2. Malignancy of any of the intrathoracic viscera.

3. Aneurysm.

4. Cardiac and aortic enlargement.

5. Lymphadenopathies. Hodgkins' disease.

Leukemia.

Lues.

Tuberculosis.

Simple infective adenitis.

6. Lordosis.

7. Enlargement of the left hepatic lobe.

Endoscopically, compression stenosis of the esophagus is manifested by a slit-like crevice which occupies the place of the lumen and which does not open up readily before the advancing tube. The long axis of the slit is almost always at right angles to the compressive ma.s.s, if the esophageal wall be uninvolved. The covering mucosa may be normal or it may show signs of chronic inflammation. Malignant compressions are characterized by their hardness when palpated with the tube.

a.s.sociated pressure on the recurrent laryngeal nerve often makes laryngeal paralysis coexistent. The nature of the compressive ma.s.s will require for its determination the aid of the roentgenologist, internist, and clinical laboratory. Compression by the enlarged left auricle has been observed a number of times. The presence of aneurysm is a distinct contraindication to esophagoscopy for diagnosis except in case of suspected foreign body.

_Treatment of compressive stenosis of the esophagus_ depends upon the nature of the compressive lesion and is without the realm of endoscopy. In uncertain cases pota.s.sium iodid, and especially mercury, should always be given a thorough and prolonged trial; an occasional cure will result. Esophageal intubation is indicated in all conditions except aneurysm. Gastrostomy should be done early when necessary.

DIFFUSE DILATATION OF THE ESOPHAGUS

This is practically always due to stagnation ectasia, which is invariably a.s.sociated with either organic or "spasmodic" stricture, existing at the time of observation or at some time prior thereto. The dilating effect of the repeatedly acc.u.mulated food results in a permanent enlargement, so that the esophagus acts as the reservoir of a large funnel with a very small opening. When food is swallowed the esophagus fills, and the contents trickle slowly through the opening.

Gases due to fermentation increase the distension and cause substernal pressure, discomfort, and belching. A very large dilatation of the thoracic esophagus indicates spastic stenosis. Cicatricial stenoses do not result in such large dilatations and the dilatation above a malignant stenosis is usually slight, probably because of its relatively shorter duration.

The _treatment of diffuse esophageal dilatation_ consists in dilating the "diaphragmatic pinchc.o.c.k" that is, the hiatal esophagus. Chronic esophagitis is to be controlled by esophageal lavage, the regulation of the diet to liquefiable foods and the administration of bis.m.u.th subnitrate. The patient can be taught to do the lavage. The local esophagoscopic application of a small quant.i.ty of a 25 per cent watery solution of argyrol may be required for the static esophagitis. The redundancy probably never disappears; but functional and subjective cures are usually obtainable.

[245] CHAPTER x.x.xI--DISEASES OF THE ESOPHAGUS (_Continued_)

SPASMODIC STENOSIS OF THE ESOPHAGUS

_Etiology_.--The functional activity of the esophagus is dependent upon reflex action. The food is propulsed in a peristaltic wave by the same mechanism as, and through an innervation (Auerbach and Meissner plexus) similar to that which controls intestinal movements. The vagus also is directly concerned with the deglut.i.tory act, for swallowing is impossible if both vagi are cut. Anything which unduly disturbs this reflex arc may serve as an exciting cause of spasmodic stenosis.

Bolting of food, superficial erosions, local esophageal disease, or a small foreign body, may produce spasmodic stenosis. Spasm secondary to disease of the stomach, liver, gall bladder, appendix, or other abdominal organ is clinically well recognized. A perpetuating cause in established cases is undoubtedly "nerve cell habit," and in many cases there is an underlying neurotic factor. Shock as an exciting cause has been well exemplified by the number of cases of phrenospasm developing in soldiers during the World War.

_Cricopharyngeal spasmodic stenosis_ usually presents the subjective symptom of difficulty in starting the bolus of food downward. Once started, the food pa.s.ses into the stomach unimpeded. Regurgitation, if it occurs, is immediate. The condition consists in a tonic contraction, ahead of the bolus, of the circular fibers of the inferior constrictor known as the cricopharyngeus muscle, or in a failure of this muscle to relax so as to allow the bolus to pa.s.s. In either case the disorder may be secondary to an organic lesion. Local malignant disease or foreign bodies may be the cause. Globus hystericus, "lump in the throat," and the sense of constriction and choking during emotion are due to the same spasmodic condition.

