A system of practical medicine. By American authors. Vol. 2 (part 3 of 8)

A system of practical medicine. By American authors. Vol. 2 (part 3 of 8)

The disease usually begins in the gums of the lower incisors, and {347} extends backward, often being confined to one side of the jaw. The gums, first swollen and then livid, become separated from the necks of the teeth. Their edges undergo ulceration. The ulcers are surrounded by fungous margins, pale or red, which bleed on the slightest contact, and some become covered with grayish-yellow detritus. The ulceration extends in depth, destroying the supports of the teeth, so that they become loosened and even detached. The inflammatory process extends to the lips, the cheek, and the tongue, which undergo tumefaction and exhibit the impressions of the teeth in grayish opalescent lines or festoons of thickened epithelium at the points of pressure. The glossitis may become intense. It is almost always present, to some extent, as a superficial or mucous glossitis. Occasionally acute oedematous glossitis has ensued, and such cases sometimes terminate fatally. Ulceration takes place in these structures similar to that which has taken place in the gums. If not arrested, gangrenous destruction ensues, not only in these tissues, but beneath them. Thus, the teeth become loosened, and even detached; the jaw-bones themselves may become bared, necrosed, and in part exfoliated; and the cheeks undergo partial destruction by gangrene. Sometimes the inflammation descends to the larynx, and this may produce oedematous infiltration of the loose connective tissue of that structure. Sometimes it mounts the pharynx and reaches the orifices of the Eustachian tubes. The salivary glands become swollen and discharge great quantities of fluid, as detailed under Symptomatology. The retro-maxillary and submaxillary lymphatic glands become enlarged by inflammatory action.

DIAGNOSIS.--In the earliest stages the inflammation of the gums in mercurial stomatitis cannot be distinguished from that which takes place in other forms of ulcerative stomatitis. The fetor of the breath, however, the profuse salivation, and the chemical reaction of the saliva, together with the history of exposure to mercury, soon place the nature of the case beyond doubt. Similar results following poisonings by copper salts and by phosphorus are differentiated by the history of the special exposure.

PROGNOSIS.--In mild cases the prognosis is favorable, provided further exposure to the cause can be avoided. This holds good almost invariably in cases due to over-medication with mercurials, but is far less applicable to cases in artisans, the result of prolonged exposure to the poisonous influences of mercury and its slow absorption. On the whole, the affection is much less serious than formerly, both because it can, in great measure, be guarded against by proper prophylaxis in risky vocations, and because its treatment has been made much more efficient. In severe cases serious results may ensue despite the most judicious treatment, and convalescence is usually very slow, weeks often elapsing before solid food can be chewed without pain or without injury to the gums.

When death ensues, it may be by asthenia, erysipelas, pneumonia, pyæmia, or colliquative diarrhoea.

TREATMENT.--Mercurial stomatitis may sometimes be prevented by the administration of potassium chlorate during exposure. Mild cases following the administration of mercurials often subside upon mere withdrawal of the drug. Should spontaneous subsidence not take place, the administration of potassium chlorate every few hours, in doses of {348} from thirty to sixty grains or more in the twenty-four hours, soon effects amelioration, which promptly terminates in recovery. The characteristic fetor often ceases within twelve hours' use of this drug. Should the inflammatory manifestations be severe, a few leeches applied beneath the edge of the lower jaw, followed by a poultice enveloping the neck to promote further flow of blood, often affords prompt relief (Watson). Lead acetate (ten grains to the ounce of water) and iodine (half a fluidrachm of the compound tincture to the ounce of water) are useful as gargles and washes. When the result of slow poisoning, elimination of the mercury by sulphur vapor baths and the administration of small doses of potassium iodide are recommended.

Cauterization of the ulcerated surfaces is sometimes serviceable, silver nitrate or hydrochloric acid (Ricord), or chromic acid 1:5 (Butlin, Canquil), being used for the purpose.

Opium in decided doses is indicated for the relief of pain. It may be added with advantage to detergent and disinfective mouth-washes (potassium chlorate, sodium borate, creasote-water, saponified emulsion of coal-tar, tincture of cinchona, tincture of myrrh, etc.), the use of which should form an important part of the treatment. Watson highly recommended a wash of gargle of brandy and water, 1:4 or 5. In severe cases difficulty is encountered in maintaining effective alimentation. When mastication is not impracticable, soft-boiled egg and finely-chopped raw beef may be given. When the patient cannot chew at all, resort is confined to milk, soups, and the juice of beef. Nourishing enemata should be administered, as in all affections where it becomes impracticable to sustain the patient by way of the mouth. Tonics and stimulants are indicated to avoid debility from the excessive salivation and its sequelæ--quinia, coffee, wine, and alcohol, the first, if required, by hypodermatic injection, all of them by enema if necessary.

Glossitis and oedema of the larynx may require the surgical procedures often necessary when they occur under other circumstances.

Other forms of toxic stomatitis hardly require special elucidation.

Abnormalities and Vices of Conformation of the Tongue.

Apart from the anomalies presented in monsters, there are a few congenital abnormalities of the tongue with which it becomes the accoucheur at least to be familiar, as their presence may interfere materially with the nutrition of the infant, whether nursed or spoon-fed.

CONGENITAL DEFICIENCY OF THE TONGUE.--A considerable portion of the tongue may be wanting anteriorly, comprising, in some instances, the entire free portion of the organ. The stump then presents as a single or a bifid protuberance of variable size. In some instances considerable power of movement exists, and even conservation of taste. Suction and deglutition are both practicable. When the child grows it can speak, though with a certain amount of difficulty. A few cases are on record, however, of ability to speak without any evidence of a tongue above the floor of the mouth.

An instance of lateral deficiency has been observed by Chollet,[16] the {349} deficient half being represented merely by the two layers of the lingual mucous membrane, without any intervening muscular substance.

[Footnote 16: Demarquay, Dict. de Méd. et de Chir. prat., xx. p. 130.]

BIFID TONGUE, separate investment of the two sides, has been occasionally observed in connection with similar arrest of development in the lower jaw and other organs.

Ankyloglossia.

DEFINITION.--An abnormal attachment or adhesion of some portion of the tongue to some portion of the surrounding structures of the mouth.

SYNONYM.--Tongue-tie.

PATHOLOGY AND MORBID ANATOMY.--The ordinary form of tongue-tie consists in an abnormal development of the frenum of the tongue, the anterior vertical portion of the duplicature of mucous membrane which connects the lower surface of the raphé of the tongue with the floor of the mouth. The tongue cannot be extended beyond the lips. Suction is interfered with in some cases. If not remedied spontaneously or by surgical interference, mastication and articulation may become seriously impeded.

Other forms of ankyloglossia, congenital and acquired, possess special interest from surgical points of view mainly.

DIAGNOSIS.--Inspection and digital exploration readily reveal the nature of the restriction in the movements of the tongue and the size of the frenum.

PROGNOSIS.--The prognosis is good, the difficulty being susceptible of relief by division of a portion of the constricting frenum. Accidents have been reported following the operation, the occasional occurrence of which should be borne in mind. These are hemorrhage, which is not dangerous except in the prolonged absence of some one competent to restrain it should it be extreme; and retroversion of the tongue, an accident which has been known to prove fatal by occluding the orifice of the larynx (Petit).

TREATMENT.--Slight cases rarely need operation; but when the movements of the tongue are restricted by a very short and deep frenum its division becomes necessary. The operation is usually performed with scissors, the ranine arteries being protected by means of a fissured plate of metal (Petit), such as has long been used as a handle to the ordinary grooved director of the physician's pocket-case. The cut should be more extensive in the lateral directions of the fold than antero-posteriorly. After-treatment is rarely necessary, unless annoying hemorrhage is produced by movements of suction. Compression between the fingers, maintained for a number of minutes, suffices to restrain the hemorrhage in most instances. When this fails, recourse may be had to cauterization with the point of a heated iron or some other form of actual cautery.

Macroglossia.

DEFINITION.--Hypertrophy of the tongue.

SYNONYMS.--Megaloglossia, Glossoptosis, Prolapsus linguæ, Lingua {350} propendula, Chronic prolapse of the tongue, Chronic intumescence of the tongue.

HISTORY.--This rare affection has been long known, the first cases on record being in the works of Galen. Other cases have been recorded by Celsus and Avicenna. Among more modern recorders may be mentioned Scaliger (1570), Bartholin (1680), Benedict and Pencer; among recent recorders, Lassus,[17] Percy,[18] Harris,[19] Humphrey,[20] Gayraud,[21] W. Fairlie Clarke,[22] Bryant,[23] and the French dictionaries in present process of publication; to all of which the reader is referred for bibliographic, descriptive, and illustrative details.

[Footnote 17: Mémoire de l'Institut National, 18--, an VI. t. i.]

[Footnote 18: Dict. Sci. Méd., t. xxvii.]

[Footnote 19: Am. Journ. Med. Sci., vol. vii., 1830, p. 17; vol. xx., 1837, p. 15--both illustrated.]

[Footnote 20: Trans. Med.-Chir. Soc. London, 1853, p. 113.]

[Footnote 21: Thèse de Montpellier, No. 68, 1865.]

[Footnote 22: Diseases of the Tongue, London, 1873.]

[Footnote 23: "Surgical Affections of the Tongue," Guy's Hosp. Reports, 1883, p. 102 et seq.]

ETIOLOGY.--This affection is usually congenital, at least to a certain extent, and augments with the growth of the child. It has been attributed, on apparently insufficient grounds, to injury received during parturition. It is probably intra-uterine in origin. Though encountered in both sexes, the majority of recorded cases have been in females. In summing up these observations, it appears that the affection often attracts little or no attention until dentition is in progress. The hypertrophy begins to augment rapidly during the second or third year of age, or a year or two later in some cases.

The gradual increase of the congenital deformity during infancy has been attributed to hypernutrition from local irritation produced by habits of sucking on the organ, induced, in some subjects, by forcible efforts at suction from a short nipple. Similarly, the rapid augmentation of volume noted as occurring during the period of dentition or a little later has been attributed to hypernutrition excited by irritation suffered by the protruding organ from the lower row of teeth. Cases commencing at this age have been supposed to be due exclusively to tongue-sucking. In some instances, due to this cause apparently, the deformity is associated with idiocy (Lawson[24]). Convulsions, epileptic seizures, and whooping cough have been regarded by some writers as occasional causes of the deformity. Indeed, idiocy and cretinism are not infrequent co-associates with the deformity (Parrot[25]). It has been observed likewise in anencephalous monsters (Brissot, idem).

[Footnote 24: Trans. Clin. Soc. London, vol. v. p. 158.]

[Footnote 25: Gaz. Méd. Paris, Dec. 10 and 17, 1881; Lond. Med. Record, Mar. 15, 1882, p. 113.]

SYMPTOMS, COURSE, DURATION, TERMINATIONS, COMPLICATIONS, AND SEQUELÆ.--The prominent symptom of macroglossia is the enlarged tongue protruding beyond the mouth. The resemblance of the protruding tongue of a child with macroglossia to the tongue hanging from the mouth of a calf gave rise to the name lingua vitulina by which it has sometimes been designated. In some instances, where the enlargement is but moderate, the organ can be retained within the mouth. When bilateral, the enlargement may be symmetrical, or may interest one side of the tongue more than the other. When the enlargement is confined to the free portion of the tongue, it interferes little with respiration and with movements of suction. When occupying the base of the organ, it may seriously embarrass respiration, and even produce suffocation in {351} some instances (Clarke). The mouth being maintained open, saliva dribbles away constantly except during alimentation. Thirst is often very great in consequence of this, and of the desiccation of the tongue and of the walls of the mouth by the unmodified air to which they are continuously exposed. The tongue is usually free from pain.

In some subjects, although the tongue, left to itself, protruded considerably, it has been found quite practicable to maintain it within the cavity of the mouth by means of bandages or other appliances secured to the back and top of the head. These bandages are removed from time to time to give relief from the restraint and to permit food and drink to be taken. Systematic compression, indeed, has been induced in this way in some instances, and has produced considerable diminution in the size of the organ--sufficient to maintain its concealment without the aid of an appliance. When the tongue cannot be retained within the mouth the patient becomes unable to close the jaws. Hence saliva dribbles constantly, save when food or drink is being taken. The protruded portion of the tongue undergoes a livid discoloration, sometimes diffuse, sometimes disseminated. Though sometimes remaining comparatively soft in texture, it usually becomes hard, dry, rough, fissured, ulcerated and sanious, covered with desiccating layers of mucus and epithelium, and marked by indentations made by the edges of the teeth, which sometimes seem almost to strangle it. Mastication, deglutition, and articulation often become very difficult, and respiration also, but less frequently. The lower lip becomes much everted. The larynx and hyoid bone become drawn upward and forward by the weight of the organ. The configuration of the lower jaw undergoes considerable change, and the teeth become pressed out of position. Dislocation of the jaw from this cause has been noticed (Chalk[26]).

[Footnote 26: Trans. Path. Soc. London, vol. viii. p. 305.]

These symptoms undergo aggravation with the growth of the subject, and, while presenting general features of resemblance in all cases, vary considerably in individual instances. Great difficulty is encountered, as a rule, in taking food, and mastication has to be performed very slowly. In some instances mastication can be performed satisfactorily by the molars, owing to a compensatory curvature of the lower jaw, even though the anterior portions of the jaw may remain permanently separated (Harris). Some patients get along by using their fingers to push the bolus far {352} enough back to permit of its deglutition. Some have used a cup with a long tube slightly curved to convey fluids to the back part of the mouth for a similar purpose. Some have been systematically fed by means of a catheter passed through a nasal passage and thus on into the oesophagus. The difficulties in nourishing patients reduce some of them to extreme emaciation.

Notwithstanding all these drawbacks, quite a number of cases are on record where the patients have reached well into adult life before being submitted to radical measures for relief. One patient is recorded as having reached the age of eighty, having worn for some sixty-five years a silver shield to conceal her deformity (Clarke).

PATHOLOGY AND PATHOLOGICAL ANATOMY.--The hypertrophy may involve all the structures of the tongue, but usually implicates the muscular tissue especially (Sédillot, Paget, Bouisson). In a case published by W. Fairlie Clarke it was found on microscopic examination that the papillæ as well as the mucous and submucous tissues were somewhat enlarged and thickened, while the bundles of muscular fibre were slightly coarser than natural. Maas reports a unilateral case of macroglossia in a male child two months of age associated with hyperdevelopment of the entire left side of the body.[27] In some instances the blood-vessels and lymphatics are chiefly involved (Virchow, Billroth, Maas), two cases of which have been described by Virchow as cavernous lymphatic tumors.

[Footnote 27: Arch. klin. Chir., p. 413, Bd. xiii. Heft 3.]

Hilliard reports[28] a congenital case from vicious growth, removed at fourteen months of age. Microscopic sections showed the large lacunæ filled with corpuscles, blood-pigment in different stages of degeneration, {353} and the papillæ much hypertrophied. Winiwarter[29] reports a congenital macroglossia associated with congenital cysts of the neck.

[Footnote 28: Brit. Med. Journ., Nov. 26, 1870, p. 591.]

[Footnote 29: Arch. klin. Chir., 1874, Bd. xvi. Heft 3.]

Sometimes there is very little true muscular hypertrophy, as in a case quoted by Bryant which was presented to the Pathological Society of London in 1872 by M. H. Arnott. In this specimen the epithelial covering was very thick and the papillæ enlarged. The blood-vessels were larger than usual, and there were large irregular spaces, thin-walled and filled with blood or clear fluid. "A few vesicular bodies which may have been enlarged lymphatics were also present"--probably cross-sections of lymphatic vessels.

The size that may be attained even in young children seems incredible, three and four inches protruding from the mouth in some instances. The free portion is more bulky than the intra-oral portion. One case reported "as thick as an arm" probably refers to the arm of the child. As a rule, both sides of the tongue are involved; exceptionally, the affection is unilateral.

In most instances the hypertrophy occupied the free portion of the tongue chiefly, the base of the organ having been implicated in but a few.

DIAGNOSIS.--The presence of the tongue outside of the mouth speaks for itself (Figs. 14 and 15). The age of the patient, usually a young child, the history of the case if it present in the adult, suffice to differentiate macroglossia from the tumefaction of glossitis on the one hand and from certain protruding tumors and malignant diseases on the other. Hypertrophy of the tongue following chronic glossitis, syphilitic or non-specific, must not be confounded with the congenital or idiopathic affection under consideration.

PROGNOSIS.--The prognosis is good as to relief from the deformity, provided the patient is submitted to surgical interference, and the prognosis of the operation depends upon the procedure selected. Sometimes additional operations are requisite to remedy the defects the lower jaw has sustained by prolonged depression. In comparatively young adults restoration of its position, configuration, and function seems likely to result spontaneously after the protruding portion of the tongue has been removed.

TREATMENT.--It has been maintained (Lassus) that the hypertrophy can be overcome by systematic compression of the tongue, by leeching the tongue, bandaging or strapping it, and forcibly maintaining it in the mouth by suitable retentive appliances. While it has been admitted that this plan may prove successful in cases of moderate enlargement of but few years' duration and unaccompanied with change in the shape of the lower jaw, the experience of more recent observers has been recorded as unfavorable, at least in pronounced cases. Clanny[30] succeeded in this way with a child five years of age whose tongue protruded three inches. This plan is said to be very painful and irritating. It requires close watching on account of the difficulty of respiration which may ensue from thus blocking up the pharynx. It has been advised as a useful and sometimes an essential preliminary (Syme) to a radical procedure consisting in the excision of a V-shaped segment. This latter operation (Boyer) has been successfully performed by Howe, Harris, Humphry, Syme, and others. {354} Frederici[31] extended the incisions to the very base of the tongue. It has been performed both with knife and with scissors, the cut surfaces being united with sutures after ligation or torsion of the bleeding vessels. Re-enlargement ensued in one of Syme's cases operated upon in this way,[32] and likewise in a case of Gies,[33] requiring subsequent excision of the exuberant portions. Operations with the ligature, though sometimes successful (Fergusson,[34] Hodgson[35]), may be followed by fatal septicæmia during the slough (Liston[36]), or, failing to strangulate the tongue sufficiently, may require the application of the knife, after all, to affect the separation (Harris[37]).

[Footnote 30: Edinb. Med. and Surg. Journ., 1805, vol. i., cited by Clarke.]

[Footnote 31: Arch. gén. de Méd., 1844; Edinb. Med. and Surg. Journ., p. 528, vol. lxiv., 1845.]

[Footnote 32: Edinb. Med. Journ., 1857, vol. ii. p. 1057.]

[Footnote 33: Arch. klin. Chir., 1873, p. 640.]

[Footnote 34: Practical Surgery, London, 5th ed., p. 518.]

[Footnote 35: Trans. Med.-Chir. Soc. London, 1858, p. 129.]

[Footnote 36: Elements of Surgery, p. 334, Philada., 1842.]

[Footnote 37: Am. Journ. Med. Sci., vol. vii. p. 17.]

Excision with the incandescent loop of the galvano-cautery seems to be the most suitable procedure. Valerani[38] operated in this manner without the loss of a drop of blood upon a congenital macroglossia in a child seven months of age. Maas[39] operated in this way on a child two months of age. Fairlie Clarke, who removed a congenital macroglossia with the écraseur in a child five months of age, recommends operation before dentition begins[40]--an opinion which appears to be justified by the belief that the pressure of the teeth contributes to the subsequent rapid enlargement of the organ. Nevertheless, the operation may be undertaken at any age. Several of those already cited were performed upon adults, and Stephen O'Sullivan[41] excised the hypertrophied tongue of a female sixty-five years of age.

[Footnote 38: Giornale della Reale Accademia di Turino, fasc. 1518; London Med. Record, Sept. 15, 1876, p. 408.]

[Footnote 39: Loc. cit.]

[Footnote 40: Lancet, March 30, 1872, p. 432.]

[Footnote 41: Dublin Journ. Med. Sci., Aug., 1875, p. 178.]

Ignipuncture with the thermo-cautery of Paquelin has been successfully used of late by Helferich and by von Bruns of Tübingen.[42] In the latter instance the subject was five years of age. Fourteen punctures were made from above downward at intervals of about one centimeter, and five were made transversely. Not a drop of blood was lost. On the third day secondary hemorrhage occurred from the intercommunication of three of the punctures; this was restrained by ferric chloride, and the case went on to a favorable conclusion. Surgical procedures must constitute our sole therapeutic reliance. The temporary subsidence of enlargement under the influence of mercury and the iodides seems sure to be followed, sooner or later, by reproduction of the deformity. It is therefore a waste of time to attempt cures by medication.

[Footnote 42: Centbl. f. Chir.; Med. Times and Gaz., Sept. 23, 1883.]

Glossitis.

DEFINITION.--Inflammation of the tongue.

The term glossitis is usually applied to inflammation of the tissues of the tongue as a whole (parenchymatous glossitis), and not to those superficial inflammations which exist associated with the different varieties of {355} stomatitis and with other affections, and which implicate the mucous membrane and its glands and papillæ only (superficial glossitis). Superficial glossitis, however, sometimes terminates in parenchymatous glossitis. Papillæ and glands are usually affected together in superficial glossitis. When the inflammation predominates in the papillæ the disease is often designated as papillary glossitis; when in the glands, it is often termed follicular glossitis. Superficial glossitis, again, is sometimes manifested by the eruption of vesicles on the tongue, under which circumstance it is often denominated vesicular glossitis, sometimes herpetic glossitis. Glossitis is sometimes restricted to a portion of the tongue (circumscribed glossitis), and it sometimes involves the whole of the tongue (diffuse glossitis). Either form may be unilateral (hemiglossitis), though both forms are more frequently bilateral. Either form may be acute or chronic.

Superficial Glossitis.

DEFINITION.--An inflammation of the mucous membrane of the tongue, usually involving likewise both papillæ and glands.

SYNONYMS.--Catarrhal glossitis, Angina lingualis. Varieties: Papillary, follicular, vesicular (herpetic and eczematous), psoriatic, ichthyotic.

ETIOLOGY.--Predisposing and Exciting Causes.--It is rarely idiopathic, is most frequently deuteropathic, and sometimes traumatic. Superficial deuteropathic glossitis usually occurs in connection with gastric and gastro-enteric affections. It occurs likewise in association with stomatitis, tonsillitis, pharyngitis, many febrile affections, scorbutus, tuberculosis, syphilis, so-called psoriasis and ichthyosis of the tongue, carcinoma of the tongue, and the various neoplasms of the organ. Irregular and sharp-cornered or jagged teeth often induce traumatic superficial glossitis. Pungent vapors, such as those of chloride of ammonium, so much used of late years in the treatment of nasal catarrhs, sometimes produce a superficial traumatic glossitis, usually localized on the superior surface of the anterior portion of the tongue. Tobacco-smoking, especially from a short-stemmed pipe, will likewise produce it occasionally at the point where the concentrated smoke strikes the organ. Attempts to drink liquids too hot, too acrid, or too caustic may be mentioned as other occasional causes. Nervous irritation, such as of the chorda-tympani nerve, is attributed as a causal influence of unilateral vesicular glossitis, herpetic or otherwise, and as a probable factor in other varieties of unilateral glossitis. Eczema of the tongue may ensue as a sequel of prolonged cutaneous eczema (De Mussy[43]).

[Footnote 43: Gaz. hebd., June 22, 1883; Med. News, Aug. 11, 1883, p. 151.]

PATHOLOGY AND MORBID ANATOMY.--Superficial glossitis, as indicated, involves the mucous membrane, glands, papillæ, and epithelium. It is hardly necessary to dwell upon the pathological conditions of the lingual mucous membrane and its epithelium in gastro-intestinal and febrile disorders, as these are described in connection with the various diseases. Ordinarily, the epithelium increases in thickness, and when detached, spontaneously or otherwise, exposes a red and swollen membrane with erect papillæ. Sometimes the condensed stratified layer of epithelium becomes dry and very hard. Under some illy-defined {356} conditions, the papillæ of the tongue undergo great hypertrophy. The filiform papillæ become elongated to several times their normal length, and feel and look like so many hairs on the tongue. Like many other lingual affections, this is often unilateral. It is quite marked in some cases of influenza and other febrile disorders, producing great annoyance in the mouth. It occurs likewise in gastro-intestinal disorders and in disorders of the mouth and teeth. It is evidently a deuteropathic phenomenon. In other cases the glands of the tongue, especially at its base, become involved, forming the follicular glossitis of some writers. In another class of cases, most frequently syphilitic or at least quasi-syphilitic, one or more whitish circumscribed patches are seen on the tongue, resembling such as are left after superficial cauterization with nitrate of silver. This condition is described as psoriasis linguæ. It is due to condensation of layers of epithelium, which may become detached in a few days in mass or in fragments, leaving the denuded mucous membrane red and the papillæ erect and somewhat swollen.

When psoriasis of the tongue has existed for a long time, a further change, and a more permanent one, takes place in the papillæ and epithelium. This condition has been denominated ichthyosis linguæ. Superficial ulceration takes place at the psoriatic patches, and the repair eventually excites such a proliferation of epithelium that it becomes quite horny to the sight and to the touch. It spreads over a much larger extent of surface than the original psoriasis, but, like it, leaves the unaffected portions of the tongue in an apparently normal condition. Both affections are usually bilateral, and the patches or series of patches most frequently symmetrical or engaging analogous vascular territory upon the two sides.

In a case reported by Mr. Hulke[44] portions of the horny substance were habitually sliced off with a razor. Microscopic examination "showed colossal papillæ; the indurated portion of the mass was altogether epithelial, the lower cells being clear, transparent, and natural, the middle ones granular, and the superficial layer felted together into a dense opaque mass" (Clarke).

[Footnote 44: Medical Times, Nov. 30, 1861, p. 556.]

Both of these affections are liable in about one-third of the cases to terminate in epithelioma. Although the opinion generally entertained classes all cases of psoriasis and ichthyosis linguæ in the category of syphilitic affections, there is reason to doubt its accuracy. Sangster[45] has drawn up a tabular statement of 44 cases, of which 1 only occurred in a female; 23 occurred in smokers, 12 being inveterate smokers. In but 12 instances (8-1/3 per cent.) was there positive proof or strong evidence of syphilis; 30 per cent. of the whole number eventuated in epithelioma.

[Footnote 45: Med. Times and Gaz., London, April 8, 1882, p. 370.]

Vesicular glossitis, usually unilateral and most frequently right-sided, has been described by Paget,[46] Stoker,[47] Barker,[48] Hill,[49] and De Mussy,[50] and doubtless by others.

[Footnote 46: Lancet, March 11, 1865; Clarke, op. cit., p. 88.]

[Footnote 47: Dub. Journ. Med. Sci., May 1, 1876, p. 401, illustrated.]

[Footnote 48: Lancet, Nov. 22, 1879, p. 764.]

[Footnote 49: Brit. Med. Journ., Oct. 7, 1882, p. 683.]

[Footnote 50: Gaz. hebd., June 22, 1883; Med. News, Aug. 11, 1883, p. 151.]

{357} SYMPTOMATOLOGY, COURSE, DURATION, TERMINATIONS, COMPLICATIONS, AND SEQUELÆ.--Dryness of the tongue, stiffness, heat, and pain--the latter especially during movements of the organ in deglutition and in articulation--are the prominent subjective symptoms of acute superficial glossitis. There are rarely any marked symptoms of febrile disturbance unless the disorder is about to undergo extension into parenchymatous glossitis.

DIAGNOSIS.--Redness of the tongue, prominence of the papillæ, slight enlargement, perhaps bearing impressions made by the teeth, and pain or sense of impediment on movement, are the main diagnostic features of superficial glossitis.

Vesicles indicate the vesicular variety of superficial glossitis; irregular whitish patches, the psoriatic variety; and hard, horny patches with intervening fissures, the ichthyotic variety. A superficial circumscribed glossitis attending the local ulcerations of syphilis, tubercle, and epithelioma is differentiated by the clinical history of the case.

TREATMENT.--In ordinary cases the treatment described under catarrhal stomatitis suffices, so far as local measures are concerned. The gastritis or gastro-enteritis requires appropriate attention, as does any systemic malady under which the patient may be laboring. Demulcent and astringent lotions may be applied by douche, spray, or gargle. Local applications of weak solutions of iodine have been recommended. In cases of considerable severity, and especially when there is reason to expect extension into the deeper tissues, superficial scarification of the dorsum of the tongue is advisable.

Ulcers are perhaps best treated locally by touching the edges daily with the pencil of sulphate of copper. Any imperfect teeth in their immediate vicinity to which the ulceration may be attributable should be extracted or put in repair. De Mussy's case of eczema was cured after five months' daily use of a large quantity of water-cress.

Glossitis Parasitica.

DEFINITION.--An inflammation of the tongue said to be due to parasitic vegetation.

SYNONYMS.--Nigrities, Glossophytia, Black tongue.

Under the term black tongue two different affections have been described, the one an epidemic erysipelatous disorder to be mentioned under parenchymatous glossitis, and the other, now to be mentioned, a peculiar black pigmentation due to parasitic disease seated upon and around the hypertrophied filiform papillæ. The ordinary parasitic vegetations found upon the tongue do not produce the affection in question.

HISTORY.--First described by H. Hyde Salter,[51] and then by Eulenburg, it has been made the subject of observation by Raynaud,[52] Fereol and others,[53] Lanceraux,[54] Dessois,[55] Hirz,[56] Pasquier,[57] Moure,[58] and a few {358} others. Outside of French literature, little had been written of it until very recently.

[Footnote 51: Article "Tongue," Encyclopedia of Anatomy and Physiology, London, 1849-52, vol. iv. pp. 1159, 1160.]

[Footnote 52: Gaz. hebd., 1869, No. 14, p. 221.]

[Footnote 53: Gaz. des Hôp., June 29, 1875.]

[Footnote 54: Union Méd., March 20, 1877.]

[Footnote 55: De la Langue noire [Glossophytie], Paris, 1878, 8vo, p. 38, illustrated.]

[Footnote 56: Gaz. Méd., Strasbourg, 1879.]

[Footnote 57: Bull. Méd. du Nord, 1883.]

[Footnote 58: Revue mensuelle de Laryngologie, etc., Sept., 1883, p. 276.]

ETIOLOGY.--The affection appears to be due to some fault of nutrition, but the cause has not been determined. The fluids of the mouth always exhibit an acid reaction. It has been seen chiefly in dyspeptics and hypochondriacs, and has seemed in one instance (Moure) to have followed the use of chlorate-of-potash lozenges. A case has been recorded by Solomon Solis Cohen[59] in a negro child the subject of congenital syphilis. Mr. George Stoker[60] and G. Y. Broatch[61] have each reported a case of long duration occurring in a painter.

[Footnote 59: The Polyclinic, Philada., July, 1884, p. 10.]

[Footnote 60: Brit. Med. Journ., March 29, 1884, p. 602--said to be first case recorded in England.]

[Footnote 61: Ibid., April 19, 1884.]

PATHOLOGY AND MORBID ANATOMY.--The disease is characterized by a grayish-black or fully black discoloration on the upper surface of the tongue, which gives it an aspect which recalls the normal appearance of the tongue of the parrot and the giraffe, and an occasional appearance of the organ in the ox, sheep, dog, cat, and some other animals. The filiform papillæ are enormously elongated, so that they closely resemble hairs, and they are described by some writers as lying upon the surface of the tongue in confusion like that of a field of wheat thrown down by the wind. The individual papillæ are surrounded with a parasitic vegetable growth. Raynaud compared the microscopic spores in his case to the microphyte of tinea tonsurans or that of herpes circinatus. According to Malassez, they do not differ from those found in the saburral tongue of the dyspeptic, and he considers that their development is favored by their very arrest by the hypertrophied papillæ. Nevertheless, the subjects of this disease are not all dyspeptics by any means. Dessois made culture-efforts to reproduce the disease upon his own tongue, but failed to inoculate it. For detailed description of the disease we cannot do better than refer the interested reader to Dessois' monograph, from whose observations, chiefly, it appears that the discoloration begins at the central portion of the tongue, increases gradually in extent and intensity for three or four days, and then gradually disappears by desquamation. The tongue is very dry while the affection is at its height. Close examination of the parts and microscopic inspection of papillæ removed for the purpose are said to show that the spores of the cryptogam are first developed at the base of the papillæ, separating them from each other. The irritation produced by the parasite causes longitudinal hypertrophy of the papilla, and the continued growth of the parasite produces a muff-like envelopment of the papilla; the spores at the same time becoming insinuated between the most superficial epithelial cells and dislocating them, so that they maintain their position around the axis of the papilla only by means of the intervening parasitic masses. The papilla continues to elongate and the cryptogam to increase, until finally it invades nearly the entire length of the papilla. This entire parasitic mass soon becomes detached, carrying with it the epithelial cells under which it has become insinuated, and leaves the papilla naked, save for a few cells remaining attached by their superior borders. In the case observed by my brother, as in Mr. Stoker's and Broatch's cases, microscopical examination of the black filaments showed them to be composed of closely-packed epithelial cells, overlapping one another, stained {359} brown, and decreasing in intensity of color from the apex toward the base of the filament. In some cells the nucleus was darker, and in others lighter, than the surrounding protoplasm. The cryptogam, therefore, cannot always be detected. Indeed, there seems reason to believe that the affection may not be parasitic,[62] although the prominence given to this feature by French writers apparently warrants its being so considered. There may be two kinds of black tongue--one non-parasitic.

[Footnote 62: Hutchinson, The Medical Press, p. 20, July 11, 1883.]

SYMPTOMS.--There are no special subjective symptoms. The objective symptoms are the peculiar dark or black discoloration of the upper surface of the tongue and the excessively elongated filiform papillæ.

DIAGNOSIS.--The chief diagnostic feature is the black discoloration of the tongue which has given the name black tongue to the disease. Discrimination is requisite from discoloration by food or medicine.

PROGNOSIS.--This is favorable, the condition subsiding under treatment, and sometimes spontaneously, though liable to recurrence. In some instances the condition becomes chronic.

TREATMENT.--The indication is to endeavor to favor desquamation of the papilla by means of potassium chloride or sodium borate, and to administer alkalines, so as to render the saliva alkaline and unfavorable for the development of the parasite. It is recommended, in addition, to scrape the tongue with a spatula, and to douche it with a spray of mercuric chloride, 1:500. Attention to the general health is requisite, especially in dyspeptics and hypochondriacs. In the case of the negro child above alluded to the discoloration of the tongue finally disappeared under the systemic use of potassium iodide, without topical treatment, although repeated recurrences took place at varying intervals.

