In cases resisting the plan of treatment suggested mercuric chloride

may be successfully used, both internally (gr. 1/16 two or three times

a day) and in spray, a drachm or less night and morning (one grain to

four ounces). External counter-irritation by repeated blistering over

the larynx and under the angles of the jaws is useful in some

instances. During treatment the voice should be used as sparingly as

practicable.

In chronic atrophic pharyngitis the treatment, constitutional and

local, should be such as favors secretion from mucous

membranes--internally, cubeb, pyrethrum, calamus, xanthoxylum,

jaborandi, ammonium chloride; topically, sprays, four or more times a

day, of hot water, glycerin and water, ammonium chloride. Patients

sleeping with the mouth open should wear an apparatus, extemporized or

made to order, to keep the lower jaw closed in sleep.

Syphilitic Pharyngitis.

DEFINITION.--A specific inflammation of the mucous membrane of the

pharynx or of the mucous membrane and submucous tissues, the result of

syphilis, and often associated with like disease in contiguous

structures.

SYNONYMS.--Pharyngitis syphilitica, Pharyngitis specifica, Syphilitic

sore throat, Syphilis of the pharynx.

ETIOLOGY.--Contamination by syphilitic virus is the sole cause, whether

by direct inoculation or by systemic poisoning, hereditary or acquired.

Direct inoculation proceeds from primary sores on the lips, tongue,

cheek, and hard palate, themselves the result of actual contact with

sores in other individuals. Initial sores have been seen upon the

tonsils, palatine folds, pharynx, and even the epiglottis. Direct

inoculation from secondary sores may be communicated by the

tooth-brush, blow-pipe, pipe-stem, trumpet, mouth-piece of

feeding-bottle, pap-boat, or similar article previously used by an

infected individual. Uncleansed surgical instruments convey the disease

in like manner.

PATHOLOGY AND MORBID ANATOMY.--Syphilitic pharyngitis--or, more

strictly speaking, syphilitic sore throat--occurs in all varieties,

primary, secondary, tertiary, and hereditary. Secondary manifestations

are the most frequent, and primary sores the most infrequent. The

primary sore is soft in some instances, and hard in others. Phagedænic

ulceration may ensue. Secondary manifestations are usually bilateral,

and often symmetric in configuration and distribution. They appear from

a few weeks to a few months after infection, and are among the most

frequent early manifestations of secondary syphilis. The inflammatory

process begins in erythema, usually diffuse, often punctated, sometimes

in patches. It extends from above downward more frequently than in the

reverse direction, but may spread in any direction. The lesion

commences upon the soft palate and tonsils more frequently than {407}

on the pharynx, but may commence in any portion of the oro-guttural

cavity. Tumefaction ensues, with lividity of the surface. The

epithelial cells become distended; the resulting opalescence, somewhat

characteristic, eventually subsides into a central opacity, the true

mucous patch or condyloma latum. Mucous patches vary in size from mere

specks to large irregular surfaces, often the result of coalescences.

They sometimes become red and granular and covered with purulent

products. Microscopically (Cornil), they consist of thickened

epithelium upon a base of proliferated lymphoid cells, which often

infiltrate the deeper tissues extensively. They may disappear in the

course of a few weeks by resolution and absorption. Sometimes

suppuration occurs in small superficial abscesses which discharge upon

the surface. Several abscesses discharging simultaneously in

coalescence, an extensive ulcer may result, which, in repair, leaves a

cicatricial trace of its site. Flat and circular bluish-white patches,

due to thickening of epithelium, appear after the first year of

constitutional syphilis, and may exist in association with the true

mucous patch. They bleed readily on rough handling, but rarely undergo

ulceration.

Tertiary manifestations may present within a few months after infection

or not until many years. Gummatous infiltration of the connective

tissue, diffused or circumscribed (syphiloma), follows diffuse or

localized erythema, and then the gummata break down, discharge by

ulceration, and leave deep-seated irregular ulcers with undermined

edges and surrounded with inflammatory areolæ. These manifestations are

much more frequent in the palate than in the pharynx, and the

ulcerative process often destroys the uvula and large portions of the

palate and palatine folds. When the pharynx and posterior surface of

the palate are both ulcerated, cicatricial adhesions are sometimes

inevitable, and thus serious stricture of the suprapalatine pharyngeal

canal may ensue. The lesion may be quite limited in extent or may

involve the entire pharynx. The ravages may become sufficiently

extensive to involve the vertebra and the skull or to perforate the

large blood-vessels. Cicatrization in the pharynx is vertical or

stellate as the rule, and the peculiar pallid lustre of the cicatrices

is quite characteristic of the syphilitic lesion. In many instances

secondary and tertiary manifestations commingle. Ulceration is then

more likely to extend superficially than in depth.