_Diagnosis_.--At esophagoscopy there will be found marked exaggeration of the usual spasm which occurs at the cricopharyngeus during the introduction of the tube. The lumen may a.s.sume various shapes, or be so tightly closed that the folds form a mammilliform projection in the center. If the spasm gradually yields, and a full-sized esophagoscope pa.s.ses without further resistance, it may be stated that the esophagus is of normal calibre, and a diagnosis of spasmodic stenosis can be made. Considerable experience is required to distinguish between normal and pathologic spasm in an unanesthetized individual. To the less experienced esophagoscopist, examination under ether anesthesia is recommended. Deep anesthesia will relax the normal cricopharyngeal reflex closure as well as any abnormal spasm, thus a.s.sisting in the differentiation between an organic stricture and one of functional character. Under deep general anesthesia, however, it is impossible to differentiate between the normal reflex and a spasmodic condition, since both are abolished. Many cases of intermittent esophageal stenosis supposed to be spasmodic are due to organic narrowness of lumen plus lodgement of food, obstructive in itself and in the esophagitis resulting from its presence. The organic narrowing, congenital or pathologic, is readily recognizable esophagoscopically.

_Treatment_.--The fundamental cause of the disturbance of the reflex should be searched for, and treated according to its nature. Purely functional cases are often cured by the pa.s.sage of a large esophagoscope. Recurrences may require similar treatment.

[247] FUNCTIONAL HIATAL STENOSIS. HIATAL ESOPHAGISMUS. PHRENOSPASM, DIAPHRAGMATIC PINCHc.o.c.k STENOSIS. (SO-CALLED CARDIOSPASM)

There is no sphincteric muscular arrangement at the cardiac orifice of the esophagus, so that spasmodic stenosis at this level is not possible and the term cardiospasm is, therefore, a misnomer. It was first demonstrated by the author that in so-called cardiospasm the functional closure of the esophagus occurred at the diaphragmatic level, and that it was due to the "diaphragmatic pinchc.o.c.k."

Anatomical studies have corroborated this finding by demonstrating a definite sphincteric mechanism consisting of muscle bands springing from the crura of the diaphragm and surrounding the esophagus at the under surface of the hiatus. An inspection of the cadaveric diaphragm from below will demonstrate an arrangement like double shears admirably adapted to this "pinchc.o.c.k" action. Further confirmation is the fact that all dilatation of the esophagus incident to spasm at its lower extremity is situated above the diaphragm. In pa.s.sing it may be stated that the pinchc.o.c.k action, plus the kinking of the esophagus normally prevents regurgitation when a man with a full stomach "stands on his head" or inverts his body. For the upward escape of food from the stomach an involuntary co-ordinated antiperistaltic cycle is necessary. The dilatation resulting from phrenospasm may reach great size (Fig. 96a), and the capacity of the sac may be as much as two liters. While the esophagus is usually dilated, the stomach on the other hand is often contracted, largely from lack of distention by food, but possibly also because of a spastic state due to the same causes as the phrenospasm. Recently Mosher has demonstrated that hepatic abnormality may furnish an organic cause in many cases formerly considered spasmodic.

The _symptoms of hiatal esophagismus_ are variable in degree.

Substernal distress, with a feeling of fullness and pressure followed by eructations of gas and regurgitation of food within a period of a quarter of an hour to several hours after eating, are present. If the esophageal dilatation be great, regurgitation may occur only after an acc.u.mulation of several days, when large quant.i.ties of stale food will be expelled. The general nutrition is impaired, and there is usually the history of weight loss to a certain level at which it is maintained with but slight variation. This is explained by the trickling of liquified food from the esophageal reservoir into the stomach as the spasm intermittently relaxes, this occurring usually before a serious state of inanition supervenes. At times the hiatal spasms are extremely violent and painful, the pain being referred from the xiphoid region to the back, or upward into the neck. Patients are often conscious of the times of patulency of the esophagus; they will know the esophagus to be open and will eat without hesitation, or will refuse food with the certain knowledge that it will not pa.s.s into the stomach. Periods of remission of symptoms for months and years are noted. The neurotic character of the lesion in some cases is evidenced by the occasionally sudden and startling cures following a single dilatation, as well as by the tendency to relapse when the individual is subject to what is for him undue nervous tension. In a very few cases, with patients of rather a stolid type, all neurotic tendencies seem to be absent.