Parenchymatous Glossitis.

DEFINITION.--An inflammation of the tongue involving its substance as well as the mucous membrane.

SYNONYMS.--Idiopathic glossitis. Interstitial glossitis. Erectile glossitis (Salter), Glossomegistus (Sauvages), Paraglossia.

HISTORY.--Albeit a comparatively infrequent disease, especially at the present day, numerous cases and collections of cases are on record from very early times; and the affection seems to have attracted the attention of medical writers ever since. Hippocrates, Galen, Aretæus, Celsus, Aëtius, Avicenna, Forestus, Rivière, Schenkins, Sauvages, Vogel, van Swieten, are referred to by more modern writers as having described the disease. Louis, De la Malle, Lassus, J. P. Frank, Jn. Frank, Fleming,[63] Clarke, and Bryant may be cited as the most prominent recent observers.

[Footnote 63: Dublin Journ. Med. Sci., 1850, vol. x.]

ETIOLOGY.--Predisposing and Exciting Causes.--Glossitis is sometimes idiopathic, sometimes deuteropathic, and sometimes traumatic. Impaired health from over-fatigue or from exhaustive disease may be regarded as a predisposing cause in the presence of the causes which more frequently give rise to traumatic glossitis. Sudden or prolonged exposure to atmospheric changes, to cold and moisture, as when working in damp and wet localities, is often the apparent determining cause in {360} both the idiopathic and deuteropathic varieties. In many instances occurring in this way it is found that the tongue has long been subjected to mechanical irritation from jagged teeth.

Idiopathic glossitis occurs at all ages, but has been supposed by some observers to be more frequent in scrofulous subjects. It occurs in the apparently healthy only after severe exposure to wet and cold, and in convalescents from acute febrile diseases usually after some moderate exposure to a draught of air or change of temperature. It appears to be more imminent after influenza (Möller, Smee, Graves, Salter) than after other febrile disorders. It has occasionally been caused by chewing acrid plants, some of them food-plants, some of them medicinal. In the list have been included celery, bilberries, Daphne mezereum and Daphne laureola, aconite, and tobacco. It has been known to follow the eating of shellfish (Watson, Salter).

Deuteropathic glossitis has occurred during the course of scarlatina, variola, epidemic erysipelas (black tongue), scorbutus, enteric fever, glanders, septicæmia from various causes, rheumatism, diffuse inflammation of the connective tissue of the cervico-mental region, herpes, syphilis, ptyalism, mercurial and other varieties of toxæmic stomatitis, tonsillitis, pharyngitis, gastritis, and epithelioma of the tongue. It appears to be occasionally endemic (Fleming[64]), and is occasionally epidemic (Reil[65]). In the United States it prevailed extensively during an epidemic of erysipelas that overran the country from 1842 to 1846, inclusive, and was frequently reported in the American medical journals of that period under the name of black tongue. In some localities more than half the cases terminated fatally, sometimes within two or three days, more frequently about the eighth or tenth day, and occasionally still later. Traumatic glossitis arises from a number of causes. Among these may be mentioned the irritation of jagged edges of broken and carious teeth; wounds from firearms and other weapons; wounds from splinters of toothpicks, spiculæ of bone, broken pipe-stems, pins, needles, nails, slate-pencils, and other pointed things inadvertently placed in the mouth; wounds from the teeth during epileptic seizures and other convulsive paroxysms; contact of the tongue with cold iron in cold weather; the inspiration of very hot air, as in burning buildings; burns, scalds, scalding beverages; acrid and corrosive substances introduced by design or accident; incautious use of tobacco in bulk, and of ammonia; incautious cauterization; concealed calculi in the tongue; concealed bulbs of teeth; rupture of the lingual frenum; the bites and stings of venomous insects, as the wasp, the hornet, and the bee. For many years writers have referred to a case reported by Dupont to the Parisian Academy of Medicine which followed a young man's attempt to win a wager that he would bite into the body of a living toad, and to two fatal cases reported by Ambrose Paré from drinking a vinous infusion of sage which was subsequently found to have been impregnated with the saliva of the toad.

[Footnote 64: Dub. Journ. Med. Sci., 1850, vol. x. p. 88.]

[Footnote 65: Memorabilia Clinica (Dict. Sciences méd.), vol. xviii.]

SYMPTOMS, COURSE, DURATION, TERMINATIONS, COMPLICATIONS, AND SEQUELÆ.--In acute parenchymatous glossitis the local symptoms often appear quite suddenly, usually unilaterally, even when they become bilateral subsequently, and they increase in severity with great rapidity. {361} These symptoms are, at first, distinct sensations of heat and tumefaction in the tongue, quickly followed by stiffness and considerable impediment in its movements, as though it were numb and weighted down. In cases where the glossitis is an extension from tonsillitis, these sensations begin in the root of the organ. They commence at the root likewise, in most instances following exposure to severe cold and moisture. In other instances the extremity of the organ is affected first. In cases resulting from local injury the symptoms commence at the injured portion. The local symptoms are sometimes preceded by rigor, followed by fever, cephalalgia, and pains in the neck and occiput. Examined at this time, the tongue is seen to be swollen and studded with indentations due to the pressure sustained from the teeth. At first the surface is punctated and red; subsequently it becomes brownish or decidedly brown. Although the organ may remain moist for several hours, it eventually becomes excessively dry, and supports a thick adhesive coating of mucus and epithelium.

In a few hours, sometimes as few as two or three, the entire organ may become involved in the inflammation, enlarging to such an extent as to keep the lower jaw depressed, to fill almost the entire oral cavity or to quite fill it, and to project like a tumor beyond the teeth and the lips (Fig. 16). In exceptional cases the enlargement of the tongue has been so great as to produce dislocation of the lower jaw. The soft palate is lifted up and the epiglottis often pressed down. The latter condition has been known to threaten suffocation. In this condition the patient cannot breathe through the mouth, widely as it may be forced open, and has great difficulty in breathing through the nose. Respiration is therefore laborious. Articulation is impeded or impossible, and deglutition difficult or impracticable. The tumefaction and congestion are often continuous into the floor of the mouth and the parts adjacent. The sublingual and submaxillary glands often become swollen, tense, and painful; and the entire neck is sometimes swollen to such a degree as to exert injurious pressure on the jugular veins. The tongue is very hard to the touch, almost or quite immovable, and is the seat of burning heat and pain. The pain often extends from the root of the tongue along the glosso-pharyngeal folds into the pharynx, and thence by way of the Eustachian tubes into the ears, the folds just named being very much upon the stretch. When the tongue protrudes far out of the mouth it becomes excessively dry, fissured, sanious, and excoriated, or even ulcerated at points where it is subjected to the pressure of the teeth. It is covered with dark viscid secretions, which often extend beyond it and over the entire aperture of the mouth. The epithelial coating often undergoes desquamation, and then the organ becomes exquisitely sensitive to the contact of food, water, or even the air. This desquamation is sometimes in mass, in sheets peeling off like a pseudo-membrane. The general symptoms vary in individual cases. As a rule, the face is turgid and its expression anxious; the conjunctiva suffused, respiration impeded, and sleep disturbed or impracticable. Saliva dribbles externally, often in considerable quantity. The {362} odor from the mouth becomes quite fetid from decomposition of the retained products of secretion. Thirst is usually intense, though immoderate only in some cases. Cough is more or less constant and quite exhausting. This and the dribbling of saliva contribute with the dyspnoea to prevent sleep. Pyrexia is often intense. The pulse is strong and quick at first, 100-120 per minute, and there is often marked throbbing of the temporal and carotid arteries. The skin is hot and dry at first, but cold sweat subsequently accumulates upon the face and neck as the dyspnoea increases. The bowels are constipated. The urine is scanty and high colored. The impediment to the return of blood to the heart from the head causes cerebral congestion, drowsiness, and even threatens asphyxia. In other cases there is intense cephalalgia, nervous irritability, restlessness, and even delirium.

The symptoms sometimes reach their acme in rather less than forty-eight hours, and then gradually subside. More frequently they continue on into the third or fourth day. Occasionally they are protracted as long as the fifth or sixth or even the eighth day, rarely longer. Resolution occasionally takes place within twenty-four hours, however (van Swieten), though more frequently occurring from the fifth to the seventh day. In some instances remittance or intermittence has been noted, the cause therefor not being apparent, although attributed to malaria.

Resolution of the inflammatory process is usually indicated by the gradual return of moisture on the tongue and progressive detumescence of the organ, accompanied by subsidence of the redness, heat, and pain. Increased secretion of saliva, general perspiration, or diuresis sometimes marks the cessation of the pyrexia.

Should the process be going to terminate in suppuration, the local distress increases, markedly about the end of the week. The pains become lancinating, and associated with throbbing of the lingual blood-vessels. The swelling becomes prominent and softer at some one point, although the sense of fluctuation is not very perceptible on palpation, and finally the abscess bursts through the surface, unless previously incised, and discharges a fetid pus. Suppuration always involves a prolonged duration of the attack.

In rare instances glossitis terminates in gangrene of the tongue, circumscribed or diffuse. This result is indicated by adynamic symptoms on the part of the constitution, and by the livid appearance of the parts undergoing mortification. The hemorrhage following extensive sloughs from gangrene has been fatal in some instances.

Fleming[66] calls prominent attention to a complication of glossitis, of which he alludes to several examples. This is "an inflammation, circumscribed or diffused, originating in the loose areolar tissue between the genio-hyo-glossi muscles, and first manifesting itself by a train of symptoms identical with those of ordinary glossitis, but soon characterized by peculiar features." These features comprise fulness under the chin like that dubbed double chin, pressure upon which, especially near the hyoid bone, being very painful; and suppuration, which, circumscribed or diffuse, burrows most freely toward the base of the tongue.

[Footnote 66: Loc. cit., p. 91.]

Chronic induration of the tongue sometimes remains unilateral, although the acute disease has not been unilateral.

{363} PATHOLOGY AND MORBID ANATOMY.--It has been advanced that in idiopathic glossitis from cold the engorgement of the vessels is probably a consequence of vaso-dilator influence of the glosso-pharyngeal nerve for the base of the organ, and of the chorda-tympani for the anterior portion. An instance of herpetic glossitis from probable irritation of the chorda-tympani nerve by an aural polypus (Berkely Hill[67]) seems to lend some force to this opinion. However engendered, there is a rapid distension of the organ by blood, followed by infiltration of fibrin and serum into the intermuscular connective tissue and into the planes of the connective tissue separating the muscular fasciculi. In some instances degeneration of muscular fibre has been observed. There is great increase in the thickness of the coats of epithelium, beneath which the mucous membrane is red and its papillæ erect. This coating sometimes peels off like a false membrane. In cases extending from tonsillitis the base of the tongue suffers most.

[Footnote 67: Brit. Med. Journ., Oct. 7, 1882, p. 683.]

The disease usually terminates by resolution, although a slight amount of hypertrophy, unilateral or bilateral, sometimes persists, and occasionally to a marked degree (Wells). In instances much less frequent suppuration ensues, usually in debilitated subjects or in cases due to traumatism or in cases inefficiently treated. The suppurative process is usually circumscribed and unilateral, and the abscess points most frequently just beneath the side of the tongue; sometimes, however, the pointing takes place at the dorsum, sometimes at the tip. The pressure of the teeth seems to be the provocative cause of the disposition to point at the edge of the tongue. The pus is usually quite fetid. Sometimes the abscess is gangrenous.

Gangrene is an infrequent result of glossitis. The pressure of the teeth, strangulating the organ at the oral outlet, seems to occasion the failure of nutrition in instances where it occurs. The losses are ordinarily insignificant, though appearing quite extensive while the tongue remains swollen. Sometimes large portions drop off, and fatal hemorrhage has resulted (Frank) in consequence. From the nature of the organ the parts separate more readily than in almost any other instance. Gangrenous abscess, ensuing even from very slight causes, such as a wound with the head of a barleycorn (Ranking[68]), sometimes proves fatal.

[Footnote 68: Provincial Med. and Surg. Journ., 1844.]

In those cases of diffuse inflammation of the interconnective tissue of the genio-hyo-glossi muscles Fleming states that the suppuration--which, whether circumscribed or diffuse, burrows toward the root of the tongue--absolutely dissects its extrinsic muscles and destroys their functions; ultimately injuring the periosteum and laying bare the inside of the inferior maxilla in the vicinity of their attachments. When an incision is made to the parts through the integument, the muscles will be found on palpation flabby and detached, and their interstices filled with purulent matter, sometimes very fetid.

DIAGNOSIS.--These is no difficulty in the diagnosis, except in the early stage of such examples as are attributed to metastatic gout and rheumatism. The subsidence of the peculiar pains elsewhere, and the onset of pain in the tongue, would lead to the inference that a glossitis of this kind {364} was in progress. The acuteness of the tumefaction would distinguish it from hypertrophy of the tongue on the one hand, and from the tumefaction attending malignant disease on the other.

Cystoma of the tongue has sometimes been mistaken for abscess due to glossitis; but even here the history of the case should serve in most instances as a satisfactory factor for the differential diagnosis.

PROGNOSIS.--The prognosis depends upon the gravity of the local symptoms and the activity of the treatment. A case left to itself will be likely to terminate fatally within five or six days. Death, indeed, has been known to take place within forty-eight hours, even in cases submitted to treatment. On the whole, however, the prognosis should be regarded as favorable in the absence of specially lethal complications. Even suppuration adds little gravity to the prognosis, the structure of the organ being but little favorable to accumulations of purulent material. Should an abscess become gangrenous, however, the prognosis becomes grave at once, as it in the presence of gangrene from pressure or other cause. Should the patient survive losses by gangrene, there may be permanent impairment in articulation.

TREATMENT.--Superficial glossitis, as a rule, merely requires active purgation, with the topical use of cold emollient mouth-washes containing mucilage of slippery elm, quince-seed, or the like, to which detergents, such as alum and borax, may be advantageously added in the proportion of five grains to the ounce. In cases resisting this mild treatment topical applications of glycerite of tannin twice or thrice a day are often serviceable.

Parenchymatous glossitis demands the most active antiphlogistic treatment. If the case be seen at an early stage of the process, before the tumefaction of the tongue has become so great as to fill the mouth and interfere with swallowing, a saline purge--say salts and senna--containing some tartar emetic can be advantageously administered to begin with. Following this, tartar emetic may be continued in small doses every two or three hours, associated with small doses of tincture of aconite-root (minim j-iij), according to the condition of the pulse and the effect of medication. Should this treatment fail to produce prompt amelioration in the local symptoms, or should the tongue be considerably swollen when the case comes under care, free leeching should be applied from the hyoid bone to the angle of the jaw on each side, including the region of the hyoid bone (fifteen to twenty-five Spanish leeches). This should be followed by emollient cataplasms, reaching from ear to ear, to favor continuous hemorrhagic oozings from the leech-bites. The internal antiphlogistic treatment is indicated just the same, and if not administrable by the mouth may be administered by the bowel; the nauseant and depressent effects of the tartar emetic and aconite being maintained by hypodermatic injection. Leeching the inflamed tongue itself is said to be often prompter in producing detumescence of the organ than leeching exteriorly, but the leech-bites are apt to add to the local irritation; besides which, the mouth is so filled by the swollen tongue as to leave little more than the tip accessible to the leeches without danger of losing control of them. Venesection from the arm, the jugular vein, or from vessels elsewhere is no longer much in vogue, it being doubtful whether general venesection is more useful than local bleedings. Debility, whether presenting originally or as the result of withdrawal of blood and other {365} antiphlogistic measures, may be met by the systematic use of tincture of chloride of iron and of quinia.

Severe cases demand one or more longitudinal incisions on each side of the raphé of the tongue, deep enough to reach nearly halfway into the substance of the organ and carried from base to tip. Cases are on record in which the patients themselves had in their despair cut into their tongues in order to obtain relief from their local sufferings, and had in this way rescued their own lives by the means most appropriate for the purpose (Camerarius, Lusitanus[69]). When the mouth is filled by the tongue, it is necessary to insert the knife on the flat until the base of the tongue is reached, and then to turn it and make the cuts as indicated. Copious bleeding usually follows these incisions, often followed by marked diminution in the volume of the organ. Deep as these cuts appear when made, they become quite shallow before the organ has shrunk to its normal volume. Bleeding from the ranular veins, recommended by some practitioners in preference to incisions into the organ, is often impracticable on account of the tumefaction preventing access to them.

[Footnote 69: Dict. Sciences méd., vol. xviii.]

If severe hemorrhage takes place from divided vessels, the vessels may be subjected to torsion, which is the preferable mode of management, or to searing with some form of the incandescent cautery (hot iron, electric cautery, Paquelin's thermo-cautery). Astringent and chemical styptics are of little use. The method of searing is open to the objection that secondary hemorrhage may ensue on detachment of the eschars, but this accident is not likely to happen under circumstances at all favorable.

In localized or circumscribed glossitis the incision to be made should interest the swollen portion only.

Should the tongue swell again, the incisions may be repeated. Whether the tongue require incision or not, it is good treatment to have the patient inhale vapor from hot vinegar, alcohol, or cologne spirits to render the parts more comfortable. Washes of weak detergent solutions containing potassium nitrate, sodium borate, or ammonium chloride may be used by syringe or spray to cleanse the parts and promote detachment of the epithelial coatings on the tongue and interior of the mouth, the accumulations of which are sometimes matters of great annoyance. The drug last mentioned exerts in addition a special action on the inflammatory process which is often quite serviceable. I have seen good results follow the prolonged use of sprays of an aqueous solution of ammonium chloride (Stuver), one drachm to the ounce, from the steam-spray apparatus, continued for fifteen to twenty minutes at a time and repeated every two or three hours.

In many instances the patient is unable to take food by the mouth. The best plan under such circumstances is to pass a catheter into the stomach through the larger of the two nasal passages, and retain it in position unless its presence interferes too much with respiration. Milk and stimulus can then be poured into the stomach from time to time with the aid of a funnel passed into the outer opening of the tube, which should be kept corked during the intervals when retained in position. This failing or impracticable, it will be necessary to nourish the patient with enemata.

On the appearance of abscess the same should be freely laid open. In cases of hesitation, the true nature of the presumable abscess can be {366} determined beforehand with the exploring-needle. The pus from an abscess of this kind is rarely copious and is usually fetid. It would be good practice to distend the sac after discharge of pus by injecting into it a solution of carbolic acid.

In resisting or advanced cases of suppurative inflammation of the planes of connective tissue between the muscles at the lower portion of the root of the tongue, Fleming recommends a free incision under the chin in the middle line, through skin and fasciæ and on through the raphé of the muscles themselves.

In cases of gangrene, washes, douches, or sprays of carbolic acid, chlorinated soda, hydrogen peroxide, or potassium permanganate are indicated to relieve fetor; while the most supporting treatment by mouth or otherwise is requisite on general principles.

Chronic Glossitis.

Chronic glossitis, like acute glossitis, may be superficial or parenchymatous.

Chronic Superficial Glossitis.

Superficial chronic glossitis is usually confined to the papillæ of the tongue, territories of which, so to speak, are mapped out on the surface of the tongue, separated by furrows reaching to the basement mucous membrane. In pronounced cases the dividing furrows are quite deep, giving the organ a mamelonnated appearance, and they penetrate into the mucous membrane (dissecting glossitis, Wunderlich), which becomes subjected to great irritation by the retention of articles of food in the fissures. Demarquay[70] has recorded a case of this kind in which, to relieve the intense sufferings with which the patient had been plagued for a number of years, he had been forced to amputate the anterior half of the organ--an operation which succeeded thoroughly.

[Footnote 70: Loc. cit., p. 142.]

In another group of cases the surface of the swollen tongue is mapped out in small ovoid patches, smooth, red, and glossy, from which the papillæ have become separated without regeneration. Sometimes chronic glossitis presents as an aphthous inflammation. Sometimes superficial ulcers occur upon the dorsum of the tongue, irritable, indolent, and indurated.

ETIOLOGY.--Chronic superficial glossitis is in rare instances a sequel of the acute form of the disease. Usually, however, it is encountered as a chronic affection from the outset, so to speak, generally as a result of long-continued irritation in connection with dyspepsia and other gastric and gastro-intestinal disorders. It is frequently encountered in subjects of chronic alcoholism.

The superficial ulcerations often occur at the sides of the organ, usually in some of the depressions formed by the contact of the teeth.

SYMPTOMATOLOGY.--The symptoms are those due to a consciousness that the tongue is too large, with occasional pain in taking acid and succulent food.

{367} PATHOLOGY.--The pathology does not differ from that of chronic inflammations elsewhere. The apparent obliteration of the papillæ in some cases is due to a filling up of the intervening furrows by permanent deposit of new-formed cells. The excoriations and superficial ulcerations are most frequently due to disturbance of nutrition by pressure.

DIAGNOSIS.--The affection may be confounded with syphilitic disease of the tongue or with papillary epithelioma, but the history of the case, the resistance to antisyphilitic treatment, and the negative results from microscopic examination of fragments of tissue removed for the purpose, serve to establish the diagnosis in cases of doubt. It must not be forgotten, however, that many cases of epithelioma begin in chronic glossitis, non-specific as well as syphilitic.

PROGNOSIS.--Though not threatening to life, the prognosis of the disease itself is bad. It resists treatment, being, in fact, a complication of some obstinate or intractable gastric or gastro-intestinal disorder, or an evidence of constitutional dyscrasia. Cure may be expected in recent cases, following cure of the dyspepsia or other malady upon which the chronic glossitis may be dependent.

TREATMENT.--Care to cleanse the tongue by washes, douches, or wet cloths after each meal, in order to remove particles of food which may have become impacted in the anfractuosities of the organ, is important in order to avoid additional sources of irritation.

Astringents and caustics of various kinds have been extensively employed, carefully applied to the floors of the fissures, but it is very rarely that any benefit ensues. Demarquay[71] reports good results in one case of dissecting papillary glossitis from biweekly applications of equal parts of chromic acid and water. Butlin reports good results from chromic acid (1:10).

[Footnote 71: Loc. cit., p. 143.]

Careful attention to the gastro-intestinal functions, and a thorough change of diet, such as the adoption of the milk cure and the like, with due attention to bathing and outdoor exercise, comprise the most rational method of constitutional treatment. Should the secretions of the mouth give an acid reaction with litmus-paper, alkalies are strongly indicated, topically and systemically. Avoidance of alcohol in all forms is often absolutely essential.

Chronic Parenchymatous Glossitis.

The chronic parenchymatous form of glossitis is usually circumscribed. When diffuse or general it has usually been a sequel of acute parenchymatous glossitis. It is not a painful disorder, and as a rule is not associated with constitutional manifestations. The circumscribed tumefaction usually presents as an induration upon some portion of the side of the tongue, being most frequently directly or indirectly due to irritation sustained from a jagged tooth. Ordinary sensibility is much diminished, and sometimes the sense of taste likewise. Sometimes the indurated mass is ulcerated superficially. The enlargement of the organ is not sufficient to keep it outside the mouth. Sometimes, indeed, the tongue, {368} as a whole, has undergone atrophy, unilateral or bilateral. Chronic abscess of the tongue sometimes supervenes, chiefly in scrofulous subjects.

PATHOLOGY AND MORBID ANATOMY.--This consists merely in interstitial connective-tissue hyperplasia, with atrophy of muscular fibres from compression.

SYMPTOMS.--In addition to the objective symptoms of induration or circumscribed tumefaction, the subjective symptoms may be summed up as general hypersensitiveness to sapid and acrid substances; diminished tactile sensibility at the part affected; slight stinging sensations while the parts are at rest; occasional or continuous local pains; and a sense of impediment in the movements of the tongue in articulation and even in deglutition.

DIAGNOSIS.--Inspection reveals the swelling, and palpation its induration. In addition, the adjacent source of irritation, a jagged tooth or two, is seen. Abscess is recognized by special prominence at one point of the swelling and by indistinct sense of fluctuation.

Cystic tumor is liable to be mistaken for abscess, but the exploring-needle will solve the difficulty. Circumscribed induration may be confounded with tumor or with epithelioma.

PROGNOSIS.--This is good, provided the source of irritation can be removed or suppressed.

TREATMENT.--The first element in the treatment is the removal or repair of any offending tooth, and next attention to any underlying malady, constitutional or local. Weak solutions of iodine locally are said to be of service. Abscesses require incision and evacuation. Their walls should be distended with solutions of carbolic acid or be touched with solutions of iodine, silver nitrate, or cupric sulphate, to promote reparative inflammation.

Glossanthrax (Carbuncle of the Tongue, Malignant Pustule of the Tongue).

This is a special variety of gangrenous ulcerative glossitis, presenting as an integral phenomenon of a disease peculiar to slaughterers, who become infected from diseased cattle, usually by means of the knife, which they are sometimes in the habit of holding in the mouth (Heyfelder and others). It has been described chiefly by Heyfelder,[72] Duhamel, Chavarrien d'Audebert, Felix Plata, Breschet et Finot, and Maisonneuve.[73]

[Footnote 72: Med. Vereins Zeitung, 1834.]

[Footnote 73: Des Tumeurs de la Langue, Paris, 1848, Thèse de Concours.]

The period of incubation occupies about one day. The tongue then undergoes rapid tumefaction and becomes the seat of intense pain. The points of inoculation become hard, covered with vesicles containing bloody serum, which blacken, rupture, and leave dark, livid, gangrenous patches of ulceration. Profound cachexia rapidly ensues under typhoid manifestations, and death may result in less than twenty-four hours, though usually not until sixty hours. The prognosis, therefore, is of the gravest character.

The chief treatment consists in thorough cauterization of the inoculated {369} points by means of the actual cautery, followed by deep incisions into the body of the tongue if the glossitis be severe.

Ulceration of the Tongue.

Apart from the ulcerations of the tongue incidentally mentioned in the foregoing pages, there are two forms of ulcer, both of sufficiently frequent occurrence in ordinary practice to require special description: these are the tuberculous ulcer and the syphilitic ulcer.

Tuberculous Ulcer of the Tongue.--Tuberculous ulceration of the tongue occurs in a certain number of cases of advanced tuberculosis of the lungs or of the lungs and larynx. It has even been asserted to precede pulmonary tuberculosis. It is most frequently observed upon the upper surface of one side of the organ, sometimes at the tip, sometimes farther back, and usually on the same side upon which the disease is most advanced in the lungs or the larynx. It is often associated with previous or subsequent tuberculous ulcerations of the palate or of the pharynx or contiguous structures. It gradually extends, and rarely if ever heals. It is characterized by a superficial excavation, and by being covered with a grayish detritus entirely different from the purulent layers seen on other kinds of ulcers. When of long standing its base is indurated, and this may give rise at first to suspicion of squamous-celled carcinoma. Small yellowish elevations are sometimes observed in the reddened mucous membrane around the ulcer--an appearance deemed sometimes characteristic of the tuberculous nature of the lesion (Trélat[74]).

[Footnote 74: Bull. de l'Acad. de Méd., 1869, or Arch. gén. de Méd., 1870.]

PATHOLOGY AND MORBID ANATOMY.--Nodular tuberculous infiltration takes place beneath the mucous membrane, which becomes elevated in small, semiglobular, yellow protuberances of one or more millimeters in diameter, around which the mucous membrane is red and swollen. The epithelium becomes shed without undergoing renewal, and thus a little point of superficial ulceration remains. When several such points are sufficiently contiguous they coalesce into a single ulcer of irregular contour, which gradually spreads without much other change. Practically, it never heals.

SYMPTOMS.--In addition to the superficial ulceration described, and in addition to the constitutional and local symptoms of advanced tuberculosis of the lungs or lungs and larynx, as may be, there are no special symptoms attending the tuberculous ulcer of the tongue. Saliva is sometimes secreted in excess, but that is not characteristic. There is little pain and little impediment to the movements of the tongue until the disease has advanced.

DIAGNOSIS.--The presence in a tuberculous subject of a unilateral, irregular ulcer of the tongue surmounted with grayish detritus and surrounded by reddened edges, should suffice for the recognition of its presumptive tuberculous character. It is most difficult perhaps to differentiate from a small ulcerated squamous-celled carcinoma, and the two indeed sometimes coexist, rendering the discrimination extremely difficult until the advanced progress of the carcinoma places the diagnosis beyond doubt.

{370} In the early stages, however, it is distinguished by lack of the peculiar lancinating pains of carcinoma, which, however, are not invariably attendant, and by lack of secondary involvements of the cervical lymphatic glands. At all times it should be distinguishable from the carcinomatous ulcer by lack of the fungus-like appearance of the bed of the ulcer which is usual in carcinoma.

From syphilitic ulcer it is distinguishable by the history of the case, its tendency to be unilateral, and its failure to respond to antisyphilitic treatment. Syphilitic ulceration of the tongue may represent the primary, the secondary, or the tertiary manifestation of the specific disease. The former will not be discussed in this connection.

Secondary ulcers occur on the upper surface of the tongue, most frequently at the anterior portion, as fissures, usually longitudinal, the floors of which are ulcerated. They occur likewise at the sides, tip, and even lower surface of the organ. They are often associated with secondary ulceration in the mucous membrane of some portion of the mouth. They are quite painful, especially to the contact of pungent articles of food. Some ulcers occur as simple superficial excoriations at some portion of the edge or tip of the tongue, giving little evidence of any specific character.

Tertiary ulcers are usually sequelæ of gummata. They are much deeper than secondary ulcers, sanious at bottom, often serpiginous in configuration, and apt to extend in depth as well as in superficies, sometimes penetrating through and through the organ. They are most frequent in the very central portion of the tongue, or are symmetrically disposed on either side of it.

PROGNOSIS.--The prognosis of tuberculous ulceration is bad, both as regards tongue and patient.

TREATMENT.--The only topical treatment offering any prospect of local cure is the bodily destruction of the ulcer and the surrounding tissue with caustics, the best of which are the incandescent metals, or else the excision, with the incandescent knife, of a portion of the tongue comprising all the affected tissue. In the former case the tuberculous process often reappears about the cicatrix; in the latter, at some more distant point.

Tincture of iodine locally, detergent washes, and the like, often secure a certain amount of comfort as palliatives. The same indications prevail as in simple chronic glossitis, superficial and deep-seated. Iodoform locally is of benefit, inasmuch as it relieves pain and reduces collateral inflammation, but it is powerless to arrest the onward march of the ulcerative process.

Hemorrhage from the Mouth.

DEFINITION.--A loss of blood from the mouth.

SYNONYM.--Stomatorrhagia.

ETIOLOGY.--Hemorrhage from the mouth is usually a symptom of some disease or injury of the mouth, tongue, gums, palate, pharynx, or nose. It may, however, occur as one of the phenomena of scorbutus or of hæmophilia. It is said to occur occasionally as a vicarious {371} menstruation. It may be slight, so as barely to tinge the saliva, or it may be profuse enough to terminate fatally. Between these extremes there is an infinity of gradations. As a result of disease it may be caused by simple hyperæmia of the mucous membrane, by rupture of dilated blood-vessels, by ulceration, by gangrene. As a result of injury it may arise from wounds of various kinds, accidental or self-inflicted.

The gums are the most frequent source of slight hemorrhage from the mouth. The pharynx, probably, is the next most frequent seat. Hemorrhage from the tongue, cheeks, lips, and palate is usually traumatic or the result of ulceration.

SYMPTOMATOLOGY, COURSE, DURATION, COMPLICATIONS, TERMINATIONS, AND SEQUELÆ.--The symptoms of hemorrhage from the mouth are the presence of blood in the saliva or in the mouth itself, or in the expelled products of expectoration, emesis, or catharsis, for sometimes the blood is swallowed, and occasionally inhaled into the air-passages. The course, duration, complications, and terminations of stomatorrhagia depend upon its cause. Prolonged hemorrhage will entail anæmia; profuse hemorrhage may terminate fatally.

DIAGNOSIS.--Careful examination of the mouth, tongue, pharynx, and posterior nares, both by direct and by reflected light, may be necessary to discover the source of the hemorrhage and discriminate it from hæmoptysis and hæmatemesis.

PROGNOSIS.--The prognosis will depend upon the nature of the cause, its susceptibility of arrest, the quantity of blood lost, and the general health of the patient. It is grave, as a rule, in the subjects of hæmophilia, as there is a constitutional malnutrition of the blood-vessel system which cannot be counteracted.

TREATMENT.--Ergot or oil of turpentine internally, astringent mouth-washes, and recumbency constitute the main features in treatment.

Morbid Dentition.

DEFINITION.--Departure from the physiological processes concerned in the eruption of teeth, entailing certain local and systemic disorders.

SYNONYMS.--Dentitio difficilis, Pathological dentition, Odontitis infantum.

The correct comprehension of the subject will be facilitated by considering its etiology, pathology, and symptomatology in connection. Indeed, morbid dentition has been assigned so prominent a part in the etiology of various affections elsewhere discussed that a satisfactory consideration of its own causation would require the repetition of much that belongs more appropriately under other titles. While in some infants the teeth erupt so quietly that the parents are astonished by the accidental discovery of their presence above the gum, few children escape a greater or less amount of local and constitutional disturbance while passing through the process of dentition. So severe may these disturbances become that, according to the mortality-tables of London, as cited by West,[75] teething was assigned as the cause of death of 4.8 per cent. of all children dying under one year old, and of 7.3 per cent. of those who died between the {372} ages of twelve months and three years. It is furthermore well recognized that the period of greatest mortality among children is that of the first dentition. Associating these facts, we see, on the one hand, that while disorders of dentition may act a causative part in the production of systemic diseases or aggravate morbid processes due to ordinary causes, on the other hand they may be but one expression of some profound constitutional disturbance; or both aberration in the eruption of the teeth and systemic disease may be dependent upon the influence of dyscrasia. The period is one of active organic processes; the child is becoming fitted for a new manner of existence; and change and development are going on throughout nervous, vascular, respiratory, and alimentary systems. Hence there exists peculiar susceptibility to morbid influences; and any process, physiological or pathological, once started, goes through its stages with excessive energy.

[Footnote 75: Lectures on the Diseases of Infancy and Childhood, Philada., 1860, p. 425.]

