through with little resistance. A retroflexed view of the cardia and fundus should be performed routinely as a double check for possible malignancy. Although there may be some resistance to intubation of the EG junction in achalasia, it is usually minimal with the endoscope passing through with a slight popping sensation. Patients with achalasia are prone to candidial esophagitis due to esophageal stasis. However focal erosive or ulcerative disease in the areas of the EG junction should raise concerns about an alternative diagnosis. A nodular mass is inconsistent with achalasia and suggests a malignancy. Malignancy masquerading as achalasia on barium studies is often infiltrating and may not involve the mucosa on either the esophageal or cardial side of the SC junction. Therefore biopsies and brushings may confirm a malignancy, but cannot rule one out. Excessive resistance to intubation should also suggest the presence of a malignancy, even in the absence of an obvious tumor. Nonetheless, pseudoachalasia is a relatively rare condition and the vast majority of patients with radiographic findings suggesting achalasia have achalasia.

Many authorities insist that all three of the tests mentioned above are required for the diagnosis of achalasia. However, I have rarely seen manometry change a diagnosis of achalasia based on the combination of barium and endoscopic findings. On the rare occasions in which the manometry appears to dictate against achalasia, the discrepancy is almost invariably due to technical problems in the performance or interpretation of the manometric study. I do not feel that manometry is a necessary test for the diagnosis of achalasia.

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