Diagnosis.—Hysteria must not be decided upon as the cause of dysphagia, until after esophagoscopy has eliminated paralysis. Dysphagia after recent diphtheria should suggest paralysis of the esophagus. The larynx, lips, tongue, and pharynx also, are usually paralyzed in esophageal paralysis of bulbar origin. The absence of the cricopharyngeal resistance to the esophagoscope passed without anesthesia, general or local, is diagnostic.
Treatment.—The internist and neurologist should govern the basic treatment. Nutrition can be maintained by feeding with the stomach-tube, which meets no resistance to its passage. Should this be contraindicated by ulceration of the esophagus, gastrostomy should be done.
LUES OF THE ESOPHAGUS
Esophageal syphilis is a rather rare affection, and may show itself as a mucous plaque, a gumma, an ulceration, or a cicatrix. Cicatricial stenosis developing late in life without history of the swallowing of escharotics or ulcerative lesions is strongly suggestive of syphilis, though the late manifestation of a congenital stenosis is a possibility.
Esophagoscopic appearances of lues are not always characteristic. As in any ulcerative lesion, the inflammatory changes of mixed infections mask the basic nature. The mucous plaque has the same appearance as one situated on the velum, and gummata resemble those seen in the mucosa elsewhere. There is nothing characteristic in luetic cicatrices.
The diagnosis of luetic lesions of the esophagus, therefore, depends upon the history, presence of luetic lesions elsewhere, the serologic reaction, therapeutic test, examination of tissue, and the demonstration of the treponema pallidum. The therapeutic test by prolonged saturation of the system with mercury is imperative in all suspected cases and no other negative result should be deemed sufficient.
The treatment of luetic esophagitis is systemic, not local. Luetic cicatrices contract strongly, and are very resistant to treatment, so that esophagoscopic bouginage should be begun as early as possible after the healing of a luetic ulceration, in order to prevent stenosis. A silk-woven endoscopic bougie placed in position by ocular guidance, and left in situ for from half to one hour daily, may prevent severe contraction, if used early in the stage of cicatrization. Prolonged treatment is required for the cure of established luetic cicatricial stenosis. If gastrostomy has been done retrograde bouginage (Fig. 35) may be used.
TUBERCULOSIS OF THE ESOPHAGUS
Esophageal tuberculosis is not commonly met, but is probably not infrequently associated with the dysphagia of tuberculous laryngitis. It may rarely occur as a primary infection, but usually the esophagus is involved in an extension from a tuberculous process in the larynx, mediastinal lymphatics, pleura, bronchi, or lungs.
Primary lesions appear as superficial erosions or ulcerations, with a surrounding yellowish granular zone, or the granules may alone be present. The mucosa in tuberculous lesions is usually pallid, the absence of vascularity being marked. Invasion from the periesophageal organs produces more or less localized compression and fixation of the esophagus. The character of open ulceration is modified by the mixed infections. Healed tuberculous lesions, sometimes resulting from the evacuation of tuberculous mediastinal lymph nodes into the esophagus may be encountered. The local fixation and cicatricial contraction may be the site of a traction diverticulum. Tuberculous esophago-bronchial fistulae are occasionally seen.