Although the periods of normal eruption of the deciduous teeth vary within extensive limits, and an invariable order in eruption is not observed in all subjects, it may be stated as a rule that the lower central incisors are cut in quick succession about the seventh month. Some infants get these teeth during the fourth month (Vogel), and others have to wait until the tenth or eleventh month, some even longer. A few weeks after the appearance of these lower incisors--within fourteen days in some subjects, not until nine or more weeks in others--the central incisors of the upper jaw are cut, and its lateral incisors shortly afterward, followed in their turn by the lateral incisors of the lower jaw. In some instances--the majority, according to Vogel--the eruption of the inferior lateral incisors is delayed until the anterior molars are about to become exposed, usually from the twelfth to the fifteenth month. Sometimes the upper molars are cut before the lower, sometimes after them. From the sixteenth to the twentieth, or even the twenty-fourth, month the canine teeth are cut, and the four posterior molars follow between the twentieth and thirtieth months, rarely delayed until the thirty-sixth month,--completing the process of the first dentition.

From this it will be seen that the teeth erupt as a rule in pairs, and that a longer or shorter interval of repose takes place between the eruption of successive pairs.

Variations from the usual order beyond the limits noted above may be considered abnormal. Numerous cases are on record both of precipitate and of tardy dentition. Tanner cites from Haller nineteen examples in which one or more of the central incisors have been found through the gums at birth, and have had to be removed to prevent injury to the mother's nipple; from Crump, a case of full dentition at birth, reported to the Virginia Society of Dentists; and from Ashburner, a case of a child beginning to cut its first tooth, an incisor in the upper jaw, during its twenty-third month, the infant being very delicate, with a large head, tumid abdomen, and peculiarly small-sized extremities. The same author quotes from Serres cases of persons passing through several years of life--in one instance seven--before cutting their first teeth, and mentions on the authority of Tomes that Boxalli and Baumes have each recorded an instance in which the patient reached old age without a single tooth having ever appeared.

Rachitis is often the cause of tardy dentition, and in the subjects of this {373} diathesis not alone are the teeth retarded in development, but they decay early and even fall from their sockets.

The first indication of approaching dentition is the markedly increased production of saliva. For some little time after birth the salivary glands seem to remain wholly inactive, and until the fourth or fifth month of extra-uterine life they furnish very little secretion. At this period a decided change occurs. The mouth is constantly filled with saliva, which dribbles from its corners. To this continual slobbering, wetting the garments covering the chest, has been attributed the bronchial catarrh which attends some infants; and diarrhoea has likewise been referred to the swallowing of large quantities of saliva, acting as a mild laxative by virtue of its saline constituents.

There may be no further manifestation until the seventh month, beyond the broadening of the dental ridge. The exact position of each tooth is usually indicated by greater prominence of the gum above it for some time before it comes through, its entire outline being very distinct in the upper central incisors. As the tooth approaches the surface the gum becomes hot, shining, tense, and tumid, often painful. A slight amount of catarrhal stomatitis is almost invariable. There is some elevation of temperature; flushing of the cheek may occur; the child is restless, peevish, and fretful; its sleep may be broken; it may cry out with pain; its thumb, its fingers, any hard substance it can obtain, are thrust into its mouth to allay the irritation of the gums. Otalgia is not uncommon, and its occurrence may be inferred from the fact that the child pokes its thumb or finger into the auditory canal or firmly presses the tragus down over the external meatus. These may comprise all the disordered manifestations, local or constitutional, or there may be in addition loss of appetite, diarrhoea, vomiting, and the various disturbances of reflex nervous origin to be alluded to later; or, in the not common yet not rare instances already mentioned, there may be absolutely no appreciable disturbance whatever.

Sometimes a disposition exists to the formation of small aphthous ulcerations on the tongue or elsewhere in the mouth, particularly at the duplicature of the lip and the outer surface of the alveoli. Ulceration occurs most frequently at the tip of the tongue, probably occasioned by friction from the new teeth. Usually there is a single flat, round ulcer, its edges somewhat infiltrated, its bed covered with a yellow lardaceous substance. It is extremely painful to the touch, and thus every movement of the tongue occasions distress. It may heal within a few days or continue for weeks. Ulcers in other situations are less obstinate.

Occasionally--and more frequently in debilitated subjects or those exposed to unhygienic surroundings--there is an unusual amount of heat and swelling of the gum, which becomes excessively tender, usually over the summit of a particular tooth--in which case there will be a little tumor-like elevation--or around a tooth which has partially pierced through it. Small sloughy ulcerations form in this situation. There is great pain, and usually high fever and severe gastro-intestinal disorder. This affection, often difficult of cure, is termed by some writers odontitis infantum. So severe is the pain, and so great its tendency to aggravate constitutional disturbances, that life may be placed in jeopardy, and even fatal results ensue.

{374} Less severe than either of the forms just described, and yet far more intense than the mild stomatitis which many authors regard as physiological, is an aggravated form of catarrhal stomatitis sometimes attendant upon morbid dentition, in which there is swelling of the submaxillary glands and infiltration of the adjacent connective tissue. In this case there is usually considerable pyrexia.

The constitutional disturbances of reflex nervous origin occasioned by morbid dentition are of the most varied character, both in their degree of gravity and in the manner and locality of their manifestation. Doubtless the extensive ramifications of the great vagus nerve, and its connections both of origin and distribution with the exquisitely sensitive fifth nerve, as well as with the facial nerve and with the sympathetic system, will explain why the irritation should now be seated in the gastro-intestinal tract, giving rise to vomiting and diarrhoea (gastritis, gastro-enteritis, enteritis, entero-colitis, cholera infantum); now in the respiratory tract, provoking cough more or less severe, or even a well-marked bronchitis; now manifest itself in various cutaneous eruptions (urticaria, eczema, impetigo, lichen, prurigo, herpes); and now accumulate in the cerebro-spinal axis, manifesting its presence by slight spasms (dysuria, muscular twitchings), or discharging with terrific force in some of those convulsive seizures which are the dread of mothers and the cause of much anxiety to physicians.

The mechanical causation of diarrhoea and bronchitis, insisted upon particularly by Vogel, has already been alluded to. While this may be one element, most certainly the nervous factor is too important to be disregarded. Bronchitis, not attributable to ordinary exposure, occurs coincidently with teething even in children who have been protected against wetting of the chest; and the fact that more purely nervous phenomena, and especially the dreaded brain symptoms, are usually absent in children who have an excessive flow of saliva, and particularly if there be also a moderate diarrhoea, would conduce to the belief that nervous irritation, discharging itself in this manner, does not accumulate in the centres.

Doubts have been expressed whether dentition can give rise to convulsions in perfectly healthy children, although its rôle as an exciting cause in predisposed subjects is admitted (Hillier). That dentition alone, in the absence of any other predisposing or exciting influence, will provoke any of the disorders with which it is associated may be doubted in view of the fact already cited, that in some infants there are no untoward occurrences. But there seems to be no valid reason for separating the disturbances purely in the domain of the nervous system from the other pathological processes originated or aggravated by morbid dentition. Doubtless predisposition often determines the direction and severity of the reflected phenomena; and in the same manner reflected irritation may bring an organ within the influence of the ordinary disease-producing cause.

The convulsive phenomena associated with dentition may take the form of general eclampsia or spasms of particular groups of muscles. These latter are very common--according to Vogel, universal--and vary in intensity from that slight contraction of the facial muscles which sends the mother into raptures of delight over the heavenly smile of her {375} sleeping babe to the distressing seizure of laryngismus stridulus. Sometimes the child may sleep with its eyes half open, the eyeballs directed upward, and only the white sclerotic to be seen through the gap between the lids, "producing an appearance which is unnatural and alarming to the laity."

The attacks of general eclampsia are usually sudden. The child has been to all appearances perfectly healthy, when, without warning, there occurs a series of tetanic spasms like a succession of electric shocks. The individual eclamptic shock cannot be distinguished from an epileptic seizure. These convulsions sometimes continue for several days, but frequently they cease after a few minutes. They may pass off and leave nothing to testify to their occurrence; very frequently they occasion permanent distressing lesions. Partial, so-called essential paralyses, squint, or even idiocy, are cited among their sequelæ; infants subject to repeated convulsions while cutting successive teeth have eventually perished from cerebro-spinal meningitis; death has not infrequently been an immediate result. In these graver cases teething is probably but one of the morbid influences at work.

Purulent otitis media follows dentition in some infants, usually, if not invariably, of a scrofulous diathesis. At the clinic of the Jefferson Medical College Hospital fully one-third of all the cases of otorrhoea in children are said to be so occasioned.

Blennorrhoeal conjunctivitis is a rare complication of teething, and when it occurs usually accompanies the eruption of the upper molars and canines (eye teeth). It is attributed to direct extension of the gingival inflammation by continuity through the antrum of Highmore and the nasal passages. By some it is said to occur only in strumous subjects. It is unilateral, and is not contagious, so that there is no cause for alarm concerning the unaffected eye. The lids soon swell enormously and the eyeball is exposed with difficulty. There is considerable pain. The secretion is more mucous, translucent, and stringy than in genuine blennorrhoea. The eyeball always remains intact and the prognosis is always favorable (Vogel). Milder forms of catarrhal conjunctivitis are not very uncommon.

Thus far, we have considered only the process of the first dentition. Before the shedding of any of the deciduous teeth, the first permanent molars inaugurate the second dentition, appearing in position at about the sixth year. Next, displacing their temporary predecessors, come the central incisors, between the sixth and eighth years, the inferior pair generally preceding the superior ones. The lateral incisors are cut between the seventh and ninth years; the anterior bicuspids between the ninth and tenth years; the posterior bicuspids between the tenth and eleventh years; the canines between the eleventh and thirteenth years; the second molars between the twelfth and fourteenth years; the third molars, or wisdom teeth, between the seventeenth and twenty-first years as a rule, occasionally much earlier, sometimes later.

The eruption of the permanent teeth does not usually occasion any very great amount of distress; nevertheless, it sometimes acts both as a predisposing and as an exciting cause of various disorders, local and systemic. The various forms of stomatitis, tonsillitis, sore throat, gastro-intestinal derangements, febrile disturbances, bronchitis, internal rhinitis, {376} diseases of the eye, of the ear, of the skin, chorea, epilepsy, etc., have all been noted as accompanying, if not occasioned by, the second dentition. Ashburner[76] records, among other similar instances, that of a lad twelve years old who presented a marked case of chorea, and after three months' continuance of the twitchings fell into a violent epileptic fit, from difficulty in the eruption of the second pair of permanent molars of the upper jaw. The use of the gum lancet relieved the convulsion, and there was no return of the chorea.

[Footnote 76: On Dentition and some Coincident Disorders, London, 1834, cited by Tanner.]

Quite frequently, the eruption of the inferior dentes sapientiæ occasions great and protracted suffering, especially when they appear very close to or partially under the coronoid processes. Considerable irritation is occasioned, in which the gums and adjacent tissues participate. Inflammation may result and extend to the fauces; mastication becomes impossible; severe odynphagia is excited. Suppuration may ensue, and then the pus burrows in various directions, finding exit at points more or less remote, internal or external. Among the consequences of the eruption of a wisdom tooth into a crowded arch, White[77] cites fistulæ, necrosis, exostosis, ulceration and sloughing of the soft tissues, cystic and other tumors, ankylosis of the jaw, amaurosis, otalgia, otorrhoea, deafness, facial paralysis, hemicrania, oesophagismus, tonsillitis, erysipelas, aphonia, hysteria, neuralgia, chorea, epilepsy, tetanus, death.

[Footnote 77: "Pathological Dentition," extract from annual supplement to the Obstet. Journ. of Great Britain and Ireland, April, 1878.]

DIAGNOSIS.--The age of the child and the appearances already described will afford a basis for diagnosis so far as the local manifestations in the mouth are concerned. The diagnosis of local disorders at a distance, or of systemic disturbances of whatever character, can be made out only by careful consideration of all the attending circumstances; and it is always to be borne in mind that while the process of dentition is to be recognized as one of the causative factors, grave injustice might be done the little patient, and its life perhaps endangered, by failure to recognize the presence of other and perhaps more potent morbid influences.

In cases of chorea or epilepsy, of eye or ear troubles, or of any morbid condition not otherwise accounted for, occurring during the period of the second dentition, especially at the sixth, twelfth, and seventeenth years, or until the wisdom teeth are fully erupted, it is well to inspect the mouth and to think of dentition as the possible cause.

PROGNOSIS.--The prognosis will depend upon the character and gravity of the associated symptoms, the presence or absence of diathesis, and the etiological importance attached to dentition. It is impossible to lay down a general law.

TREATMENT.--The treatment of the deuteropathic or associated disorders is to be conducted on the general principles applicable to those diseases; for a consideration of which the reader is referred to the appropriate articles of this work. We have here to consider general prophylaxis and local measures. The proper management of the child during the period of the first dentition is a matter of great importance, and may avert serious complications. The child should be as much as possible in the open air whenever the weather is favorable. The head may be daily sponged with cold water, and caps and warm head-coverings of all kinds should {377} be forbidden.[78] Frequent rubbing of the gums with a crust or other hard substance, or with the finger, is advisable; and something for the child to bite on, preferably a silver piece, should be provided. Orris-root, calamus, and other vegetable substances frequently given to children for this purpose are objectionable; their fermentation is apt to lead to thrush. The secretions must be kept active. The diet should be carefully regulated, and cooling drinks be freely given in order that the child may not overload its stomach by too frequent suckling in its efforts to relieve the local heat by moisture. The mother should be warned not to put it too frequently to the breast. Weaned children will often be found unable to digest their ordinary food, and in that case still greater care will be required. Slight diarrhoea does not call for interference, and is often beneficial in relieving nervous tension and thus averting a tendency to convulsions. Indeed, when the bowels are not relaxed gentle aperients should be given, especially in plethoric subjects or in those with cutaneous eruptions (Clarke). Cutaneous eruptions do not call for treatment, and there seems to be ground for the popular fear that they may be driven inward; at least, cases are on record in which their disappearance under treatment, and even spontaneously, has been followed by more or less severe convulsions.

[Footnote 78: Tanner after Clarke.]

In cases where bronchitis can be traced wholly or in part to soaking of the clothing, due protection of the chest by an oil-cloth or waterproof bib may be prophylactic against future attacks. In children who have suffered from any special set of morbid manifestations during the eruption of one pair of teeth, similar disturbances may be expected, and should be guarded against, in the future.

Aphthous ulcerations are usually associated with disorders of digestion, the relief of which must be the main object of treatment. Locally, the treatment does not differ from that of aphthous stomatitis in general. Obstinate ulceration of the tongue may require the use of silver nitrate. In that form of ulceration called odontitis infantum, in addition to proper attention to the diet and secretions and mild antiphlogistic medication, local depletion by leeches, preferably at the angle of the jaw, is often beneficial. Some writers advise the application of leeches directly to the gum. Potassium chlorate internally, two grains every four hours to a child twelve months old, is curative in the majority of cases. It may be given dissolved in sweetened water. Solutions of borax, and, in severe cases, of silver nitrate, may be applied locally. The use of the lancet is contraindicated, for the cut surfaces would be liable to ulceration.

The propriety of resort to the lancet for cure of systemic disturbances by obviating the source of local irritation is one which deserves consideration. It can only be decided upon the indications presented by the individual case. The knife is not a panacea for all the disorders of childhood occurring during dentition, and its indiscriminate use is to be discountenanced. Nevertheless, there can be no doubt that engorged and inflamed gums demand incision for their relief, on the same general principles of surgery applicable to similar conditions elsewhere. Where it is probable that systemic disease, even if not solely caused, is aggravated by the irritation and pain of a tooth unable to make its way to the surface unaided, it is clearly the duty of the physician to give his little patient that modicum of relief, if not of cure, which will be afforded by a proper incision of {378} the gum. It will not do merely to score the gums, but cuts should be made deep enough to reach the presenting surface and extend even beyond its boundaries. The developing enamel cannot be injured unless undue force be exerted. The best instrument to employ is a curved double-edged bistoury, so wrapped as to prevent injury to tongue, cheek, or lips. The child should be firmly held by another person, and in such a position that the parts may be well illuminated. The jaws can be separated by the operator's left hand, and the fingers so disposed as to protect the tongue and lips. Sometimes the insertion of a small cork between the jaws will be of advantage. The cuts should be made with special reference to the form of the presenting tooth. James W. White[79] recommends for the incisors and cuspids a division of the gum in the line of the arch; for the molars a crucial incision, thus X, the centre of the crown as near as can be determined indicating the point of decussation. A cuspid partially erupted needs severance of the fibrous ring on the anterior and posterior as well as on the lateral surfaces (Fig. 17). All the cups of a molar may have erupted, and yet strong fibrous bands maintain a decided resistance. In this case White thinks that all the boundaries of the tooth should be traced by the lancet and all such bands completely severed, or else a crucial incision, as in the figure (Fig. 18), should be made so as to ensure perfect release from pressure. The only contraindication to the use of the lancet, except in ulcerative odontitis, as before mentioned, is the existence of a hemorrhagic diathesis.

[Footnote 79: Op. cit.]

{379}

DISEASES OF THE TONSILS.

BY J. SOLIS COHEN, M.D.

Tonsillitis.

DEFINITION.--An acute inflammation of the tonsil or tonsils; or inflammation of the tonsil or tonsils, with inflammation of the peritonsillar connective tissue and of the palatine folds.

VARIETIES.--When the inflammatory process is confined to the mucous membrane the disease is erythematous, superficial, or catarrhal tonsillitis; when it involves the lacunæ it constitutes lacunal or follicular tonsillitis; when it involves the gland as a whole it constitutes parenchymatous, phlegmonous, or suppurative tonsillitis. The two latter varieties may present in combination. When the superficial inflammatory process is a vesicular one, eventually sheathing the surface of the organ in whole or in part with a membranous envelope, it constitutes herpetic or membranous tonsillitis. This variety may complicate superficial tonsillitis. When the inflammation of the tonsil, usually superficial, is due to the presence of a cryptogamic growth, it is a mycotic or parasitic tonsillitis, benign or malignant (diphtheria), as may be. When the inflammation of the tonsil is due to rheumatism, it is rheumatic or constitutional tonsillitis.

SYNONYMS.--Inflammation of the tonsils, Amygdalitis, Quinsy, Angina tonsillaris, Angina phlegmonosa, Phlegmonous sore throat, Cynanche tonsillaris. Lacunal tonsillitis is more generally known as folliculous tonsillitis (tonsillitis follicularis). Common membranous or pseudo-membranous sore throat (angina membranosa communis) is used as a synonym for herpetic or membranous tonsillitis (tonsillitis herpetica seu membranosa). Mycosis tonsillaris is a synonym for mycotic tonsillitis (tonsillitis mycotica benigna or tonsillitis parasitica). The tonsillitis of diphtheria is sometimes termed tonsillitis diphtheritica, tonsillitis mycotica maligna; that of rheumatism, tonsillitis rheumatica, angina rheumatica, rheumatic sore throat.

HISTORY.--Tonsillitis was described by Hippocrates. Of recent authors, Sauvages, Cullen, Louis for researches on the effects of blood-letting; Bell on the specific value of guaiacum; Velpeau as to the use of powdered alum and nitrate of silver; Bourgeoise on the use of tartar emetic; Maingault on paralytic sequelæ; Hering on mycosis; and the authors of the various encyclopædias and dictionaries,--may be mentioned as chief among the numerous observers whose contributions have been of most value. The bibliographical references appended to the {380} compilations last cited will guide the student in gaining access to the more important special observations of anomalous cases.

ETIOLOGY.--Predisposing and Exciting Causes.--Tonsillitis may be idiopathic, deuteropathic or symptomatic, or traumatic.

The predisposing cause of idiopathic tonsillitis is usually diathetic, and is associated with congenital or inherited vulnerability of the organ. Of diathetic causes, scrofula is undoubtedly the most provocative, but even rheumatism and gout are likewise so considered, though in a far more limited degree. Acute articular rheumatism is, in fact, sometimes preceded by rather a sharp attack of tonsillitis (rheumatic tonsillitis), which subsides spontaneously in a very few days, sometimes within one day, sometimes suddenly and synchronously with the onset of the ordinary manifestations of rheumatism, though the latter are often slight and transient, as if the force of the attack had been spent on the tonsils. Tonsillitis, non-specific in character, is apt to be prevalent during epidemics of scarlatina, diphtheria, rubeola, and variola. Membranous tonsillitis is common before and after epidemics of diphtheria. Epidemics of tonsillitis have been recorded, but in the face of their extreme rarity it becomes questionable whether they were not extensive examples of the proclivity just alluded to.

Tonsillitis is more frequent in individuals with chronically diseased tonsils than in individuals in whom these glands are healthy. Such individuals, too, are more liable to recurrences; and such recurrences often follow very slight provocations.

Idiopathic tonsillitis is rare in infancy. At the period of eruption of the permanent teeth it is much more liable to occur than before that period, and the liability increases progressively until the second dentition has been completed. It is most frequent during the decennium immediately following puberty--that is to say, in adolescents and young adults--or from the fifteenth to the twenty-fifth year. The disposition or predisposition to renewed attacks continues marked during the decennium immediately succeeding; after which attacks are more and more infrequent. Certain anatomical changes occurring in the tonsils, as the rule about the fortieth year, may diminish their proclivity to inflammation. Nevertheless, the disease occasionally occurs in advanced age.[1]

[Footnote 1: Solomon Solis Cohen, "Abscess of the Tonsil in an Octogenarian," Med. News, Philada., Feb. 16, 1884, p. 186.]

Deuteropathic tonsillitis is quite frequent in infancy, being excited by the infection of scarlet fever, diphtheria, measles, and small-pox, as discussed under these headings respectively. Under similar circumstances it occurs in the adolescent and the adult likewise. It is also produced in carcinoma and sarcoma of the tonsil.

Rheumatic tonsillitis, a deuteropathic variety, is most prevalent during atmospheric changes.

Herpetic tonsillitis, often a deuteropathic variety, seems sometimes of nervous origin exclusively. It is sometimes traceable to defective drainage. It is sometimes prevalent during epidemics of diphtheria, when its membranous character renders it extremely liable to be mistaken for the tonsillitis of diphtheria.

Traumatic tonsillitis occurs occasionally. The causes are--inspiration of irritant gases, the deglutition of chemically acrid substances, the {381} accumulation of calcareous concretions in the crypts or in the lacunæ, direct and indirect gunshot and other wounds, the impaction of fish-bones, fragments of toothpicks, cherry-stones, and other foreign bodies, and the like.

Mycotic tonsillitis is due to the development of a cryptogam upon tonsils probably already in a state of catarrhal inflammation in individuals with health impaired by previous disease or unfavorable hygienic influences.

SYMPTOMATOLOGY, COURSE, DURATION, TERMINATIONS, COMPLICATIONS, AND SEQUELÆ.--The onset of tonsillitis, sometimes preceded by headache and general malaise, is often accompanied by a chill, pyrexia following within twenty-four hours. The temperature may reach 105° F., being at its maximum, as a rule, about the third day. It is rarely below 101° F. The pulse is accelerated to 120 beats per minute. Simultaneously with the constitutional symptoms local distress is usually manifested, but either set of disturbances may precede the other by several hours or by an entire day. Heat and soreness of the throat are early complained of, gradually increasing in severity to actual pain. The pain may become intense, especially during deglutition. When the posterior palatine fold is put upon the stretch, additional pain is referred to the ear, for this fold encloses the staphylo-salpingeus muscle, which runs from the palate to the pharyngeal orifice of the Eustachian tube. This pain in the ear, sometimes the principal cause of complaint, is often premonitory of suppuration. Noises in the ears on the one hand, and impairment of hearing on the other, often attend extension of the inflammation in this direction, the enlarged tonsil sometimes pressing the posterior palatine fold against the pharyngeal orifice of the Eustachian tube.

On inspecting the throat early in the disease, one of the tonsils will be seen to be swollen into an irregularly tumid, much-inflamed mass, usually of a vivid red color. Occasionally both tonsils are involved simultaneously, but this is far less frequent than involvement of the second tonsil a few days later or after subsidence of the process in its fellow. In many instances the inflammation affects one tonsil only.

The inflammatory process is seldom confined to the tonsil. All the structures of the throat, even to the base of the tongue, are often involved, and it is rarely indeed that the anterior palatine fold, distended over the surface of the tumefied gland, escapes inflammation. It is this stretching of the anterior palatine fold which occasions much of the exquisite pain that forms so prominent a subjective symptom in severe cases. The soft palate, hanging forward in the cavity of the pharynx, is often inflamed or intensely congested, and the uvula tumefied, elongated, and oedematous. It may be flaccid upon the posterior part of the tongue or hang immediately over the epiglottis or upon it, and induce painful and tiresome efforts at deglutition and expectoration to relieve the consequent titillation. Sometimes it adheres by viscid secretion to the side of the swollen tonsil.

The inflamed tonsil or the tonsil and its coverings project far into the cavity of the pharynx, often as far as the middle line, touching its fellow when both are involved, so that ulceration sometimes ensues at the points of contact. The posterior surface of the anterior palatine fold sometimes becomes unfolded, as it were, in the tumefaction of the gland, and remains {382} stretched over it in a thin continuous layer without any line of demarcation. The swollen palate projects upon the enlarged tonsil like a shelf, from which depends the uvula, the latter being often oedematous, usually anteriorly, but sometimes posteriorly.

Inflammation of the connective tissue about the lower jaw, especially when at or near the articulation, often renders it difficult or even impracticable to open the mouth sufficiently to permit direct inspection of the parts; but it is rarely that sufficient space cannot be made to allow partial protrusion of the tongue on the one hand, and the introduction of a fore finger for exploratory purposes on the other, though both of these acts are sometimes impossible. The tumefaction of the parts impairs the freedom and ease of deglutition, which may become so painful as to prevent the swallowing of the saliva, which then may dribble from the mouth.

The pain experienced in swallowing is often manifested by convulsive action of the muscles of deglutition and of the muscles of the face. The swollen tonsils prevent the soft palate from being applied to the surface of the pharynx, as usual in deglutition; and as the upper or retro-nasal portion of the pharynx thus fails to be shut off from the lower oesophageal portion, liquids are often forced up into the nasal passages posteriorly, and are regurgitated through the nostrils, thus rendering it impracticable, for the time, to slake thirst or to swallow liquid nourishment.

At first sensations of dryness and pastiness in the throat are complained of, but in a few hours these symptoms become relieved by a more copious secretion of mucus or mucus and saliva. This secretion soon becomes viscid, and so adherent to the parts as to be detached only with difficulty, thus causing harassing efforts for its dislodgment by hawking and expectoration, or equally distressing efforts to swallow it. Should the inflammatory process extend to the salivary glands, as is not infrequently the case, secondary ptyalism often results, with increased distress from this source, and the patient lies or sits with his head inclined upon the diseased or most diseased side to favor the uninterrupted flow of saliva from the mouth.

Extension of the inflammatory process to the submaxillary glands, or to the parotid, or to the connective tissue surrounding them, is indicated by tumefaction externally, which is often exquisitively sensitive to pressure.

The timbre or quality of the voice is often impaired in a peculiar manner by the tumefaction of the throat and the immobility of the soft palate. The voice is thick, throaty, or guttural, having a characteristic harsh, rasping aspiration in enunciation, while articulation is much impeded by impairment in the movements of the jaw, palate, tongue, and lips. At times it is also painful. Speech is sometimes indistinguishable or impossible, and the voice may even become suppressed, so that signs and writing remain the sole means of communication.

Impairment of respiration, at least to any considerable degree, does not occur, unless both tonsils are involved and swollen to an intense degree--conditions under which dyspnoea may become pronounced, severe, and even urgent, and suffocation become imminent. Painful respiration is not uncommon in rheumatic tonsillitis.

The fever is sthenic in type. There are often severe aching pains in {383} the limbs. Headache, restlessness, insomnia, nausea, and even vomiting, may occur. The tongue is heavily coated, the breath is fetid, appetite is impaired, and the bowels are constipated. The urine is diminished in quantity, high-colored, and of high specific gravity. It usually shows slight increase of urea and great diminution of chlorides. Albuminuria occurs in rare instances.

The symptoms are proportionate to the severity of the attack. A first attack is usually much severer than subsequent ones, and suppurative cases more severe than those terminating by resolution. Resolution is the usual termination, and the parts are restored to a normal condition at the end of ten to fourteen days, sometimes earlier; in exceptional cases not until three or four weeks. Sometimes permanent hypertrophy of the tonsil remains.

Where the inflammatory process fails to subside, suddenly at the end of five or six days, or a little later, or not until ten days to a fortnight have passed, slight rigors supervene, announcing suppuration, and the local distress is very great, with pulsation and lancinating pains in the tonsils, until all at once the abscess bursts and its contents are discharged with immediate relief. Sometimes the pus or much of it is involuntarily swallowed; sometimes it is expectorated. In exceptional instances the pus has escaped into the larynx and suffocated the patient, usually during sleep.[2] In rare instances the abscess, having burrowed beneath the pharyngeal muscles, may open at the external angle of the jaw or behind the sterno-mastoid muscle. It may discharge into the epiglotto-pharyngeal fold, and thence reach and distend the epiglottis. It has been known to descend along the planes of connective tissue into the mediastinum or into the lungs. Even ulceration into the maxillary and carotid arteries has occurred, usually with fatal result, occasionally with an opportunity to save life by ligating the carotid (Erhmann).[3]

[Footnote 2: Stokes, Med. Times and Gaz., Aug. 29, 1874, p. 251; Littlejohn, Brit. Med. Journ., Jan. 2, 1875, p. 16.]

[Footnote 3: Gaz. méd., Paris, 1878, p. 42.]

The most frequent point of spontaneous rupture externally is at the upper portion of the gland anteriorly, just beneath the anterior palatine fold. Sometimes internal rupture occurs into the lacunæ.

Termination by gangrene is exceptional, and is confined to individuals with debilitated constitutions. It is much less frequent than formerly--as a result, perhaps, of better methods of treatment.

Metastasis is one of the methods of termination as to joints or muscles in rheumatic tonsillitis--to lungs, brain, or gastro-intestinal tract--as formerly occurred with much more frequency under direct depletory treatment.

In rare cases extension of the inflammation occurs to the epiglottis, even to the larynx, and the laryngitis may be so severe as to threaten life from the occurrence of oedema. Diffuse inflammation of the retro-pharyngeal connective tissue or of the connective tissue of the neck may constitute an unpleasant complication of the disease.

In a few instances paralysis of the palate occurs as a sequel of tonsillitis, and in exceptional cases the paralysis may also affect the arytenoid muscles of the larynx, and even the accommodator muscles of the eyes.

PATHOLOGY AND MORBID ANATOMY.--Tonsillitis is almost always {384} associated with inflammation of the tissues surrounding the tonsil and those contiguous to it, even in the mildest and most frequent manifestations of the affection. Thus, inflammation of the palate (staphyllitis) and uvula, and even of the pharynx (pharyngitis), are anatomically included with tonsillitis in angina or sore throat.

The mildest form of the malady is a catarrhal inflammation of the mucous membrane covering the gland, and does not extend along the lacunæ which dip inward from the surface and divaricate toward the interior of the organ. It is termed catarrhal tonsillitis, and, as has been intimated, is almost always associated with catarrhal sore throat. It is attributed to hyperæmia, with passive engorgement of the vessels, following retrocession of blood from the cutaneous surface after undue exposure to cold and moisture. A severer form of the malady involves the lacunæ in addition--several or all of them. This should be termed lacunar tonsillitis, as suggested by Wagner. Primarily, at least, it does not involve the follicles of the tonsils which open into the lacunæ, and is therefore incorrectly denominated follicular tonsillitis, although it is most generally so described. The lacunæ are involutions of the mucous membrane, and in health furnish a slightly turbid mucoid secretion which serves to lubricate the parts and, as is generally believed, to facilitate deglutition. When the lacunæ are inflamed these products become pent up in them to a certain extent, accumulate, and project in part at their orifices in turbid creamy or curdy masses, plastered over the parts when thin in consistence, or tightly imbedded when thick or desiccated. These masses are usually white, but sometimes, owing to various admixtures, they are more or less yellowish or gray or brown. They consist of epithelium chiefly, with more or less pus and accumulation of cells similar to those of which the follicles are composed--whether from follicles which have become distended by proliferation of their constituents, and have then burst, is not known. This epithelium has often undergone fatty degeneration in part. Cholesterin is an occasional constituent, and swarms of micrococci and bacteria abound when the masses are not recent, especially if the inflammation is occurring in a tonsil long the seat of chronic disease of the lacunæ.

The tonsil itself is moderately swollen and its mucous membrane hyperæmic. If the parenchyma of the tonsil be involved likewise, as often occurs, the swelling will be much greater, so that the gland will project a considerable distance beyond the margins of the palatine folds. When a hypertrophied tonsil is the seat of the inflammation the tumefaction will be much greater than when the inflamed tonsil has been normal.

Acute inflammation of the palatine folds often coexists, especially of the anterior fold. The soft palate may also be engaged in the morbid process, which may involve the uvula likewise. Pharyngitis is an occasional accompaniment, and stomatitis quite a rare one.

Lacunar tonsillitis sometimes subsides by spontaneous evacuation of the pent-up contents of secretion and desquamation, the parts returning to their normal condition. More frequently a desiccation of some of these products ensues, with permanent chronic inflammation. Decomposition then often takes place, fouling the breath by the escape of the gases. Butyric acid has been recognized as one of the most prominent of these fetid {385} gases. Calcareous change occurs in these contents of the lacunæ in some instances. Lacunar or follicular tonsillitis is often associated with severe inflammation of the peritonsillar connective tissue and the contiguous palatine fold, with serous or cellular infiltration into these structures almost always terminating in suppuration. This form of tonsillitis is very frequent, and is often confounded with parenchymatous tonsillitis or with tonsillar abscess. In these cases the abscess is in the peritonsillar tissue or in the posterior leaflet of the anterior palatine fold. It bursts above the tonsil at the angle between the two folds in the greater number of cases. In some instances the suppurative inflammation affects the anterior surface of the posterior palatine fold, sometimes contiguously to the antero-tonsillar abscess, sometimes independently, constituting a retro-tonsillar abscess. The follicles in the posterior palatine fold are sometimes involved, the thickened anterior surface of this structure becoming studded with small projections the size of ordinary pinheads or larger, distended with whitish-yellow contents.

