A system of practical medicine. By American authors. Vol. 2

by Unknown

DISEASES OF THE OESOPHAGUS.

BY J. SOLIS COHEN, M.D.

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Oesophagitis.

DEFINITION.—Inflammation of the oesophagus.

SYNONYMS.—Inflammatory dysphagia, Inflammation of the gullet.

Oesophagitis may be acute or chronic. Either form may be idiopathic, deuteropathic, or traumatic.

Acute Oesophagitis.

DEFINITION.—Acute inflammation of the gullet.

SYNONYM.—Oesophagitis acuta.

HISTORY.—Until the publication in 1829 of a thesis by J. T. Mondière entitled Recherches sur l'Inflammation de l'Oesophage, et sur quelques points de l'anatomie pathologique de cet organ, little study had been devoted to acute inflammation of the oesophagus; and since that time Mondière's researches have been largely utilized by subsequent writers. It has been taken for granted that Galen's mention of pain in the oesophagus¹ has indicated his recognition of the disease. Fernel² mentions phlegmon of the oesophagus; Honkoop³ describes inflammation of the oesophagus; J. P. Frank⁴ describes an oesophageal angina; and Joseph Frank⁵ seems to have been the first author to use the term oesophagitis. Since the publication of Mondière's monograph the principal systematic descriptions have been those of Hamburger⁶ Von Oppolzer⁷ Zenker and Ziemssen⁸ Luton,⁹ and Bernheim.¹⁰

¹ De locis affectis, lib. iv. cap. iii.; lib. v. cap. v.

² De partium mortis et sympt., lib. vi. p. 277.

³ Specimen inaugurale de morbo oesophagi inflammatorie, Lugd. Batav., 1774.

⁴ De curandis hominem morbis, Epitome prælectionibus academicis dicata, Mannheim, Stuttgardt, and Vienna, 1792-1820.

⁵ Praxeous medica præcepta universa, Lipsiæ, 1826-32.

⁶ Klinik der Oesophaguskrankheiten, Erlangen, 1871.

⁷ Vorlesungen über specielle Pathologie und Therapie, Erlangen, 1872; Englished in abstract by the writer in Philada. Med. Times, 1872.

⁸ Handbuch der speciellen Pathologie und Therapie, 1877; English translation, New York, 1878, vol. viii.

⁹ Dictionnaire de Médecine et de Chirurgie pratiques, Paris, 1877, vol. xxiv.

¹⁰ Dict. Encyclopediques des Sciences médicales, Paris, 1880, vol. xiv.

ETIOLOGY.—Acute oesophagitis is quite a rare disease. It occurs idiopathically, deuteropathically, and traumatically—traumatically far the most frequently, and idiopathically least frequently. It is doubtful whether any special predisposing causes of oesophagitis can be indicated. Nevertheless, infancy has been so cited by some authors (Mondière, Billard, Behier, and Steffan). Slight idiopathic catarrhal—or rather erythematous—oesophagitis occasionally ensues in the adult from sudden or prolonged exposure to cold and moisture, and under such circumstances may sometimes be regarded as rheumatic in origin, subsiding after a few hours' continuance, to be immediately succeeded by manifestations of articular rheumatism, acute or subacute, as in some analogous examples of rheumatic pharyngitis. Exceptionally, severe oesophagitis may follow a simple cold (Noveene, cited by Bernheim), or presents as an extension of sore throat, the result of cold (Graves¹¹). It is induced also by the habitual use of very hot drinks and food, and occasionally by the opposite extremes, the use of very cold articles of food and drink (Mondière, Bourguet, Hamburger). The abuse of tobacco and alcohol is alleged as quite a frequent cause of mild oesophagitis, usually occurring, however, in association with pharyngitis from the same causes.

¹¹ Lon. Med. and Surg. Journ., 1836-37, No. 172, and Clinical Lectures, Dublin, 1864, p. 592.

Oesophagitis sometimes follows the deglutition of irritating medicines or moderately caustic poisonous substances not sufficiently acid to produce veritable traumatic oesophagitis. Mercury, codeina, and particularly tartar emetic, are cited as capable of exciting oesophagitis.

Large doses of tartar emetic, as formerly administered in pneumonia (Laennec¹²), sometimes produced a peculiar form of pustulous oesophagitis, not unlike the pustulous oesophagitis sometimes occurring as part of the local manifestations of small-pox.

¹² Traité de l'Auscultation médicale, etc., Paris, 1837, vol. iii. p. 560, illustrated; Laboulbène, Anatomie pathologique, and Nouveau Dict. de Méd. et de Chir., vol. xxiv. p. 370, illustrated; Von Oppolzer, op. cit., p. 109.

Deuteropathic catarrhal oesophagitis occurs sometimes as an extension of catarrhal pharyngitis on the one hand, and of catarrhal gastritis on the other. It also occurs in scarlet fever, measles, and typhus fever. It is likewise consecutive to the various diseases and surgical lesions of the tube itself. Parasitic oesophagitis occurs as an extension of parasitic stomatitis or thrush. Deuteropathic circumscribed phlegmonous oesophagitis is sometimes produced by extension of inflammation from softened caseous bronchial glands at the bifurcation of the trachea, and by pressure from mediastinal tumors, aneurism of the aorta, etc.

Pseudo-membranous oesophagitis is almost always deuteropathic. It has been encountered chiefly in association with pseudo-membranous pharyngitis or diphtheria, and with croupous pneumonia, but likewise in enteric and typhus fever, in cholera and in dysentery, in measles, scarlatina, and small-pox, in nephritis, tuberculosis, carcinoma, and pyæmia.

In a case of hysteria, to be mentioned later, the entire epithelial coat of two-thirds of the oesophagus was discharged by emesis. In this respect the local disease—in that instance at least—resembles pseudo-membranous enteritis.

Traumatic oesophagitis is produced by the deglutition of corrosive substances, which destroy portions of the mucous membrane in their passage or excite a suppurative inflammatory process, or is produced by the passage of foreign bodies of sharp and irregular contour, or by the passage of surgical appliances, whether used for actual operations or for explorations merely.

In rare cases traumatic oesophagitis is the result of wounds with firearms or other weapons.

Phlegmonous oesophagitis may be the result of disease or injury of the interior of the oesophagus, or of its external coat by extension of disease from tissues surrounding it. Foreign bodies, arrested in the oesophagus or wounding it in their passage to the stomach; injuries from surgical appliances, exploratory or operative, employed in treatment for foreign bodies in the tube or in cases of stricture and morbid growth; and chemical irritants swallowed by accident or design,—are the chief causes in the former class of cases; but pustulous and pseudo-membranous oesophagitis must likewise be regarded as occasional causes. The causes operating upon the exterior of the tube primarily are suppurative laryngitis and tracheitis, tumefaction and softening of bronchial and tracheal lymphatic glands, and caries of the spine. Isolated cases have been attributed to emboli in connection with valvular diseases of the heart (Parenski, cited by Daton), and to fits of anger (J. Frank and Rigal, cited by Daton). In certain cases the cause is unassignable, and is then usually attributed to some dyscrasia, syphilis in particular.

PATHOLOGY AND MORBID ANATOMY.—Acute oesophagitis presents both as a diffused inflammation and a circumscribed process, annular or irregular in contour. It does not appear from the post-mortem records consulted that any special portion of the tube is particularly liable to circumscribed inflammation, though the lower fourth appears most frequently affected. The inflammatory process may be simply superficial or erythematous, catarrhal or desquamative (Zenker and Ziemssen), or it may be phlegmonous, and thus interest the submucous tissues as well as the mucous membrane. This may terminate in abscess or in diffuse suppuration with ulcerations. In occasional instances gangrene ensues. Both in diphtheria and in croupous pneumonia, pseudo-membranous oesophagitis is an occasional complication; and the same process is said to have been observed in typhus fever, measles, scarlatina, cholera, pyæmia, dysentery, tuberculosis, and carcinoma (Von Oppolzer and others).