Hereditary manifestations pursue much the same course as tertiary

manifestations. They usually occur before puberty, but are occasionally

delayed until after maturity. Deferred tertiary and late hereditary

manifestations sometimes present the characteristic ulceration of the

commingled secondary and tertiary disease; and this form of ulceration

is often incorrectly attributed to scrofulosis and to lupus.

SYMPTOMATOLOGY, COURSE, DURATION, COMPLICATIONS, AND SEQUELÆ.--The

subjective symptoms of syphilitic pharyngitis are those of erythematous

and ulcerative pharyngitis of like grade, except that there is very

little pain. The course is chronic unless specific treatment be

instituted, when prompt repair may be expected unless the general

health has been much undermined. The duration is indefinite. The

manifestations subside under treatment, and recur if it is not

sufficiently prolonged. Complications occur with similar manifestations

of syphilis in adjacent or contiguous or distant structures, as may be.

The most frequent sequel in neglected cases is cicatricial stricture.

{408} DIAGNOSIS.--Bilateral inflammation in symmetric distribution is

very characteristic of syphilis. Irregular ulcers with undermined

borders and surrounded by inflammatory areolæ are similarly

characteristic. Acknowledged history of syphilis or the detection of

syphilitic manifestations elsewhere serves to confirm the diagnosis. In

cases of doubt a few days' treatment with specific remedies in large

doses will almost invariably serve to clear up the diagnosis.

PROGNOSIS.--The prognosis as to life is good unless the ulcerations

have become so extensive as to threaten perforation into blood-vessels

or the patient has become greatly debilitated. The prognosis as to

freedom from cicatricial adhesions and stricture is not good in the

presence of lesions which have destroyed large territories of tissue,

even under very careful management.

TREATMENT.--Specific medicines in positive doses constitute the most

effectual treatment. Mercury is indicated in secondary lesions.

Extensive ulcerative tertiary and hereditary lesions are peculiarly

susceptible to large doses (30 to 90 or more grains daily) of potassium

iodide, under the influence of which they often heal without any local

applications whatever. As soon as a positive impression has been

produced the dose may be diminished. The parts should be kept clean and

comfortable by periodic douching with sprays of alkaline solutions, or,

what is still more serviceable, with a ten-volume solution of hydrogen

peroxide diluted with one or more parts of distilled water. The best

local application to the edges of the pharyngeal syphilitic ulcers is

the solid cupric sulphate. Chromic acid (1:8) is a serviceable local

stimulant to indolent ulcers. Necrosed fragments of bone should be

removed. Should any impediment to respiration take place during

administration of the iodides, oedema of the larynx may be suspected,

and should be looked for. Professional supervision is requisite for

many months after the lesions have healed. Cicatricial sequelæ of

stricture require surgical interference.

{409}

DISEASES OF THE OESOPHAGUS.

BY J. SOLIS COHEN, M.D.

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

oesophagus[1] has indicated his recognition of the disease. Fernel[2]

mentions phlegmon of the oesophagus; Honkoop[3] describes inflammation

of the oesophagus; J. P. Frank[4] describes an oesophageal angina; and

Joseph Frank[5] 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 Hamburger[6] Von

Oppolzer[7] Zenker and Ziemssen[8] Luton,[9] and Bernheim.[10]

[Footnote 1: _De locis affectis_, lib. iv. cap. iii.; lib. v. cap. v.]

[Footnote 2: _De partium mortis et sympt._, lib. vi. p. 277.]

[Footnote 3: _Specimen inaugurale de morbo oesophagi inflammatorie_,

Lugd. Batav., 1774.]

[Footnote 4: _De curandis hominem morbis, Epitome prælectionibus

academicis dicata_, Mannheim, Stuttgardt, and Vienna, 1792-1820.]

[Footnote 5: _Praxeous medica præcepta universa_, Lipsiæ, 1826-32.]

[Footnote 6: _Klinik der Oesophaguskrankheiten_, Erlangen, 1871.]

[Footnote 7: _Vorlesungen über specielle Pathologie und Therapie_,

Erlangen, 1872; Englished in abstract by the writer in _Philada. Med.

Times_, 1872.]

[Footnote 8: _Handbuch der speciellen Pathologie und Therapie_, 1877;

English translation, New York, 1878, vol. viii.]

[Footnote 9: _Dictionnaire de Médecine et de Chirurgie pratiques_,

Paris, 1877, vol. xxiv.]

[Footnote 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 {410} 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 (Graves[11]). 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.

[Footnote 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

(Laennec[12]), sometimes produced a peculiar form of pustulous

oesophagitis, not unlike the pustulous oesophagitis sometimes occurring

as part of the local manifestations of small-pox.

[Footnote 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 {411} 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 {412}

patches. One case, however, has been recorded (Birch-Hirschfeld[13]) 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.

[Footnote 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.

[Footnote 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. {413} 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._).

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