The Diagnosis of Cardiospasm

Abstract

SUMMARY Cardiospasm, or achalasia, is a nonorganic stenosis of the lower end of the esophagus. This condition must be distinguished from esophageal spasm (diffuse spasm) and reflex spasm at the cardia. During a twelve-year period, 601 patients with cardiospasm were seen and treated at the Mayo Clinic. There were 327 males and 274 females. The ages of these patients at the time of the onset of their symptoms and at the time of consultation is depicted in Figure 1. The patients varied in age from two to 88 years. There were 17 children included in the group who were less than 15 years of age. Data concerning the duration of symptoms are included in Table I. The symptoms of cardiospasm are obstruction to swallowing, regurgitation and pain. Although obstruction and regurgitation are common symptoms, pain occurred in only 29 per cent of the cases. Hemorrhage from the esophagus occurred in but 2.5 per cent. Pulmonary complications of cardiospasm were recognized in 10 per cent of the entire group and are reported elsewhere. The most important diagnostic procedure in these cases is the roentgenologic examination. The roentgenoscopic diagnosis is based on observation of a barium-filled esophagus. A number of roentgenologic observations are necessary for the diagnosis of cardiospasm. These are as follows: (1) the outline of the constricted segment at the cardia; (2) the degree of obstruction at the cardia; (3) the extent of the enlargement or dilatation of the esophagus above the constricted segment; (4) the length and course of the esophagus; (5) evidence of retained food and fluid within the esophagus, and (6) alterations in the muscular activity of the esophagus. From a roentgenologic point of view, cardiospasm may be divided into four stages based on the degree of dilatation of the esophagus. Stage 1 is essentially a normal appearing esophagus but with evidence of obstruction at the cardia. Diagnosis is often difficult at this stage. Stages 2, 3 and 4 represent advancing degrees of dilatation. The incidence of these stages in our series can be ascertained from Table I. In general, it may be stated that the motility of the esophagus is increased during stages 1 and 2 and either reduced or absent in stages 3 and 4. Stages 2, 3 and 4 are illustrated in Figure 2. The roentgenographic appearance of the esophagus after mechanical dilatations of the cardia deserves special comment. Some degree of motility is recovered by the esophagus and the appearance is similar to that noted in diffuse spasm. In the differential diagnosis of cardiospasm, carcinoma of the cardiac end of the stomach is the most important condition to be considered. At times carcinoma of the cardia may closely simulate cardiospasm, as illustrated in Figure 4b. Esophagoscopy is usually unnecessary in making the diagnosis of cardiospasm but is sometimes desirable in the effort to exclude carcinoma. Esophagoscopy was performed 110 times in our 601 cases. Seventy-two esophagoscopic examinations were done for diagnostic purposes and the rest were done to assist in the treatment. In our experience, the passage of sounds often has more diagnostic value than esophagoscopy. Diffuse spasm of the esophagus must likewise be differentiated from cardiospasm. It should be pointed out that cardiospasm and diffuse spasm may occur in the same patient. Although the coexistence of cardiospasm and megacolon has been reported commonly in South America, these diseases occurred together only once in our series. In this instance a boy, six years old, had both cardiospasm and megacolon. The associated occurrence of esophageal diverticula, diaphragmatic hernias and bulbar palsy in patients with cardiospasm introduced interesting speculations as to the etiology of this condition. Degenerative changes in Auerbach's plexus are commonly demonstrated in patients who have had cardiospasm. The reason for these changes is not clear and the etiology of cardiospasm remains obscure. In our opinion, it is probably not primarily a psychosomatic disease. It is important that the diagnosis of cardiospasm be made early, before the decompensated stages have set in.