In another class of cases of tonsillitis the inflammatory process may be chiefly parenchymatous, for rarely is it wholly so. That is to say, it may involve the glandular structure of the organ wholly or in main part. The disease is then an adenitis, an inflammation of gland-tissue--tonsillitis per se. It is associated with superficial inflammation of the surrounding mucous membrane, secondarily if not primarily, and often with inflammation of the lacunæ. In many instances the parenchymatous inflammation is a direct extension of the lacunar inflammation.

Parenchymatous tonsillitis may subside by resolution, or, as is quite frequent, terminate by suppuration. A number of small abscesses may be formed, which usually become confluent and rarely remain discrete. Sometimes a single large abscess is formed. The confluent abscess may discharge by several points. It is always associated with a severe inflammation of the palatine folds and palate, especially the anterior fold; sometimes of the adjoining half of the soft palate and the uvula; sometimes of the entire velum and uvula. Sometimes these parts become oedematous; sometimes suppuration ensues. Severe pharyngitis is not uncommon. Glossitis, involving the posterior portion of the tongue especially or exclusively, is an occasional accompaniment of parenchymatous tonsillitis. (See GLOSSITIS.) Occasionally oedema takes place in the epiglottis and upper margin of the larynx.

The character of the secretions varies. Sometimes these are semifluid; sometimes soft, caseous, or pultaceous; sometimes fibrinous and arranged in pseudo-membranes; sometimes hemorrhagic; sometimes moist and viscid, sometimes very dry; often adherent, and always containing cryptogams (leptothrix, Oïdium albicans, bacteria, and micrococci). Collections of caseous products accumulate not only in the crypts of the tonsils and in their overlying mucous membrane, but likewise in the follicles of the palatine folds below the tonsil, and thence toward the base of the tongue.

The submaxillary glands often undergo engorgement, and become so tender that external manipulation is painful, and sometimes they undergo suppuration. The tumefaction due to the swollen glands and infiltrated connective tissue around it is frequently incorrectly referred to the tonsil itself, rather than to the accompanying inflamed palate, with the {386} lymphatics of which these glands are in more direct anatomical connection. The tonsil is at a considerable distance from the inflamed glands, and cannot be felt from the exterior except under unusual circumstances.

Herpetic tonsillitis is a rare form of inflammation of the tonsil, or rather of its investing mucous membrane, characterized by the eruption of herpetic vesicles on its surface. The vesicles soon undergo rupture, and the resulting ulcers coalesce and become covered with a fibrinous exudation. The disease is usually associated with similar vesicles upon the palatine folds and upon the soft palate, and exceptionally with vesicles on the pharynx. (See Herpetic Pharyngitis.) It is by some fortuitous circumstance only that it is observed in the vesicular stage. It is confined to one side of the throat in most instances, but may be bilateral also.

Mycosis tonsillaris has been described by a few observers. B. Fraenkel[4] has recorded three cases, E. Fraenkel[5] one, and Bayer[6] two. In these cases the disease was not confined to the tonsils, but implicated the calciform papillæ of the tongue also, and one of Bayer's cases some pharyngeal follicles in addition. E. Fraenkel's case was in a male, and occupied but the right tonsil and base of tongue. The white masses in this case were formed of spores and filaments (Bacillus fasciculatus, Sadebeck), which are described as penetrating some millimeters into the gland-tissue. These masses were tenacious, and were reproduced rapidly after removal. In Bayer's cases, both females, the same microphyte was recognized. In a female patient observed at the Philadelphia Polyclinic[7] this affection followed rheumatic tonsillitis, diphtheria being prevalent near her residence, which was in a very unsalubrious locality. The deposit, confined to the left tonsil, was so firmly adherent to the mucous membrane that the implicated portion had to be torn away to get rid of the growth, which was twice reproduced. The fungus was in its mycelial state, a few spores and conidiferous filaments being recognized microscopically.

[Footnote 4: Berlin. klin. Woch., 1873, S. 94; ibid., 1880, No. 18.]

[Footnote 5: Zeitschrift für klin. Med., iv., 1882.]

[Footnote 6: Rev. mens. de Laryngologie, etc., Nov., 1882, p. 329.]

[Footnote 7: S. Solis-Cohen, The Polyclinic, March, 1884, p. 133.]

Quite recently, and since the above was written, the results of an elaborate study of this affection by Theodor Hering of Warsaw have been published in a paper entitled "Pharynxmycosis leptothricia,"[8] read before the Society of German Naturalists and Physicians. The author collates fourteen cases, six of which were observed by himself. He claims that the microphyte is simply the Leptothrix buccalis.

[Footnote 8: Zeitschrift für klinische Medicin, Bd. vii. H. 4, 1884.]

The local subjective symptoms as collated by Hering vary from the merest sense of discomfort in chronic cases to intense pain, difficulty in speech and in deglutition, and various grades of cough in acute ones. In some cases they are altogether wanting. Constitutional disturbance may be entirely absent or may be presented in various febrile or sub-febrile manifestations.

DIAGNOSIS.--The history of the attack, the appearances described, and the symptoms narrated should ordinarily suffice for a correct diagnosis. Still, mistakes do occur. An unsuspected tumor of the tonsil observed for the first time during an ordinary sore throat might be taken for an inflamed tonsil, but the progress of the case would soon lead to its due {387} recognition. While tonsillitis is infrequent after the fourth decennium, it occasionally occurs late in life, and has been observed even in the ninth decennium; and reserve is proper as to the cause of enlarged tonsils in the sore throats of those advanced in life.

The deposit in follicular or lacunar tonsillitis or angina is pulpy and not membraniform. It can be wiped from the surface with a fragment of sponge, and does not tear from the surface in strips, as is the case with the pseudo-membrane of diphtheria or of common membranous sore throat. There is no abrasion of the mucous membrane beneath the deposit. The patches are more prominent, usually more circumscribed, and dip down into the lacunæ, or rather project from the crypts upon the surface of the tonsil. In its physical aspect the deposit more closely resembles that observed in the sore throats accompanying cachectic conditions, as in chronic tuberculosis, advanced syphilis, some forms of scarlatina, typhus and typhoid fever, extreme old age (agine pultacée, Fr.; cachectic angina); but the existence of previous constitutional disease and actual debility should prevent the mistake in diagnosis. In susceptible subjects the oncoming of an attack of rheumatic tonsillitis may often be inferred, previous to the manifestation of local symptoms, from the existence of otherwise inexplicable odynphagia, the pain being especially intense upon attempts to swallow saliva. Sometimes laryngoscopic inspection at this early stage of the disease will reveal vivid redness of the mucous membrane in the neighborhood of the crico-arytenoid articulations.[9] The value of this early diagnosis lies in the opportunity it affords to try abortive treatment.

[Footnote 9: S. Solis Cohen, The Medical News, Aug. 11, 1883, p. 146.]

PROGNOSIS.--The prognosis of catarrhal tonsillitis is almost invariably favorable, except under very obviously unfavorable conditions, the inflammatory process subsiding spontaneously within a few days. It is favorable, as a rule, in phlegmonous tonsillitis subsiding within ten or twelve days in most instances, even though all the stages be completed to suppuration and discharge of the abscess. Sometimes two or three weeks are consumed in the process. A certain amount of reserve is requisite, nevertheless, in severe cases, in view of the possible complications which may prevent recovery. If both tonsils are affected to such an extent as to interfere seriously with respiration, death by suffocation may ensue should the obstruction be not relieved by excision of portions of the swollen glands or an artificial opening be not made into the air-passage. Suppuration may perforate the internal carotid or the external maxillary artery and produce sudden fatal hemorrhage. The remembrance of such occurrences should screen a surgeon from the imputation of carelessness should he be unfortunate enough to incise an abscess under similar conditions. Some cases are on record of fatal hemorrhage but a short period before a proposed operation could have been performed.

Suffocation has ensued from discharge of the abscess into the air-passage, usually during sleep; but it has occurred even during the moment of speaking (Stokes).[10] Such results are accidental and exceptional.

[Footnote 10: Med. Times and Gaz., Aug. 29, 1874, p. 251.]

Recurrences are frequent, especially in scrofulous subjects, and such recurrences are apt to result in permanent hypertrophy and induration.

TREATMENT.--Mild cases of tonsillitis require no treatment except to {388} keep the patient protected from exposure to abrupt changes of temperature. The course of the affection both in mild cases and in severe ones may often be materially shortened by prompt resort to the use of guaiacum, both internally and topically. A gargle containing an ounce each of ammoniated tincture of guaiacum and compound tincture of cinchona to the pint, with the addition of three ounces of clarified honey, and saturated with potassium chlorate (twenty grains to the ounce), may be used, a drachm at a time, every two hours, hour, or half hour, according to the urgency of the symptoms, and may likewise be administered internally in drachm doses for an adult every two or more hours. The beneficial effects will often be manifested within less than twelve hours. Pellets of ice held in the mouth from time to time often relieve pain and repress inflammation. Sodium bicarbonate locally, in powder, affords great relief in some instances. In the presence of marked pyrexia tincture of aconite may be given in drop doses every hour until an impression has been made upon the heart, when its continuance at intervals of four or more hours will be a matter for consideration.

Guaiacum and aconite may be given with equal benefit in any form preferred by the prescriber. At the same time saline laxatives may be required from time to time. Regulation of the diet is often necessary.

When the tonsils are very much swollen, gargling of all kinds becomes too painful, and therefore sprays of sedative and emollient mixtures are to be substituted, or steam from water impregnated with volatile substances, as benzoin, paregoric, hops, chamomile, and sage. When the cervical glands are swollen, continuous hot and moist applications externally afford great relief. If the suffering from the inflamed tonsil be intense, scarification should be practised and the bleeding be encouraged by warm water. When suppuration exists, the abscess should be promptly evacuated by incision at the most prominent accessible point.

Special symptoms require appropriate management on general principles. The pain in swallowing can often be diminished by pulling on the lobe of the ear at the moment of deglutition (Grewcock).[11] In debilitated subjects, or during epidemics of diphtheria, quinia, iron, and supporting measures are indicated.

[Footnote 11: Lancet, Nov., 1882, N.Y. reprint, p. 399.]

The rheumatic cases are best treated with sodium salicylate, ten to fifteen grains every hour or two until relieved. Instituted in the formative stage above alluded to, this treatment frequently seems to be veritably abortive, especially when preceded by a full dose of an alkaline purgative--say one ounce of Rochelle salts. Oil of gaultheria may be used in small doses as an agreeable flavor to the mixture, or in doses of ten to twenty minims, well diluted, as an adjuvant to the salicylate, or even as a substitute for it. After subsidence of the acute symptoms cinchonidine salicylate may be continued for a few days in appropriate doses.

Herpetic tonsillitis requires the ordinary treatment for erythematous tonsillitis, with additional topical treatment by sprays of alkaline solutions, such as sodium borate or bicarbonate, five grains to the ounce, or lime-water. Internally, small doses of mercuric chloride will be of service, the dose varying, according to the age and size of the patient, from one-forty-eighth to one-sixteenth of a grain every two hours, until the stomach shows signs of irritation therefrom. In cases of doubt as to {389} diagnosis from diphtheria the treatment for diphtheria will be indicated as the safer measure. Here, again, the mercuric chloride is sometimes equally valuable.

Mycosis of the tonsil does not seem amenable to medicinal treatment. Thorough removal of the fungus with forceps or sharp spoons is required, even though mucous membrane be detached with it. When this is impracticable, ablation of the tonsil may be necessary. Raw or cut surfaces left by any of these manipulations should be subjected to thorough cauterization, electric cauterization being the most feasible method.

{390}

DISEASES OF THE PHARYNX.

BY J. SOLIS COHEN, M.D.

Acute Pharyngitis.

DEFINITION.--An acute inflammation of the mucous membrane of the pharynx, whether implicating the glandular structures or not, and usually associated with inflammation of contiguous structures.[1] Acute pharyngitis may be catarrhal or erythematous, phlegmonous or suppurative, ulcerative, herpetic or membranous, gangrenous, and erysipelatous.

[Footnote 1: In deference to the plan suggested by the editor of this work, separate articles have been prepared under the heads of Pharyngitis and Tonsillitis respectively. The two processes, however, are so frequently associated that they should be studied together, the more that both of them are likewise associated with extensions of the inflammatory process to the palate, palatine folds, base of the tongue, and other contiguous structures. The writer has always preferred to describe these diseases under the head of sore throat, which does not presuppose any limitation to individual anatomical structures.]

SYNONYMS.--Sore throat; Angina.

ETIOLOGY.--Acute pharyngitis may be idiopathic, deuteropathic, traumatic, toxic, or parasitic. The predisposing cause may be diathetic, as scrofula, rheumatism, gout, and syphilis; it may be a depression of the vital powers from any cause, such as continued exposure to foul air or impure water, improper diet or sedentary occupations. There exists in some individuals a predisposition to "catching cold," independent of any cachexia. Pharyngitis may occur at any age, but is more frequent in the young. One attack increases subsequent liability to the disease.

The exciting cause is usually exposure to cold and damp. Hence the disease is more frequent at the seasons when these conditions prevail or when sudden changes of temperature are taking place. Sudden chilling of the body when overheated may occasion it in warm weather; for instance, a plunge into the ocean while covered with perspiration. The ulcerative variety, when not due to syphilis or tuberculosis, is usually of septic origin, and is apt to occur in the debilitated especially. The gangrenous form, which is rare, results from profound blood-poisoning. The herpetic or membranous variety may be due to disturbance of the trophic nervous system, and has been attributed to mental emotion (Feron), to uterine disturbances (Bertholle), to the contact of irritating substances and to miasmatic or fetid exhalations (Peter). It prevails principally during epidemics of diphtheria or of scarlet fever, and may be of cryptogamic origin. The cryptogam of thrush is sometimes developed on the mucous membrane of the pharynx, either primitively or as an extension of the disease from the oral cavity. Certain conditions of the {391} atmosphere give rise at times to so-called epidemic pharyngitis. Paludal or malarial pharyngitis may arise from the same causes as malarial fevers. Pharyngitis occurs in the various exanthemata as an essential part of the morbid process, and is always more or less prevalent during epidemics of measles or scarlet fever. It occurs not rarely in typhoid fever, and is an occasional complication of pneumonia, rheumatism, herpes, pemphigus, and other acute affections. It is one of the complications of facial erysipelas, but erysipelatous pharyngitis may occur primarily. Pharyngitis may be excited by the inhalation of deleterious solid, fluid, and gaseous substances in the atmosphere which act mechanically or chemically on the mucous membrane. Many drugs administered in poisonous or even in medicinal doses may give rise to an attack of inflammation of the pharynx; among them may be cited preparations of mercury, antimony, iodine, arsenic, copper, lead, zinc, silver, stramonium, belladonna, and most of the Solanaceæ. Traumatic pharyngitis results from deglutition of boiling water or of acrid or caustic substances; from inhalation of hot air, of steam, or of flame, and is most usually associated with traumatic oesophagitis or with laryngitis.

PATHOLOGY AND MORBID ANATOMY.--Acute pharyngitis, as most commonly encountered, is a simple erythematous inflammation of the mucous membrane; the palate and tonsils being likewise involved. In most instances there is simply an active hyperæmia which may subside in a day or two. When more intense than this the mucous membrane of the palate, tonsils, and pharynx becomes congested and swollen, uniformly or in circumscribed areas. In some instances the submucous tissue of the pharynx is greatly relaxed, and the mucous membrane lies upon the substructure in thick folds. In others there is more or less oedema. The mucous follicles, especially those of the posterior palatine folds, are frequently swollen. There is an abnormal though not excessive secretion of viscid mucus, clear or turbid. The uvula is often swollen or distended with serum, and its mucous membrane is relaxed. Sometimes it appears as though pasted to one of the folds of the palate by viscid secretion. The posterior palatine folds may be distended with serum, and their arched appearance thus become obliterated. Resolution occurs gradually in some instances, quickly in others.

Phlegmonous pharyngitis exhibits a still higher grade of inflammation. It involves the submucous structures as well as the mucous membrane, including at times the fibrous sheaths of the muscles. It may, in addition, involve the palate, the tonsils, the base of the tongue, and contiguous structures. Suppuration is common, usually circumscribed, but not infrequently diffuse in patients of enfeebled constitution.

One variety of the disease is essentially a deep-seated pharyngitis; and this form almost always progresses to suppuration (suppurative pharyngitis). The process becomes then, not infrequently, a diffuse suppurative inflammation of the subpharyngeal connective tissue, extending sometimes downward along the oesophagus, into which the pus may be discharged by spontaneous rupture, with a result of permanent stricture from irregular cicatrization. Sometimes the suppurative process extends anteriorly beneath the cervical fascia, and the pus may gravitate so as to occlude the air-passages, partly or completely, by direct pressure; or in other instances the entrance of {392} the larynx may become blocked by the tumefaction of the pharynx. When phlegmonous pharyngitis is of traumatic origin, there will be more or less destruction of the mucous membrane according to the nature of the injury, whether accidental or designed, whether due to burn, scald, inhalation of hot air or steam, or to deglutition of alkaline, acid, or other corrosive substances. In these cases the morbid process is rarely confined to the pharynx, but the larynx, the oesophagus, and even the stomach, are liable to be involved. If regurgitation of hot air or of caustic fluids takes place through the nasal passages, the injury will of course involve those regions.

Ulcerative pharyngitis is a low form of inflammation present in sore throat, probably dependent upon septicæmia. The tonsils are somewhat congested and swollen, and one or more white superficial ulcers form on their surface, or on the palate, or on the pharynx. These ulcers are generally round or oval, and vary greatly in size. When two or more ulcers exist, they exhibit no tendency to confluence. Healing takes place rapidly, usually without leaving any traces of the lesion.

Membranous pharyngitis, or herpes of the pharynx, is one of the infrequent phenomena of a not uncommon sore throat, which exhibits at first a collection of small vesicles the size of millet-seeds or larger, isolated here and there or clustered in groups on the palate and uvula, less frequently on the tonsils. Herpes of the mouth and lips sometimes coexists. These vesicles are surrounded by inflammatory areolæ. Their contents are more or less turbid. In rare instances they disappear without trace after a day or two. Usually they soon undergo rupture, sometimes within a few hours, so that small ulcers are left, which almost immediately become covered with a grayish-white exudation. A number of patches will coalesce, forming limited sheets of false membrane not unlike those of diphtheria. The disease is usually confined to one side of the throat, the corresponding submaxillary or cervical glands being affected moderately when at all involved. The tonsil is swollen, and the mucous membrane of the palate and the palatine folds is congested and often tumefied. There is an abnormal secretion of viscid, ropy, turbid mucus. In a few days the ulcers heal beneath the exudation, which becomes disintegrated and detached, the inflammatory process subsiding by gradual resolution. Sometimes the ulcers cicatrize without previous deposit of false membrane. Occasionally there are at longer or shorter intervals successive crops of vesicles, which may or may not undergo ulceration.

Gangrenous pharyngitis may supervene upon any form of pharyngitis, but in the majority of instances its malignant character is inevitable from the outset; so that some authors have even restricted the term gangrenous to a form of sore throat characterized by primitive gangrene of the pharyngeal mucous membrane originating independently of any other malady. Whether an idiopathic disease, or whether it follows scarlatina, measles, small-pox, dysentery, or enteric fever, it is associated with that depraved condition of the system denominated typhoid. At times it occurs in tuberculous phthisis. The initial manifestations may be simply those of intense inflammation. The tongue is covered with a dark creamy, pultaceous deposit consisting of broken-down epithelium, pus-cells, bacteria, and molecular débris, while similar masses are occasionally seen upon other mucous surfaces of the mouth and throat. The tonsils, {393} palate, and pharynx are livid and swollen, and sometimes oedematous. At an early period the tonsils, the palatine folds, and the posterior wall of the pharynx become covered with dark, ashy-colored ulcers with excavated edges. Sometimes these spots are black from the first, and appear slightly elevated. These soon slough out with more or less of the surrounding tissues, and the ulcers left are covered with sanious, ichorous, fetid secretion. In some instances a delicate pseudo-membrane has been found in the bed of the ulcer after death (Mackenzie). The destructive process rapidly extends--sometimes to the oesophagus in one direction or to the nares in the other. The larynx is less frequently implicated; should it be attacked, oedema is liable to occur. Occasionally the process is limited to the tonsil, and there is no pharyngitis at all. Erosion of the blood-vessels may give rise to fatal hemorrhage. In those instances where the gangrene is circumscribed there are found, post-mortem, depressed oval or circular patches from one-twentieth to one-half an inch in diameter, varying in color from dark gray to absolute black. The edges are of a brownish color and are perpendicular. The bundles of muscular fibre are laid bare by destruction of the mucous membrane and submucous connective tissue, but as a rule escape implication of their substance. Similar patches have been noted in the epiglottis and the upper part of the larynx as well as in the mouth and pharynx--in some cases, indeed, in the trachea, the lungs, the oesophagus, the stomach, and the intestines.

Erysipelatous pharyngitis is usually an extension of erysipelas from the facial integument, which may take place by the lips and mucous membrane of the mouth, by the nasal fossæ, by the Eustachian tube from the tympanum and external ear, or by the nasal fossæ from the conjunctiva and eyelids through the lachrymal duct. When the disease begins in the pharynx the order of communication may be reversed. The pathological processes are the same as in cutaneous erysipelas. The mucous membrane of the pharynx will be diffusely red or purplish and shiny. Sometimes little bullæ are formed and become ruptured, leaving a patch of softened whitish-yellow tissue, which is sometimes torn from the surface beneath by the act of coughing or of deglutition. The inability to swallow is not due to swelling of the tissues, but to actual paresis of the muscles, probably from interstitial infiltration, but perhaps from implication of their substance. The cervical and submaxillary glands are rarely involved. Erysipelatous pharyngitis usually terminates by resolution, desquamation of the greater part of the epithelium of the mucous membrane often taking place; but it may be followed by abscess or by gangrene. Extension may take place to the larynx, and oedema may follow.

Exanthematous pharyngitis accompanies some cases of cutaneous exanthemata. The pharyngitis of small-pox is occasioned by an eruption upon the mucous membrane similar to that which appears on the skin. Often in advance of the cutaneous eruption it occupies the inside of the cheeks, the palate, uvula, and pharynx; sometimes the larynx as well. Maturation occurs more rapidly than upon the skin, and there is more or less purulent infiltration of the submucous connective tissues. Ulceration of the larynx or trachea may ensue so severe in character as to cause fatal termination by the local lesion.

{394} In measles an eruption similar to the cutaneous manifestation occupies the air-tract from nostril to bronchi rather than the food-passages. The Eustachian tubes may be involved, and the inflammation is sometimes propagated along the lachrymal duct. The throat may be affected a day or two before the external integument. Small red points the size of a millet-seed or larger appear on the palate, the tonsils, the posterior palatine folds, and the wall of the pharynx. These disappear in a few days, though sometimes in bad cases fibrinous exudation may accumulate. In other instances abscess or ulceration takes place, chiefly in the larynx.

The pharyngitis of scarlatina develops a day or two prior to the cutaneous eruption, the mucous membrane of the palate, tonsils, and pharynx being deeply congested, uniformly or in patches, with slight papulous elevations here and there. In the course of a day or two an opalescent or milky deposit, consisting chiefly of detached epithelium and viscid mucus, is observed on the swollen palate and tonsils. In the anginose variety the hue of the inflamed structures is more dusky. There is a pseudo-membranous deposit of a dirty-white, ash, or even yellow color. It is not limited to the tonsils, but accumulates rather on the palate, palatine folds, and posterior wall of the pharynx. The mucous membrane beneath the patches is often ulcerated, and sometimes gangrenous. There is much greater tumefaction of all the parts than in simple scarlatina, the enlargement of the cervical and submaxillary glands and the infiltration of contiguous connective tissue being so great in some instances as to prevent the mouth from being opened. A viscid and turbid secretion accumulates in the mouth. The nasal secretions sometimes desiccate into firm crusts. Suppuration may occur. Sometimes otitis media results from extension along the Eustachian tube, and sometimes suppuration of the membrana tympani, suppurative external otitis, or disease of the internal ear with extension to the cerebrum. In malignant cases all the processes are aggravated. Ulceration or gangrene soon ensues, the pseudo-membranous deposit being dark, almost black, from extravasated blood. Oedema of the uvula and soft palate is liable to occur, and if the larynx be involved there may be oedema of the epiglottis and ary-epiglottic folds.

SYMPTOMATOLOGY.--Simple pharyngitis very often gives rise to but little discomfort. There is usually more or less heat and dryness in the parts, especially at first. There is some dysphagia, principally from pain in swallowing, but in part from actual debility in the muscles of deglutition. Hoarseness is not usual, and cough is infrequent if there be no elongation of the uvula. Speech may be embarrassed by difficulty of articulation. There is usually some febrile movement, with acceleration of pulse and respiration. Some cases exhibit more intense inflammatory action, with a corresponding aggravation of the constitutional symptoms. The skin becomes markedly heated, the body-temperature rises to 101° F. or higher, the pulse reaching 100-120, in some instances 140, beats per minute, even in the adult.

In that variety known as rheumatic sore throat there will be in addition pain and soreness in the neck, back, and limbs, often severe, and increased by motion. There will be great accumulation of saliva in the mouth because of the intense pain in swallowing it. Speech, and even respiration, may become painful. These manifestations are frequently {395} followed by the ordinary phenomena of acute articular rheumatism, but they may subside in a few days, leaving only a general feeling of muscular soreness or slight stiffness in one or more of the joints. Sometimes a temporary torticollis follows.

In some cases of pharyngitis the cervical glands become swollen and painful, but this is not common. In children the constitutional disturbance is much greater than in adults. In malarial districts or in subjects of malarial poisoning the manifestations may assume a periodic character. Recovery takes place, as a rule, in from three to ten days.

In many instances the local phenomena are most prominently manifested on one side of the throat. There will then exist great liability to similar involvement of the other side after convalescence of a day or two, and without care and avoidance of exposure the second attack may be far more severe than the first.

The severe variety of pharyngitis denominated phlegmonous is often ushered in with a decided chill, the phenomena of fever following within twenty-four hours. The symptoms, both local and general, are of much greater severity than in catarrhal pharyngitis, especially in cases proceeding to suppuration.

Paralysis of the palate and other paralyses may follow either of the forms of sore throat just described. Albuminuria sometimes results. In extremely rare cases it is an accompaniment of the disease.

Superficial ulceration of the mucous membrane may occur in almost any form of pharyngitis or of sore throat. Some authors have separated a special form of ulcerative sore throat occurring in those enfeebled from long exposure to unwholesome influences, such as nurses, hospital attendants, etc., in whom the first symptom is pain in deglutition, especially of saliva. The tongue is furred and the breath is offensive. There is loss of appetite, with general lassitude, feebleness of circulation, and more or less elevation of temperature. Intense headache is often present. Under suitable treatment recovery is rapid.

The ulcerative sore throats of syphilis and of tuberculosis require separate consideration.

Common membranous pharyngitis frequently gives rise to but slight symptoms, differing very little from those of other forms of pharyngitis; but there may be high fever of sthenic or of asthenic type, very often preceded by general malaise, sometimes by a decided chill. The pain in deglutition and the local heat and dryness are sometimes much greater than in the more ordinary forms of pharyngitis. The distress may extend into the ear, sometimes to the nasal passages, in rare instances to the larynx. The disease lasts for a week or ten days, usually terminating in recovery. In occasional instances, chiefly in children, it terminates fatally by apnoea from extension of the membrane into the larynx. Paralytic sequelæ are not rare.

The advent of gangrenous pharyngitis is sometimes indicated by sthenic phenomena, but usually from the first it is marked by extreme prostration, comparable in some instances to the collapse of cholera. There is a low type of fever. The pulse is feeble and infrequent. The skin, especially of the extremities, is cold and blue. The eye is glassy, the countenance haggard. The pain, as a rule, is not severe, sensation being benumbed. The disease is often accompanied by an irregular erythematous cutaneous {396} eruption. The secretions and excretions escape by the mouth and nose, and they are extremely fetid. There is indeed a peculiar odor, which once encountered can scarcely be mistaken. If the lungs become affected there will be copious hæmoptysis. In some cases the tendency to hemorrhage is general, blood oozing or gushing simultaneously from lungs, bowels, nose, and mouth, and sometimes extravasating beneath the skin. Sphacelus ultimately takes place at the points of ecchymosis. Diarrhoea, abundant and fetid, due to invasion of the alimentary tract, often sets in before the close, and may be regarded as a sure precursor of death. Death usually takes place from syncope, intelligence often remaining unaffected to the last. When these cases recover a horrible amount of deformity often remains to mark the ravages of the disease. During cicatrization the positions of contiguous parts become very much altered. The palate may become adherent by its sides, and by more or less of its posterior surface, to the pharynx, sometimes resulting in complete occlusion of the nasal portion of the pharynx.

The constitutional symptoms of erysipelas of the pharynx are those that attend the usual manifestations of external erysipelas, the febrile phenomena, epigastric pain, nausea, and so on, being increased in severity. There will be great pain and difficulty of deglutition. If there be serious oedema, symptoms of suffocation will occur. Laryngitis will be indicated by pain referred to the larynx. The duration of the disease varies from forty-eight hours to a week, rarely longer. Death may occur within two or three days from oedema of the larynx or from other causes frequently indiscernible. Resolution usually takes place in those cases which recover. Occasionally abscess occurs.

DIAGNOSIS.--The diagnosis rests upon the conditions already described under the heads of Pathology and Symptomatology. Under ordinary circumstances it presents no difficulty, but during the prevalence of epidemics of scarlatina or diphtheria even the mildest sore throat demands careful attention and frequent inspection until the exclusion of the graver maladies may be positively determined. The greatest difficulty will present in cases of common membranous sore throat, for it is sometimes impossible to make the differentiation from diphtheria, especially as the vesicular stage is rarely seen. Sometimes, it is said, it is possible to detect one or more of the small ulcers left by the rupture of the vesicles; sometimes small isolated spots of false membrane will by their transparency indicate recent formation, and by their circular shape the previous existence of a vesicle (Peter, cited by Mackenzie). The coexistence of cutaneous herpes is corroborative of the diagnosis, but by no means an infallible sign. It must not be forgotten in this connection that membranous sore throat may predispose to an attack of diphtheria. In gangrenous sore throat the grayish-black patches may be mistaken for the pseudo-membranes of diphtheria, but their color is dark from the outset, while in diphtheria they become dark only as the disease progresses. They always represent actual death of the tissues, which is not an essential lesion of diphtheria. Swelling of the cervical glands is unusual. Finally, the characteristic odor of gangrene is almost unmistakable.

PROGNOSIS.--The prognosis is favorable in catarrhal pharyngitis and in the milder forms of the phlegmonous, non-specific, ulcerative, and {397} common membranous varieties. It is unfavorable in intense suppurative pharyngitis, though cases often get well. In gangrenous pharyngitis the prognosis is extremely grave, but recovery is not impossible. In traumatic pharyngitis the prognosis will of course depend upon the nature and extent of the injury, being not unfavorable if this be confined to the pharynx, though even in limited cases there may be stenosis or other ill results from cicatrization. Erysipelatous pharyngitis is of grave prognosis when the result of extension of the disease from the face, but recovery is frequent when the pharyngeal disease is primary.

TREATMENT.--The treatment of superficial pharyngitis is very simple. Unless the case be so light that no special medicinal treatment seems advisable, the patient should be confined to a bed or lounge to secure rest, a light coverlid being thrown over the body to equalize the heat of the surface. If a meal has recently been taken, a mild emetic is often of service to empty the stomach and save the labors of digestion. A gentle laxative or, if the patient be of costive habit, a saline purge is indicated to facilitate the passage of matters already in the intestinal canal. In cases of actual constipation a drastic cathartic may be required. If there be considerable pain a small dose of morphine may be advantageously combined with the aperient. If frequent pulse or high temperature exist, especially in severe cases, tincture of aconite, in doses of one or two drops every hour or two hours at first, will be useful. As soon as any marked effect has been produced the aconite may be discontinued or the intervals between administrations lengthened. Locally, the free use of demulcent drinks, and of pellets of ice when cold is agreeable, will relieve the pain in the throat and sometimes repress excessive secretion. Cold compresses to the neck anteriorly are often soothing, and sponging the entire surface of the body with tepid water, acidulated or alcoholized, will allay the intense heat of the skin. The diet should be light and nutritious. Very often the emetic, rest, and regulation of diet will constitute the entire treatment required.

When the local distress is very great, astringent lozenges (catechu, krameria) may be allowed to dissolve in the mouth, or sprays of weak solutions of alum or of carbolic acid may be propelled upon the mucous membrane. Tannin, potassium chlorate, and cupric sulphate are often used for this purpose. When the uvula is elongated or oedematous it is often a constant source of irritation and discomfort. Scarification to give vent to pent-up blood or puncture to allow the escape of effused serum will afford prompt relief. Excision is never necessary.

In phlegmonous pharyngitis the treatment will necessarily be more active. Here an early emetic is of great service. A saline laxative may be administered every three or four hours for a day or two, each dose containing a drop or two of the tincture of aconite, with the addition of morphine if indicated by pain. Drop-doses of aconite at more frequent intervals sometimes serve a better purpose. Inhalation of steam, or of steam from water impregnated with hops, chamomile-flowers, paregoric, compound tincture of benzoin, juice of conium, or the aqueous extract of opium, belladonna, or conium, will afford great relief, as will the frequent projection of sprays of warm water, simple or slightly aromatized with cologne-water or with toilet vinegar. Warm and moist applications externally are often very soothing. Gargling entails too much pain to be of {398} service, but medicated sprays may be used of aqueous solutions (twenty grains to the ounce) of tannin, alum, zinc sulphate, or cupric sulphate, care being taken to guard against the swallowing of any of these drugs. Powders of alum, tannin, krameria, etc., diluted with liquorice, acacia, bismuth, lycopodium, and the like, may be blown upon the parts, and are often efficient. Sodium bicarbonate frequently affords relief. The topical application of silver nitrate is rarely practicable and generally unnecessary.

