Part 68

The local treatment consists in systematic mechanical dilatation with bougies or mechanical dilators properly constructed. These are employed {426} daily, every other day, or at more prolonged intervals, according to the tolerance of the parts and the progressive improvement. They are retained several moments at each introduction, and followed by the passage and immediate withdrawal of an instrument of larger size. It is often advisable that the final dilatation of each series be made with a stomach-tube, so that liquid food may be poured through it from a syphon or a small-lipped vessel, that there may be no necessity for swallowing food for some hours thereafter. This method is continued until it becomes evident that nothing further is to be gained by its continuance. In cases that have been at all successful, the introduction of the instrument should be repeated every week or two for a long time, to prevent or retard recurrence of the constriction, which is very liable to take place. M. Krishaber has reported cases in which a tube passed through the nose was retained from forty to three hundred and five days; and from this success he deduces the practicability of continuous dilatation in this manner. Billroth and Rokitansky have encountered cases in which frequent dilatation had set up inflammation of the surrounding connective tissue, which had caused fatal pleurisy by continuity.

Forcible dilatation by mechanical separation of the sides of a double metallic sound has been employed with success in some instances. It is a risky procedure.

Destruction of cicatricial tissue by caustics has been attempted, and, though successes occasionally attend the practice, it is hardly considered sufficiently promising.

Division of the stricture by internal oesophagotomy, with subsequent dilatation, has been practised of late years, and offers some chances of success. Oesophagostomy and gastrostomy have been performed in some cases of impassable stricture, and the latter operation is gaining in favor. For surgical details, however, we must refer to works on surgery.

Carcinoma of the Oesophagus.

DEFINITION.--Carcinomatous degeneration of the oesophagus, whatever the variety.

SYNONYM.--Cancer of the oesophagus.

ETIOLOGY.--Carcinoma is the most frequent disease of the oesophagus that comes under professional observation. The most frequent variety is the squamous-celled (53 out of 57, Butlin). Spheroidal-celled and glandular-celled varieties are much less frequent. In some instances the morbid product is a combination of the two. Colloid degeneration is occasionally met with. Carcinoma is usually primitive. Its cause is undetermined, but, as it is most frequent at the constricted portions of the tube, pressure is supposed to be the exciting cause. It does not always give rise to secondary infection. Sometimes it is an extension from the tongue, epiglottis, or larynx, or from the stomach. It is most frequent in males, and more so in the intemperate than in the abstinent.

The immediate exciting cause is often attributed to local injury from retention of foreign bodies or the deglutition of hot, acrid, or indigestible substances.

{427} There appears to be some disposition to carcinoma of the oesophagus in tuberculous subjects (Hamburger), while the children of tuberculous parents may have carcinoma of the oesophagus, and their offspring, again, tuberculosis.

SYMPTOMS.--The earliest local symptom is slight dysphagia, with impediment to completion of the act of glutition--an evidence of commencing stricture. Subsequently, inverted peristaltic action is added, an evidence of dilatation above the stricture, with partial retention of food. At a later stage vomiting will occur, with admixtures of pus and sanguinolent fragments of cancerous tissue.

Progressive emaciation and impaired physical endurance usually precede these local symptoms, but actual cachectic depression may come on quite tardily. At first there is no pain; subsequently there comes on considerable uneasiness at some portion of the tube. Finally, there may be severe local burning or lancinating pains, particularly after meals. If the disease be high up, there may be pain between the shoulders, along the neck, and even in the head, with radiating pains toward either shoulder and along the arm. If low down, there may be intense cardialgia and even cardiac spasm. If the trachea or larynx be compressed or displaced, dyspnoea will be produced. If the recurrent laryngeal nerve be compressed, there will be dysphonia or aphonia. Perforation of the larynx will be indicated by cough, expectoration, hoarseness, or loss of voice; of the trachea, by paroxysmal cough, dyspnoea, or suffocative spasm; of the lungs, by acute pneumonitis, especially if food shall have escaped, and expectoration of blood, pus, and matters swallowed, as may be; of the pleura, by pneumothorax; of the mediastinum, by emphysema; of the pericardium, by pericarditis; of the large vessels, by hemorrhage. Perforation of the aorta or pulmonary artery is often followed by sudden death from hemorrhage, and of the lungs by rapid death from pneumonitis.

PATHOLOGY AND MORBID ANATOMY.--Primitive carcinoma is usually circumscribed. It is most frequent at the cardiac extremity, but often occurs where the oesophagus is crossed by the left bronchus, and sometimes occupies the entire length of the tube. The greater proclivity of the lower third of the oesophagus has been attributed to mechanical pressure where it passes through the diaphragm; that of the middle third, to pressure of its anterior wall against the left bronchus by the bolus. It begins, either nodulated or diffuse, in the submucous connective tissue, implicates the mucous membrane, encroaches upon the calibre of the tube, undergoes softening and ulceration, and becomes covered with exuberant granulations. When the entire circumference of the oesophagus is involved stricture results, sometimes amounting eventually to complete obstruction. Ulceration taking place, the calibre again becomes permeable. The oesophagus becomes dilated above the constriction and collapsed below it.