Pustulous oesophagitis occurs in small-pox, and occasionally follows the use of tartar emetic in large doses.

The morbid anatomy of acute idiopathic oesophagitis, though usually detailed in descriptions of the disease, must be known by theory much more than by demonstration, few examples coming under the inspection of the pathologist in time to distinguish the progressive stages of the inflammatory process, and still fewer being revealed by oesophagoscopy during life. The lesions most frequently observed post-mortem are thickening, softening, and desquamation of the epithelium, with very scanty accumulations of viscid mucus here and there upon the mucous membrane. The mucous membrane is seen to have suffered numbers of pinhead or slightly larger superficial circumscribed erosions, rounded or longitudinal, and likewise a few actual ulcerations. The follicles of the mucous membrane are often both swollen and hypertrophied, reaching the size of peas, especially in the upper portion of the tube.

The desquamation of the epithelium usually takes place in small patches. One case, however, has been recorded (Birch-Hirschfeld¹³) in which a young hysterical woman, after suffering three days with acute oesophagitis without assignable cause, ejected by emesis a membranous tube two-thirds of the entire length of the oesophagus, and shown under examination to have been the completely detached epithelial coat of the oesophagus, wholly normal in its upper layers and infiltrated with agglomerated round cells in its lower layers. It was supposed that the mass had been detached in consequence of acute subepithelial suppuration.

¹³ Lehrbuch der pathologische Anatomie, Ziemssen, 1877, p. 818; English translation, vol. viii. p. 140.

In addition to swollen and hypertrophied follicles there may be some evidence of ulcerative destruction of these follicles. Mondière and others declare that this folliculous inflammation and ulceration may exist without any other change whatever in the remaining constituents of the mucous membrane; and therefore this form of oesophagitis was termed folliculeuse by Mondière (folliculous oesophagitis). This form of the disease has been observed in typhus fever, in croup (Mondière), and in tuberculosis. Ulceration of the oesophagus occurs, likewise, in carcinoma and in oesophagitis from corrosive fluids, wounds, and other injuries.

In pseudo-membranous oesophagitis the exudation occurs usually in small circumscribed gray-yellow or brownish flakes or stripes distributed over different portions of the surface, more closely, however, at the upper portion of the tube. Superficial erosions are sometimes observed beneath these deposits, and occasionally ulcerations, at times sufficient to give rise to severe hemorrhage (Zenker and Ziemssen). Usually the mucous membrane is but slightly hyperæmic. In some instances pseudo-membrane is so massed in plugs as to occlude the cavity of the tube, as with obturators. In cases associated with pseudo-membranous gastritis the oesophageal manifestations are greatest in the vicinity of the cardiac extremity. Somewhat allied to pseudo-membranous oesophagitis, and apt to be confounded therewith, is the parasitic deposit of the Oïdium albicans in cases of thrush; in connection with which subject this point has already received attention.

The pustules of small-pox may interest any portion of the mucous membrane, but are most numerous at the upper portion of the tube. They may be discrete or confluent. The pustules from tartar-emetic poisoning are most numerous at the two extremities of the canal. It is contended that the so-called pustules of variolous oesophagitis are really superficial variolous ulcers, the antecedent specific lesions having been lenticular papules merely, with abrasion of the softened epithelial layer.¹⁴ Variolous oesophagitis may excite an accompanying catarrhal or pseudo-membranous oesophagitis. The local lesions, be they pustular or ulcerous, heal without cicatrices.

¹⁴ Virchow's Deutsche Klinik, 1858, No. 31, p. 306; Zenker and Ziemssen, op. cit., p. 146.

Phlegmonous oesophagitis presents both as a diffuse and as a circumscribed inflammation. Examined after death, there is abundant purulent infiltration into the submucous connective tissue, which has undergone destruction in portions of its extent. The infiltration pushes the folds of mucous membrane outward to the interior of the tube, and thus diminishes its calibre considerably when the infiltration is annular. The mucous membrane is congested, ecchymosed, and covered with mucus, and has usually suffered desquamation of portions of its epithelium. Ulcerations through the mucous membrane will have taken place in some instances. Cicatrices mark the location of ulcers which have healed.

In the diffuse variety the oesophagus is inflamed and swollen, as a whole, in proportion to the extent of the disease. In the circumscribed variety the morbid appearances are circumscribed. It has been known to continue into the stomach (Belfrage and Hederius, cited by Zenker and Ziemssen), and to extend therefrom (Ackermann, idem).

As described by Zenker and Ziemssen, chiefly from ten autopsies by themselves and one by Belfrage and Hederius, phlegmonous oesophagitis begins with a submucous purulent infiltration, transforming the areolar tissue into an apparent layer of pus, although microscopic examination shows the bundles of connective tissue to be intact at first. At a later period they become really destroyed, leaving mere crevices filled with pus. The mucous membrane, but little involved, may remain normal or may present the evidence of catarrhal inflammation, desquamation of epithelium, congestion, and slight deposits of mucus. The muscular coat, intact to the unaided eye, under the microscope gives some evidence of purulent infiltrations. The pus may finally escape through the mucous membrane, in extensive infiltrations, at several points, which give the parts a sieve-like appearance when the perforations are closely grouped.

Gangrene sometimes occurs as a result of intense phlegmonous oesophagitis, but this is far more rare than the gangrene supervening after injuries by caustic substances. Sometimes it results from capillary embolism (Rokitansky, Virchow, cited by Luton, op. cit.).

SYMPTOMATOLOGY, COURSE, DURATION, TERMINATION, COMPLICATIONS, AND SEQUELÆ.—The main subjective symptoms of oesophagitis are pain and difficulty in swallowing, with febrile phenomena superadded in severe cases. In simple oesophagitis of mild character these symptoms may be so slight as to be attributed to other causes or be disregarded altogether. In most instances there is a dull, steady pain beneath the sternum, some sense of impediment to deglutition or absolute pain in swallowing (odynphagia), and occasional regurgitation of viscid, glairy mucus, food, or acid products from the stomach. In severe cases the substernal pain is more acute and more diffused, and is frequently associated with pain between the scapulæ and to the left side. This latter pain may be attributable to acid from the stomach. Sometimes the pain is described as acute, especially during the passage of large boluses, particularly if they are very hot, or even very cold. The seat of pain, however, does not always indicate the seat of inflammation, even though the pain be always referred to the same locality. When the cervical portion of the tube is implicated, tenderness may sometimes be detected by external pressure or by special movements of the head and vertebræ.

The amount and character of the dysphagia vary greatly. Sometimes there is a sense of impediment to the passage of food, solid or liquid, or solid only, through and beyond the painful region. This sensation may be accompanied or be followed at a brief interval by regurgitation of food or mucus, or food enveloped with mucus, the latter in some instances tinged with blood. The deglutition or the regurgitation may be accompanied by spasm of the muscular coat of the oesophagus. The dysphagia is not always due to tumefaction of the mucous membrane, but usually in part to coexisting inflammation of the muscular coat or infiltration between the sheaths of muscular fibres, paralyzing their efforts at contraction.

There are no subjective symptoms which permit discrimination between desquamative catarrhal oesophagitis and folliculous oesophagitis. The only symptom particularly indicating pseudo-membranous oesophagitis is the expulsion of shreds of the membrane by hawking or by emesis; but a strong inference is justifiable when the ordinary symptoms of oesophagitis occur in cases of pseudo-membranous pharyngitis or croupous pneumonia.

Phlegmonous oesophagitis is indicated by the presence of pus or of dead mucous membrane in the matter regurgitated or vomited. In severe cases there is considerable febrile reaction. In children, convulsions may supervene from reflex irritation conveyed along the pneumogastric nerve.