When the inflammatory process is of a higher grade and not likely to yield to purely medicinal treatment, leeching or venesection may be employed, but should not be resorted to without urgent reason. The recognition of abscess is an indication for its immediate discharge by incision or aspiration. In suppurative cases quinia and iron should be given in large doses. The general treatment is like that of simple sore throat. When liquid food cannot be swallowed, nourishment by enema is requisite. Efforts at deglutition should be spared as much as possible, and with this view medicines which can be administered by inhalation, by enema, or by hypodermatic injection are to be preferred.

In pharyngeal sore throat, whether catarrhal or phlegmonous, depending on rheumatic or gouty diathesis, salicylic acid or the salicylates will prove useful, either alone or in conjunction with other measures.

The treatment of ulcerative pharyngitis is practically the same as that recommended for phlegmonous pharyngitis. Antiseptic gargles may be used locally, but as a rule the pain is so great that inhalations of soothing vapors, as before recommended, will answer a better purpose. When the process is very acute fragments of ice will be most useful. Ice to the head will afford relief to pain. A little good wine, with quinia and iron, comprises the medicinal measure requisite.

Gangrenous pharyngitis calls for the most active and supporting treatment. Eggs, milk, cream, nutritious soups (up to the limits of the patient's capacity for swallowing, and by enema when necessary), quinia, tincture of the chloride of iron, and alcohol in large doses, are indicated. Local treatment is of high importance. Agents to destroy diseased tissue promptly and prevent the extension of the gangrenous process, such as bromine, strong nitric or hydrochloric acid, acid solution of mercuric nitrate, or caustic potassa, are to be thoroughly applied, in the hope of exposing a healthy surface beneath which will heal by granulation. When this treatment is unsuccessful or too hazardous, as in cases where the blood-vessels are probably involved, we can only palliate the symptoms by applying weak solutions of acids and astringents, to which opium may be added, relying on constitutional measures for restraining the destructive process. Washes and sprays of potassium chlorate, eucalyptol, thymol, hydrogen peroxide, etc., or the agents employed in common sore throat, are often agreeable to the patient, and may be useful in restraining fetor, but they have no direct therapeutic influence on the progress of the disease. If the ulceration is extending into the vicinity of the great vessels of the neck, measures for compression should be at hand, in the use of which the nurse should be instructed, and preparations be made to facilitate ligation of the carotid artery in an emergency. Tracheotomy may be necessitated by oedema of the larynx. The deformities resulting from gangrenous sore throat in cases that recover usually require surgical treatment.

{399} Traumatic pharyngitis must be treated on general principles. When due to contact of caustic or corrosive substances, an attempt may be made to neutralize the effects by a chemical antidote, but the physician is usually summoned too late to accomplish much in this manner. Morphine should be given in full doses, hypodermatically. Insufflations of morphine in powder, soothing inhalations, fragments of ice in the mouth, cold compresses, and, where possible, oleaginous drinks, are indicated to relieve topical distress. Rectal alimentation should be resorted to where the difficulties of deglutition are at all great. If symptoms of suffocation occur, tracheotomy must be performed. The results of traumatic pharyngitis require treatment according to their special indications.

Erysipelatous pharyngitis is to be treated by the administration, by enema if necessary, of large doses of quinia, tincture of the chloride of iron, brandy, and diffusible stimulants. Alimentation is to be kept up by mouth or rectum, as may be necessary, with as much food as can be given containing the most nutrition in the smallest bulk possible. Locally, a strong solution of silver nitrate (sixty grains to the ounce) should be so applied as to cover a margin of unaffected structures. Sedative inhalations are of service. Extension to the larynx demands scarification or tracheotomy.

When the diagnosis of common membranous sore throat can be made out with certainty, there is nothing calling for special treatment, but the treatment pursued in ordinary sore throat may be generally followed with advantage. When fetor exists, as during the detachment of patches of exudation, antiseptic and detergent sprays may be employed. Solutions of borax, boric acid, carbolic acid, potassium chlorate, potassium permanganate, etc. are appropriate. In some individuals, especially strumous and tuberculous subjects, there is a constitutional proclivity to chronicity or to the recurrence of the peculiar manifestations. More active measures will be required in these cases. Locally, frequent application of the dilute acids (i.e. every day or two) affords the most satisfactory results. Internally, iron and cinchona preparations should be administered. Opium in small doses has a special application--not as a narcotic, but as a gentle stimulant or nervous tonic. Nux vomica or arsenic may be employed for a similar purpose. The diet should be highly nutritious and easily assimilable. Unnecessary exposure should be avoided, and supporting measures generally, hygienic, as well as medicinal, should be persisted in. Membranous pharyngitis sometimes exhibits a tendency to phagedæna. The treatment for gangrenous sore throat is then indicated. It may invite an attack of diphtheria or the diagnosis may be in doubt. In that case the prudent course is to treat it as diphtheria, but to avoid the recommendation for diphtheria of some indifferent remedy, during the exhibition of which a case of membranous sore throat has recovered. When extension to the larynx occurs threatening suffocation, tracheotomy to avert death should be performed, as in croup or diphtheria.

The sore throats of the exanthemata, of typhoid fever, etc., are to be treated on the general principles applicable to catarrhal or phlegmonous pharyngitis. Oedema or tumefaction, as in malignant scarlatina, of a sufficient extent to obstruct respiration, is to be relieved by scarification, and when this is inefficient resort must be had to tracheotomy. The sore {400} throats caused by drugs are to be treated first by removal of the cause, and afterward according to the special indications.

Tuberculous Pharyngitis.

DEFINITION.--An acute ulcerative pharyngitis due to infiltration with miliary and granular tubercle and the consequent destructive metamorphosis.

SYNONYMS.--Acute tuberculous sore throat, Acute tuberculous pharyngitis, Tuberculosis of the pharynx, Phthisis of the pharynx.

HISTORY.--Only of late years has tuberculosis of the pharynx been distinctly recognized as a tuberculous disease. The tubercular sore throat or pharyngitis described by Green of New York, and other authors following him, is an affection of entirely different character, and not tuberculosis at all. The chronic tuberculous sore throat of advanced tuberculosis is likewise a different affection clinically, though of the same histological character.

To the late Isambert[2] of Paris belongs the credit of definitively recognizing the specificity of acute tuberculous sore throat or pharyngitis, and to him likewise the credit of indicating its differentiation from syphilitic sore throat, with which it had long been confounded. To B. Fraenkel of Berlin[3] is likewise due the credit of an accurate comprehension and elucidation of the clinical and histological pathology of this disease.

[Footnote 2: Annales des Maladies de l'Oreille, du Larynx, etc., vol. xi., 1875, p. 162; Conférences cliniques sur les Maladies du Larynx et des premières Voices, Paris, 1877, p. 219.]

[Footnote 3: Berlin. klin. Woch., Nov., 1876; London Med. Record, Jan. 15, Feb. 15, 1877.]

ETIOLOGY.--Acute tuberculous pharyngitis is quite a rare disease. Its predisposing causes, in all probability, are identical with those of acute tuberculosis. Its exciting cause, in some cases at least, is some unusual exposure to cold and wet. It is not certain that the throat is affected before the lungs; but if this be the case, it is certain that the lungs become affected soon afterward. The disease occurs in young children, Isambert having recorded a case at four and a half years of age, but it is much more frequent in adolescents and young adults. It is impossible, as yet, to assign the reason why the pharynx rather than other structures undergoes tubercularization in these exceptional cases of pharyngitis. Syphilis sometimes coexists in the adult certainly, and it may be questioned whether hereditary taint may not be an important factor in determining tuberculosis in a region so frequently ravaged by syphilis.

PATHOLOGY AND MORBID ANATOMY.--The local disease is essentially an ulcerative pharyngitis or pharyngo-laryngitis, as may be, extremely rapid in its progress, and terminating fatally within a few weeks, or a few months at farthest. The ulcerative process usually begins on the palatine folds or else on the lateral wall of the pharynx, thence extending to the palatine folds, soft palate, uvula, and hard palate in one direction, and toward the posterior wall of the pharynx in the other. The uvula sometimes becomes thickened into a club-shaped, gelatinous-looking mass, somewhat characteristic. Previous to ulceration the mucous membrane is subjected to abundant infiltration with miliary and granular tubercle just beneath the epithelial layer. Macroscopically, these infiltrated portions of {401} tissue present as irregular chagrinated groups of patches, generally confluent, which when abundant or prominent are liable to be confounded with syphilitic patches. Just beneath the surface the collections of tubercle project as little semi-transparent grayish nodules, in size and form recalling the appearance of vermicelli-seeds or fish-eggs. They steadily increase in volume and in number, lose their translucency, and finally undergo disintegration into lenticular ulcers with caseous bottoms and undermined hyperæmic edges. The ulcers extend steadily in periphery and in depth, and coalesce by necrosis of intervening mucous membrane. Polypoid excrescences springing from the beds of the ulcers have been described (Fraenkel). Collateral tumefaction takes place in some instances, due, it is stated (Isambert), to infiltration of the tissues by a gelatinous material, possibly a mucoid degeneration of the connective tissue. The usual tendency of the disease, however, is to incite atrophic metamorphosis of the adjacent tissues not undergoing actual tubercularization. In many instances extension to the upper portion of the larynx takes place; in some, extension to the vault of the pharynx. Extension to the oesophagus, as has been remarked by Mackenzie, and to the posterior nasal outlets, has not been noticed. Enlargement of the cervical lymphatic glands is quite common.

Microscopic examination of the tissues of the pharynx has revealed profuse infiltration with round cells--most frequently in the mucous membrane and submucous connective tissue only, occasionally in the muscular fibres likewise. The muscles sometimes undergo the fatty degeneration, and the mucous glands both fatty and colloid degeneration.

SYMPTOMATOLOGY.--The chief and characteristic subjective symptom is extreme pain in swallowing (odynphagia)--pain much more intense than in other morbid processes in the same locality, and inexplicable by the extent of the visible disease merely. This pain often extends toward the ears. Cough, adynamic fever, rapid emaciation, and so on are present, as in acute tuberculosis generally.

DIAGNOSIS.--It cannot be stated that the diagnosis is easy. The two distinguishing characteristics are the exquisite pain in swallowing and the absence of pus from the surface of the ulcers. The aspect of the ulcers differs, furthermore, from that of syphilitic ulcers by the lack of opalescence and of inflammatory areolæ. The gray nodules in the affected mucous membrane are different from what is observed in any other disease. These points, with the history of the attack, the family history, and the probable evidence of tuberculosis in the lungs, will usually serve to discriminate the disease from syphilis, for which it is most likely to be mistaken. In cases of doubt ophthalmoscopic examination of the choroid and iris may reveal tubercle. The bacillus tuberculosis has been found in the detritus from the ulcers (Guttman, Gurovitch). The fact must not be ignored that syphilitic and tuberculous pharyngitis may exist together. Febrile symptoms, typhoidal in type, in a case of supposed syphilitic sore throat will most likely be indicative of tuberculosis.

PROGNOSIS.--The disease is rapidly fatal, apparently inevitably so. An exceptional case has been recorded, however (Cadier[4]), living {402} several years after the diagnosis had been made by Isambert and many others.

[Footnote 4: Annales des Maladies de l'Oreille, du Larynx, etc., July, 1883, p. 136.]

Death takes place by asthenia in from six weeks to six months; occasionally within a fortnight from the apparent onset.

TREATMENT.--The little that can be accomplished in the way of treatment is limited to improving the diet and hygienic surroundings, with the administration of such constitutional remedial agents as are given in acute tuberculosis, and palliative treatment of the local suffering. For the latter purpose insufflations of iodoform and morphine are to be recommended, two or three grains of the former with one-fourth to one-half grain of the latter, once a day or oftener. Such insufflations should be preceded by douches or sprays of sodium borate or bicarbonate, to rid the parts of mucus and detritus. A drop or two of carbolic acid, of eucalyptol, or of a solution of thymol may be advantageously added for purposes of disinfection. Solution of hydrogen peroxide (2 per cent. or weaker) is a very valuable agent for use in spray or douche. It may be rendered more agreeable by the addition of a few drops of some balsamic.

When swallowing is impracticable, nourishment by enema is indicated, with forced feeding by means of a catheter passed through the larger of the two nasal passages into the oesophagus.

Chronic Pharyngitis.

DEFINITION.--A chronic inflammation of the mucous membrane of the pharynx, whether implicating the glandular structures or not, and commonly associated with similar chronic inflammation of contiguous structures.

SYNONYMS.--Chronic sore throat, Chronic angina.

Chronic pharyngitis presents in two varieties: 1, simple chronic pharyngitis (chronic catarrhal pharyngitis, chronic catarrhal sore throat), in which the disease does not affect, or affects but slightly, the glandular structures of the mucous membrane; and 2, follicular pharyngitis (granular pharyngitis, clergyman's sore throat), in which groups of the follicular glands of the mucous membrane are enlarged, and sometimes inflamed.

ETIOLOGY.--The predisposing causes of chronic catarrhal pharyngitis are those enumerated under the head of the acute form of the affection, and the exciting causes are repeated attacks of the acute malady.

The predisposing causes of chronic follicular pharyngitis are overcrowding, and sedentary occupations; and the exciting causes are chiefly improper use of the voice and exposure to local irritations, mechanical and chemical, including too free use of condiments, tobacco, and alcohol, gormandizing, and the alternations of hot food, cold drinks, ices, and hot drinks at meals. It is not so often a direct sequel of attacks of acute sore throat as a result of prolonged catarrhal pharyngitis; and sometimes it appears to be chronic, so to speak, from the outset.

Both forms of chronic pharyngitis are frequently associated with chronic inflammations of the mucous membranes elsewhere, particularly of the nasal passages and of the stomach, and, to a less extent, of the genito-urinary apparatus; the entire train of phenomena, in some instances, {403} being due to passive congestion dependent upon impaired cardiac power. Similarly, it presents at times as one of the accompaniments of exophthalmic goitre. It is often associated with phthisis, and is sometimes found in phthisical subjects prior to the detection of the pulmonary disease. It is sometimes coincident with chronic cutaneous eruptions, and may depend on the same causes, whether dietetic or nervous.

Uterine disturbances may give rise to chronic pharyngitis, probably by reflex nervous influence, and so do other chronic and dispiriting complaints. In like manner, depression of spirits and impairment of bodily vigor from domestic, financial, and social chagrin provoke a train of phenomena in which chronic pharyngitis may be a prominent manifestation.

PATHOLOGY AND MORBID ANATOMY.--Simple chronic pharyngitis is a chronic catarrhal inflammation of the mucous membrane and submucous connective tissue of the pharynx, with irregular hyperplasia of all the histological elements, chiefly affecting the epithelial layers and the most superficial strata of the submucosa. The pharynx, the posterior surface of the palate, and the pharyngo-palatine folds are the structures most generally implicated, but the glosso-palatine folds, the base of the tongue, and even the anterior surface of the palate, are sometimes involved. At an advanced stage of the affection extension may take place to the vault of the pharynx and the posterior nasal outlets, and in occasional instances to the larynx.

The initial hyperæmia of diffuse congestion finally leads to permanent dilatation of tracts of capillaries varying in area and mode of distribution, sometimes recalling the territorial outlines upon a map. The mucous membrane is bright red in color and irregularly thickened, sometimes into prominent welts or folds. The palate is often relaxed. Hypersecretion takes place over the entire diseased surface, and there is considerable desquamation of turbid epithelium, which sometimes accumulates in masses. Glands are dilated and hypertrophied here and there, but not in every instance, or if so indiscernibly, at least, to the naked eye.

In some cases enlarged follicles are very prominent in the infra-tonsillar space, between the anterior and posterior palatine folds, and along the lateral walls of the pharynx down toward the base of the tongue. The circumvallate papillæ may also be enlarged, and the fungiform papillæ are sometimes very prominent and deeply congested.

In the folliculous variety of the disease the hyperplasia affects chiefly the mucous glands and follicles, isolated or in groups, together with zones of connective tissue surrounding them and the epithelial investment of the mucous membrane in their immediate neighborhood. A number of small projections, from the size of pinheads to that of peas, mostly somewhat hemispheroidal, sometimes ellipsoidal or quite irregular in configuration, stud the pharynx irregularly. When clustered they are more apt to occupy the lateral angles of the pharynx. In this locality indeed the chains of glands and their enveloping mucous membrane sometimes present in longitudinal ridges which simulate additional or adventitious post-palatine folds. The projections are usually opaque, deeper in color than the surrounding congested mucous membrane, and velvety from loss of squamous epithelium. Sometimes they are translucent, as if filled with colloid material, probably retained and degenerated secretion. {404} Very often their contents undergo caseous degeneration, and sometimes even calcification--a variety designated tubercular by Green, Gibb, and others, but far different histologically from true tuberculosis of the pharyngeal glands, which does occur occasionally in phthisical patients.

Delicate red lines of engorged capillaries usually surround the base of these projections. There is great disposition to the accumulation of viscid, discolored mucus on the surface of the mucous membrane. As the disease progresses all the processes become more widely extended, until finally nearly the entire pharyngeal and oral mucous membrane becomes involved. The soft palate becomes relaxed and the uvula thickened and elongated, sometimes to an extreme degree. Chronic folliculous tonsillitis exists in many cases.

When either form of chronic pharyngitis continues for a long while unchecked, there may result atrophy of the glandular structures and epithelial elements generally, giving rise to pharyngitis sicca or atrophic pharyngitis (so-called dry catarrh). There is then but scanty secretion, and this dries rapidly upon the surface of the thin mucous membrane, which becomes rough, inflexible, and glazed.

SYMPTOMATOLOGY.--Cough, expectoration, impairment of voice, dysphagia, and uncomfortable sensations in the throat present in various degrees according to the stage of the disease and the temperament of the patient. Hemming and hawking to clear the throat often become habitual, especially in cases associated with chronic internal rhinitis, being provoked in many instances by secretory products which drop into the pharynx or glide along its walls. It is sometimes important to distinguish this habit from the cough of laryngeal or bronchial irritation.

In cases associated with chronic gastritis the loss of appetite and consequent emaciation accompanying the symptoms of pharyngitis sometimes lead friends of the patient to a mistaken diagnosis of consumption; and when, as is not infrequent, chronic bronchitis also coexists, even the physician may be misled.

In many instances of chronic folliculous pharyngitis evidently of long standing, and accidentally discovered at times to the surprise of the patient, no history of the classical group of symptoms can be obtained.

DIAGNOSIS.--The diffuse congestion of the mucous membrane and the absence of marked involvement of the follicles are, with the history of the case, the main discriminative features in the diagnosis of chronic catarrhal pharyngitis. The regular or irregular masses of tissue projecting beyond the general surface of the mucous membrane are the distinguishing characteristics of chronic folliculous pharyngitis. The vascular network of dilated capillaries mapping the surface into numerous irregular small areas of different sizes is not peculiar to either variety.

PROGNOSIS.--The prognosis of chronic catarrhal pharyngitis is favorable when no irremediable malady of body or mind exists. Much depends on the practicability of improving the dietetic and hygienic environment of the patient. The prognosis is likewise good in chronic folliculous pharyngitis under favorable surroundings, so far as relief from suffering is concerned; but the follicles, when long hypertrophied, so rarely undergo absorption under any treatment that their destruction becomes necessary--quite a different thing from their cure. The enlarged follicles once destroyed, the collateral irritative inflammation caused by {405} them usually subsides. Impairment of voice, a result of the disease, may be remedied in young subjects, who will learn to use the voice with the abdomen in distension; but much improvement cannot be expected in old subjects and in those in whom the disease has been produced by improper methods of declamation, which are beyond correction.

TREATMENT.--In chronic catarrhal pharyngitis constitutional treatment adapted to the diathetic condition is required in the first instance. Alkaline laxatives are usually indicated by the irregularly coated tongue and the tendency to costiveness. These may be advantageously administered in half a pint of hot water one hour or so before meals, with a view of washing the stomach free from accumulations of mucus, epithelium, and retained products of digestion and decomposition, so that its condition may be improved for the reception and digestion of the ensuing meal. Topical medication of the throat is likewise requisite. This should be of a soothing character. Mild astringents are applicable, but strong astringents are often actually injurious. Silver nitrate and cupric sulphate in stick or strong solution should not be used; but sprays of dilute solutions (one or two grains to the ounce of distilled water), twice or thrice a day, are often of service. Zinc sulphate (five grains to the ounce) may be used in the same manner. Zinc chloride (ten grains to the ounce), carefully applied to the surface daily with a broad brush or soft cotton wad, is a useful remedy. Tannin in ether sometimes answers admirably, a delicate film being left for some time on the surface. Solutions of bismuth nitrate or borate in glycerin applied locally often relieve uneasiness. A broad flat brush is the best instrument for making these applications, placed low in the pharynx so as to paint the entire posterior wall by a single movement from below upward.

For home use, sprays, three or four times a day, of tar-water, containing five or ten grains to the ounce, of sodium borate or bicarbonate, or sodium, potassium, or ammonium chloride, or sodium, potassium, or ammonium iodide, are soothing and efficacious, and much superior to gargles. They are often preferred warm. Demulcent lozenges (gelatin, acacia, althæa, glycyrrhiza) slowly dissolved in the mouth often relieve topical discomfort.

Much more active treatment is required in chronic folliculous pharyngitis. Judicious constitutional treatment is of great importance. Topical medication is of equal importance. In recent cases of moderate intensity the ordinary treatment for the catarrhal variety sometimes suffices. In cases of long standing strong solutions of silver nitrate (sixty to one hundred and twenty grains to the ounce), carefully applied with the broad flat brush twice or thrice a week, are often of great remedial effect. Iodine (one drachm to the ounce of glycerin), alone or in combination with equal parts of carbolic acid, applied daily, may be serviceable in cases unimproved by the silver nitrate. Dilatation of the capillaries may sometimes be benefited by applications of ergot (fluid extract) or ergotin (grs. x-xx to the ounce). Enlarged follicles of long standing are rarely amenable to astringent and alterant topical treatment. They require destruction. The agent to be used is a matter of indifference as a rule, and, according to the taste or resources of the practitioner, may be the solid silver nitrate, caustic potash, London paste, zinc chloride, {406} or the incandescent cautery, whether heated by fire, hot naphtha, or electricity.

The sprays and lozenges already mentioned are useful in this variety of pharyngitis also. They may be medicated with sedative ingredients according to indications for the relief of pain and discomfort.

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.).

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 {414} 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 {415} 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, {416} 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 {417} 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 {418} 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 {419} 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.

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

[Footnote 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 {420} 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 {421} 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. {422} 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 Homes[17]), 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.

[Footnote 17: Biblioth. méd., t. viii. p. 260; Michel, Dict. Encyclopedique, t. xiv. p. 466.]

[Footnote 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, {423} 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.

[Footnote 19: The Lancet, 1872.]

[Footnote 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.

{424} 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 {425} 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 {426} daily, every other day, or at more prolonged intervals, according to the tolerance of the parts and the progressive improvement. They are retained several moments at each introduction, and followed by the passage and immediate withdrawal of an instrument of larger size. It is often advisable that the final dilatation of each series be made with a stomach-tube, so that liquid food may be poured through it from a syphon or a small-lipped vessel, that there may be no necessity for swallowing food for some hours thereafter. This method is continued until it becomes evident that nothing further is to be gained by its continuance. In cases that have been at all successful, the introduction of the instrument should be repeated every week or two for a long time, to prevent or retard recurrence of the constriction, which is very liable to take place. M. Krishaber has reported[21] 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.

[Footnote 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.

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

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

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

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

As the disease progresses the adjoining tissues become involved. Adhesions may take place with trachea, bronchi, bronchial glands, lungs, diaphragm, or even the spinal column (Newman[22]). Perforation may take place into the trachea, usually just above the bifurcation, or into the lungs, pleura, mediastinum, pericardium, aorta, or pulmonary artery. Abscesses are formed, the contents of which undergo putrefaction. There {428} may be involvement of the pneumogastric nerve, with reflex influence on the spinal nerves and the sympathetic (Gurmay[23]).

[Footnote 22: N.Y. Med. Journ., Aug., 1879, p. 158.]

[Footnote 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 (Reid[24]).

[Footnote 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.

{429} Paralysis of the Oesophagus.

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

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

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

The paralysis may be due to disease or wounds of the nerves themselves or of their motor roots, or of the cerebro-spinal axis, implicating their origin, or to pressure and atrophy of a trunk-nerve in some portion of its tract. It is likewise due to neurasthenia from hemorrhage or from protracted disease (enteric fever, yellow fever, cholera), or to systemic poisoning in diphtheria, syphilis, and plumbism. It may be due to muscular atrophy or intermuscular proliferations of connective tissue, to dilatation of the oesophagus, and to disease in the tube. It may be due to mechanical restraint from external adhesions of the oesophagus to intrathoracic tumors (Finny[25]). 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.

[Footnote 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 {430} 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.

[Footnote 26: Edinb. Med. and Surg. Journ., July, 1883.]

[Footnote 27: Traité Élément. de Path. int., Paris, 1883, ii. p. 358.]

{431} 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 (Rokitansky[28]) 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 Billroth[29]) to partial closing of one of the branchial fissures externally, while the internal opening has remained patent.

[Footnote 28: Archiv. gén. de Méd., 1840, p. 329.]

[Footnote 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 Hankel[30] 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.

[Footnote 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 {432} 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).

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 (Rokitansky[31]); in rare cases, even a capacity nearly equal to that of the stomach (Luschka[32] and others). (See Fig. 19.)

[Footnote 31: Path. Anat.]

[Footnote 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 (Raymond[33]).

[Footnote 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 {433} 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 {434} 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 (Davy[34]), 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.

[Footnote 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 (Lindau[35]). 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 (Hannay[36]).

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

[Footnote 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.

{435} 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.

[Footnote 37: Dict. Encyclop., xiv. p. 465.]

{436}

FUNCTIONAL AND INFLAMMATORY DISEASES OF THE STOMACH.

BY SAMUEL G. ARMOR, M.D., LL.D.

Functional Dyspepsia (Atonic Dyspepsia, Indigestion).

To difficulty in the physiological process of digestion the familiar name of dyspepsia has been given, while to a merely disturbed condition of the function the term indigestion is more frequently applied. This distinction, difficult at all times to make, may appear more arbitrary than real; and inasmuch as it involves no important practical point, the author of the present article will use the terms interchangeably as indicating functional disturbance of the stomach--i.e. disturbance of the digestive process not associated with changes of an inflammatory character, so far as we know.

Since it is one of the most common of all complaints from its association with various other morbid conditions, the term is not unfrequently vaguely employed. It is difficult, of course, to define a disease whose etiology is so directly related to so many distinct morbid conditions. Indeed, there are few diseases, general or local, which are not at some time in their history associated with more or less derangement of the digestive process. For purposes of limitation, therefore, it will be understood that we now refer to chronic functional forms of indigestion which depend largely, at least, on a purely nervous element, and for this reason are not infrequently described as sympathetic dyspepsia. Doubt has been expressed as to whether such forms of disease ever exist, but that we encounter purely functional forms of dyspepsia, corresponding to the dyspepsia apyretica of Broussais, would appear to be a well-recognized clinical fact.

What the precise relation is between digestive disturbances and the nervous system we may not fully understand, no more than we understand how a healthy condition of nervous endowment is essential to all vital processes. Even lesions of nutrition are now known to depend upon primary disturbance of nervous influence. This is seen in certain skin diseases, such as herpes zoster, which closely follows the destruction of certain nerves. And it is well known that injury of nerve-trunks is not unfrequently followed by impaired nutrition and failure in reparative power in the parts to which such nerves are distributed. Indeed, so marked is the influence of the nervous system over the nutritive operations that the question has been considered as to whether there are {437} trophic nerves distributed to tissue-elements themselves whose special function is to keep these elements in a healthy state of nutrition. The proof, at least, that the digestive process is, in some unexplained way, under the immediate influence of the nervous system, either cerebro-spinal or trophic, is both varied and abundant. The digestive secretions are known to be the products of living cells which are abundantly supplied with nerve-fibres, and we can readily believe that the potential energy of this cell-force is probably vital and trophic. At any rate, it is unknown in the domain of ordinary chemistry. The digestive ferments, as clearly pointed out by Roberts, are the direct products of living cells. Their mode of action, he claims, bears no resemblance to that of ordinary chemical affinity. It has a distinctly physiological character. Nor do they derive their vital endowments from material substances. "They give nothing material to, and take nothing from, the substances acted on. The albuminoid matter which constitutes their mass is evidently no more than the material substance of a special kind of energy--just as the steel of a magnet is the material substratum of the magnetic energy, but is not itself that energy" (Roberts). That this living cell-force is partly, at least, derived from the nervous system is clear from the well-known effects of mental emotion, such as acute grief, despair, etc., in putting an immediate stop to the digestive process. Experiments on the lower animals have also shown the direct influence of the nervous system over gastric secretion. Wilson Philip showed by various experiments on rabbits and other animals that if the eighth pair of nerves be divided in the neck, any food which the creatures may afterward eat remains in the stomach undigested, and after death, when the nerve has been divided, the coats of the stomach are not found digested, however long the animal may have been dead. Bernard also excited a copious secretion by galvanization of the pneumogastric, and by section of the same nerve stopped the process of digestion and produced "pallor and flaccidity of the stomach." Recently doubt has been thrown on these statements of Bernard and Frerichs. Goltz concludes, from observations made on frogs, that nerve-ganglia, connected by numerous intercommunicating bundles of nerve-fibres, exist in the walls of the stomach, the irritation of which gives rise to local contractions and peristaltic movements of the stomach, and that these ganglia influence the gastric secretion. However this may be, it still remains true that these gastric ganglia are in connection, through the vagi, with the medulla oblongata, and are thus influenced by the cerebro-spinal nerve-centres. And clinical observation confirms what theoretical considerations would suggest. Thus, strong mental impressions are known to produce sudden arrest of secretion, and that which arrests secretion may, if continued, lead to perversion of the same.

Impressions made upon the nerves of special sense are also known to affect the salivary and gastric secretions. The flow of saliva is stimulated by the sight, the smell, the taste, and even thought, of food. Bidder and Schmidt made interesting experiments on dogs bearing upon this point. They ascertained by placing meat before dogs that had been kept fasting that gastric juice was copiously effused into the stomach. Other secretions are known to be similarly affected. Carpenter by a series of well-observed cases has shown the direct influence of mental conditions on the {438} mammary secretion. The nervous association of diabetes and chronic Bright's disease is interesting in this connection, and the direct nervous connection betwixt the brain and the liver has been shown by numerous experiments. It is maintained by modern physiologists that "the liver--indeed each of the viscera--has its representative area in the brain, just as much as the arm or leg is represented in a distant localized area" (Hughlings Jackson). And in harmony with this view Carpenter long since pointed out the fact that if the volitional direction of the consciousness to a part be automatically kept up for a length of time, both the functional action and the nutrition of the part may suffer. It has been described by him as expectant attention, and it has, as we shall see, important practical bearings on the management of gastric affections. Sympathetic disturbance of the stomach is also connected with direct disease of the brain. This is seen in cases of concussion. The almost immediate effects of a blow are nausea and vomiting, and the same thing is observed in local inflammation of the meninges of the brain.

Many forms of functional dyspepsia due to nervous disturbance of a reflex character will be pointed out when discussing the etiology of the disease.

ETIOLOGY.--Among the agencies affecting the digestive process in atonic forms of dyspepsia may be mentioned--

First, predisposing causes;

Second, exciting causes.

In general terms it may be said that all conditions of depressed vitality predispose to the varied forms of atonic dyspepsia. These conditions range through an endless combination of causes, both predisposing and exciting. There is not a disturbed condition of life, extrinsic or intrinsic, that may not contribute to this end. In some cases it may be the effects of hot and enervating climates; in others the alterations in the elementary constituents of the blood may be apparent; while in still others the cause may be exhausting discharges, hemorrhages, profuse suppuration, venereal excesses, sedentary occupations, and long-continued mental and moral emotions.

Heredity may also predispose to functional dyspepsia. Certain faulty states of the nervous system are specially liable to be transmitted from parent to offspring--not always in the exact form in which they appeared in the parent, but in forms determined by the individual life of the offspring. For obvious reasons, growing out of our modern American civilization, the inheritance of a faulty nervous organization is apt to spend itself upon the digestive apparatus. The inordinate mental activity, the active competitions of life, the struggle for existence, the haste to get rich, the disappointments of failure,--all contribute to this end. The general tendency of American life is also in the direction of a highly-developed and morbidly sensitive nervous system, and functional dyspepsia is a natural sequence of this. The symptoms of dyspepsia thus caused usually manifest themselves at an early period of life.

Age also predisposes to weak digestion. The stomach becomes weak as age advances, in common with all the functions of the body, and consequent upon this weakness there is diminished excitability of the gastric nerves, with diminished muscular action of the walls of the stomach and deficient secretion of the gastric juice. Chronic structural changes are {439} also apt to occur in advanced life. The gastric glands become atrophied and the arteries become atheromatous, so that with symptoms of indigestion there are often associated loss of consciousness at times, vertigo, irregular action of the heart, etc. These general facts have an important bearing upon the hygienic management of dyspepsia in the aged. They require, as a rule, less food than the young and vigorous. In times when famine was more frequent than now it was found that the older a human being was, the better deficiency of food was borne. Hippocrates tells us, in his Aphorisms, that old men suffer least from abstinence. Their food should be such, both in quantity and quality, as the enfeebled stomach can digest. There is less demand for the materials of growth, and consequently for animal food. Moderate quantities of alcohol, judiciously used, are also specially adapted to the indigestion of the aged. It has the double effect of stimulating the digestive process and at the same time checking the activity of destructive assimilation, which in old age exhausts the vital force. And in order to more effectively arrest destructive metamorphosis great caution should be taken against excessive muscular fatigue, as well as against sudden extremes of temperature. Loss of appetite from deficient formation of gastric juice is a common symptom in old age. This is not often successfully treated by drugs, and yet medicines are not without value. The sesquicarbonate of ammonium acts as a stimulant to the mucous membrane and to the vaso-motor nerve, and in this way becomes a valuable addition to the simple vegetable bitters. Dilute hydrochloric acid with the vegetable bitters may also be tried. Condiments with the food directly stimulate the action of the enfeebled stomach. The old remedy of mustard-seed is not unfrequently useful, and pepper, cayenne, horseradish, and curries act in a similar manner in torpid digestion. And in cases of great exhaustion associated with anæmia benefit may be derived from small doses of iron added to tincture of columbo or gentian.