The _diagnosis of hiatal esophagismus_ requires the exclusion of local organic esophageal lesions. In the typical case with marked dilatation, the esophagoscopic findings are diagnostic. A white, pasty, macerated mucosa, and normally contracted hiatus esophageus which when found permits the large esophagoscope to pa.s.s into the stomach, will be recognized as characteristic by anyone who has seen the condition. In the cases with but little esophageal distension the diagnosis is confirmed by the constancy of the obstruction to a barium mixture at the phrenic level, while at esophagoscopy the usual resistance at the hiatus esophageus is found not to be increased, and no other local lesion is found as the esophagoscope enters the stomach. It is the failure of the diaphragmatic pinchc.o.c.k to open, as in the normal deglut.i.tory cycle, rather than a spasmodic tightness, that obstructs the food. The presence of organic stenosis at the hiatus may remove the case altogether from the spasmodic cla.s.s, or a cicatricial or infiltrated narrowing may be the result of static esophagitis. A compressive stenosis due to hepatic abnormality may simulate spasmodic stenosis as shown by Mosher, who believes that 75 per cent of so-called cardiospasms are organic.

_Treatment of hiatal esophagismus (so-called cardiospasm)_ consists in the over-dilatation of the "diaphragmatic pinchc.o.c.k" or hiatus esophageus, and in proper remedial measures for the removal of the underlying neurosis. The simple pa.s.sage of the esophagoscope suffices to cure some cases. Further dilatation by endoscopic guidance may be obtained by the introduction of Mosher's divulsor through the esophagoscope, by which accurate placement is obtained. The distension should not usually exceed 25 mm. Numerous water and air bags have been devised for stretching the hiatus, and excellent results have been obtained by their use. Possibly some of the cures have been due to the dilatation of organic lesions, or to the crowding back of an enlarged malposed, or otherwise abnormal left lobe of the liver, which Mosher has shown to be an etiologic factor.

Certain cases prove very obstinate of cure, and require esophageal lavage for the esophagitis, and feedings through the stomach tube to increase nutrition and to dilate the contracted stomach. Gastrostomy for feeding rarely becomes necessary, for a stomach tube can always be placed with the esophagoscope if it will not pa.s.s otherwise.

Retrograde dilatation with the fingers through a gastrostomy opening has been done, but seems hardly warranted in view of the excellent results obtainable from above. Instructions should be given concerning the proper mastication of food, and during treatment the frequent partaking of small quant.i.ties of liquid foods is recommended. Liquids and foods should be neither hot nor cold. The neurologist should be consulted in cases deemed neurotic.

[96a.-Functional hiatal stenosis. Cramp of the diaphragmatic pinchc.o.c.k (so-called cardiospasm).]

Endocrine imbalance should be investigated and treated, as urged by MacNab.

_Esophageal antiperistalsis_ is the name given by the author to a heretofore undescribed disease a.s.sociated with regurgitation of food from the esophagus, the food not having reached the stomach. It may be continuous or paroxysmal and may be of so serious a degree as to threaten starvation. The best treatment in severe cases is gastrostomy to put the esophagus at rest. Milder cases get well under liquid diet, rest in bed, endocrine therapy, cure of a.s.sociated abdominal disease, etcetera.

[251] CHAPTER x.x.xII--DISEASES OF THE ESOPHAGUS (_Continued_)

CICATRICIAL STENOSIS OF THE ESOPHAGUS

_Etiology_.--The accidental swallowing of caustic alkali in solutions of lye or proprietary washing and cleansing powders, is the most frequent cause of cicatricial stenosis. Commercial lye preparations are about 95 per cent sodium hydroxide. The cleansing and washing powders contain from eight to fifty per cent of caustic alkali, usually soda ash, and are sold by grocers everywhere. The labels on their containers not only give no warning of the dangerous nature of the contents nor antidotal advice, but have such directly misleading statements as : "Will not injure the most delicate fabric," "Will not injure the hands," etc. Utensils used to measure or dissolve the powders are afterward used for drinking, without rinsing, and thus the residue of the powder remaining is swallowed in strong solution. At other times solutions of lye are drunk in mistake for water, coffee, or wine. These entirely preventable accidents would be rare if they were as conspicuously labelled "Poison" as is required by law in the case of these and any other poisons, when sold by druggists. The necessity for such labelling is even greater with the lye preparations because they go into the kitchen, whereas the drugs go to the medicine shelf, out of the reach of children. "Household ammonia," "salts of tartar" (pota.s.sium carbonate), "washing soda" (sodium carbonate), mercuric chloride, and strong acids are also, though less frequently, the cause of cicatricial esophageal stricture. Tuberculosis, lues, scarlet fever, diphtheria, enteric fever and pyogenic conditions may produce ulceration followed by cicatrices of the esophagus. Spasmodic stenosis with its consequent esophagitis and erosions, and, later, secondary pyogenic infection, may result in serious cicatrices. Peptic ulcer of the lower esophagus may be a cause. The prolonged sojourn of a foreign body is likely to result in cicatricial narrowing.