As the disease progresses the adjoining tissues become involved. Adhesions may take place with trachea, bronchi, bronchial glands, lungs, diaphragm, or even the spinal column (Newman). Perforation may take place into the trachea, usually just above the bifurcation, or into the lungs, pleura, mediastinum, pericardium, aorta, or pulmonary artery. Abscesses are formed, the contents of which undergo putrefaction. There {428} may be involvement of the pneumogastric nerve, with reflex influence on the spinal nerves and the sympathetic (Gurmay).

DIAGNOSIS.--The diagnosis will rest on due appreciation of the symptoms enumerated and the ultimate evidence of the cancerous cachexia. Auscultation will often reveal the location of the disease. This may be further confirmed by palpation with the bougie, but the manipulation should be made without using any appreciable force. Laryngoscopic inspection and digital exploration are sufficient when the entrance into the oesophagus is involved.

Differential diagnosis is difficult at an early stage, and often to be based solely on negative phenomena. At a later stage it is easy, especially when cancerous fragments are expelled. In some instances a tumor can be felt externally. Such a tumor, however, has been known to have been the head of the pancreas (Reid).

Cancer of the oesophagus is liable to be confounded with chronic oesophagitis, cicatricial stenosis, diverticulum, extraneous compression, abscess, and non-malignant morbid growths.

PROGNOSIS.--The prognosis is unfavorable, the disease incurable. Death may be expected in from one to two years, though sometimes delayed for longer periods. Inanition or marasmus is the usual cause of death in uncomplicated cases. Sometimes it takes place by hæmatemesis, sometimes following involvement of the stomach, and sometimes wholly unassociated with any direct disease of the walls of the stomach. Death takes place not infrequently from perforation into adjoining organs, and sometimes from secondary inflammation of other vital organs, as the brain and the lungs.

TREATMENT.--There is little to be done in the way of treatment apart from the constitutional measures indicated in carcinoma generally and in chronic diseases of the oesophagus. The cautious use of the stomach-tube to convey nourishment into the stomach is allowable during the earlier stages of the disease only. It is dangerous after ulceration has taken place, from the risk of perforating the walls of the oesophagus, and thus hurrying on the fatal issue by injury to the intrathoracic tissues.

When deglutition becomes impracticable or the passage of the oesophagus absolutely impermeable to nutriment, food and alcoholic stimuli should be administered by enema. Indeed, it is good practice to begin to give nourishment occasionally by the bowel before it becomes absolutely necessary, so as to accustom the part and the patient to the manipulation. Narcotics to relieve pain are best administered hypodermatically, so as to avoid unnecessary irritation of the rectum.

The passage of dilators, as in stricture of cicatricial origin, is very hazardous. They produce irritation, which hastens the softening of the tissues, and are open to the risk of penetrating the softened tissues and passing through the walls of the oesophagus into the pleura, lung, or mediastinum. Fatal accidents of this nature are on record.

Gastrostomy is sometimes performed to prolong life.

{429} Paralysis of the Oesophagus.

DEFINITION.--Loss of motive-force in the muscular tissue of the oesophagus, whether intrinsic or reflex in origin.

SYNONYMS.--Gulæ imbecillitas, Paralytic dysphagia, Atonic dysphagia.

ETIOLOGY.--Paralysis of the oesophagus may be caused by impairment of function in one or more of the nervous tracts distributed to the muscles concerned in dilating the upper orifice of the gullet or in those concerned in the peristaltic movements which propel the bolus to the stomach. These impairments of function may be nutritive in origin, as in softening and atrophy of the nerve-trunk, or, as is more frequent, they may be pressure-phenomena from extravasations of blood, purulent accumulations, exostoses, tumors, and the like.

The paralysis may be due to disease or wounds of the nerves themselves or of their motor roots, or of the cerebro-spinal axis, implicating their origin, or to pressure and atrophy of a trunk-nerve in some portion of its tract. It is likewise due to neurasthenia from hemorrhage or from protracted disease (enteric fever, yellow fever, cholera), or to systemic poisoning in diphtheria, syphilis, and plumbism. It may be due to muscular atrophy or intermuscular proliferations of connective tissue, to dilatation of the oesophagus, and to disease in the tube. It may be due to mechanical restraint from external adhesions of the oesophagus to intrathoracic tumors (Finny). It may result from sudden shock or fright. It may follow the sudden reaction of cold upon the overheated body. It is one of the manifestations of hysteria and of the hysteria of pregnancy.

SYMPTOMS.--Partial paralysis may give rise to no symptoms at all. The earliest manifestations are those of impediment to the prompt passage of the bolus to the stomach, repeated acts of deglutition or additional swallows of food or drink being necessary. Large masses are swallowed and propelled onward more readily than small ones, and solids more readily than fluids. There is often a characteristic gurgling attending the passage of fluids along the tube. Swallowing is best performed in the erect posture. These symptoms increase in severity as the paralysis increases. There is little pain or none at all. In some cases there is no regurgitation of food; in others, this is more or less frequent. When the paralysis is complete, deglutition becomes impossible, and the food attempted to be swallowed is expelled from the mouth and nose in a paroxysm of cough. Sometimes the food enters the larynx and produces paroxysms of suffocation or threatens asphyxia.