Nor should it be forgotten that in the opposite extreme of life the digestive capacity is extremely limited. The infant's digestion is readily disturbed by unsuitable alimentation. For obvious reasons it does not easily digest starchy substances. The diastasic ferment does not exist in the saliva of young sucking animals, at least to any extent. No food is so suitable for early infantile life as the mother's milk, provided the mother herself is healthy. It contains in an easily digestible form all the constituents necessary to the rapidly-growing young animal. Van Helmont's substitute of bread boiled in beer and honey for milk, or Baron Liebig's food for infants, cannot take the place of nature's type of food, which we find in milk. If a substitute has to be selected, there is nothing so good as cow's milk diluted with an equal quantity of soft water, or, what in many cases is better, barley-water, to which may be added a teaspoonful of powdered sugar of milk and a pinch of table-salt and phosphate of lime. Lime-water may be added with advantage. Dilution of alimentary substances is an important condition of absorption in the infant stomach.

Anæmia is a common predisposing cause of indigestion. Indeed, as a widely-prevailing pathological condition few causes stand out so prominent. It affects at once the great nutritive processes, and these in turn disturb the functional activity of all the organs of the body. Not only are the gastric and intestinal glands diminished in their {440} functional activity by impoverished or altered blood, but the movements of the stomach are retarded by weakened muscular action. It is impossible to separate altered blood from perverted tissue-structure and altered secretion. Indigestion produced by anæmia is difficult of treatment, on account of the complexity of the pathological conditions usually present, the anæmia itself being generally a secondary condition. Careful inquiry should be made, therefore, into the probable cause of the anæmia, and this should, if possible, be removed as an important part of the treatment of the dyspepsia. Nothing will more promptly restore the digestive capacity in such cases than good, healthy, well-oxidized blood. Indeed, healthy blood is a condition precedent to the normal functional activity of the stomach.

To these general predisposing causes may be added indigestion occurring in febrile states of the system. The cause here is obvious. In all general febrile conditions the secretions are markedly disturbed; the tongue is dry and furred; the urine is scanty; the excretions lessened; the bowels constipated; and the appetite gone. The nervous system also participates in the general disturbance. In this condition the gastric juice is changed both quantitatively and qualitatively, and digestion, as a consequence, becomes weak and imperfect--a fact that should be taken into account in regulating the diet of febrile patients. From mere theoretical considerations there can be no doubt that fever patients are often overfed. To counteract the relatively increased tissue-metamorphosis known to exist, and the consequent excessive waste, forced nutrition is frequently resorted to. Then the traditional saying of the justly-celebrated Graves, that he fed fevers, has also rendered popular the practice. Within certain bounds alimentation is undoubtedly an important part of the treatment of all the essential forms of fever. But if more food is crowded upon the stomach than can be digested and assimilated, it merely imposes a burden instead of supplying a want. The excess of food beyond the digestive capacity decomposes, giving rise to fetid gases, and often to troublesome intestinal complications. The true mode of restoring strength in such cases is to administer only such quantities of food as the patient is capable of digesting and assimilating. To this end resort has been had to food in a partially predigested state, such as peptonized milk, milk gruel, soups, jellies, and beef-tea; and clinical experience has thus far shown encouraging results from such nutrition in the management of general fevers. In these febrile conditions, and in all cases of general debility, the weak digestion does not necessarily involve positive disease of the stomach, for by regulating the diet according to the digestive capacity healthy digestion may be obtained for an indefinite time.

Exhaustion of the nerves of organic life strongly predisposes to the atonic forms of dyspepsia. We have already seen how markedly the digestive process is influenced by certain mental states, and it is a well-recognized fact that the sympathetic system of nerves is intimately associated with all the vegetative functions of the body. Without a certain amount of nervous energy derived from this portion of the nervous system, there is failure of the two most important conditions of digestion--viz. muscular movements of the stomach and healthy secretion of gastric juice. This form of indigestion is peculiar to {441} the ill-fed and badly-nourished. It follows in the wake of privation and want, and is often seen in the peculiarly careworn and sallow classes who throng our public dispensaries. In this dyspepsia of exhaustion the solvent power of the stomach is so diminished that if food is forced upon the patient it is apt to be followed by flatulence, headache, uneasy or painful sensations in the stomach, and sometimes by nausea and diarrhoea. It is best treated by improving in every possible way the general system of nutrition, and by adapting the food, both in quantity and quality, to the enfeebled condition of the digestive powers. Hygienic measures are also of great importance in the management of this form of dyspepsia, and especially such as restore the lost energy of the nervous system. If it occur in badly-nourished persons who take little outdoor exercise, the food should be adapted to the feeble digestive power. It should consist for a time largely of milk and eggs, oatmeal, peptonized milk gruels, stale bread; to which should be added digestible nitrogenous meat diet in proportion to increased muscular exercise. Systematic outdoor exercise should be insisted upon as a sine quâ non. Much benefit may be derived from the employment of electric currents, and hydrotherapy has also given excellent results. If the indigestion occur in the badly-fed outdoor day-laborer, his food should be more generous and mixed. It should consist largely, however, of digestible nitrogenous food, and meat, par excellence, should be increased in proportion to the exercise taken. Medicinally, such cases should be treated on general principles. Benefit may be derived from the mineral acids added to simple bitters, or in cases of extreme nervous prostration small doses of nux vomica are a valuable addition to dilute hydrochloric acid. The not unfrequent resort to phosphorus in such cases is of more than doubtful utility. Some interesting contributions have been recently made to this subject of gastric neuroses by Buchard, Sée, and Mathieu. Buchard claims that atonic dilatation of the stomach is a very frequent result of an adynamic state of the general system. He compares it to certain forms of cardiac dilatation--both expressions of myasthenia. It may result from profound anæmia or from psychical causes. Mathieu regards mental depression as only second in frequency. Much stress is laid upon poisons generated by fermenting food in the stomach in such cases. It may cause a true toxæmia, just as renal diseases give rise to uræmia. Of course treatment in such cases must be addressed principally to the general constitution.

But of all predisposing causes of dyspepsia, deficient gastric secretion, with resulting fermentation of food, is perhaps the most prevalent. It is true this deficient secretion may be, and often is, a secondary condition; many causes contribute to its production; but still, the practical fact remains that the immediate cause of the indigestion is disproportion between the quantity of gastric juice secreted and the amount of food taken into the stomach. In all such cases we have what is popularly known as torpidity of digestion, and the condition described is that of atony of the stomach. The two main constituents of gastric juice--namely, acid and pepsin--may be deficient in quantity or disturbed in their relative proportions. A certain amount of acid is absolutely essential to the digestive process, while a small amount of pepsin may be sufficient to digest a large amount of albuminoid food. {442} Pure unmixed gastric juice was first analyzed by Bidder and Schmidt. The mean analyses of ten specimens free from saliva, procured from dogs, gave the following results:

Gastric Juice of a Dog. Water 973.06 Solids 26.94 Containing--Peptone and pepsin 17.19 Free hydrochloric acid 3.05 Alkaline chlorides 4.26 Ammonium chloride 0.47 Chlorine 5.06 | Lime 1.73 Phosphates | Magnesia 0.23 | Iron 0.08

They proved by the most careful analyses that fresh gastric juice contains only one mineral acid--namely, hydrochloric; since which time Richet has been able to prove that "this acid does not exist in a free state, but in loose combination with an organic substance known as lucin," the chloride of lucin. And just here the curious and puzzling question arises as to the secretion of a mineral acid from alkaline blood. Ewald, the distinguished lecturer in the Royal University of Berlin, tells us that "a brilliant experiment of Maly's has thrown unexpected light upon this. There are fluids of alkaline reaction which may contain two acid and alkaline mutually inoffensive salts, but still have an alkaline reaction, because the acid reaction is to a certain extent eclipsed; for instance, a solution of neutral phosphate of soda (Na_{2}HPO_{4}) and acid phosphate of soda (NaH_{2}PO_{4}) is alkaline. Such a solution placed in a dialyzer after a short time gives up its acid salt to the surrounding distilled water, and one has in the dialyzer an alkaline fluid outside an acid fluid." He thus proved that the acid phosphate of sodium is present in the blood in spite of its alkaline reaction.

Lack of the normal amount of the gastric secretion must be met by restoring the physiological conditions upon which the secretion depends. In the mean time, hydrochloric and lactic acids may be tried for the purpose of strengthening the solvent powers of the gastric secretion.

EXCITING CAUSES.--The immediate causes of dyspepsia are such as act more directly on the stomach. They embrace all causes which produce conditions of gastric catarrh, such as excess in eating and drinking, imperfect mastication and insalivation, the use of indigestible or unwholesome food and of alcohol, the imperfect arrangement of meals, over-drugging, etc.

Of exciting causes, errors of diet are amongst the most constantly operative, and of these errors excess of food is doubtless the most common. The influence of this as an etiological factor in derangement of digestion can scarcely be exaggerated. In very many instances more food is taken into the stomach than is actually required to restore tissue-waste, and the effects of such excess upon the organism are as numerous as they are hurtful. Indeed, few elements of disease are more constantly operative in a great variety of ailments. In the first place, if food be introduced into the stomach beyond tissue-requirements, symptoms of indigestion at once manifest themselves. The natural balance betwixt {443} supply and demand is disturbed; the general nutrition of the body is interfered with; local disturbances of nutrition follow; and mal-products of digestion find their way into the blood. Especially is this the case when the excessive amount of food contains a disproportionate amount of nitrogenous matter. All proteid principles require a considerable amount of chemical alteration before they are fitted for the metabolic changes of the organism; the processes of assimilative conversion are more complex than those undergone by fats and amyloids; and it follows that there is proportional danger of disturbance of these processes from overwork. Moreover, if nitrogenous food is in excess of tissue-requirement, it undergoes certain oxidation changes in the blood without becoming previously woven into tissue, with resulting compounds which become positive poisons in the economy. The kidneys and skin are largely concerned in the elimination of these compounds, and the frequency with which these organs become diseased is largely due, no doubt, to the excessive use of unassimilated nitrogenous food. Then, again, if food be introduced in excess of the digestive capacity, the undigested portion acts directly upon the stomach as a foreign body, and in undergoing decomposition and putrefying changes frets and irritates the mucous membrane. It can scarcely be a matter of doubt that large groups of diseases have for their principal causes excess of alimentation beyond the actual requirements of the system. All such patients suffer from symptoms of catarrhal indigestion, such as gastric uneasiness, headache, vertigo, a general feeling of lassitude, constipation, and high-colored urine with abundant urates, together with varied skin eruptions. Such cases are greatly relieved by reducing the amount of food taken, especially nitrogenous food, and by a systematic and somewhat prolonged course of purgative mineral waters. Europe is especially rich in these springs. The waters of Carlsbad, Ems, Seltzer, Friedrichshall, and Marienbad, and many of the alkaline purgative waters of our own country, not unfrequently prove valuable to those who can afford to try them, and their value shows how often deranged primary assimilation is at the foundation of many human ailments. The absurd height to which so-called restorative medicine has attained within the last twenty years or more has contributed largely to the production of inflammatory forms of indigestion, with all the evil consequences growing out of general deranged nutrition.

The use of indigestible and unwholesome food entails somewhat the same consequences. This may consist in the use of food essentially unhealthy or indigestible, or made so by imperfect preparation (cooking, etc.). Certain substances taken as food cannot be dissolved by the gastric or intestinal secretions: the seeds, the skins, and rinds of fruit, the husks of corn and bran, and gristle and elastic tissue, as well as hairs in animal food, are thrown off as they are swallowed, and if taken in excess they mechanically irritate the gastro-intestinal mucous membrane and excite symptoms of acute dyspepsia, and not unfrequently give rise to pain of a griping character accompanied by diarrhoea. Symptoms of acute dyspepsia also frequently follow the ingestion of special kinds of food, such as mushrooms, shellfish, or indeed fish of any kind; and food not adapted to the individual organism is apt to excite dyspeptic symptoms. Appetite and digestion are also very much influenced by the life and {444} habits of the individual. The diet, for instance, of bodily labor should consist largely of digestible nitrogenous food, and meat, par excellence, should be increased in proportion as muscular exercise is increased. For all sorts of muscular laborers a mixed diet is best in which animal food enters as a prominent ingredient. Thus, it has been found, according to the researches of Chambers, that in forced military marches meat extract has greater sustaining properties than any other kind of food. But with those who do not take much outdoor exercise the error is apt to be, as already pointed out, in the direction of over-feeding. It cannot be doubted at the present time that over-eating (gluttony) is one of our popular vices. Hufeland says: "In general we find that men who live sparingly attain to the greatest age." While preventive medicine in the way of improved hygiene--better drainage, better ventilation, etc.--is contributing largely to the longevity of the race, we unfortunately encounter in more recent times an antagonizing influence in the elegant art of cookery. Every conceivable ingenuity is resorted to to tempt men to eat more than their stomachs can properly or easily digest or tissue-changes require. The injurious consequences of such over-feeding may finally correct itself by destroying the capacity of the stomach to digest the food.

But, on the other hand, in many nervous forms of dyspepsia the weak stomach is not unfrequently made weaker by severely restricted regimen, and especially is this the case with mental workers. Theoretical and fanciful considerations sometimes lead to physical starvation. This is apt to be the case with dyspeptics. Men who toil with their brain rather than their muscles, whether dyspeptic or not, require good, easily-digested mixed diet. It is a popular error to suppose that drugs can take the place of such food, especially drugs which are supposed to have a reconstructive influence over the nervous system, such as iron and phosphorus. The expression of Büchner, "No thinking without phosphorus," captivating to theoretical minds, has gained much notoriety, and has doubtless led to the excessive use of that drug in nervous forms of indigestion. There never was a period when phosphorus was so universally prescribed as the present. It enters into endless combinations with so-called nerve-tonics. Of the injurious influence of the drug in many cases of functional indigestion there can be no doubt; and the statement itself, so often quoted, that "the amount of phosphorus in the blood passing through the brain bears an exact proportion to the intensity of thought," is calculated to mislead. T. K. Chambers, author of the excellent Manual of Diet, makes the statement that "a captive lion, tiger, leopard, or hare assimilates and parts with a greater amount of phosphorus than a hard-thinking man; while the beaver, noted for its power of contrivance, excretes so little phosphorus that chemical analysis cannot find it in its excreta." In the wonderful adaptations and regulative mechanisms of nature we may trust largely to the natural law of supply and demand in maintaining a proper equilibrium. It may be doubted, indeed, whether we require at any time more phosphorus for brain- and nerve-tissue than can be found in such food as contains digestible phosphatic salts. The natural demand for food grows out of healthy tissue-change. An appetite to be healthy should commence in processes outside of the stomach.

Food may also be introduced into the stomach in an undigestible form {445} from defects of cookery. The process of cooking food produces certain well-known chemical changes in alimentary substances which render them more digestible than in the uncooked state. By the use of fire in cooking his food new sources of strength have been opened up to man which have doubtless contributed immeasurably to his physical development, and has led to his classification as the cooking animal. With regard to most articles the practice of cooking his food beforehand is wellnigh universal; and especially is this the case with all farinaceous articles of food. The gluten of wheat is almost indigestible in the uncooked state. By the process of cooking the starchy matter of the grain is not only liberated from its protecting envelopes, but it is converted into a gelatinous condition which readily yields to the diastasic ferments. Roberts, in his lectures on the Digestive Ferments, points out the fact that when men under the stress of circumstances have been compelled to subsist on uncooked grains of the cereals, they soon fell into a state of inanition and disease.

Animal diet is also more easily digested in the cooked than in the raw state. The advantage consists chiefly in the effects of heat on the connective tissue and in the separation of the muscular fibre. In this respect cooking aids the digestive process. The gastric juice cannot get at the albumen-containing fibrillæ until the connective tissue is broken up, removed, or dissolved. Hot water softens and removes this connective tissue. Hence raw meat is less easily digestible. Carnivorous animals, that get their food at long intervals, digest it slowly. By cutting, bruising, and scraping meat we to a certain extent imitate the process of cooking. In many cases, indeed, ill-nourished children and dyspeptics digest raw beef thus comminuted better than cooked, and it is a matter of observation that steamed and underdone roast meats are more digestible than when submitted to greater heat.

Some interesting observations have been made by Roberts on the effects of the digestive ferments on cooked and uncooked albuminoids. He employed in his experiments a solution of egg albumen made by mixing white of egg with nine times its volume of water. "This solution," says Roberts, "when boiled in the water-bath does not coagulate nor sensibly change its appearance, but its behavior with the digestive ferments is completely altered. In the raw state this solution is attacked very slowly by pepsin and acid, and pancreatic extract has no effect on it; but after being cooked in the water-bath the albumen is rapidly and entirely digested by artificial gastric juice, and a moiety of it is rapidly digested by pancreatic extract."

It is a mistake, however, to suppose that cooking is equally necessary for all kinds of albuminoids. The oyster, at least, is quite exceptional, for it contains a digestive ferment--the hepatic diastase--which is wholly destroyed by cooking. Milk may be indifferently used either in the cooked or uncooked state, and fruits, which owe their value chiefly to sugar, are not altered by cooking.

The object in introducing here these remarks on cooking food is to show that it forms an important integral part of the work of digestion, and has a direct bearing on the management of all forms of dyspepsia.

Haste in eating, with imperfect mastication, is a common cause of indigestion in this country. Mastication is the first step in the digestive {446} process. It is important, therefore, that we have good teeth and that we take time to thoroughly masticate our food, for by so doing we prepare it for being acted upon by the juices of the stomach. Time is also necessary in order that the salivary secretion may be incorporated with the alimentary substances. By the salivary diastase starch is converted into sugar and albuminoids are prepared for the action of the gastric juice. If these changes take place imperfectly, the stomach can scarcely regain in gastric digestion what was lost in imperfect mastication and insalivation. Haste in eating is one of the American vices. It grows out of the temperament of our people. We are jealous of lost time, and unfortunately this time is too often taken from the stomach. We bolt our food with unseemly haste, and pay the penalty in ruined stomachs. Many cases of indigestion are greatly relieved, if not permanently cured, by simply doubling or quadrupling the time occupied in eating.

Irregularity in the intervals between meals, such as taking one meal only in twenty-four hours or taking food before the preceding supply has been digested, is another fruitful source of indigestion. The digestive process, in the natural order of change, is confused; changes which should take place are delayed; and the results are such as arise from excessive eating. Moreover, the stomach lacks the rest so essential to digestion. The necessary interval, however, between meals varies with the nature of the food taken. "Between the extremes of the carnivoræ," says Ewald, "which feed once in twenty-four hours, and the herbivoræ, which never have done with the business of feeding, man holds a middle place, but not without permitting the recognition in the course of his life of a sort of transition from the herbivora to the carnivora. Infants should have the breast during the first three weeks as often as they wake; after that every two hours to the third month; then up to dentition every three hours; and later there should be five meals in twenty-four hours." But to this general statement there are, of course, many exceptions. Under certain pathological conditions food should be taken in small quantities at short intervals. This is especially the case in chronic gastric catarrh and in feeble digestion of nervous subjects. Such patients are not unfrequently improved by becoming again infants or herbivoræ. By the use of an exclusive milk diet or peptonized milk gruels, given in small quantities at comparatively short intervals of time, the stomach may be so accommodated that it will digest without discomfort a large amount of nourishment within a given time. To S. Weir Mitchell of Philadelphia we are indebted for some valuable observations bearing upon this point of forced alimentation.

To the causes of indigestion already alluded to may be added the habit of spirit-drinking, especially the habit of taking alcohol undiluted on an empty stomach, which rarely fails after a time to engender dyspeptic symptoms. It is a prominent factor in the production of chronic gastric catarrh--a condition more frequently present in painful indigestion than any that have been named. It is one of the most common diseases met with in practice. Indeed, all causes already alluded to involve, sooner or later, if they are constantly operative, irritative and catarrhal conditions of the mucous membrane of the stomach, so that we find it difficult at times--indeed impossible--to separate purely functional from subacute inflammatory forms of dyspepsia. Practically, we simply study the {447} subject in the relative degrees of prominence of the one condition or the other.

But, in a still more comprehensive sense, indigestion is caused by disturbance of organs directly associated with the stomach in the digestive process. All organs closely associated with each other in their physiological functions are apt to become associated in morbid action. The clinical recognition of this is a matter of great importance in the management of gastric affections. And first in the order of importance in such association is the liver. So closely, indeed, are the liver and stomach functionally associated in the process of primary assimilation that they may be considered parts of the same great digestive apparatus. Hence disturbance of the liver--either in the formation of glycogen, the destruction of albuminoid matter, or the secretion of bile--is immediately communicated to the stomach. It may be difficult to say which of these separate and distinct functions of the liver is most at fault; that can only be a matter of physiological inference. In the one case, for instance, the dyspeptic may be fairly well nourished, yet his elimination may be bad. In the other there is no failure of the destructive and excreting functions, but those concerned in the assimilation of fat and peptones are disordered, so that the patient is not well nourished, so far as the fatty element is concerned. This is the more common form, and a form not unfrequently associated with pulmonary consumption. The liver finally becomes fatty--a condition usually found associated with the constitutional forms of phthisis.

The pancreas is also closely associated with the stomach, and its secretion is of essential value in the digestive process. It is to be regretted that our precise knowledge of its diseases is in such striking contrast with its importance in the animal economy, and yet it can scarcely be doubted that in dyspeptic symptoms associated with failure of digestion of starchy, albuminous, and fatty elements of food there is disorder of the secretion of the pancreas. Hence in the treatment of the early stages of pulmonary consumption and other disorders associated with deficient digestion and assimilation of fatty substances the importance of directing our attention to the condition of the liver and pancreas, as well as to the stomach.

That morbid states of the intestinal track occupy a prominent place in the etiology of dyspepsia is also a well-recognized clinical fact. Indeed, constipation of the bowels is an almost universal accompaniment of deranged digestion, and when persistent for years it is apt to lead to the most disastrous consequences. These are mainly in the direction of lessened elimination from the intestinal glandulæ. The general symptomatology of deficient excretion from these glandulæ is closely analogous to the same condition of the liver: there is impairment of the general health; the clear florid complexion disappears; the patient becomes of a greenish or sallow hue; the blood is altered in quality; fatigue is experienced after the slightest exertion; the nights are restless; and there is great tendency to mental despondency. Moreover, constipation often precedes the gastric symptoms. The diminished muscular activity of the intestinal track extends to the stomach; its movements are diminished; food is not properly mixed with the gastric juice, and by being too long retained in the stomach in a comparatively undigested state acetous fermentation in the saccharine and starchy articles of diet is set {448} up, acid eructations and a sour taste in the mouth being commonly complained of. Dyspepsia associated with this condition of the intestinal track cannot be relieved until the constipation is relieved, and by overcoming the constipation the dyspeptic symptoms often disappear.

Mention has been made of the baneful influence of certain mental states in the production of dyspeptic symptoms. But there are forms of indigestion due to local nervous disturbance existing elsewhere than in the nerve-centres. This was ascribed by the older writers to what they termed consensus nervorum, or sympathy, by which "the operation of a stimulus is not limited to the nerves immediately irritated, but is extended to distant parts in known or unknown connection with the irritated nerves." An intimate acquaintance with this law of sympathy is of the utmost importance in the study of the functional forms of dyspepsia, for no other organ of the body is subjected to such a wide range of reflected nervous disturbance as the stomach. Morbid sympathetic impressions are transmitted mainly through branches of the vaso-motor nerve of the semilunar ganglia of the abdomen, and from the pneumogastric to the stomach. Thus, a pregnant uterus not unfrequently produces very troublesome vomiting; some females suffer from nausea and indigestion during each menstrual period; and the more chronic forms of pelvic irritation, such as a flexed uterus, and endometritis, cervicitis, or tender ovary, may be the continuous exciting cause of most troublesome forms of nervous dyspepsia. There is also close sympathy of the stomach with the lungs and heart through the distribution of the pneumogastric. So also may fixed points of irritation in any part of the nervous system be reflexly transmitted to the stomach, giving rise to most pronounced symptoms of indigestion. And it is evident that in all such cases but little can be accomplished in the way of relieving the dyspeptic symptoms until the cause upon which they depend is removed. The treatment must have reference mainly to the removal of such cause.

Lastly, all the causes mentioned finally concur in producing irregularities of the mechanism of digestion; and this may be done by disturbing either the muscular movements of the stomach or in suspending or perverting the gastric solvents, or in these two conditions combined.

SYMPTOMS.--1st. Referable to the Stomach.--The symptoms which attend and indicate the presence of functional dyspepsia are such as accompany in a greater or less degree almost all cases of chronic gastritis. Clinically, so far as the direct gastric symptoms are concerned, it is difficult to separate them. The more prominent of the local symptoms are--a sense of fulness and distension after meals, discomfort during the digestive process, derangement of appetite, acid eructations, flatulence, regurgitations of food, and sometimes nausea and vomiting. There is seldom severe pain; the sensation is rather that of uneasiness. Exceptionally, however, there may be pain, which radiates from the stomach to the shoulders, and may pass down the left arm so as to simulate angina pectoris. But it may be readily distinguished from that complaint by coming on after food, and not after exertion. In other cases a sense of constriction may be accompanied by dyspnoea, arising from impeded movements of the diaphragm from being pushed upward by the distended stomach, or there may be heartburn, with an ill-defined sense of burning felt in the epigastrium; {449} but thirst, so frequently present in chronic gastritis, is, as a rule, absent in functional dyspepsia. These symptoms are manifested in varying degrees of prominence in individual cases, and some of them are rarely found present. Thus, nausea and vomiting are not characteristic features of the chronic forms of functional dyspepsia, and as a rule epigastric tenderness is entirely absent. In markedly hysterical subjects or in persons whose nervous system has been unduly excited by alcohol there may be shrinking from the slightest touch upon pressure; but in these cases the tenderness is not confined to the stomach, nor is it increased by deep pressure. In some cases there is an unnatural craving for food--a symptom rarely if ever observed in structural lesions of the stomach--and now and then it happens that the appetite becomes depraved, especially with hysterical patients. They crave indigestible and unnatural substances, such as earth, chalk, and substances wholly devoid of alimentary properties. Impairment of appetite, however, is the more common feature of this form of indigestion.

Flatulence and eructations are generally complained of, the flatulence being accompanied by a painful sense of fulness, affecting in equal degree the stomach and small intestines. It is derived principally from putrefactive or fermentative changes of the ingesta, which are imperfectly elaborated in the stomach. The gases consist of carbonic acid, sulphuretted hydrogen, hydrogen, nitrogen, and the hydrocarbons, the butyric and acetic fermentations furnishing the hydrogen and carbonic acid gas. In addition to these marsh gas is formed by a special fermentation, the basis of which exists in the cellulose taken with vegetable food. In excessive meteorism from paralysis of the intestines the gas is principally nitrogen; the marsh-gas fermentation results from the ingestion of certain easily-fermentable vegetables, such as cabbage, cauliflower, etc.

In a certain proportion of cases regurgitation occurs from the stomach. The liquor regurgitated may be intensely acid from the presence of some of the fatty acids, probably butyric, lactic, or acetic. Exceptionally, it may be insipid or brackish, constituting what is known as pyrosis, or water-brash. The fluid is usually tasteless and without smell, and in reaction it is neutral to test-paper. It contains sulphocyanuret of potassium, and it has been supposed therefore to be only saliva. The quantity thrown up may vary from a spoonful to a pint or more. It affects females more than males, and especially those who subsist upon coarse and indigestible food. It is best treated by astringents--such as kino, krameria, logwood, or tannin--administered in the intervals between digestion, so that they may act directly on the mucous membrane. The oxide and nitrate of silver are thought by some to be superior to the vegetable astringents.

Cardialgia is a painful condition of the stomach, usually referred to its cardiac orifice, and is popularly known as heartburn. It is met with in both functional and organic disease of the stomach. It is very constantly present in chronic catarrhal gastritis, and evidently depends upon the presence of an acid, for it is usually promptly relieved by alkalies, such as chalk, magnesia, soda, or alkaline saline waters. Food containing much fat, starch, or sugar should be avoided.

Nausea and vomiting are only occasional symptoms of functional dyspepsia. When vomiting does occur it may take place at different times {450} and with varying degrees of severity, differing in this respect from the nausea and vomiting of subacute gastritis, which takes place, if at all, soon after the ingestion of food. The time of vomiting and the character of the matter ejected are liable to great variation in functional dyspepsia. It may be the result of direct irritation of morbidly sensitive gastric nerves, or it may be a reflex phenomenon; it may follow soon after the ingestion of food, or it may come on when the stomach is empty; the material vomited may be simply food but little altered or an alkaline ropy mucus; it may consist in the acid juices of the stomach or in a neutral watery fluid; or the ingesta may have undergone fermentative and putrefactive changes from either insufficient amount of the gastric solvent or from narrowing (constriction) of the pyloric extremity, in which case the yeast fungus (Torula cerevisiæ) or the Sarcina ventriculi may be found in great abundance in the vomited matter. Vomiting of this kind usually occurs some time after eating. The gastric juice itself checks putrefaction; so also does the admixture of bile. In the absence of these natural antiseptics fermentation takes place. But it would be erroneous to suppose that the fermentative dyspepsia is the primary disease; it is a symptom which can be permanently corrected only by correcting the condition upon which it depends.

Among the most noticeable of the phenomena referable to other organs than the stomach are those connected with the liver and the alimentary canal. The tongue in dyspeptic troubles varies much in character. In reflex sympathetic indigestion it is not unfrequently clean; in hepatic dyspepsia it is generally thickly coated with a white or yellow fur. The symptoms are such as pertain more especially to chronic gastro-duodenal catarrh, such as nausea, epigastric oppression, furred tongue, heartburn, acid eructations, flatulent distension of the stomach and bowels, unpleasant taste in the mouth, offensive breath, loaded urine, frontal headache, irritability, and hypochondriasis.

Constipation, as we have seen, is an almost universal accompaniment of functional dyspepsia, sustaining to it not unfrequently a causative relation. It is undoubtedly one of the most common of the slighter ailments of civilized life, and exerts a wide influence in deranging the general health. "It is quite extraordinary how many different derangements of health may result from imperfect action or a torpid state of the secreting and expelling structures of the large bowel. There may be violent and persistent nerve-pains, referred to the back, or hip, or groin, and certain other symptoms which lead pessimist practitioners, excelling in the discovery of neuroses, to diagnose structural changes in some part of the spinal cord or the antecedent state which is supposed to lead to them" (Beale). Pains in the loins and thighs, violent lumbar pain, and certain remediable forms of sciatica are sometimes due to imperfect excretion of the lower part of the alimentary canal. And it is even possible that a condition of hypochondria bordering on insanity may be brought about by long-continued defective action of the bowels. In exceptional cases of dyspepsia diarrhoea may be present. This is more frequently the case when indigestion is associated with a congested state of the liver, in which case the symptom should be regarded as curative. Excessive irritability of the muscular walls of the stomach, superadded to weak digestion, may also be followed by lienteric forms of diarrhoea. Undigested {451} food hastily finds its way into the intestinal track, and not unfrequently appears in the fecal evacuations.

Functional derangements of the stomach are often accompanied by pale urate deposits in the urine. It may contain an excess of phosphates, and in microscopical examination crystals of the oxalate of lime are frequently found, constituting a special affection described by Golding-Bird as oxaluria. He associated it with irritative dyspepsia, hypochondriasis, and exhaustion of nerve-power. This form of dyspepsia is best managed by the mineral, vegetable, and acid tonics, to which may be added small doses of nux vomica, with the usual adjuvants of good air and exercise, freedom from anxiety and care, cold sea-water baths, and well-selected, generous animal diet.

Another form of dyspepsia is sometimes associated with a peculiar form of dizziness--gastric vertigo. German writers speak of it as abdominal dizziness, and Trousseau calls it vertigo stomicale. It is usually an acute symptom, begins without any premonition, and is liable to be confounded with disease of the brain. It sometimes occurs soon after a meal, but more often when the stomach is empty (Trousseau). It perhaps, in a majority of cases, depends upon dyspepsia, but it has to be differentiated from organic brain disease, from cerebral anæmia, cerebral hyperæmia, the slighter forms of epilepsy, Minière's disease, and general nervous exhaustion and depression. But in many cases it will be found that treatment directed against the dyspepsia cures the vertigo.

Dyspeptic patients are also liable to skin diseases, and especially is this observed in the gastro-duodenal forms of indigestion. Disorders of the skin, such as urticaria, erythema, lichen, eczema, and other allied conditions, are well-recognized external indications at times of disordered conditions of the gastro-intestinal mucous membrane. Thus, it is a matter of common observation that the gastric symptoms increase when the eruption on the surface disappears.

The general influence of the nervous system over the function of digestion is perhaps the most remarkable feature of the disease, so that disturbed innervation becomes conspicuous in its symptomatology. The phenomenon varies in individual cases. Languor, drowsiness after taking food, depression of spirits, irritability, hypochondriasis, sleeplessness, palpitation, dry cough, dyspnoea, are all of common occurrence; and the mental disturbance--the anxiety, gloom, and sadness--is to many dyspeptics more distressing than absolute pain.

It is impossible, however, to present, in this connection, a complete clinical history of functional dyspepsia, for the reason that it is associated with so many separate and distinct affections, the dyspepsia itself being symptomatic of these affections.

PATHOLOGY.--But little is known of the pathology of the purely functional forms of dyspepsia beyond what is expressed by the terms atony and asthenia. These express simply certain states of the system with which atonic dyspepsia is so frequently found associated. Pathological anatomy has shown, however, that some cases are dependent upon, or associated with, certain appreciable alterations of the stomach, such as atrophy of the mucous membrane or fatty degeneration of its walls; and not unfrequently it is the seat of the so-called amyloid or lardaceous degeneration, although this albuminoid infiltration or cloudy {452} swelling is more frequently the accompaniment of chronic inflammatory process. But Jones and Fenwick have shown that these conditions may occur independently of inflammation. However, upon this point we are compelled to speak with caution. The boundary-line between functional and structural diseases is not always clearly defined. Functional and structural troubles of the stomach are certainly very intimately associated. Moreover, symptoms of purely functional dyspepsia are so frequently associated with the subacute forms of gastritis that the pathology of the disease becomes, from necessity, doubtful and complex. It can only be studied in connection with certain states or conditions of which functional derangement of the stomach is a symptom readily recognized during life. In the light of more advanced physiological and pathological researches we may expect the limits of purely functional dyspepsia to be much restricted.