The course of acute catarrhal oesophagitis is, as a rule, short, the pain and dysphagia usually subsiding in a few days, with complete resolution and no unfavorable sequelæ. When due to obstruction, the course is indefinitely prolonged. Sometimes it subsides into a mild or unsuspected chronic oesophagitis. In the symptomatic oesophagitis of febrile diseases, the course is longer and unequal. In severer forms and in phlegmonous oesophagitis, the disease may be protracted by suppuration, abscess, gangrene, perforation of the oesophagus, and other complications. It often terminates fatally—in three or four days in some cases—sometimes under symptoms of collapse. Cases may recover without important sequelæ, but stricture very often results from cicatricial complications. Chronic oesophagitis is a more frequent sequel of the phlegmonous variety than of the catarrhal. It, in its turn, may give rise to dilatation of the oesophagus, annular or diverticular, from detention of food and consequent pressure.

DIAGNOSIS.—The diagnosis will rest upon the interpretation of the coexistence of a certain number of the symptoms mentioned. Idiopathic phlegmonous oesophagitis may readily be mistaken for dorsal myelitis by the location of the pain—the more so that the spinal disease is occasionally attended with spasm of the oesophagus, and the myelitis by difficulty in deglutition; but the differentiation may be determined by the inability to produce oesophageal pain by pressure made along the dorsal vertebræ. In deuteropathic or traumatic phlegmonous oesophagitis, the history of the attack will indicate the probable nature of the malady, and prevent the mistake. Diffused oesophagitis is suspected when the general pain or the painful dysphagia appears to extend along the entire tract of the oesophagus, or at least a large portion of it.

Circumscribed oesophagitis is usually indicated by odynphagia at a certain point of the tube after completing the act of deglutition. The location of the inflammation can sometimes be determined by auscultation of the descent of the alimentary bolus or of a swallow of water (Hamburger), which may yield evidence to the ear of arrest or impediment to its passage. Auscultation of the oesophagus, however, is less useful in acute oesophagitis than in stenosis, stricture, and mechanical obstruction. When available in oesophagitis, the normal sound of the passage of water down the gullet becomes masked, and accompanied by that of regurgitative ascent of small bubbles of air. Sometimes there is a slight friction sound during the act of deglutition itself. In circumscribed oesophagitis, especially when annular, as is most frequently the case, sounds are heard attributable to marked obstruction to the descent of the bolus. Abscess cannot be positively diagnosticated until after its rupture and the appearance of pus in the matters regurgitated or otherwise expelled from the oesophagus.

Catheterism of the oesophagus is hardly justifiable as a method of diagnosticating oesophagitis, though proper enough when it becomes important to determine the locality of attendant obstruction.

It is important that inflammation of the oesophagus be differentiated from spasm, stricture, stenosis, carcinoma, and other oesophageal maladies; nearly all of which present the same main subjective symptoms—pain and impediment to deglutition. The history of the case is in itself a guide of great diagnostic value, often quite sufficient for the purpose; but in its absence or retention other data must be gathered.

Spasm of the oesophagus is most frequent in neurotic subjects. Its manifestations are often sudden. It is evanescent or intermittent. It is not a febrile affection. It is often overcome in a moment by catheterization.

Stricture presents often an additional symptom of oesophagitis, the regurgitation of mucus and food. The differentiation is made, in cases of doubt, by the passage of the bougie or catheter.

Carcinoma of the oesophagus, while recent, may present much similitude to oesophagitis, but as the case advances, the glandular involvements, the cachexia, the expulsion of cancerous fragments, and the vomiting of blood seem sufficient to prevent further confusion.

PROGNOSIS.—The prognosis is favorable in acute catarrhal oesophagitis, the manifestations often subsiding within a few days; sometimes, indeed, within a few hours, and that, too, without special medication. It is therefore largely dependent on the cause of the oesophagitis and the severity and extent of the malady. The only unfavorable prognostications arise from the impediment to nourishment and the complications which may ensue.

In presumptive pustulous oesophagitis from the use of preparations of antimony, the manifestations usually subside within a few days upon suspension of the remedy. Sometimes, however, these cases terminate fatally.

Pseudo-membranous oesophagitis is usually fatal in its significance, and the same may be said of the pustulous or ulcero-papular oesophagitis of small-pox.

Phlegmonous oesophagitis is of grave augury, though many cases recover. It may prove fatal within two or three days, though life is usually prolonged for several days, even in fatal cases. When not fatal, abscesses are apt to form, which, discharging internally or externally, are followed by stricture or fistulæ.

Both ulcerative oesophagitis and intense catarrhal oesophagitis may terminate in chronic thickening of the walls of the oesophagus and in cicatricial adhesions more or less extensive.

TREATMENT.—Mild oesophagitis requires no special treatment. The patient should be kept within doors, and be fed on rice-water, barley-water, and other mucilaginous articles of diet, so as to avoid all sources of local irritation. These drinks are usually better borne hot than cold, but sometimes cold is quite agreeable. When cold can be well borne the frequent deglutition of pellets of ice is useful as well as agreeable, and ice-cream becomes a medicinal article of diet.

In severe cases the measures indicated become still more requisite, and the use of the voice should be restrained in addition. All unnecessary efforts at deglutition should be avoided, and anodyne medicaments (opium, hyoscyamus, belladonna) should be added to the demulcent food or beverages. When swallowing is impracticable or very painful, nutriment should be given by the bowel, and medicines by the bowel or by the skin. Thirst may be allayed by retaining fragments of ice in the mouth from time to time, by rinsing the mouth with simple or acidulated water, by sucking the juice of acid fruits, or by allowing compressed effervescent lozenges to dissolve slowly in the mouth.

The external application of cold compresses, continuously or in frequent renewals, is also indicated.

Febrile phenomena require ordinary antiphlogistic medication. When this is impracticable, the indications may be met by using the cold bath or the wet sheet, and by administering antipyretics hypodermatically. Traumatic oesophagitis from a foreign body requires removal of the object if still in the oesophagus; that from swallowing alkalies is met by the use of acidulated beverages (vinegar and water, Orfila); that from swallowing acids, by the use of alkaline drinks, of which the handiest is usually soap and water. As soon as they can be procured this may be changed for lime-water and calcined magnesia. Theoretically, the carbonates of the alkalies are indicated likewise, but it is contended (Hamburger, Oppolzer) that the extrication of the carbonic acid gas renders mechanical rupture of the corroded oesophagus imminent. Subsequently, fresh water should be freely drunk, or be injected into the oesophagus when swallowing is impracticable. The subsequent treatment is to be instituted upon general principles.

Chronic Oesophagitis.

DEFINITION.—A chronic inflammation of some of the tissues of the oesophagus.

SYNONYM.—Oesophagitis chronica.

ETIOLOGY.—Chronic oesophagitis is sometimes a sequel of the acute affection. More frequently it is the result of excessive use of strong alcoholic beverages or of very hot drinks. It is said to be sometimes the result of passive congestion in chronic pulmonary and cardiac diseases. It follows the prolonged sojourn of foreign bodies in the oesophagus. It exists in connection with carcinoma of the oesophagus, with dilatation, and with stricture of the oesophagus, and with other diseases obstructing the tube externally or internally. It is sometimes produced by caries of the vertebræ, both scrofulous and syphilitic, and by the pressure of aneurismal and other tumors.

PATHOLOGY AND MORBID ANATOMY.—Hypertrophy of the mucous membrane of the oesophagus, of the submucous connective tissue, and even of the muscular coat, are the processes which take place in chronic oesophagitis, especially when it has been of long continuance. This hypertrophy, when at or near the cardiac extremity, may produce stricture (Rokitansky and others), with subsequent dilatation of the oesophagus from its frequent and prolonged distension by food which should have passed on at once into the stomach.

On post-mortem examination the main evidences of disease are most frequent in the lower third of the organ. Its folds of mucous membrane are thick and prominent, dirty red, brownish-red, or gray, as may be, abraded here and there, and covered with viscid muco-purulent secretions. Abscesses and ulceration are not uncommon in cases due to prolonged pressure or extension of disease from outside the tube. Such ulceration has not uncommonly been the source of serious hemorrhage.