[FIG. 97.--Schematic ill.u.s.tration of a series of eccentric strictures with interstrictural sacculations, in the esophagus of a boy aged four years. The strictures were divulsed seriatim from above downward with the divulsor, the esophageal wall, D, being moved sidewise to the position of the dotted line by means of a small esophagoscope inserted through the upper stricture, A, after divulsion of the latter.]

_Location of Cicatricial Esophageal Strictures_.--The strictures are often multiple and their lumina are rarely either central or concentric (Fig. 97). In order of frequency the sites of cicatricial stenosis are: 1. At the crossing of the left bronchus; 2. In the region of the cricopharyngeus; 3. At the hiatal level. Stricture at the cardia has rarely been encountered in the Bronchoscopic Clinic.

Stenosis of the pylorus has been noted, but is rare.

_Prognosis_.--Spontaneous recovery from cicatricial stenosis probably never occurs, and the mortality of untreated small lumen strictures is very high. Blind methods of dilatation are almost certain to result in death from perforation of the esophageal wall, because some pressure is necessary to dilate a stricture, and the point of the bougie, not being under guidance of the eye, is certain at sometime or other to be engaged in a pocket instead of in the stricture. Pressure then results in perforation of the bottom of the pocket (Fig. 98). This accident is contributed to by dilatation with the wrinkled, scarred floor which usually develops above the stricture. Rapid divulsion and internal esophagotomy are mechanically very easily and accurately done through the esophagoscope, and would yield a few prompt cures; but the mortality would be very high. Under certain circ.u.mstances, to be explained below, gentle divulsion of the proximal one of a series of strictures has to be done. With proper precautions and a gentle hand, the risk is slight. Under esophagoscopic bouginage the prognosis is favorable as to ultimate cure, the duration of the treatment varying with the number of strictures, the tightness, and the extent of the fibrous tissue-changes in the esophageal wall. Mortality from the endoscopic procedure is almost nil, and if gastrostomy is done early in the tightly stenosed cases, ultimate cure may be confidently expected with careful though prolonged treatment.

[FIG. 98.--Schema ill.u.s.trating the mechanism of perforation by blind bouginage. On encountering resilient resistance the operator, having a false conception, pushes on the bougie. Perforation results because in reality the bougie is in a pocket of the suprastrictural eccentric dilatation.]

_Symptoms_.--Dysphagia, regurgitation, distress after eating, and loss of weight, vary with the degree of the stenosis. The intermittency of the symptoms is sometimes confusing, for the lodgment of relatively large particles of food often simulates a spasmodic stenosis, and in fact there is often an element of spasm which holds the foreign body in the strictured area until it relaxes. Static esophagitis results in a swelling of the esophageal walls and a narrowing of the lumen, so that swallowing is more or less troublesome until the esophagitis subsides.

_Esophagoscopic Appearances of Cicatricial Stenosis_.--The color of the cicatricial area is usually paler than the normal mucosa. The scars may be very white and elevated, or they may be flush with the normal mucosa, or even depressed. Occasionally the cicatrix is annular, but more often it is eccentric and involves only a part of the circ.u.mference of the wall. If the amount of scar tissue is small, the lumen maintains its mobility; opens and closes during respiration, cough, and vomiturition. Between two strictures there is often a pouch containing food remnants. It is rarely possible to see the lumen of the second stricture, because it is usually eccentric to the first.

Stagnation of food results in superjacent dilatation and esophagitis.

Erosions and ulcerations which follow the stagnation esophagitis increase the cicatricial stenosis in their healing.

_Differential Diagnosis_.--When the underlying condition is masked by inflammation and ulceration, these lesions must be removed by frequent lavage, the administration of bis.m.u.th subnitrate with the occasional addition of calomel powder, and the limitation of the diet to strained liquids. The cicatricial nature of the stenosis can then be studied to better advantage. In most cases the cicatrices are unmistakably conspicuous. Spasmodic stenoses are differentiated by the absence of cicatrices and the yielding of the stenosis to gentle but continuous pressure of the esophagoscope. While it is possible that spasmodic stenosis may supplement cicatricial stenosis, it is certainly exceedingly rare. Nearly all of the occasions in which a temporary increase of the stenosis in a cicatricial case is attributed to an element of spasm, the real cause of the intermittency is not spasm but obstruction caused by food. This occurs in three ways: 1. Actual "corking" of the strictured lumen by a fragment of food, in which case intermittency may be due to partial regurgitation of the "corking"

ma.s.s with subsequent sinking tightly into the stricture. 2. The "cork"

may dissolve and pa.s.s on through to be later replaced by another. 3.