DIAGNOSIS.--The diagnosis of atonic dyspepsia must have special reference to its etiology. It is usually a chronic disease, and has to be discriminated from subacute or chronic inflammation of the stomach. This is the more difficult because many symptoms exist in common in both varieties of indigestion. But in functional or atonic dyspepsia the symptoms are not so continuous; there is less epigastric uneasiness, less tenderness, less nausea or loathing of food, less thirst, and less acidity and heartburn, less emaciation, less cerebral and nervous disturbance, and the constitutional symptoms are also less severe. The tongue, as a rule, is not so thickly coated, is not so red or broad and flabby, the papillæ are less marked, the breath less offensive, and the urine, instead of showing a condition of lithæmia, is not unfrequently pale and sometimes neutral, depositing oxalates and phosphates, especially in feeble, broken-down conditions of the nervous system.

With other painful affections of the stomach, such as ulcer and cancer, it is not likely to be confounded, especially when in these affections pain, vomiting, and hæmatemesis are present.

TREATMENT.--The first and leading indication is to remove, as far as possible, all causes of the disease, and this requires patient research and much diagnostic skill. Suggestive hints of treatment may be found in connection with the discussion of the varied etiology of the disease. We can, in conclusion, only allude to the matter in a very general way. Special cases must furnish their own indications of treatment.

In many cases a condition of nervous asthenia will be found prominently present. A leading indication, therefore, irrespective of the special determining cause, is to improve the general health of the patient; and this is accomplished by all means which invigorate the system generally. And first in the order of importance are diet and regimen. It is evident that if a patient eat too much or too often, or if he eat indigestible or unwholesome food, or lead an indolent and luxurious life, nothing can be accomplished by way of drugs in the relief of the disease. Excessive alimentation is, as we have seen, a most prolific source of the disease. Tempted to excess by great variety and by the ingenuity of culinary refinements, the stomach is burdened beyond its capacity of digestion and beyond the actual requirements of the system; and especially is this the case with those who live sedentary, indoor lives. In all such cases it is absolutely essential that the digestive organs have rest. {453} Better even in cases of doubt reduce the diet for a time below the actual wants of the system until waste products are thoroughly removed and appetite is revived. The benefit derived in some instances from the protracted use of purgative mineral waters is largely attributable to the restricted regimen enforced and to the washing out of the system the waste products.

On the other hand, too great or too protracted abstemiousness may equally impair the digestive process. In ordinary forms of atonic dyspepsia we should seek rather, by appropriate treatment, to raise the digestive capacity to the level of digesting good, healthy, nutritious food, than to reduce the food to the low standard of feeble digestion. But it is a mistake to suppose that this can be accomplished by simply forcing food upon a stomach that lacks capacity of digestion.

As to the kind of diet, no precise rule is suited to all cases. Within certain limits individual experience must be consulted. But these experiences are not always reliable. Dyspeptic patients, more than any others, are apt to have fancies. Certain general rules, therefore, should be insisted upon. The food should be wholesome and digestible; it should be well cooked, well masticated, and taken at regular and not too long intervals. The intervals of time between meals depend upon circumstances already referred to. In some cases small quantities of easily-digested food should be taken at short intervals. In cases of feeble digestion of nervous subjects milk diluted in Seltzer water, or milk and lime-water, or peptonized milk, may be taken in liberal quantities at comparatively short intervals of time. Sometimes isinglass, arrowroot, or ground rice may be advantageously combined with the milk, to which tender, undone meats may be added.

Peptonized Food.--Recently the attention of the profession has been attracted to artificially digested food. The essential acts of digestion are known to be chemical transmutations. Albuminoid substances are changed into peptones and starchy matters are changed into dextrin and sugar. To Roberts, in his excellent lectures delivered in the Lumleian course before the Royal College of Physicians of London in 1880, we are indebted for valuable information on the digestive ferments and in the preparation and use of artificially-digested food; and from these lectures we shall derive most of the information we possess at present. It has been demonstrated that an extract of the stomach or pancreas, in water, has to a certain extent the same powers as the natural secretions of these organs. Hence, says Roberts, it is possible for us to subject articles of food beforehand to complete or partial digestion. Heat approximatively accomplishes the same thing. In the practice of cookery we have, as it were, a foreshadowing of this art of artificial digestion. Heat and digestive ferments alike aid gastric digestion. In case of the lower animals the whole process has to be accomplished by the labor of their own digestive organs.

Artificially digested food may be prepared in two ways--either by following the gastric method with pepsin and hydrochloric acid, or by following the intestinal method and using extract of pancreas. Both of these plans have had special advocates. Roberts claims that the latter yields by far the better results. "The pancreas not only acts upon albuminous substances, but also upon starch. Pepsin, on the other hand, is {454} quite inert in regard to starch. Moreover, the products of artificial digestion with pepsin and acid are much less agreeable to the taste and smell than those produced by pancreatic extract." The pancreas of the pig, according to Roberts, yields the most active preparation, but the pancreas of the ox or the sheep may be employed. The pancreas of the calf is not active on starchy materials. A very active extract of pancreas is now prepared, and is easily obtainable, with directions for making peptonized milk, milk gruel, milk punch, soups, jellies, blanc-manges, beef-tea, enemata, etc. It is important to remember that peptonized foods do not keep well, especially in warm weather. If a quantity sufficient for twenty-four hours be prepared at any one time, the quantity which remains over twelve hours should be reboiled before using. Food thus peptonized is indicated in feeble conditions of digestion and when the derangement of digestion results from causes pertaining to the condition of the stomach itself--i.e. catarrhal forms of dyspepsia.

As a rule, the food should be such as will require the least possible exertion on the part of the stomach. Raw vegetables should be forbidden; pastries, fried dishes, and all rich and greasy compounds should be eschewed; and whatever food be taken should be eaten slowly and well masticated. Many patients digest animal better than vegetable food. Tender brown meats, plainly but well cooked, such as beef, mutton, and game, are to be preferred. Lightly-cooked mutton is more digestible than beef, pork, or lamb, and roast beef is more digestible than boiled. Pork and veal and salted and preserved meats are comparatively indigestible. Bread should never be eaten hot or fresh--better be slightly stale--and bread made from the whole meal is better than that made from the mere starchy part of the grain. Milk and eggs and well-boiled rice are of special value.

But to all these general dietetic rules there may be exceptions growing out of the peculiarities of individual cases. These should be carefully studied. The aged, for obvious reasons, require less food than the young; the middle-aged, inclined to obesity and troubled with feeble digestion, should avoid potatoes, sweets, and fatty substances and spirituous liquors; persons suffering from functional derangements of the liver should be put, for a time, on the most restricted regimen; while, on the contrary, the illy fed and badly-nourished require the most nutritious food that can be digested with comfort to the patient.

The general regimen should be tonic and invigorating. The patient should have the benefit of the best possible hygiene. Under this head may be mentioned suitable clothing, fresh air, moderate exercise, sunlight, baths, rest, regular hours, and the abandonment of all bad habits. No single measure has such marked influence on the digestive powers of the stomach as systematic, well-regulated muscular exercise in the open air, and especially if the exercise be accompanied by a cheerful mental state. For this reason outdoor sports are of benefit. Hunting, fishing, boating, are known to excite the keenest appetite for food, and the stomach will digest substances that would distress it under other circumstances. Exhaustion, however, is to be carefully avoided. Horseback exercise is a remedy of much value, especially in the hepatic forms of indigestion.

The mental and moral treatment of the purely functional forms of {455} indigestion are amongst the most powerful means we possess. As an etiological factor certain morbid mental states rank first, as we have seen, in the order of importance. Grief, despondency, and despair are effectual barriers to digestion, and in a less degree mental worry seriously interferes with the process. It is a matter of prime importance, therefore, that the patient's mind be pleasantly occupied, that he should be free from all care and mental worry, and that he especially be kept from dwelling, if possible, upon his own bodily ailments. This is often best accomplished by travel, when practicable, in foreign countries, where everything will be novel and new and calculated to lead him away from himself. Get him to travel, says Watson, in search of his health, and the chances are in favor of his finding it. We have the authority of Sir James Johnson also for saying that no case of purely functional dyspepsia can resist a pedestrian tour over the Alps.

We come now to discuss the medical treatment of dyspepsia, which, though not unimportant, is subordinate to the general hygienic measures already referred to. General hints of treatment have been made in connection with special causes mentioned in the text. We seek, in a general way, by therapeutic measures--

1st. To stimulate the secreting and muscular coats of the stomach;

2d. To supply materials in which it is supposed the gastric juice is defective;

3d. To lessen abnormal irritability;

4th. To combat special symptoms or conditions which may hinder the digestive process.

To meet these indications innumerable remedies have been recommended, but they are of benefit only as they counteract the conditions upon which the dyspepsia depends. For loss of appetite, if there are no contraindications to their use, the vegetable bitters are often useful, such as quassia, gentian, and columbo. Of these columbo is the simplest of its class, but none more generally useful than mistura gentianæ with soda. The Hydrastis canadensis has also peculiar claims as a bitter stomachic. It, perhaps more than any of the bitters, promotes gastric secretion in feeble digestion, and has at the same time peculiar salutary effects on the enfeebled condition of the chronically inflamed gastric mucous membrane. It is supposed also to have a stimulating effect on the pancreatic secretion. It may be given in the form of a fluid extract combined with glycerin and small doses of nux vomica.

Among the specific stimulating nerve-tonics, nux vomica, or its alkaloid, strychnia, deserves special mention. In small tonic doses it is specially indicated in conditions of general nervous prostration associated with a tendency to hypochondriasis. In such cases we frequently observe pale urine, containing an excess of the phosphates. The mineral acids are valuable additions to the bitter tonics in all broken-down conditions of the nervous system. In administering nux vomica care should be taken as to limitation of time and dose. The excessive or prolonged use of the drug is apt to produce serious general nervous disturbance, the secondary condition being often the opposite to that for which it was prescribed. Temporary saccharine diabetes is not unfrequently one of the results.

In atony of the mucous membrane, with morbid sensibility and slow {456} digestion, ipecacuanha is a remedy of much value. It was first brought into prominent notice in connection with gastric affections by Budd, since which time it has been more or less used by the profession. In torpid, slow digestion, with depraved or lessened gastric secretion, it is of undoubted value. It should be given on an empty stomach at least half an hour before meals. The dose should be short of producing nausea. We may commence with two to four drops of the tincture or wine of ipecac, and gradually increase until we find the point of tolerance; or it may be given in the form of pill in doses of a quarter or a half grain before meals, combining it with rhubarb in three- or four-grain doses. Ipecacuanha may be administered at the same time we are giving the mineral acids, or mineral acids with pepsin.

Adjuvants to Digestion.--In atony of the stomach the gastric mucous membrane responds feebly to the stimulus of food. There is failure in both muscular movement and gastric secretion, with slowness of digestion as a result. To meet this condition we seek to increase the digestive power by the addition of certain principles natural to the digestive process--viz. the mineral acids, pepsin, and pancreatin. Of these acids, the hydrochloric should be preferred, because it is the natural acid of the gastric juice. Lactic, nitro-hydrochloric, and phosphoric acids have also been used with benefit. There can be no doubt of the efficacy of either of these preparations. They are best given when the stomach is empty, so that they may directly act on the relaxed atonic mucous membrane. Half an hour before or two hours after a meal is the best time for their administration, and to be of benefit they should be administered for a length of time. From fifteen to twenty minims of the dilute hydrochloric or nitro-hydrochloric acid may be given in some bitter tincture or infusion for months. An elegant preparation may be made by adding the acid to tincture of orange-peel and syrup of lemon. Aromatic tincture, tincture of ginger, or glycerin may be added in some cases. It is important that remedies administered in gastric affections should be made pleasant as possible to the patient.

Metallic preparations are of use in some cases. If for any reason they are preferred, the perchloride of iron is one of the very best preparations. Arsenic and zinc may also be tried in small doses.

Pepsin and its Uses.--Of the efficacy of pepsin as an artificial substitute for the normal solvent of the food adverse opinions have been expressed, but in spite of the most critical scepticism as to its action its use since first introduced into medicine has steadily increased. It has been shown to be the natural constituent of the gastric juice and glands, and as a natural ferment, when combined with hydrochloric acid, it constitutes the most important solvent of the nitrogenous portions of our diet (Habershon). There is a vast number of different preparations of pepsin in the market, and some of them are doubtless of little value. We ought to be quite sure that the article is what it purports to be. The pepsina porce is the best preparation, one grain of which, says Beale, ought to thoroughly digest one hundred grains of boiled white of egg in three or four hours at a temperature of 100° F. His test as to the value of pepsin is as follows: "One hundred grains of hard-boiled white of egg, cut into thin slices, may be placed in a wide-mouthed bottle or flask with one ounce of water and twenty drops of dilute hydrochloric acid. One {457} grain of pepsin powder is to be added, and the mixture placed before a fire at a temperature of about 100° F. The flask is to be shaken from time to time. In about an hour the white of egg begins to look transparent at the edges, and in about four hours it will be completely dissolved if the pepsin is good." In cases of feeble digestion from deficiency of gastric juice pepsin is a valuable adjuvant to the digestive power, and may be given with advantage in connection with the mineral acids or with ipecacuanha or capsicum before meals.

Special Remedies.--There are certain symptoms characteristic of the different forms and complications of dyspepsia that require special remedies. Bismuth is often useful. It is especially indicated where there is a morbid painful condition of the gastric nerves. The subnitrate or carbonate of bismuth may be given in ten- or twenty-grain doses, suspended in water by means of mucilage of acacia, and flavored with ginger or peppermint. It should always be given on an empty stomach. Other elegant preparations supposed to be improvements upon these have been recommended, and may be tried.

In cases of anæmia, if there are no contraindications, iron may be tried. If digested and assimilated, it improves the blood, and this is often the first step in the direction of restoring functional activity. Of the preparations of iron, none is perhaps superior to the perchloride. The saccharo-carbonate and the ammonio-citrate are also valuable and unirritating salts of iron, and may be given with other tonics. Ferruginous mineral waters slightly charged with carbonic acid are well tolerated in small doses. The free dilution favors the action, and is frequently more acceptable to the stomach than the more concentrated forms. From one-half to one glassful may be taken at a time; and the use of iron in this form may be preceded or accompanied by the administration of small doses of quinia and of the bitter tonics. But it is a mistake to commence the treatment by the indiscriminate use of iron, quinine, and nerve-tonics. The contraindications to the use of iron are irritable and inflammatory states of the mucous membrane, or dyspepsia associated with deranged conditions of secretion, as manifested by dirty tongue and loaded urine.

When the nervous system is prominently at fault, nux vomica, arsenic, and the nitrate and oxide of silver often prove to be valuable remedies. Here also benefit may be derived from the lighter ferruginous preparations; indeed, few combinations have greater influence over the nervous system than the joint action of arsenic and iron. Much benefit may also be derived, in special cases, from methodical hydro-therapeutic treatment. If judiciously used it strengthens the nervous system, stimulates the organic functions, and increases the power of vital resistance. And in some cases of nervous dyspepsia electricity gives good results. In all cases of nervous prostration as much wholesome food should be taken as the stomach can easily digest.

In hepatic forms of indigestion there is no substitute for an occasional mercurial cathartic, for, notwithstanding adverse criticism, clinical experience has taught the great value of this drug upon the upper portion of the intestinal track. The mode of operation may be doubtful, but the result is unquestionable. In functional disturbance of the liver or morbid conditions of the upper portion of the intestinal track, as indicated {458} by the loaded tongue, sallow complexion, want of appetite, and lithæmia, no remedy will give so much relief as a few broken doses of calomel, followed by a saline aperient; or eight or ten grains of blue mass, with a grain of ipecacuanha, may be administered at bedtime, followed by a saline draught in the morning. After the bowels are thoroughly unloaded by a mercurial, great advantage may be derived from a systematic course of the aperient mineral waters--the Friedrichshall, the Hunyadi, Carlsbad, or some of the mineral waters of our own country. The hepatic form of indigestion cannot be relieved until we relieve the congested hepatic portal system, and this is best accomplished by the general line of treatment here indicated. The simple vegetable bitters, with or without alkalies, may be used at the same time or subsequent to this treatment; but they are often worse than useless until we secure freedom of abdominal circulation. The diet should be light and nourishing, and the patient should spend most of his time out of doors. Horseback exercise is peculiarly advantageous.

But in many cases of the more chronic forms of dyspepsia the colon is as atonic as the stomach, and therefore the bowels require special attention. In colonic dyspepsia all active purgation should be avoided, and salines, such as sulphate of magnesia, the Hunyadi and other saline mineral waters, should be specially prohibited. The most useful aperients in such cases are rhubarb, aloes, senna, colocynth, or podophyllin. Few laxatives answer a better purpose than the ordinary compound rhubarb pill. It may be improved, in special cases, by combining with it extract of nux vomica or belladonna. When there is no affection of the rectum to forbid its use, the watery extract of aloes answers very well, and, unlike many cathartic substances, the dose need not be increased, nor does it disturb the digestive process. It may be given in one-sixth of a grain up to a grain or more, and its purgative action may be improved by being reduced to a state of very minute division and combining with it small doses of belladonna. Belladonna itself is a useful remedy. According to the observations of Harley, it "tones and tightens the longitudinal fibre, while it relaxes the circular;" and long before this theory of its action was suggested, Trousseau called attention to its singular efficacy in producing easy and natural evacuations from the bowels. It is important to observe its mode of use. It should be given in sixth of a grain doses of the extract in the morning a half hour or hour before breakfast. Its efficacy may be increased by combining with it small doses of the watery extract of aloes. In colicky conditions of the bowels two- or three-drop doses of tincture of colocynth sometimes act wonderfully well. In obstinate constipation the free use of diluents at the termination of digestion is often attended with excellent results. But the hygienic and dietetic treatment of constipation is even more important than the medicinal, such as outdoor exercise, the cold bath, rubbing, kneading the bowels, and the use of bread made of whole meal, oatmeal, and an abundant supply of fresh vegetables and fruits.

Nausea and vomiting, occasional symptoms of functional dyspepsia, may be relieved by various agents, such as effervescing draughts, lime-water, oxalate of cerium, hydrocyanic acid, creasote, ice, and alkalies.

When vomiting is dependent on fermentation or putrid action of the contents of the stomach with development of sarcinæ, it may be checked {459} by carbolic acid or by creasote, or by the sulphite of soda or sulphurous acid; and in irritable conditions of the stomach bismuth is a valuable remedy. It may be given with alkalies or with finely-triturated animal charcoal.

Gastric pain needs treatment appropriate to the circumstances under which it arises. Sometimes it is relieved by regulating the ingesta or the intervals at which it is taken; sometimes by warm carminative stimulants or by chloric ether, ginger, or brandy. If the pain is more constant, approaching a condition of gastralgia, hydrocyanic acid and bismuth are more effective remedies. But it cannot be too strongly stated, in conclusion, that in the management of the atonic forms of dyspepsia hygienic treatment is of prime importance. The hopeful future of medicine lies in the direction of promoting healthy nutrition, and this is best accomplished by the careful adaptation of food and exercise and modes of living to individual cases of disease.

Gastralgia (Gastrodynia, Cardialgia, Spasm of the Stomach).

Under the head of neuroses of the stomach have been variously described the conditions indicated in the heading of this section; and a certain amount of confusion has arisen in the use of these terms from the fact that they represent subjective sensations common alike to organic and functional forms of indigestion: pain, for instance, is felt in gastritis, cancer of the stomach, and ulcer of the stomach. Indeed, it rarely occurs independently of some disorder of digestion or structural lesion of the stomach.

By gastralgia, considered as a distinct affection, however, we mean a purely neuralgic condition of the sensory fibres of the stomach, excluding inflammatory and structural changes on the one hand and chronic forms of atonic dyspepsia on the other. The attacks are usually periodical in character, with constricting pain in the pit of the stomach, and the intervals are not necessarily associated with symptoms of dyspepsia. It chiefly occurs in females of nervous temperament at the catamenial periods.

Two forms of the disease have been described--one depending on hyperæsthesia of the sensory fibres of the pneumogastric, the other on hyperæsthesia of the solar plexus. This may be correct in theory, but practically it can be of little importance to make the discrimination, even if it were possible to do so.

Clinically, the disease is presented to us in two forms. In one the pain is agonizing, comes on without premonition, is sometimes intermittent or remittent in character, and conveys to the sufferer the idea of spasm; hence it has often been described as colic of the stomach. If not relieved by appropriate remedies, the pain may last for hours or days. This is the acute form. In the other the pain is more of a neuralgic character and is not so severe. There may be varying exacerbations which may last for months or years. This is not an unfrequent form, and may consist simply in the more acute form becoming chronic.

ETIOLOGY.--With the limitation indicated, we have naturally to seek the causes of the affection, says Ziemssen, in two directions: either in the abnormal nature of the irritants to which the gastric nerves are subjected, {460} or in an altered condition of the nerves themselves, which therefore react abnormally with the normal degree of irritation. This briefly covers the whole ground of the etiological relations of the disease.

The predisposing causes are such as produce general depressed vitality, embracing at the same time special conditions of extreme nervous excitability. Some of these general conditions were pointed out while speaking of atonic forms of dyspepsia. Indeed, the two conditions are often associated, and practically it may be difficult to separate them, although the connection between them is not necessarily an invariable one. Like atonic dyspepsia, gastralgia is apt to affect anæmic persons, and notably anæmic females at menstrual periods. Thus, the association between gastralgia, chlorosis, and hysteria is a matter of common observation. Of 350 cases noted by Briquet, only 30 had no signs of gastralgia; and this observation is a fair average expression of the experience of others.

Certain blood-poisons are also known to give rise to the disease. Infection of the blood by malaria was observed by Niemeyer to produce spasm of the stomach instead of the paroxysms of intermittent fever; and in malarious regions of the United States the same observation has been made. Gout and rheumatism are also known to sustain causative relations to the disease. Certain idiosyncrasies also enter as a factor into the somewhat complex etiology of the disease. Thus, some persons suffer immediately from eating certain kinds of food and fruits, such as shellfish, strawberries, honey, and even milk and coffee. The pain and spasm are produced by direct contact with the sensory fibres of the stomach; i.e. they react abnormally to normal stimulation. But disease of the nerve-centres may enter into the causation. This is seen by the effects of morbid growths impinging upon nerve-trunks; their terminal branches often become extremely irritable and painful, and this condition may be intensified by idiosyncrasy. Excessive acidity of the stomach, seeds of fruit, certain articles of food, the presence of worms in the stomach, and draughts of ice-water may simply act as exciting causes to a centric predisposition.

Of the more direct causes operating upon nerve-centres, all the depressing passions and emotions deserve special mention; so do all causes which produce an exhausted state of innervation, such as venereal excesses, onanism, the abuse of narcotics, etc.

But chief among the causes are those of a reflex kind. Painful affections of the kidneys, irritable conditions of the bladder, diseases of the liver, and, above all, morbid conditions of the female genital organs, sustain a direct and close relation to painful and spasmodic conditions of the stomach. It is a common accompaniment of versions, flexions, prolapses, inflammations, erosions of the os, as well as diseased conditions of the ovaries. When such local conditions are associated with anæmia and hysteria, patients rarely fail to have painful gastric complications.

SYMPTOMS.--The symptoms of gastralgia, like most of the neuroses, are characterized by severe pain occurring in paroxysms, followed by remissions, and sometimes by complete intermissions, again to recur with varying degrees of severity. The pain in the acute variety is of a violent, spasmodic character, and is referred to the epigastrium immediately beneath the ensiform cartilage. Frequently it extends from the epigastrium to the back and chest and into the right and left hypochondrium. {461} No one has so briefly and so accurately described the immediate attack of gastralgia as Romberg: "Suddenly, or after a precedent feeling of pressure, there is severe griping pain in the pit of the stomach, usually extending into the back, with a feeling of faintness, shrunken countenance, cold hands and feet, and small, intermittent pulse. The pain becomes so excessive that the patient cries out. The epigastrium is either puffed out like a ball, or, as is more frequently the case, retracted, with tension of the abdominal walls. There is often pulsation in the epigastrium. External pressure is well borne, and not unfrequently the patient presses the pit of the stomach against some firm substance or compresses it with his hands. Sympathetic pains often occur in the thorax under the sternum, in the oesophageal branches of the pneumogastric, while they are rare on the exterior of the body. The attack lasts from a few minutes to half an hour; then the pain gradually subsides, leaving the patient much exhausted, or else it ceases suddenly with eructation of gas or watery fluid, with vomiting, with a gentle soft perspiration, or with the passage of reddish urine."

Besides the violent paroxysmal pain referred to the stomach, symptoms of derangement of other organs are often present. Prominent among these are hysterical phenomena which are protean in their manifestations, and if not recognized they are liable to mislead. Thus, with gastric pain there may be violent palpitation of the heart, with shortness of breath, cough, globus, hiccough, and convulsive affections, and in a certain proportion of cases there is marked melancholia or hypochondriasis.

The stomach is variously modified in its function. In many cases it is entirely unaffected. The desire for food may be indeed increased, and its ingestion may give a sense of relief. In others vomiting may be severe, while in still others there may be merely a condition of anorexia. The tongue is, as a rule, clean, the skin cool, the temperature undisturbed, and there is absence of tenderness over the epigastrium. Generally pressure relieves the pain.

DIAGNOSIS.--Functional and structural troubles of the stomach very markedly simulate each other; therefore the diagnosis requires to be made with great caution, and this is best done by a most rigid and careful exclusion; and this becomes difficult because the symptoms are mainly subjective.

It is a matter of great moment in differentiating the disease to take into account all constitutional states which predispose to nervous asthenia. Thus in conditions of chlorosis and hysteria the presumption is strong that the pain is neurotic or spasmodic in character; and this presumption is intensified if there be no accompanying constitutional symptoms which indicate inflammatory action. We exclude inflammatory conditions of the stomach by the frequent and complete intermissions, by the absence of thirst, tenderness, and all febrile movement. Moreover, the pain of inflammatory affections, unless produced by corrosive poisons, is rarely so severe as in neuralgic affections; nor are nausea and vomiting so uniformly present in neurotic affections. Then the time at which the pain is experienced is a matter of importance. In inflammatory affections it is felt immediately on taking food. In neurotic affections it may occur when the stomach is empty, and it is not unfrequently relieved by food. In ulcer and cancer of the stomach pain is a common element, and, as in {462} gastralgia, it is referred to the epigastrium. But in gastric ulcer the pain is rarely absent; it is of a dull, gnawing character, is strictly localized in the centre of the epigastrium, and is aggravated by pressure and by food. Moreover, the vomited matter often contains blood. In cancer of the stomach the pain is not as severe and spasmodic in character as in gastralgia, the vomiting is a more prominent symptom, and the material vomited has the characteristic cancerous look. Cancer is more apt to occur too in advanced life, and it is characterized by a steady progressive emaciation.

Gastralgia may also be confounded with rheumatism of the abdominal muscles as well as neuralgia of the inferior intercostal nerves, and it is liable to be confounded with colic resulting from biliary calculi. Colicky pains in the transverse portions of the colon may also be mistaken for pains in the stomach. "It is no exaggeration to say," says Trousseau, "that in perhaps half the cases which are called gastralgia the affection is nothing more than cholalgia." The more fixed the pain is to one spot, and the nearer it is to the median line, the greater is the probability of its being gastric.

PROGNOSIS.--Notwithstanding the severe and apparently alarming nature of the symptoms, the prognosis of gastralgia is in the main favorable, although the prospect of a permanent and speedy cure is small. The duration of the disease depends on the nature and persistence of the exciting causes, and these are so often associated with an exhausted state of innervation that speedy recovery from the disease cannot be promised. In the simpler varieties, caused by improper food, the disease will disappear by removing the cause, and the hysterical forms are liable to disappear with advancing life. So also cases arising from malaria, anæmia, chlorosis, uterine disease, rheumatism, and gout may be relieved by removing the cause. But there are cases produced by unknown causes, and especially cases associated with a general and unexplained cachexia, in which the prognosis is not good.

TREATMENT.--This is both radical and palliative. The radical treatment must have reference to the diseases which have given rise to it. If, for instance, the gastralgia can be traced to sympathetic disturbances of the uterine organs, no remedy can be permanently effective until the cause is removed. Since chlorosis and anæmia are so often found associated with it, benefit may be expected from the ferruginous preparations in some form. Iron occupies a prominent place as a remedial agent. The precipitated carbonate is to be preferred on account of its peculiar influence over the nervous system, and especially over painful neuralgic conditions. It may be given in drachm doses, or even larger, combined with ginger or aromatic powder. If the stomach will not tolerate it, other preparations may be tried.

Quinia is a valuable addition to iron, and it is specially valuable in cases of suspected malarious origin. Sometimes a few large doses will break up the paroxysmal pains as no other agent will.

In the more chronic forms of the disease arsenic is one of the most reliable remedies we possess. It has a well-deserved reputation in the treatment of a great variety of nervous affections, and in none more than in the disease now under consideration. It should be given for a length of time--three or four minims of Fowler's solution, gradually increased and {463} given immediately after food--and in cases of anæmia it should be associated with iron.

In irritable, broken-down conditions of the nervous system nux vomica, or its alkaloid strychnia, is a useful remedy. But it is a powerful stimulant to the spinal nerve-centre, and care should be used in the too protracted use of the remedy or in its administration in too large doses. It may be combined with the phosphate or the valerianate of zinc, or either may be given separately. The nitrate and oxide of silver have also been used with asserted success. Nitrate of silver may be given in pill form with opium.

If there is a strong hysterical element, the bromides and antispasmodics may be tried in connection with remedies calculated to strengthen the nervous system. The judicious employment in such cases of hydro-therapeutic measures is of great value. Good results are also obtained from electricity. The constant current should be preferred.

Among palliative remedies--i.e. remedies that act directly on the painful gastric nerves--the subnitrate of bismuth has long been regarded with great favor. Its action is mainly local; it may be given, therefore, in drachm doses or more three or four times a day. If there is nothing to contraindicate its use, aconite or dilute hydrocyanic acid may be given with the bismuth.

For the immediate relief of pain, however, there is no substitute for opium. The subcutaneous injection of morphia will generally give immediate relief. But there are many reasons why we should try other palliative remedies. In a disease so painful in character a remedy that gives such prompt relief is liable to abuse. The formation of the opium habit should be carefully guarded against. Spirits of chloroform may be tried, therefore, as a substitute for opium, followed by large draughts of hot water--hot as the patient can possibly sip it. Hot water of itself often gives immediate relief.

An important part of the treatment consists in well-regulated hygiene. Change of air, travel, pleasant mental surroundings, together with carefully regulated diet, are in a majority of cases more efficacious than drugs.

Acute Gastritis (Acute Gastric Catarrh).

Reasoning from the great functional activity of the stomach, from its daily periodical change of blood-supply, from its extensive glandular arrangement, and from its important relations to the functions of vegetative and animal life, we might readily infer that it would be frequently the seat of acute and destructive inflammation. But it is remarkable, all things considered, how seldom that is the case. Indeed, acute spontaneous inflammation of the stomach is almost unknown. When it occurs it most frequently results from toxic causes. In less severe forms, however, not attended with immediate danger to life, it is undoubtedly a disease of frequent occurrence, and in this more comprehensive sense the subject will be considered in the present section.

The mucous membrane alone is usually the seat of the disease, and for this reason it has become the custom of late years to describe it as gastric {464} catarrh. This may be objectionable, for the reason that it does not include gastric inflammation of every grade of intensity. The term catarrh is generally applied to much more simple anatomical structures than those pertaining to the stomach. We shall consider the subject therefore under two forms--namely, (1) Catarrhal; (2) Erythematous gastritis.

ETIOLOGY.--Certain conditions predispose to the disease. Acute catarrhal gastritis is specially liable to occur in those who habitually suffer from a disordered stomach. This may arise from functional disturbance of the digestive process on the one hand, or mechanical obstruction on the other. Mechanical causes are widespread in their influence. Thus, weak heart-action from any cause tends to disturb the normal adjustment between the two sides of the circulation--arterial and venous. An abnormal amount of blood accumulates on the venous side of the circulation, and chronic passive hyperæmia of the abdominal viscera is the result. The effect of this upon the stomach is to lower its functional activity and to invite inflammatory action. The same condition results from structural diseases of the heart, lungs, or liver. Persons suffering from valvular diseases of the heart, emphysema of the lungs, or cirrhosis of the liver are strongly predisposed to diseases of the stomach. Gastric troubles are also apt to supervene during the progress of various diseases.

Gouty and rheumatic persons are specially prone to suffer from gastric catarrh; and eruptive disorders, such as scarlatina, diphtheria, etc., tend to erythematous forms of gastric inflammation. Catarrhal gastritis is also a very common sequence of the whole class of malarious fevers, including yellow fever, intermittents, and remittents. In its more acute form gastric inflammation supervenes in the course of yellow fever; and what is observed here in an extreme degree exists in a minor degree in all the so-called malarious fevers. Intermittent and remittent fevers are always attended with gastro-duodenitis and gastro-hepatitis. The degree of this inflammatory complication determines the continued character of the fever. Upon this point the writer has very decided views based upon a wide field of observation in malarious regions of country. We have lost ground in the treatment of these diseases by directing our attention almost exclusively to the febrile and malarious, to the exclusion of the inflammatory, elements. Quinia is inoperative in the cure of these troublesome and often fatal complications. Indeed, it is more than that: it is often positively injurious. Arrest the local phlegmasia and secure freedom of abdominal circulation, and we at once get the action of the specific remedy. It may be going too far to affirm, as did Broussais, that gastritis sustains a causative relation to all forms of fever, but that gastro-duodenitis is an important secondary condition in all forms of malarious fever, complicating and perpetuating the febrile state, there can be no doubt; and it is equally clear that it constitutes one of the most dangerous complications. Excessive alimentation, with the injudicious use of tonics and stimulants, so often resorted to in the treatment of these fevers in their early stages, only serves to intensify the local inflammation. Abolish the congestive and inflammatory element of a remittent, and it at once becomes an intermittent.