Diffuse inflammation of the peri- or retro-oesophageal connective tissue has been noted as an occasional sequel to the inflammatory process in the walls of the oesophagus.

SYMPTOMATOLOGY, ETC.—The symptoms of simple chronic oesophagitis are similar in the main to those of mild acute oesophagitis, but are often still more moderate, and therefore likely to be overlooked. In severe cases the symptoms are chiefly those of the disease, usually stenotic, which has excited the chronic inflammatory process. The course is prolonged and the duration indefinite. Stricture is a frequent sequel.

DIAGNOSIS.—The diagnosis rests on the same principles and inferences as in acute oesophagitis, the symptoms, however, being of longer duration. The auscultatory signs of arrest or impediment in the descent of the solid or liquid bolus are usually more definite than in acute oesophagitis. The same differentiations are available in excluding spasm, stricture, and malignant diseases. The use of the sound or catheter is much more justifiable than in the acute variety.

PROGNOSIS.—The prognosis is usually unfavorable, on account of the great liability to stricture and occlusion from organization of inflammatory products.

TREATMENT.—Chronic oesophagitis may require both local and constitutional treatment. The constitutional treatment will have to be adapted to the cause of the disease. If due to obstructed circulation in consequence of valvular disease of the heart, digitalis and remedies of its class will be indicated. If due to obstructive pulmonic disease, chloride of ammonium and alkaline remedies will be indicated. Syphilitic inflammation requires the mixed treatment, with mercuric chloride and potassium iodide or their equivalent. Iodides, indeed, are often required in non-specific cases, and are useful particularly in ordinary circumscribed oesophagitis. Under all conditions alcoholic beverages should be interdicted, and so should the deglutition of all irritating food and drink. Mild, bland, and mucilaginous substances should be largely employed in food and drink. The copious use of carbonic-acid waters is also recommended (Oppolzer). Sinapisms and revulsives to the side of the cervical and dorsal vertebræ are also recommended by some writers (Oppolzer).

The topical treatment consists in the systematic use every few days of aqueous solutions of astringents (alum, tannin, ten to thirty grains to the ounce) or alterants (compound solution of iodine, twenty minims to the ounce) passed gently over the diseased surfaces by means of a piece of soft surgical sponge securely attached to a flexible staff.

Severe pain of rather sudden occurrence is usually attributable to circumscribed ulceration, and is best treated by superficial cauterization, as above, with a dilute solution of silver nitrate (ten grains to the ounce). These remedies may be used in the form of ointments of the same strength smeared upon a rather large flexible bougie. To relieve pain and sense of constriction belladonna or stramonium ointment, applied in the same manner, sometimes fulfils a useful indication. Before making these applications attempts should be made by auscultation to locate the seat of disease or obstruction. After subsidence of the disease, occasional catheterization may be practised at intervals of several weeks, in order to detect any recommencing stenosis.

Ulcerations of the Oesophagus.

DEFINITION.—Circumscribed destruction of portions of the mucous membrane of the oesophagus, the result of inflammatory processes.

ETIOLOGY.—Ulceration of the oesophagus occurs as a result of inflammation of the organ, as discussed in connection with Oesophagitis, and the cause varies with the character of the oesophagitis, whether idiopathic, traumatic, or symptomatic of disease elsewhere. Diseases, constitutional or local, provocative of ulceration of the oesophagus, usually implicate some portion of either the alimentary or the respiratory tract.

SYMPTOMATOLOGY.—The symptoms are in the main those described under Acute Oesophagitis, particularly the expulsion of sanguinolent products or of unmixed blood. Perforation into the trachea is indicated by expectoration of food or drink; perforation into the great vessels, by hæmatemesis, usually fatal; and perforation into the mediastinum, by emphysema and purulent cellulitis. When large or extensive ulcerations have cicatrized they occasion symptoms of organic stricture.

PATHOLOGY AND MORBID ANATOMY.—Referring to the corresponding section under Oesophagitis, attention may be directed here to the liability of deep-seated ulcers of the oesophagus to perforate the gullet and establish fistulæ with the trachea, bronchi, mediastinum, aorta, and carotid artery, according to the locality of the lesion. These lesions are usually necessarily fatal.

DIAGNOSIS.—The presence of blood in matters regurgitated or vomited forms the chief diagnostic indication of ulceration of the oesophagus, taken in connection with the usual symptoms of acute or chronic oesophagitis.

PROGNOSIS.—The prognosis is altogether dependent on the nature of the disease which has given rise to the ulceration.

TREATMENT.—The constitutional treatment will depend on the nature of the disease which has occasioned ulceration. Ergot and turpentine are administered in case of hemorrhage—the former best, perhaps, hypodermatically. Attempts are sometimes made to cauterize the ulcer or ulcers with nitrate-of-silver stick conveyed in a covered slotted canula, to be exposed when the fenestrum reaches the ulcerated locality, previously determined by catheterization, or inferred to be reached by the sensations of the patient. The practice is uncertain in its manipulation and questionable in its results.

Stricture of the Oesophagus.

DEFINITION.—A constriction of the calibre of the oesophagus, whether spasmodic or organic in character. This definition excludes stenosis due to pressure from without.

Spasmodic Stricture of the Oesophagus.

DEFINITION.—A contraction of the muscles of the oesophagus, of variable duration, causing partial or complete stenosis of the gullet and interfering with the passage of food or of food and drink to the stomach.

SYNONYMS.—Oesophagismus, Spasm of the oesophagus, Cramp of the oesophagus, Convulsive dysphagia, Spasmodic dysphagia, Spasmodic stenosis of the oesophagus, Spastic stricture of the oesophagus.

HISTORY.—On this subject there is little of importance in medical annals previous to the observations of Frederick Hoffmann,¹⁵ and little of importance subsequently save the observations of Mondière,¹⁶ though numerous personal observations are on record, as well as a number of excellent compilations in various monographs, text-books, encyclopædias, and dictionaries.

¹⁵ De spasmo gulæ inferioris, Halæ, 1733; De morbis oesophagi spasmodicis, Opera omnia, vol. iii., Geneva, 1761.

¹⁶ "Recherches sur l'Oesophagisme ou Spasme de l'Oesophage," Arch. gén. de Méd., April, 1833.

ETIOLOGY.—Spasmodic stricture of the oesophagus is a neurosis often hysterical. It is much more frequent in females than in males, and, although observed in young subjects and less frequently in old ones, is most common between the ages of twenty and fifty. It is sometimes observed in several members of a neurotic family. It is often associated with other evidences of neurosis, but sometimes constitutes the sole manifestation. Sometimes the cause defies detection. Sometimes it can be traced to a fear of strangulation, induced primarily by some accidental impediment to deglutition or the entrance of a foreign body. Strong mental emotion, such as the dread of hydrophobia after having been bitten by a dog, sometimes produces the affection.

It occurs in connection with organic lesions of the oesophagus, organic lesions of the stomach, organic lesions of the larynx and trachea, and organic lesions of the lungs, heart, large blood-vessels, and perioesophageal tissues, but likewise as a reflex disorder, with lesions of distant organs, as the genito-urinary tract, the intestines, the brain and spinal cord. Even pregnancy may produce reflex oesophagismus. It sometimes occurs as a direct or reflex manifestation of gout and of rheumatism. In a few instances it occurs as one of the manifestations of tetanus and of hydrophobia.

