SPASMODIC STENOSIS OF THE ESOPHAGUS
Etiology.—The functional activity of the esophagus is dependent upon reflex action. The food is propulsed in a peristaltic wave by the same mechanism as, and through an innervation (Auerbach and Meissner plexus) similar to that which controls intestinal movements. The vagus also is directly concerned with the deglutitory act, for swallowing is impossible if both vagi are cut. Anything which unduly disturbs this reflex arc may serve as an exciting cause of spasmodic stenosis. Bolting of food, superficial erosions, local esophageal disease, or a small foreign body, may produce spasmodic stenosis. Spasm secondary to disease of the stomach, liver, gall bladder, appendix, or other abdominal organ is clinically well recognized. A perpetuating cause in established cases is undoubtedly "nerve cell habit," and in many cases there is an underlying neurotic factor. Shock as an exciting cause has been well exemplified by the number of cases of phrenospasm developing in soldiers during the World War.
Cricopharyngeal spasmodic stenosis usually presents the subjective symptom of difficulty in starting the bolus of food downward. Once started, the food passes into the stomach unimpeded. Regurgitation, if it occurs, is immediate. The condition consists in a tonic contraction, ahead of the bolus, of the circular fibers of the inferior constrictor known as the cricopharyngeus muscle, or in a failure of this muscle to relax so as to allow the bolus to pass. In either case the disorder may be secondary to an organic lesion. Local malignant disease or foreign bodies may be the cause. Globus hystericus, "lump in the throat," and the sense of constriction and choking during emotion are due to the same spasmodic condition.
Diagnosis.—At esophagoscopy there will be found marked exaggeration of the usual spasm which occurs at the cricopharyngeus during the introduction of the tube. The lumen may assume various shapes, or be so tightly closed that the folds form a mammilliform projection in the center. If the spasm gradually yields, and a full-sized esophagoscope passes without further resistance, it may be stated that the esophagus is of normal calibre, and a diagnosis of spasmodic stenosis can be made. Considerable experience is required to distinguish between normal and pathologic spasm in an unanesthetized individual. To the less experienced esophagoscopist, examination under ether anesthesia is recommended. Deep anesthesia will relax the normal cricopharyngeal reflex closure as well as any abnormal spasm, thus assisting in the differentiation between an organic stricture and one of functional character. Under deep general anesthesia, however, it is impossible to differentiate between the normal reflex and a spasmodic condition, since both are abolished. Many cases of intermittent esophageal stenosis supposed to be spasmodic are due to organic narrowness of lumen plus lodgement of food, obstructive in itself and in the esophagitis resulting from its presence. The organic narrowing, congenital or pathologic, is readily recognizable esophagoscopically.
Treatment.—The fundamental cause of the disturbance of the reflex should be searched for, and treated according to its nature. Purely functional cases are often cured by the passage of a large esophagoscope. Recurrences may require similar treatment.
[247] FUNCTIONAL HIATAL STENOSIS. HIATAL ESOPHAGISMUS. PHRENOSPASM, DIAPHRAGMATIC PINCHCOCK STENOSIS. (SO-CALLED CARDIOSPASM)
There is no sphincteric muscular arrangement at the cardiac orifice of the esophagus, so that spasmodic stenosis at this level is not possible and the term cardiospasm is, therefore, a misnomer. It was first demonstrated by the author that in so-called cardiospasm the functional closure of the esophagus occurred at the diaphragmatic level, and that it was due to the "diaphragmatic pinchcock." Anatomical studies have corroborated this finding by demonstrating a definite sphincteric mechanism consisting of muscle bands springing from the crura of the diaphragm and surrounding the esophagus at the under surface of the hiatus. An inspection of the cadaveric diaphragm from below will demonstrate an arrangement like double shears admirably adapted to this "pinchcock" action. Further confirmation is the fact that all dilatation of the esophagus incident to spasm at its lower extremity is situated above the diaphragm. In passing it may be stated that the pinchcock action, plus the kinking of the esophagus normally prevents regurgitation when a man with a full stomach "stands on his head" or inverts his body. For the upward escape of food from the stomach an involuntary co-ordinated antiperistaltic cycle is necessary. The dilatation resulting from phrenospasm may reach great size (Fig. 96a), and the capacity of the sac may be as much as two liters. While the esophagus is usually dilated, the stomach on the other hand is often contracted, largely from lack of distention by food, but possibly also because of a spastic state due to the same causes as the phrenospasm. Recently Mosher has demonstrated that hepatic abnormality may furnish an organic cause in many cases formerly considered spasmodic.
The symptoms of hiatal esophagismus are variable in degree. Substernal distress, with a feeling of fullness and pressure followed by eructations of gas and regurgitation of food within a period of a quarter of an hour to several hours after eating, are present. If the esophageal dilatation be great, regurgitation may occur only after an accumulation of several days, when large quantities of stale food will be expelled. The general nutrition is impaired, and there is usually the history of weight loss to a certain level at which it is maintained with but slight variation. This is explained by the trickling of liquified food from the esophageal reservoir into the stomach as the spasm intermittently relaxes, this occurring usually before a serious state of inanition supervenes. At times the hiatal spasms are extremely violent and painful, the pain being referred from the xiphoid region to the back, or upward into the neck. Patients are often conscious of the times of patulency of the esophagus; they will know the esophagus to be open and will eat without hesitation, or will refuse food with the certain knowledge that it will not pass into the stomach. Periods of remission of symptoms for months and years are noted. The neurotic character of the lesion in some cases is evidenced by the occasionally sudden and startling cures following a single dilatation, as well as by the tendency to relapse when the individual is subject to what is for him undue nervous tension. In a very few cases, with patients of rather a stolid type, all neurotic tendencies seem to be absent.
The diagnosis of hiatal esophagismus requires the exclusion of local organic esophageal lesions. In the typical case with marked dilatation, the esophagoscopic findings are diagnostic. A white, pasty, macerated mucosa, and normally contracted hiatus esophageus which when found permits the large esophagoscope to pass into the stomach, will be recognized as characteristic by anyone who has seen the condition. In the cases with but little esophageal distension the diagnosis is confirmed by the constancy of the obstruction to a barium mixture at the phrenic level, while at esophagoscopy the usual resistance at the hiatus esophageus is found not to be increased, and no other local lesion is found as the esophagoscope enters the stomach. It is the failure of the diaphragmatic pinchcock to open, as in the normal deglutitory cycle, rather than a spasmodic tightness, that obstructs the food. The presence of organic stenosis at the hiatus may remove the case altogether from the spasmodic class, or a cicatricial or infiltrated narrowing may be the result of static esophagitis. A compressive stenosis due to hepatic abnormality may simulate spasmodic stenosis as shown by Mosher, who believes that 75 per cent of so-called cardiospasms are organic.
Treatment of hiatal esophagismus (so-called cardiospasm) consists in the over-dilatation of the "diaphragmatic pinchcock" or hiatus esophageus, and in proper remedial measures for the removal of the underlying neurosis. The simple passage of the esophagoscope suffices to cure some cases. Further dilatation by endoscopic guidance may be obtained by the introduction of Mosher's divulsor through the esophagoscope, by which accurate placement is obtained. The distension should not usually exceed 25 mm. Numerous water and air bags have been devised for stretching the hiatus, and excellent results have been obtained by their use. Possibly some of the cures have been due to the dilatation of organic lesions, or to the crowding back of an enlarged malposed, or otherwise abnormal left lobe of the liver, which Mosher has shown to be an etiologic factor.