Reactionary swelling of the esophageal mucosa due to stagnation. Here again the obstruction may be prolonged, or it may be quite intermittent, due to a valve-like action of the swollen mucosal surfaces or folds intermittently coming in contact. Cancerous stenosis is accompanied by infiltration of the periesophageal tissue, and usually by projecting bleeding fungations. Cancer may, however, develop on a cicatrix, favored no doubt by chronic inflammation in tissue of low resistance. Compression stenosis of the esophagus is characterized by the sudden transition of the lumen to a linear or crescentic outline, while the covering mucosa is normal unless esophagitis be present. The compressive ma.s.s can be detected by the sensation transmitted to the touch by the esophagoscope.

_Treatment_.--Blind bouginage should be discarded as an obsolete and very dangerous procedure. If the stenosis be so great as to interfere with the ingestion of the required amount of liquids, gastrostomy should be done at once and esophagoscopic treatment postponed until water hunger has been relieved. Gastrostomy aids in the treatment by putting the esophagus at rest, and by affording the means of maintaining a high degree of nutrition unhampered by the variability or efficiency of the swallowing function. Careful diet and gentle treatment will, however, usually avoid gastrostomy. The diet in the gastrostomy-fed patients should be as varied as in oral alimentation; even solids of the consistency of mashed potatoes, if previously forced through a wire gauze strainer, may be forced through the tube with a gla.s.s injector. Liquids and readily liquefiable foods are to be given the non-gastrostomized patient, solids being added when demonstrated that no stagnation above the stricture occurs. Thorough mastication and the slow partaking of small quant.i.ties at a time are imperative. Should food acc.u.mulation occur, the esophagus should be emptied by regurgitation, following which a gla.s.sful of warm sodium bicarbonate solution is to be taken, and this also regurgitated if it does not go through promptly. The esophagus is thus lavaged and emptied. In all these cases, whether being fed through the mouth or the gastrostomic tube, it is very important to remember that milk and eggs are not a complete dietary. A pediatrist should be consulted.

Prof. Graham has saved the lives of many children by solving the nutritive problems in the cases at the Bronchoscopic Clinic. Fruit and vegetable juices are necessary. Vegetable soups and mashed fruits should be strained through a wire gauze coffee strainer. If the saliva is spat out by the child because it will not go through the stricture the child should be taught to spit the saliva into the funnel of the abdominal tube. This method of improving nutrition was discovered by Miss Groves at the Bronchoscopic Clinic.

_Esophagoscopic bouginage_ with the author's silk-woven steel-shank endoscopic bougies (Fig. 40) has proven the safest and most successful method of treatment. The strictured lumen is to be centered in the esophagoscopic field, and three successively increasing sizes of bougies are used under direct vision. Larger and larger bougies are used at the successive treatments which are given at intervals of from four to seven days. No anesthesia, general or local, is used for esophagoscopic bouginage. The tightness of the grasping of the bougie by the stricture on withdrawal, determines the limitation of sizes to be used. When the upper stricture is dilated, lower ones in the series are taken seriatim. If concentric, two or more closely situated strictures may be simultaneously dilated. For the use of bougies of the larger sizes, the special esophagoscopes with both the light-carrier ca.n.a.l and the drainage ca.n.a.l outside the lumen of the tube are needed. Functional cure is obtained with a relatively small lumen at the point of stenosis. A lumen of 7 mm. will allow the pa.s.sage of any well masticated food. It is unwise and unsafe to attempt to restore the lumen to its normal anatomic size. In cicatricial stricture cases it is advisable to examine the esophagus at monthly periods for a time after a functional cure has been obtained, in order that tendency to recurrence may be early detected.

_Divulsion_ of an upper stricture may be deemed advisable in order to reach others lower down, especially in cases of multiple eccentric strictures (Fig. 97). This procedure is best done with the author's esophagoscopic divulser, accurately placed by means of the esophagoscope; but divulsion requires the utmost care, and a gentle hand. Even then it is not so safe as esophagoscopic bouginage.

_Internal esophagotomy_ by the string-cutting instruments and esophagotome are relatively dangerous methods, and perhaps yield in the end no quicker results than the slower and safe bouginage per tubam.

_Electrolysis_ has been used with varying results in the treatment of cicatricial stenosis.

_Thermic bouginage_ with electrically heated bougies has been found useful in some cases by Dean and Imperatori.