SYMPTOMATOLOGY, COURSE, DURATION, ETC.—The spasm may affect the oesophagus only, or may be associated with spasm of the muscles of the pharynx. It is usually manifested in a sudden inability to swallow or to complete the acts of deglutition. This may be transitory or may continue for a number of hours. The relaxation of the spasm is sometimes followed by the discharge of flatus and the copious secretion of pale urine. The spasm may recur at irregular intervals or be more or less distinctly intermittent. Sometimes it precedes every effort at deglutition. In some instances it occurs only upon attempts to swallow certain kinds of food, and the articles of food vary with different patients. Cold viands sometimes produce spasm when warm and hot food is tolerated. Consciousness of a liability to spasm increases the dysphagia for the time being, or brings it on suddenly when this liability had been forgotten. The spasm is sometimes painless and sometimes painful. In some instances it is associated with partial regurgitation of a mass of air (the globus hystericus).

The dysphagia is rarely complete, instances in which no liquids can be swallowed being infrequent. The aliment swallowed usually passes on into the stomach, upon relaxation of the spasm, after a certain period of detention varying from a number of seconds to many minutes. In cases of prolonged or persistent spasm the aliment is usually rejected, either at once or after a time, according as the contraction takes place at the pharyngeal extremity of the oesophagus or lower down. When rejected after some detention in the gullet, the aliments are usually enveloped with mucus or followed by expulsion of mucus and of flatus.

In some subjects the pain in swallowing is severe. Sometimes it is associated with spasm of the diaphragm (hiccough), spasm of the air-passages, palpitation of the heart, and syncope.

The liability to spasm sometimes continues for years. Sometimes it ceases permanently as suddenly and as unexpectedly as it began.

The seat of the spasm is referred by the patient to different regions, which in their totality comprise the entire extent of the oesophagus. In some patients the seat varies on different occasions. The actual seat of any individual spasm is best determined by exploration with the oesophageal bougie or by auscultating the oesophagus during the passage of a bolus. It is most frequent perhaps at the upper extremity, and then perhaps at the cardiac extremity. When habitually low down, there is some liability to permanent distension of the oesophagus from repeated retentions of food at the same place for hours together. In some instances food is regurgitated from the oesophagus after its retention for a day or even longer. When the spasm is high up, the regurgitation may follow the act of deglutition almost immediately.

PATHOLOGY AND MORBID ANATOMY.—The affection being usually a pure neurosis, there is no oesophageal lesion to be cited. In some of the few autopsies recorded, constriction has been noted without lesion of tissue.

DIAGNOSIS.—The diagnosis is based on the sudden onset of the spasm without assignable cause, its intermittent or recurrent character, its manifestation in advance of the effort at deglutition, the symptoms of regurgitation, the coexistence of some of the affections mentioned in connection with its etiology, and on the satisfactory result of exploration with the oesophageal bougie; which differentiates the affection from organic stricture or mechanical obstruction. In catheterization of the oesophagus in cases of pure spasm, although the sound is usually arrested at the seat of constriction, it passes onward after a few moments by sudden relaxation of the spasm. Sometimes, indeed, the very first manipulation of this kind overcomes the spasm permanently.

In the absence of other indications the differentiation from spasm of organic origin rests, in great measure, on the conservation of nutrition, cases being few in which the spasm is persistent enough to interfere so materially with the ingestion of aliment as to produce emaciation.

PROGNOSIS.—The prognosis is usually favorable in spasm of the oesophagus, except in cases where the underlying malady is itself a grave one. Patients do not die of neurotic spasm of the oesophagus. In the majority of cases it is susceptible of cure within a few weeks, sometimes much more promptly. Even when it continues for months or for years there is little fear of permanent injury to the general health, inasmuch as sufficient nutriment of some kind or other can be ingested to sustain the patient.

The duration of the affection depends upon the surroundings of the patient, his amenability to treatment, and the existence or absence of disease in the oesophagus or elsewhere. In cases dependent upon diseased conditions in the oesophagus or elsewhere the character of the disease controls the prognosis, both immediate and ultimate. Thus, aneurism of the aorta, tuberculosis, ulceration of the larynx and trachea, carcinoma of the stomach, tetanus, and hydrophobia present the highest unfavorable indications. Purely neurotic cases are extremely prone to recurrence.

TREATMENT.—The treatment to be pursued will depend upon the nature of the case. If due to organic lesion in the oesophagus or in some other organ, the treatment will be directed to that affection, whatever it may be. If due to emotional disturbance, therapeutic efforts will be directed to their suppression or removal. If purely hysterical, appropriate constitutional remedies for that condition will be prescribed. These comprise asafoetida, valerian, camphor, musk, oxide of zinc, bromides, belladonna, conium, and so on, best administered in small doses at frequent intervals.

Local treatment is almost always necessary, both for its beneficial mechanical effects and for its emotional influence. This consists in the systematic passage of the bougie; and it is by far the best practice to insist upon the patient's submission to it without an anæsthetic. In cases of intense hyperæsthesia, which are rare, and in the initial exploratory passage of the instrument in highly excitable or uncontrollable subjects, anæsthesia may be resorted to if there be no contraindication. The mere passage of the bougie will often effect immediate relaxation of the spasm. When required, the manipulation may be repeated a few times at intervals of several days. Should the passage of the bougie determine the stricture to be purely spasmodic, the patient should be made to partake of food in the physician's presence at first, and afterward under the supervision of an efficient attendant, until it becomes evident that there is no absolute impediment to the passage of food. The presence of the physician during early attempts at taking ordinary food imparts such confidence in the patient that he soon overcomes his dread of strangling and learns to eat again as he should do. Meantime, it may be necessary from time to time to pass the bougie just before food is taken. In such cases it is well to smear the instrument with ointment of belladonna, so as to deposit it more or less along the entire tract of the oesophagus. Failing by these methods, success may follow the occasional passage, at intervals of a few days, of a sponge probang saturated with a very weak solution of iodine or of silver nitrate.

Counter-irritation along the course of the pneumogastric nerve or along the spine is sometimes useful.

Electricity is sometimes employed to overcome the spasm; but intra-oesophageal electrization of every kind is risky from the danger of exciting fatal syncope from irritation of the pneumogastric nerve. This objection is not applicable to percutaneous electrization, save in a much more limited degree. Caution is requisite even with external manipulations along the tract of the pneumogastric nerve; and such manipulations, therefore, should not be undertaken without sufficient familiarity with the effects of electric currents in that situation.

Taken all in all, the best results seem to follow the systematic use of the bougie and enforced deglutition under the eye of an attendant in whom the patient feels reliance can be placed in case the food should "go the wrong way" or become impacted in the gullet.

Organic Stricture of the Oesophagus.

DEFINITION.—Diminution in the calibre of the oesophagus in consequence of organic alterations in its walls, whether interstitial, cicatricial, or malignant.

SYNONYM.—Stenosis of the oesophagus.

HISTORY.—As mentioned in connection with other affections of the oesophagus, so with organic stricture: though much more has been written on the subject, it is to the observations and publications of Mondière, so frequently cited, that we must credit medical literature with a due appreciation of this topic. The last thirty years especially have been prolific in the record of cases, and their study has been further stimulated by the attention directed to the operation of gastrostomy as a means of prolonging life in cases otherwise hopelessly fatal.

ETIOLOGY.—Organic stricture of the oesophagus is occasionally congenital. As a rule, life is rarely prolonged under such conditions, but cases are on record in which it has been preserved to quite advanced age. Thus, in a female who died from inanition at fifty-nine years of age, after lifelong symptoms of stricture (Everard Homes¹⁷), there was an annular stricture behind the first ring of the trachea; and in a male subject who died with pneumonia at seventy-four years of age, after lifelong symptoms of stricture,¹⁸ the stricture was found at the cardiac extremity of the oesophagus, which was enormously dilated its entire length above the constriction.

¹⁷ Biblioth. méd., t. viii. p. 260; Michel, Dict. Encyclopedique, t. xiv. p. 466.

¹⁸ Wilks, Path. Trans. London, xvii. p. 130; Holmes, The Surgical Treatment of the Diseases of Infancy and Childhood, 2d ed., p. 137.

In the majority of cases the stricture is due to cicatricial obliteration of more or less of the calibre of the oesophagus, the result of losses of substance following scalds produced by caustic substances swallowed, mostly by accident and sometimes by design. Wounds of all kinds, whether from the interior, as in the case of foreign bodies and instruments of extraction, or from the exterior, as in the case of surgical operations, wounds from firearms, and the like, are apt in their cicatrization to give rise to this form of stricture.

Though denied by some authorities, syphilitic disease of the oesophagus is an undoubted cause of stricture. Setting aside disputed records of older authorities, we may cite recent cases reported by Lancereaux, West,¹⁹ Wilks, Virchow, and Lublinski,²⁰ the latter-named going deeply into the bibliography, pathology, and therapeutics of stricture from syphilis. The author could add his personal testimony were it requisite.

¹⁹ The Lancet, 1872.

²⁰ Berlin. klin. Woch., Aug. 20, 1883; London Medical Record, Nov. 15, 1883, p. 489.

Stricture of the oesophagus is likewise occasioned by the presence of papillomatous, fibroid, and other morbid growths. Carcinoma is quite a frequent cause.

The frequent deglutition of undiluted spirituous liquors is said to give occasion at times to stricture of the oesophagus, but in these instances this result is usually due to precedent chronic oesophagitis thereby excited, and terminating in infiltration and hyperplasia of the submucous connective tissue, and sometimes great thickening of the epithelium as well.

Males are more frequently the subjects of stricture of the oesophagus, and early adult life the most frequent period for its occurrence, though it may present at any age.

SYMPTOMATOLOGY.—Except in traumatic cases, the earliest symptoms, preceded in some instances by indications of mild oesophagitis, perhaps unnoticed or unrecognized, are occasional impediments to deglutition of large and firm boluses, or rather a mechanical obstacle to completion of the act of glutition occurring at intervals of a few meals or a few days. After a while the swallowing of a large solid bolus becomes permanently impracticable. Then, sometimes, repeated efforts become necessary to swallow small masses of solid food; and even to do this may require external manipulation, or at least the additional pressure of liquids swallowed immediately after the solid bolus. These efforts are sometimes attended with spasm, regurgitation, and pain, and may be accompanied in addition with tracheal dyspnoea, and with nervousness in consequence. As the disease progresses it becomes impossible to swallow solid food, and subsequently even fluid food in extreme cases. The bolus is then often regurgitated immediately after its deglutition, and may be covered with mucus, blood, pus, or fragments or detritus of ulcerated malignant growth, according to the nature of the case. Pain and sensations of rawness are often felt at the point of constriction, whence the pain often radiates toward one or both scapulæ. If the tube is much dilated above the stricture, the food may be detained in the sac for several hours, and then be regurgitated in a softened, partially-decomposed condition. Should the mass be so situated as to compress the trachea, suffocative symptoms may be produced.

In stricture due to organic disease there may be dysphonia from pressure or injury to the recurrent laryngeal nerve producing paralysis of the vocal band. The anatomical relations of the left recurrent nerve renders it the much more liable of the two to become implicated. Moderate dyspnoea may result from this paralysis by reason of the reduced space of the glottis.

PATHOLOGY AND MORBID ANATOMY.—Organic stricture of the oesophagus is usually due to disease or structural change involving the mucous membrane and submucous connective tissue; but the muscular structure may become involved likewise. It may, however, be due to abnormal laxity of the mucous membrane, permitting a fold to occupy a position impeding the passage of the bolus.

In cases which are not carcinomatous the diminution in the actual calibre of the tube is usually due to submucous proliferation of connective tissue and to thickening of the mucous membrane. The encroachment on the calibre of the tube may be quite slight, or may be so great as to amount to almost complete occlusion.

The seat of stricture is at the upper portion of the oesophagus most frequently, then at the cardiac extremity, at the point of crossing by the left bronchus, and at the point of passage through the diaphragm—all localities slightly constricted normally—but it may occur at any portion.

In most instances the stricture is single. There may, however, be two, three, or even four strictures. Multiple strictures are most common after deglutition of caustic substances which have made their way clear down into the stomach.

Syphilitic strictures are usually single, and so, as a rule, are strictures of malignant origin. The latter are much larger in extent.

Cicatricial strictures from caustic substances may be in the form of bands, rings, or longitudinal stripes or folds. Sometimes they are quite extensive, and have been known to interest fully one-third of the length of the oesophagus. The circumference, length, calibre, and thickness of the stricture, however, vary within the most extreme limits. Occasionally occlusion of the tube is complete.

The detention of food above the stricture usually dilates the oesophagus, producing hypertrophy of the mucous membrane and submucous connective tissue, followed in its turn by fatty degeneration. Atrophy of the oesophagus may ensue below the stricture if at all tight, and the mucous membrane becomes thrown into longitudinal folds.

DIAGNOSIS.—The diagnosis of organic stricture of the oesophagus rarely presents difficulty. Dysphagia, spasm, and regurgitation are quite characteristic of stricture. When the constriction is high up, the vomiting or regurgitation of food may closely follow its deglutition; when low down, this act may be delayed ten or fifteen minutes, in some cases for hours. Alkaline reaction of the vomited matters is indicative of their having failed to reach the stomach. The presence of blood-cells, pus-cells, and cancer-cells indicates ulceration, suppuration, and malignant disease, respectively.

Auscultation of the oesophagus during deglutition of water will indicate the seat of stricture by revealing the ascent of consecutive air-bubbles even when palpation with bougies fails. The passage of oesophageal bougies or the stomach-tube into the oesophagus will often reveal the point of stricture. Its length is estimated by the distance of the resistance offered to the passage of the instrument; its diameter, by the size of the largest instrument which can be passed through it; and its consistence, by the character of the resistance. Care is requisite in manipulating with these instruments, lest by undue exertion of force they be passed through an ulcerated portion of the wall of the tube or a diverticulum. The character of the resistance is sometimes the sole means of differentiating stricture from stenosis due to compression of the oesophageal wall from its outside.

It sometimes happens, in individuals with impaired sensitiveness of the epiglottis or vestibule of the larynx, that the exploratory bougie is introduced into the air-passage instead of the gullet. The usual premonitory phenomena of suffocation will indicate the mistake. There is some likelihood, too, of entering the larynx in individuals with unusually prominent cervical vertebræ and in cases of stricture at the extreme upper portion of the oesophagus. In introducing these instruments into the oesophagus, therefore, it is well that they be guided along the fore finger of the disengaged hand, and passed deeply into the throat, either to the side of the larynx or behind it. By keeping to the side and reaching the oesophagus by way of the laryngo-pharyngeal sinus the risk of entering the larynx may be avoided. Before introducing the tube the case should be carefully examined for aneurism, which by pressure sometimes gives rise to the ordinary subjective symptoms of stricture. Should aneurism be detected, passage of the tube would be hazardous.

PROGNOSIS.—The prognosis is in most instances unfavorable. It is comparatively favorable in cases of moderate stricture due to causes apparently remediable. The extent and volume of the stricture progress more or less slowly according to the nature of its cause, and in non-malignant cases, such as are due to the action of caustic substances, it may last for years before the patient, if not relieved, succumbs, as he does, from gradual inanition. In the earlier stages, before the hypertrophied muscles above the stricture undergo fatty metamorphosis, the increased muscular power is sufficient to force nourishment through the stricture; but when this becomes no longer possible progressive marasmus must ensue. Meantime, abscess may become developed in consequence of the pressure of retained food, and tuberculous degeneration of the lung and local gangrene may take place in consequence of the malnutrition.

TREATMENT.—The treatment of organic stricture of the oesophagus resolves itself into maintenance of the general health, the administration of the iodides to promote absorption of effusions into the connective tissue or the muscles, mechanical and operative measures for removal of the causes of the constriction or the strictured tissues themselves, and operations for securing artificial openings below the point of stricture for the introduction of nourishment (oesophagostomy and gastrostomy). Nourishment by enema is of great value.

In carcinomatous stricture local measures are in the main unjustifiable, as they usually entail injury which may prove very serious. Arsenic internally is thought to retard the progress of malignant disease when administered early and persistently. Morphine is used hypodermically to assuage pain.

In cancerous and tuberculous disease great caution is requisite in determining upon mechanical or surgical procedures. In cicatricial stenosis from the effects of caustic substances, such measures may be undertaken with much less consideration.

The local treatment consists in systematic mechanical dilatation with bougies or mechanical dilators properly constructed. These are employed 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 reported²¹ 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.

²¹ Trans. Internat. Med. Congress, London, 1881, vol. ii.

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.

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 (Newman²²). 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 may be involvement of the pneumogastric nerve, with reflex influence on the spinal nerves and the sympathetic (Gurmay²³).

²² N.Y. Med. Journ., Aug., 1879, p. 158.

²³ Bull. méd. de l'Aisne, 1869; Gaz. méd. Paris, April, 1872.

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 (Reid²⁴).

²⁴ N.Y. Med. Journ., Oct., 1877, p. 404.

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.

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 (Finny²⁵). 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.

²⁵ Dub. Journ. Med. Sci., Oct., 1877.

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.

There is more or less flow of saliva from the mouth in consequence of the inability to swallow it; and in some cases the losses of material from the blood are so great as to reduce the patient very rapidly.

PATHOLOGY AND MORBID ANATOMY.—Paralysis of the oesophagus may be partial or complete. It may be associated with paralysis of the pharynx, palate, tongue, epiglottis, or larynx; with so-called bulbar paralysis; with general paralysis; with cerebro-spinal disseminated sclerosis.

DIAGNOSIS.—The diagnosis rests mainly on the symptoms of dysphagia, especially when associated with paralyses elsewhere. It is differentiated from paralysis of the pharynx by the ability to swallow the bolus and the apparent arrest of the bolus at some portion of the tube. Auscultation of the oesophagus will determine the locality of the arrest. It likewise affords presumptive evidence of an alteration in the usual form of the bolus, which, being subjected to compression at its upper portion only, assumes the form of an inverted cone. The remaining auscultatory indications are similar to those of dilatation.

There is no impediment to the passage of the stomach-tube or oesophageal sound, or to its free manipulation when within the oesophagus.

When the symptoms quickly reach a maximum, they indicate a paralysis due to apoplexy, and so they do when the symptoms are sudden, hysteria being eliminated. Paralysis due to gumma or other cerebral tumor is much slower in its course.

PROGNOSIS.—In idiopathic paralysis, the local or special affection to which it is due being curable, the prognosis is favorable, especially if the paralysis be confined to the oesophagus. Recovery, however, is often slow, even in curable cases. In hysterical paralysis the prognosis is good. In deuteropathic paralysis the prognosis is much less favorable, and will depend upon the nature of the causal disease—apoplexy, insanity, cerebral tumor, syphilis, etc.

TREATMENT.—The treatment varies with the nature of the cause as far as combating the origin of the disease is concerned. With regard to the intrinsic paralysis of the oesophagus itself, strychnine and its congeners are indicated, and may be administered hypodermatically if the difficulty in swallowing be very great. If the paralysis be partial, it is better to give nux vomica or Ignatia amara by the mouth, in hopes of getting some beneficial astringent influence on the walls of the oesophagus.

In all instances the feeding of the patient is an important element in treatment. Masses of food arrested in the tube should be forced onward with the sound. In some cases nourishment must be habitually introduced through the stomach-tube and nutritive enemata be resorted to.

Electricity, though sometimes successful, is a risky agent to employ, because, as announced by Duchenne, the use of an oesophageal electrode is attended with some risk of unduly exciting the pneumogastric nerve and thereby inducing syncope.

Dilatation of the Oesophagus.

DEFINITION.—An abnormal distension of a portion of the oesophagus or of the entire tube, whether general, annular, or pouched.

SYNONYMS.—Oesophagocele, Hernia of the oesophagus, Diverticulum of the oesophagus.

ETIOLOGY.—Dilatation of the oesophagus is occasionally met as a congenital affection (Hanney,²⁶ Grisolle,²⁷ and others). The cause under these circumstances is obscure. Usually, however, dilatation of the oesophagus is of mechanical origin, due to distension by food or water above a stricture or an impacted foreign body. Presumptive paralysis of the muscular coat in chronic oesophagitis is alleged as a source of similar distension.

²⁶ Edinb. Med. and Surg. Journ., July, 1883.

²⁷ Traité Élément. de Path. int., Paris, 1883, ii. p. 358.

General dilatation is presumed to be the mechanical result of constriction of the cardiac extremity, leading to distension of the oesophagus by the accumulation of large quantities of liquids. Sometimes it is due to paralysis of the muscular coat, permitting its distension by food.

Annular dilatation is sometimes due to distension just above the seat of a stricture. Sometimes it is due to impaction of a foreign body; sometimes there is no mechanical impediment; occasionally it is observed as a congenital anomaly.

Pouched dilatation (diverticulum) is usually due to retention of food immediately above an impacted foreign body or some obstruction of another character. Some of the muscular fibres of the oesophageal wall become separated and spread asunder, allowing the mucous membrane to be gradually forced through them by repeated efforts of deglutition upon retained masses of food or drink, until finally a pouch is formed, hernia-like, outside of the tube. Another mode of production is said (Rokitansky²⁸) to consist in the subsidence of tumefied glands outside the oesophagus, after adhesions had been contracted with the oesophagus during the inflammatory process. The shrinking of these enlarged glands to their normal volume sometimes draws the tube outward into a funnel-shaped sac constricted at its margin by the muscular coat, which has receded from the pouch or has been stripped loose. The same form of dilatation is likewise an occasional result of rupture of the muscular coat sustained in blows or falls. It occasionally exists, too, as a congenital defect, and this has been attributed (Bardeleben and Billroth²⁹) to partial closing of one of the branchial fissures externally, while the internal opening has remained patent.

²⁸ Archiv. gén. de Méd., 1840, p. 329.

²⁹ Trans. Clin. Soc. London, 1881, p. 130.

SYMPTOMATOLOGY.—The symptoms, at first, are usually those of obstruction to the passage of food, but before this obstruction occurs dilatation may have existed without symptoms. In some cases of diverticulum high up, there is a tumor, usually on the left side of the neck. Rokitansky has reported one the size of the fist situated on the right side of the neck, and Hankel³⁰ and others a tumor upon each side. The tumor varies in bulk from time to time according as it may be empty or may be distended with food, drink, or gas.

³⁰ Rust's Mag., 1833; Dict. Encycl., loc. cit.

Food caught in the pouch can often be forced out into the pharynx by external pressure over the tumor in the neck. The retention of food above a constriction or in a sac is usually accompanied by some distress after indulgence in too much food. This uneasiness becomes relieved upon regurgitation or vomiting. Deglutition is impeded to a less extent when the disease does not implicate the upper portion of the gut.

Complete dilatation is sometimes indicated by long addiction to habits of rumination. In some instances this rumination is an agreeable sensuous process. In pouched dilatation it is very often disagreeable, the regurgitated matters being acrid, owing to acid fermentation of the contents of the sac.

While the dilatation remains moderate there may be little dysphagia or none at all, the muscles continuing sufficiently vigorous to propel the food; but after the muscles become paralyzed by distension the dysphagia gradually increases and may culminate in complete aphagia. One of the special indications of diverticulum is that the regurgitation does not take place until several hours after a meal. As the sac enlarges there may be less and less complaint of dysphagia, because it becomes able to contain larger quantities of food. At the same time it may so compress the main tube as to occlude its calibre and prevent access of food to the stomach.

The symptoms of annular dilatation are similar to those of stricture with retention of food above it, the regurgitation usually following deglutition more quickly.

In some cases of dilatation, circumscribed and general, food is sometimes retained for an entire day or more before it is ejected. The decomposition of the retained food usually produces a more or less continuous foul odor from the mouth.

The course of the affection is progressively from bad to worse, and entails ultimate emaciation. Some patients succumb early, and some live to advanced age. Perforation of the oesophagus ensues in some instances, and death results in consequence of the injuries sustained by perioesophageal structures by the escape of the contents of the oesophagus. Perforation is indicated by sudden collapse and by emphysema from swallowed air.

PATHOLOGY AND MORBID ANATOMY.—Dilatation of the oesophagus is either general or partial, according as it takes place in the whole or greater portion of the oesophagus or in a circumscribed portion. Partial dilatation may involve the entire circumference of the canal (annular dilatation), or it may implicate but a portion of the wall, which becomes pouched into a sac externally (diverticulum or saccular dilatation).

FIG. 19.

Fusiform Dilatation of Oesophagus (Luschka). A, Larynx; B, Thyroid gland; C, Trachea; D, Oesophagus; E, Stomach.

General dilatation, though sometimes congenital, is, as mentioned under Etiology, more frequently the mechanical result of distension of the oesophagus by food or drink prevented from ready entrance into the stomach by a constriction at the cardiac orifice. This form of dilatation is sometimes discovered as a post-mortem curiosity. The muscles have usually undergone great hypertrophy, and the mucous membrane some thickening and congestion, with erosions and sometimes ulcerations, indicative of chronic oesophagitis. In some instances all the coats of the oesophagus have undergone hypertrophy. The dilatation may vary from slight enlargement to the thickness of an ordinary man's arm or larger (Rokitansky³¹); in rare cases, even a capacity nearly equal to that of the stomach (Luschka³² and others). (See Fig. 19.)

³¹ Path. Anat.

³² Arch. für Anat., etc., March, 1868, p. 473.

The oesophagus is usually fusiform or spindle-shaped, being constricted at those portions at which it is normally slightly constricted. Sometimes the dilatation takes place between the lobes of the lungs (Raymond³³).

³³ Gaz. méd. de Paris, 1869, No. 7, p. 91.

Annular dilatation is usually due to circumferential distension just above a stricture. When not due to stricture its seat is usually just above the diaphragm, where the oesophagus is normally liable to constriction. The upper portion of the dilatation is larger than the lower portion, and the muscular walls are usually hypertrophied.

Pouched dilatation (diverticulum) is usually formed chiefly of mucous membrane and submucous tissue pushed through gaps in the fibres of the muscular coat, produced by distension. It sometimes involves the entire coat in cases in which the oesophageal wall has become adherent to enlarged lymphatic glands, which subsequently undergo subsidence in volume and drag the adherent portion of the wall after them (Rokitansky). The muscular walls are then usually hypertrophied, the mucous membrane sometimes hypertrophied, sometimes atrophied. The diverticulum is usually located in the upper portion of the oesophagus, just below the inferior constrictor muscle of the pharynx. It may thus be, in part, a pharyngocele also. It may be located behind the point of bifurcation of the trachea or where the oesophagus is crossed by the left bronchus. Its direction may be to the left side in the upper portion of the oesophagus, to the right side, or upon both sides; but when situated lower down it is usually directed backward, between the posterior wall of the tube and the spinal column. Hence its distension with food completely blocks up the calibre of the oesophagus. The orifice by which the oesophageal wall remains in communication with the pouch is round or elliptic in shape and variable in size, sometimes being about an inch in its long diameter, sometimes much smaller. The size of the diverticulum varies; a common size is that of a duck egg, but the size of a fist has been attained. Sometimes the diverticulum drags the oesophagus out of position and forms a sort of blind pouch in the direct line of its axis, so that it becomes filled with food which fails to reach the stomach. Sometimes there are several dilatations.

The dilatations become enlarged by retention of food, and are liable to undergo inflammation, ulceration, and perforation.

DIAGNOSIS.—The diagnosis will depend upon the symptoms of dysphagia, regurgitation, and so on, and upon the evidence furnished by auscultatory indications, palpation with the oesophageal sound, and, in some instances, the existence of a tumor in the neck, enlarging after meals, and from which food or mucus can be forced up into the pharynx by pressure externally.

Stethoscopic auscultation of the oesophagus during the deglutition of water indicates an alteration in the usual form of the gulp, which seems to trickle rapidly in a larger or smaller stream according to the degree of dilatation. If the dilatation be annular and located high up, auscultation is said to give the impression of a general sprinkling of fluid deflected from its course. The peculiar gurgle is often audible without the aid of stethoscopy. Palpation with the oesophageal bougie is competent to reveal the existence of a large sac by the facility with which the terminal extremity of the sound can be moved in the cavity. In the case of a diverticulum, however, the sound may glide past the mouth of the pouch without entering it, although arrested at the bottom of the sac in most instances.

In annular dilatation any constriction below it is usually perceptible to the touch through the sound; but, on the other hand, the ready passage of the bougie into the stomach, while excluding stricture, does not positively disprove the existence of a circumscribed dilatation. If high up, the dilatation may be detected externally by its enlargement when filled with food after a meal, and the subsidence of tumefaction when the sac is emptied by pressure from without, or by regurgitation. If the dilatation occupy a position which exercises compression of the trachea, dyspnoea will ensue when it is distended. The intermittence of the tumefaction serves to differentiate the swelling from abscess or morbid growth. From aneurism of the aorta, which it may simulate (Davy³⁴), it is to be discriminated by absence of the usual stethoscopic and circulatory manifestations. The diagnosis of congenital dilatation is based upon a history of difficulty in deglutition dating from the earliest period of recollection.

³⁴ Irish Hosp. Gaz., 1874, p. 129; Med. Press and Circular, May, 1874.

PROGNOSIS.—The prognosis is not favorable in any given case unless the cause can be removed, and not even then unless food can be prevented from accumulating in the distended portion of the tube. Nevertheless, cases sometimes go on into advanced age. On the other hand, they may terminate fatally within a year (Lindau³⁵). The danger of perforation adds additional gravity to the prognosis, for life may be suddenly lost by this accident. Death usually takes place by inanition. A case of death by suffocation has been recorded, attributed to the pressure of the distended oesophagus upon the intrathoracic vessels (Hannay³⁶).

³⁵ Casper's Wochenschrift, 1840, No. 22; Arch. gén. de Méd., 1841, p. 498; Dict. de Méd et de Chir., xxiv. p. 410.

³⁶ Edinb. Med. and Surg. Journ., July 1, 1833.

TREATMENT.—If the dilatation be due to stricture or to an impacted foreign body, the treatment should be directed to overcoming the one and removing the other.

General dilatation from chronic oesophagitis requires treatment for that disease.

Much depends upon preventing the accumulation of food in a sac or diverticle; the best means of accomplishing which is the systematic administration of all nutriment by means of the stomach-tube. When this is not advisable, care must be exercised in the selection of such food as is least likely to irritate the parts if detained in the pouch.

As far as general treatment is concerned, stimulants are usually indicated, as the patients become much reduced. If paralysis of the muscular coat of the oesophagus is believed to exist, the administration of preparations of phosphorus and of strychnine are indicated on general principles of therapeutics. Stimulation of muscular contractility by the oesophageal electrode has been recommended, but the prospects of success hardly justify the risks of serious injury in the domain of the pneumogastric nerve.

It has not yet been determined whether surgical procedures are competent to relieve dilatation. In cases of pouched dilatation high up it would not be difficult, as suggested by Michel,³⁷ to expose the sac and excise it in such a manner that the sutures uniting the walls of the oesophagus shall occupy the site of the mouth of the diverticulum, and, thus obliterating it by cicatrization, restore the normal path of the food from the pharynx to the oesophagus. Gastrostomy, too, should hold out some hope of rescue, no matter what portion of the oesophagus be dilated.

³⁷ Dict. Encyclop., xiv. p. 465.