Mention has been made of weak heart-action as a factor in catarrhal {465} gastritis; also mechanical impediments to the return of blood from the stomach to the heart. The stomach is thereby kept in a constant state of congestion, the nutrition of the mucous membrane is less active than in health, and its solvent juices are more sparingly secreted. Thus in long-continued congestion produced by mitral disease of the heart Samuel Fenwick found the formation of pepsin impaired. He made artificial gastric juice from the mucous membrane of three males dying of heart disease, and he found, on the average, only 2-9 grs. of albumen were dissolved, whereas the amount digested by the mucous membrane of persons who had died of other maladies was 4 grains. In the cases of three females a still smaller amount of solvent power was displayed. These facts have important bearings upon the question of alimentation in fevers and the conditions in which there is chronic congestion on the venous side of the circulation. Long-continued passive hyperæmia of the stomach from any cause not only impairs its functional activity, but strongly predisposes to inflammatory complication.

Acute erythematous gastritis is most frequently met with in children. It is a very common form of disease in early life, and the local nature of the malady is frequently overlooked. Few questions in practical medicine are more embarrassing to the physician. It has been known and described as gastric and remittent fever, as continued typhoid, and even as acute hydrocephalus. Writers and teachers describe and dogmatize, while practical men hesitate at the bedside. There is little doubt but in the background of these febrile manifestations in children there is often an acute erythematous gastritis, which is more successfully treated by a rigid milk diet, small doses of calomel and bismuth, mucilaginous drinks, cooling saline laxatives, and sometimes leeches applied to the epigastrium, than by the heroic doses of quinia so frequently resorted to.

We must not, in this connection, lose sight of the fact, so clearly pointed out by Broussais, that inflammation of the stomach is often secondarily repeated in the brain. The whole field of clinical observation abounds in illustrations of this. How often, for instance, we can trace the sick headache, the delirium, and even convulsive movements of the voluntary muscles, to primary gastro-intestinal irritation! In the play of the sympathies morbid irritative action is transmitted from the organic to the cerebro-spinal nerves; and of all portions of the abdominal viscera the stomach and upper portion of the intestinal track are the most frequent seat of these intense morbid sympathies. Remedies which cool the stomach and lessen inflammatory action diminish the excitement of the brain, and vice versâ.

EXCITING CAUSES.--Among the direct exciting causes of gastric inflammation--exclusive of acrid or corrosive poisons--the most frequent in this country is the excessive use of alcohol. It acts most injuriously when it is but slightly diluted and taken on an empty stomach. And next to this pernicious habit, in the order of importance, is the use of large quantities of food--more than the stomach has capacity to digest, and more than is necessary for the wants of the system. Excessive alimentation is a prolific source of gastric inflammation. It generally manifests itself, however, in a chronic or subacute form.

Acute erythematous gastritis, so frequently met with in children, is {466} often present in scarlatina. It is evidently not catarrhal in character, for in the earlier stages there is no increased secretion of mucus and but little injection of the mucous membrane. The changes are observed in the deeper structures of the stomach, and principally in the gastric tubules. They are much distended by granular, fatty, and albuminous matter; and in this respect it is analogous to erythematous affections of the skin with which it is associated in scarlatina.

Finally, acute gastric catarrh may be excited by all causes that weaken the digestive power either by weakening the gastric juice or by retarding the movements of the stomach.

ANATOMICAL CHARACTERS.--No disease requires more knowledge and caution in determining post-mortem changes than those of the stomach. In the first place, it presents in inflammatory conditions markedly different degrees of intensity, with corresponding differences in anatomical changes. Its diseases also present many special forms, and changes take place after death which simulate morbid processes during life. Moreover, intense vascular injections are apt to disappear in the small superficial vessels after death. This applies to all mucous membranes, but specially to the mucous membrane of the stomach, which is the seat of varying amounts of blood in their physiological limits during life. For this reason the observations of Beaumont made upon a living subject are invested with peculiar interest. It will be remembered that in the case of Alexis St. Martin the appearances noted were such as belong to the milder forms of inflammation. Beaumont noticed in this case, after indiscretions in eating or abuse of ardent spirits, a livid erythematous redness of the gastric mucous membrane, with, at the same time, dryness of the mouth, thirst, accelerated pulse, and, at the height of the injection, an entire absence of gastric secretion. At other times there was considerable muco-purulent matter, with oozing of grumous blood, "resembling the discharge from the bowels in cases of chronic dysentery." The fluid taken out through the fistulous opening consisted mostly, however, of mucus and muco-pus which showed an alkaline reaction. He describes also a condition of ecchymosis and oozing of blood from certain red spots of the gastric mucous membrane, and when thus limited the constitutional symptoms experienced by the patient were correspondingly slight. Ecchymoses may be present in large number, with exudates of false membrane, which Beaumont describes as aphthous. Brinton also describes a severe form of gastritis which he terms ulcerative, in which he observed hemorrhagic erosions.

In the catarrhal form of gastritis the mucous membrane is covered with a thick, tenacious, stringy mucus; it is softer than usual, and generally thickened. It presents at the same time a dead-white appearance, corresponding to Virchow's cloudy swelling--a condition analogous to that which is observed in acute Bright's disease. Even casts of the tubes are sometimes met with.

This inflammatory change in the substance of the mucous membrane is especially observed in the acute erythematous form of gastritis complicating scarlatina. In the early stage there is no increased secretion of mucus, and at a more advanced stage the membrane may be even paler than usual.

In cases of acute toxic gastritis intense redness is seen over the entire {467} surface of the mucous membrane, followed by rapid exudations and sloughing of portions of the membrane.

In all forms of the disease there is a tendency to extension of the inflammation into the duodenum and small intestines. In the more chronic forms we almost invariably encounter the condition of gastro-duodenitis.

SYMPTOMS.--The symptoms of inflammation of the stomach present wide differences in their intensity, depending upon the degree of severity in different cases. In acute inflammation caused by the direct action of poisonous irritants they are pronounced and highly diagnostic. The patient immediately complains of burning pain, referred to the epigastrium, followed by intense thirst and vomiting. The thirst is apt to be very great and the act of vomiting painful. The vomited matters contain mucus, saliva, sometimes bile, and not unfrequently, in fatal cases, black, grumous, coffee-ground material. There is marked tenderness on pressure, the pulse is frequent and small, coldness of the surface is marked, and hiccough is apt to occur. The expression of the patient is anxious, the abdominal muscles rigid, and, in fatal cases, the prostration becomes rapidly extreme. The patient dies by asthenia. These symptoms apply to acute cases of marked severity, usually of toxic origin.

In the milder forms of catarrhal gastritis more frequently met with there is seldom complaint of pain. The sensation is rather that of fulness, uneasiness, with more or less tenderness on pressure. The symptoms are such as belong to acute indigestion and the embarras gastrique of French authors. The phenomena may be those of a slight bilious attack. The tongue is foul, the breath offensive, the bowels confined, and the urine high-colored and scanty. There is also generally a sense of fatigue, and soon secondary cerebral symptoms supervene, such as cerebral hyperæmia, headache, vertigo, noises in the ears, palpitation, sighing, yawning, dyspnoea, faintness, and in severe cases marked physical and mental depression. Nausea and vomiting are common, and if the inflammation extends to the duodenum and liver, symptoms of gastro-hepatic catarrh manifest themselves. If fever supervenes, urticaria sometimes complicates these attacks.

In young children the inflammation is apt to involve a general catarrh of the whole intestinal track. Thirst is excessive, followed by vomiting and diarrhoea. The discharges are liquid, watery, offensive, acid, and out of all proportion to the amount of fluid absorbed by the stomach. The pulse becomes weak and fluttering, the skin pale, the features pinched, the eyes sunken, and the extremities cold. The tendency is toward rapid collapse and fatal issue. The symptoms describe what is usually known as cholera infantum. It has its analogue in the cholera morbus of adults.

In erythematous gastritis nausea and vomiting are as general as in the catarrhal form, but, unlike the catarrhal, pain at the epigastrium is a prominent symptom. It comes on directly after taking food. In phthisical cases the sensation is rather that of rawness of the oesophagus and stomach. Thirst is a troublesome symptom; the tongue is red or dry and glazed; tenderness of the epigastrium is marked; diarrhoea is generally present; and, as in the catarrhal form, the stools are fetid and unhealthy. The disease shows a marked tendency to become chronic.

{468} DIAGNOSIS.--In the more acute forms of the disease the symptoms are all highly diagnostic. Vomiting, burning pain of the stomach, tenderness on pressure, intense thirst, with frequent and small pulse, point with almost unerring certainty to acute gastric inflammation. But vomiting of itself, however persistent, is not evidence of gastritis, for it may be present from many other causes. If the vomiting be attended by headache, it may be confounded with gastric irritability from brain disease. Thus, chronic meningitis with persistent vomiting strongly simulates gastritis, and in the case of children it is liable to be mistaken for it. In gastritis the nausea is from the first a pronounced feature of the disease. Vomiting in affections of the brain is often unattended by nausea. In gastritis the tongue is more frequently coated or red and glazed. Diarrhoea is also more frequently present, especially in early life. In affections of the brain the tongue may be clean and the bowels are usually obstinately confined. When there is much fever, gastritis may be confounded with remittent or typhoid fever. In periods of childhood this mistake is specially liable to occur, for there are many symptoms in common. In all such cases the early history of the case ought to be carefully inquired into. In gastritis we may be able to detect the cause in any particular case. The gastric symptoms are apt to occur suddenly, and, as already stated, are prominent from the first. In meningitis the skin is more frequently dry; in gastric catarrh perspirations are common. The more prominent and characteristic symptoms of typhoid should also be carefully excluded, such as the gradual invasion, peculiar eruption, bronchial catarrh, enlargement of the spleen, gurgling in the right iliac fossæ, with tympanitic abdomen. Peritonitis, with vomiting, may be mistaken for gastritis, but the diffuse tenderness, the fixedness of position, the rigidity of the abdominal muscles, and the tympanitic distension serve to guide us in our diagnosis.

PROGNOSIS.--The prognosis must have reference to the cause. The more violent forms of the disease resulting from corrosive poisons are generally fatal. Death is apt to take place in a few hours from a condition of collapse. The immediate cause of death is failure of heart-action. It is also a dangerous disease in the extremes of life. In its acute form in children it is apt to terminate fatally, especially if it is not recognized early and judiciously treated. The complications of the disease may also render the prognosis unfavorable. Milder cases tend to recovery.

TREATMENT.--The most important indication of treatment, applicable to all forms of gastric inflammation, is to secure complete or partial rest for the inflamed organ. In dangerous cases no food should be taken into the stomach. The patient should be nourished exclusively by nutrient enemata. If food is permitted, it should be restricted to milk and lime-water, administered in small quantities at short intervals. In acute and dangerous cases, suddenly manifesting themselves, the exciting cause should be carefully inquired into, and speedily removed, if possible, by an emetic, or, if need be, by the stomach-pump, if the poison be one which can be ejected; and following this antidotes are to be administered according to the nature of the poison.

To allay the intense thirst small pieces of ice should be swallowed at frequent intervals, or, what is often more grateful to the patient, iced {469} effervescing drinks in small doses oft repeated. Injections of water may also tend to relieve thirst. To allay vomiting the physician is often tempted to try a great variety of remedies which are usually worse than useless, for they aggravate rather than relieve the distressing symptom. For the purpose of quieting the stomach opium is the most reliable remedy we possess. It is best administered hypodermically. Fomentations may be applied over the epigastrium. Stimulants are, of course, contraindicated on account of their irritating action on the inflamed membrane, but in case of rapid tendency to death by failure of heart-action they should be administered by the rectum or hypodermically.

In milder cases--which are much the more common--physiological rest of the organ is also a cardinal principle of treatment. Rest of the body is equally essential. In cases of any severity the patient should be kept quiet in bed. For the condition of acute indigestion known as embarras gastrique ipecacuanha in six- or eight-grain doses, given three times within twenty-four hours, will often produce healthy bilious stools, and in this manner accomplish the cure. One or two grains of calomel may be added to each dose of ipecacuanha with benefit. In all forms of catarrhal gastritis, especially if symptoms of portal congestion are present, mild mercurial cathartics are attended with benefit. Six or eight grains of calomel may be rubbed up with sugar of milk and placed dry on the tongue, followed by a cooling saline aperient. When diarrhoea is present in such cases, it should be regarded as conservative, and encouraged by the administration of half-grain or grain doses of calomel, combined with bismuth and bicarbonate of soda. The diet should be restricted to milk and lime-water or milk mixed with Vichy or Seltzer water. Demulcent drinks should be freely given. In the slighter attacks effervescing drinks are grateful to the patient; and if there be excessive formation of acid in the stomach, antacids and sedatives should be administered.

Bismuth has a peculiar sedative and antiseptic effect in the milder forms of inflammatory action of mucous membranes. It is especially valuable in gastro-intestinal troubles of children. Its action is mainly local surface action, and may therefore be given in liberal doses if necessary. Children may take from five to ten grains, and adults twenty grains or more. Hydrocyanic acid adds to its sedative qualities, or when pain is present, with diarrhoea, opium in some form may be added. The salicylate of bismuth is specially indicated when we want to add to the antiseptic qualities of bismuth.

The general principles of treatment indicated here are applicable to the so-called remittent fevers of children--namely, calomel in small doses, combined with bismuth and bicarbonate of soda, followed by occasional cool saline laxatives. Ipecacuanha is also a valuable agent in correcting morbid gastro-intestinal secretions. When there is early epigastric tenderness, with hot skin and elevation of temperature, two or three leeches should be applied to the epigastrium, followed by warm poultices of linseed meal. Dry cupping may also be used with benefit; and if decided remissions occur, with suspicions of a complicating malarious element, a few liberal doses of quinia may be tried. In many such cases, however, it will be found unnecessary, and not unfrequently hurtful. In acute gastro-intestinal inflammations of children--the {470} temperature reaching 105° or more--no febrifuge, in the opinion of the writer, is equal to the cool or cold bath, repeated from time to time until there is a decided reduction of temperature. But the gastric inflammation, rather than the fever, should mainly claim our attention.

Great care is necessary during convalescence from acute gastric disease, particularly as regards the hygienic management. The apparent debility of the patient too often tempts the physician to the early and injudicious use of tonics, stimulants, and excessive alimentation, which, if persisted in, can scarcely fail to perpetuate a chronic form of inflammatory action.

Chronic Gastritis (Chronic Gastric Catarrh).

There is perhaps no malady more frequently met with than chronic gastric catarrh, and none more frequently misunderstood. It comprises many different forms of gastric derangement, which are grouped under the general head of inflammatory dyspepsia, with many symptoms strongly simulating ordinary functional dyspepsia. It includes, in the author's opinion, a large number of cases of obstinate chronic dyspepsia, which are badly managed because not recognized as of inflammatory origin.

ETIOLOGY.--In a more or less chronic form it is frequently met with as a result of the acute affections. Hence the etiology is mainly that of acute gastric catarrh. It may be caused--

1. By functional disorders of the stomach.

2. By mechanical causes which interfere with the portal circulation.

3. In connection with certain constitutional states, such as gout, rheumatism, phthisis, renal disease, certain eruptive diseases, and as a sequence of malarious fevers.

4. By the excessive use of alcohol and other gastric irritants.

5. By errors of diet, especially excessive alimentation.

6. By decomposition of ingested aliment owing to deficiency of gastric juice.

7. By all causes that weaken the digestive power and lower the general tone of the system.

Of all these causes, errors of diet are most apt to produce it, and to perpetuate it when once established. And next to this, in the order of importance, is the immoderate use of alcohol, especially by persons whose general health and digestive power are below a healthy standard. Such persons are apt to suffer from irritative and inflammatory forms of dyspepsia, which, in various degrees of intensity, alternate with the acuter forms of embarras gastrique.

The injudicious use of drugs may also be mentioned. There can be no doubt that many transient and functional forms of indigestion merge into the more chronic inflammatory forms of dyspepsia from the abuse of stimulants, tonics, and purgatives. Anxious for relief, and urged on by hope of recovery, the victims of functional dyspepsia are apt to have recourse to every grade of quacks and to be subjected to every form of harassing and mischievous treatment. Indeed, the use of potential and irritating drugs, administered for all kinds of ailments, real or imaginary, enters largely into the etiology of chronic gastric catarrh.

Mechanical causes deserve also special consideration. These are mainly {471} such as offer impediment to the return of blood from the stomach to the heart. In acute cases the congestion may be very intense. Congestion of the same kind, but more gradual in its occurrence and less in degree, may be present from all conditions affecting the circulation of venous blood through the liver. General anæmia, by producing weak heart-action, disturbs the normal adjustment between the arterial and venous sides of the circulation. Blood accumulates in the veins and capillaries, and morbid action propagates itself in a direction contrary to the circulation. Hence in all conditions of general anæmia there is tendency to dyspnoea, pulmonary oedema, bronchorrhoea, special forms of liver disease, gastric catarrh, and even temporary albuminuria. All mechanical obstructions to the free transit of blood through the heart, lungs, or liver are followed by the same results. A free secretion of mucus into the stomach is one of the most commonly recognized. It is often vomited in large quantities. This alkaline mucus, while it dilutes the digestive juices of the stomach, furnishes favorable conditions for the development of low micro-organisms, which contribute to the fermentative process. We may not duly estimate the effects of these organisms on a mucous membrane softened by long-continued passive hyperæmia.

Malarious fevers, from their congestive tendency, give rise to the more acute forms of gastro-enteric inflammation. In the more chronic forms of intermittent and remittent fevers more or less gastric inflammation is invariably present. Indeed, in all forms of fever gastric inflammation is a complicating element, and the recognition of the fact has an important bearing on the treatment.

Certain constitutional diseases appear to involve special liability to this affection, such as scrofula, phthisis, gout, rheumatism, syphilis, and many chronic forms of skin disease; and in many cases the cause is not apparent.

ANATOMICAL CHARACTERS.--The gross appearance of the stomach in chronic gastritis is thus admirably described by Broussais, who faithfully recorded what he "observed during many years in the bodies of those who have long suffered from distaste for food, nausea, and vomiting." These observations were made long before morbid anatomy had thrown much light on the more minute structural changes of organs, and the general picture will be recognized as faithful to-day: "Softening, friability, and the reduction into a kind of gelatinous mass commonly occurs in the region of the lower part of the larger curvature of the stomach; and when closely examined it is perceived that it is not only the mucous membrane that has undergone that species of decomposition, but that the muscular has participated in it, and that the whole of the cellular tissue which united the three membranes has entirely disappeared. The parietes of the viscus are then reduced to a very thin lamina of serous membrane, commonly so fragile as to tear on the slightest handling, or even already perforated without any effort on the part of the anatomist. The pyloric region, on the contrary, has manifestly acquired more consistence and thickness; the mucous membrane there presents large folds, the muscular appears more developed, and the cellular and vascular are injected; sometimes even a true scirrhous state is observed there. The portion of the mucous membrane which covers this scirrhus is sometimes {472} ulcerated, but that in the surrounding parts and at the border of the ulcer, far from being softened, is, on the contrary, tumefied, indurated, and injected. Finally, though there may or may not be ulceration of the pylorus, it is always manifestly hypertrophied, whilst the lower part of the great curvature is the seat of softening and atrophy."

These were the observations of the great anatomist apparent to the naked eye. At the present time we can only confirm them by stating that structural changes are particularly noticed in the pyloric region of the stomach. The mucous membrane generally is vascular and covered with a grayish, tough, transparent mucus. It is more opaque and thicker than natural. The surface is usually changed in color: it may be red, brown, ash-gray, slate-colored, or even black in spots. The darkened spots are due to pigmented matter, and this is generally most marked in the pyloric half of the stomach. It is most commonly met with in cases of prolonged passive congestion of the stomach from portal obstruction, and requires for its production the rupture of capillaries in the superficial layers of the membrane and the transformation of the hæmatin into pigment. The same condition often produces ecchymoses and hemorrhagic erosions in spots. In other cases the mucous membrane is strikingly uneven, being studded with numerous little prominences separated from each other by shallow depressions or furrows. This condition, which has been compared to granulations upon wounds, is called mammillation. It is the état mamelonne of Louis, and is considered by him as a sure and constant sign of inflammatory action. Like many other structural changes, it is usually found in the neighborhood of the pylorus. More rarely polypoid growths project from the membrane, and little cysts also frequently appear in the mucous membrane.

Chronic inflammation tends to thickening of the mucous membrane. It sometimes is not only greatly thickened, but acquires an extreme degree of toughness. Exceptionally, however, the membrane, either entire or in spots, may be abnormally thin. The thickening of the walls of the stomach, when it involves the pylorus, gives rise to constriction of the orifice and consequent dilatation of the stomach.

When the disease has been of long standing the interstitial tissue between the tubules becomes thickened, the stomach is changed in its normal structure, and the tubules themselves become confused, compressed, and much less straight and parallel than in the normal state. Or they may in some cases be enlarged, according to Flint, in consequence of swelling and parenchymatous or fatty degeneration of their epithelial cells. Microscopic examination often shows changes such as occur in other glandular organs. The glands and tubules become the seat of degenerative changes, such as are observed in Bright's disease of the kidney, and they are frequently found associated in the same case. The mouths of the gastric tubules become blocked up, while deeper parts are dilated into cysts; and at times they are atrophied or filled with granular fatty matter.

Many cases of persistent anæmia may be traced, according to Flint, to this degenerative process of the gastric tubules.

The SYMPTOMS of chronic gastritis are mainly those of difficult digestion of an aggravated kind, and are liable to be mistaken for those of {473} ordinary functional dyspepsia. Some points of distinction were referred to in the section treating of functional dyspepsia; and while there are many symptoms in common, it is vastly important that the two forms of the disease should be early recognized, for they are radically distinct in their pathology and treatment.

We now speak of what is usually known as inflammatory, irritative, or gastric dyspepsia--a persistent and aggravated form of indigestion which has its origin in the stomach itself, in contradistinction to dyspepsia which originates largely from causes outside of the stomach and transmitted to it through nervous impression. The one is functional and indirect; the other is inflammatory and direct.

The symptoms referable directly to the stomach are mainly those of difficult and painful digestion, and are alike characteristic of all forms of indigestion, such as loss of appetite, sense of weight and fulness of the epigastrium, distress after taking food, acidity, eructations of gas, etc. But chronic gastritis is more frequently accompanied by a burning sensation in the epigastric region, accompanied by tenderness on pressure, which is generally increased after meals. Sometimes this tenderness amounts to actual pain, which is increased after meals. But we are liable to be misled by pain: gastric pain is not a characteristic symptom; subacute forms of the disease may exist without any fixed pain; the sensation is rather that of burning, uneasiness, and oppression of the epigastric region. The appetite, as a rule, is greatly impaired--indeed, the sense of hunger is rarely experienced--and nausea and vomiting frequently follow the ingestion of food. This is especially the case when catarrh of the stomach is associated with renal disease, portal congestion, or chronic alcoholism. Large quantities of mucus are brought up, the vomiting taking place usually in the morning, and on examination of the mucus it will frequently be found to contain sarcinæ and large numbers of bacterial organisms. When stricture of the pylorus is present the vomiting of putrid, half-digested food usually takes place about the termination of the digestive process.

The tongue presents characteristics peculiar to chronic inflammation of the stomach. In some cases it is small and red, with enlarged and red papillæ; in others, it is broad and flabby and somewhat pale; but in either case, on close inspection, the papillæ will be found red and enlarged, this being more apparent on the tip and edges. In children of scrofulous habits and in older persons of tubercular tendency the whole organ is redder than natural, the papillæ standing out as vivid red spots.

In other cases the catarrh of the stomach extends to the mucous membrane of the mouth. In all cases of oral catarrh the tongue, instead of being red and pointed, is large and apparently oedematous. It is uniformly covered with a white or dirty brownish coat, and frequently shows the impression of the teeth upon its edges. The secretions of the mouth are depraved, the breath heavy and offensive, and the gums spongy and unhealthy in appearance. Acidity is also common.

Thirst is a common symptom. It is rarely absent either in the acute or chronic form of the disease. It is most marked in the intervals between meals and in the evenings.

It is rare in gastric catarrh of long standing that it does not extend to the intestines, and occasionally from the duodenum to the ductus {474} choledochus; in which case we have the combined symptoms of gastro-intestinal catarrh associated with jaundice. The nutritive system becomes implicated, and patients are especially prone to develop any diathesis to which they may be liable.

There remains a group of symptoms of great interest in the study of gastric inflammation--important because liable to mislead as to the real nature of the difficulty--namely, morbid conditions of the nervous system. Few diseases have such a wide range of morbid sympathies, and few, it may be added, are so generally misunderstood and misinterpreted. Two main facts, as formulated by Broussais, deserve to be restudied by the profession:

First, that irritations of the visceral parenchyma which do not implicate their serous membranes only give rise to ill-defined sensations, and they not painful;

Second, that most of the acute pains arising from visceral irritation are rather referred to external parts than to the viscera themselves.

Unless the seat of very acute inflammation, mucous membranes are remarkably free from pain, and yet the gastric mucous membrane is the seat of a most exquisite internal visceral sense and has a wide range of morbid sympathetic disturbances. These sympathetic phenomena are often treated for primary neuralgias. No fact in the clinical study of disease deserves more careful consideration than this. Absence of pain, then, is calculated to mislead. It is often only the sensation of uneasiness, depression and melancholy, want of appetite, thirst, nausea, loathing of food, and derangement of the bilious and gastric secretions, that directs our attention to the stomach. Moreover, in gastro-enteric inflammations pain is more frequently felt in parts sympathetically affected than in the stomach itself. "It is only when irritations of mucous membranes are in the vicinity of the openings of cavities that the irritations are distinctly perceptible in the seat they occupy" (Broussais). Morbid irritative action commencing in the stomach repeats itself in the cerebro-spinal system of nerves, and the secondary irritation may develop a more immediately dangerous inflammation than the primary. This is frequently observed in children, who are specially prone to irritation of the visceral apparatus. Many cases of primary gastric irritation terminate in acute cerebral inflammation. Indeed, the greater number of phlegmasiæ of the brain are only sympathetic irritations issuing from primary inflammation of the stomach. Short of inflammation, the transmitted irritation may merely give rise to reflex convulsions, and in adults to sick headache, or, if long continued, to conditions of hypochondria. Headache is a prominent symptom of gastric irritation. It is not usually acute, but rather a sense of fulness and pressure, sometimes felt in the frontal, at other times in the occipital, region. Many cases commonly called cerebral hyperæmia and cerebral anæmia are nothing more than malassimilation from chronic gastric catarrh. This fact deserves to be specially emphasized at present, for we are apt to consider the cerebral the primary lesion. Vertigo, as in functional dyspepsia, is also an occasional symptom, and very commonly patients complain of extreme degrees of sleeplessness and disturbed dreams and nightmare.

The heart's action is often disturbed in its rhythm, and sympathetic dyspnoea leads to suspicion of disease of the lungs. And to all these {475} nervous phenomena may be added unusual languor, lassitude, irritability of temper, and a feeling of inability for either mental or physical exertion.

But in the play of morbid sympathies it must be borne in mind that the stomach may be secondarily affected. Irritations of all organs are constantly transmitted to the stomach from their very commencement. Hence the frequent loss of appetite, the thirst, the embarrassed digestion, the deranged gastric secretion, and the altered color of the tongue. This is markedly the case in all the malarious and essential forms of fever. Gastric complication in these fevers is rarely, if ever, absent, and if aggravated by the too early use of tonics and stimulants and by harsh irritating cathartics, it becomes too often a fatal complication.

Gastric symptoms are also associated with other constitutional disorders, such as phthisis, renal disease, rheumatism, gout, and almost all forms of chronic eruptive diseases.

Intestinal symptoms are rarely absent. Constipation is often obstinate, and especially is this the case if the catarrhal condition is confined to the duodenum. The lower down the inflammation the greater the probability of diarrhoea, and when present the stools are offensive and frothy; sometimes they are dry and scybalous and coated with a tough, tenacious mucus which may form casts of portions of the intestinal track. In other cases patients suffer from distressing intestinal flatulence and a sense of general discomfort. Piles is a complication frequently present without reference to complication of the liver.

The urine is more frequently disordered than in any other form of disturbance of digestion. The most common changes consist in an abundant deposit of the urates; exceptionally, however--especially in cases of long standing in which there are marked nervous symptoms associated with defective secretion of the liver and pancreas--it may be of low specific gravity and pale in color from the presence of phosphates. Slight febrile movement is not uncommon.

Finally, in all cases of chronic gastric catarrh the nutritive system becomes deeply implicated--much more so than in functional disturbances of the stomach. Emaciation is almost constantly present, the patient often showing signs of premature decay.

DIAGNOSIS.--The disease with which chronic gastritis is most liable to be confounded is atonic dyspepsia, the chief points of distinction from which have been already alluded to. In general terms it may be said that in chronic gastritis there is more epigastric tenderness, more burning sensation and feeling of heat in the stomach, more thirst, more nausea, more persistent loss of appetite, more steady and progressive loss of flesh, more acidity, more eructations of gas, more general appearance of premature decay, and greater tendency to hypochondriasis. And yet all these symptoms, in varying degrees of prominence, may be present in all forms of indigestion. To the points of distinction already mentioned, then, a few circumstances may be added which will afford considerable assistance in coming to a correct diagnosis:

1. The length of time the disease has uninterruptedly lasted. It is essentially a chronic disease.

2. The local symptoms are never entirely absent, as is not infrequently the case in functional dyspepsia.

{476} 3. The uneasy sensations, nausea, oppression, or pain, as the case may be, follow the ingestion of food. They are not so prominently present when the stomach is empty.

4. The result of treatment. In chronic gastritis it will be found that all the local symptoms are exasperated by the usual treatment of functional dyspepsia.

5. Stimulants and stimulating food are not well borne. Alcohol, especially on an empty stomach, produces gastric distress. There is also frequently slight febrile disturbance.

Chronic gastritis, with nausea, vomiting, hæmatemesis, general pallor, and loss of flesh, may be mistaken for cancer of the stomach. But in cancer vomiting is about as apt to take place when the stomach is empty as during the ingestion of food; pain is usually greater, especially when the orifices of the stomach are involved; the tenderness is more marked; the emaciation and pallor more steadily progressive; the vomiting of coffee-ground material takes place more frequently; and the disease is more rapid in its progress. The age and sex of the patient may also aid us in our diagnosis. Cancer is more frequently a disease of middle and advanced life, and localizes itself oftener in the stomach of males than females. Finally, the discovery of a tumor would remove all doubts. Hæmatemesis in chronic catarrh of the stomach is almost invariably associated with obstruction to venous circulation in the liver, heart, or lungs.

In rare cases it may be difficult to distinguish chronic gastric catarrh from ulcer of the stomach. In ulcer of the stomach pain is a more prominent and constant symptom; it is more centrally located; the vomiting after taking food is more immediate and persistent; the tongue may be clean; flatulence is not a constant symptom; the appetite is seldom much affected; the bowels are generally confined; and there is nothing characteristic about the urine.

TREATMENT.--In this, as in the more acute forms of the disease, rest of the stomach is important. From mistaken notions of disease we are prone to over-feed our patients, and thus seriously impair the digestive and assimilative processes. In chronic inflammation of the stomach a restricted diet is of prime importance. The physician should most carefully select the patient's food, and urgently insist on its exclusive use. This of itself, if faithfully persevered in, will often effect a cure.

The exclusive use of a milk diet--especially skim-milk--should be thoroughly tested. In testing it we should allow two or three weeks to elapse before any other food is taken. At the end of that time soft-boiled eggs, stale bread, and well-cooked rice may be added, with an occasional chop once a day. Some patients do not tolerate raw milk well. In such cases we should thoroughly test the peptonized or pancreatized milk or the peptonized milk-gruel, as suggested by Roberts. This artificially-digested milk agrees wonderfully well with many stomachs that cannot digest plain milk. Milk, in whatever form administered, should be given at comparatively short intervals of time, and never in quantity beyond the digestive capacity. Better err on the side of under- than over-feeding. Nothing should be left to the fancy or caprice of the patient. The food should be carefully selected by the medical adviser, and given in definite quantities at definite times. Even the moral {477} effect of such discipline is healthful for the patient. After testing milk diet for a time, we may gradually add small quantities of rare and thoroughly minced meat. Milk, eggs, and rare meat are more easily digested, as a rule, than starchy substances. Farinaceous food is apt to give rise to excessive acidity. But stale bread may be added to the milk, and, if there is tendency to acidity, better have it toasted thoroughly brown.

In addition to the dietetic treatment of the disease, diluents, timeously administered, are of essential service. As a rule, patients are too much restricted from their use, under the supposition that they dilute the gastric juice and thereby impair the digestive power. This restriction is proper at, and for some time after, the ingestion of food. But at the end of the first hour after taking food several ounces of gum-water, or some mucilaginous fluid sweetened and rendered palatable by a few drops of dilute muriatic acid, should be administered, and repeated every hour during the digestive process. Diluents, thus administered, are not only grateful in allaying the thirst of the patient, but are at the same time an essential part of the treatment. The free use of demulcents at the termination of digestion in the stomach is especially useful.

Beyond these general principles of treatment, applicable to all varieties of gastric catarrh, we must have reference to the varied etiology of the disease. This, we have seen, is most complicated. Hence the difficulty in prescribing any rules of treatment applicable to all cases. We should seek here, as in all cases, to generalize the disease and individualize our patient.

Chief among remedial agents may be mentioned the alkaline carbonates. When combined with purgative salines they are specially valuable in gastro-duodenal catarrhs associated with disease of the liver. These are a very numerous class of cases, especially in malarious regions of country, and when present in a chronic form lay the foundation of widespread disorders of nutrition. No treatment in such cases is effective until we diminish engorgements of the liver and spleen, and nothing accomplishes this so well as the use of alkaline saline laxatives. These may be assisted in their action by small doses of mercurials. It was a cardinal principle among the older practitioners, in the absence of more minute means of diagnosis, to look well to the secretions; and what was their strength is, I fear, our weakness.

Wonderful results often follow a course of the Carlsbad, Pullna, or Marienbad waters, taken on an empty stomach, fasting, in the morning. While taking the waters a rigid and restricted diet is enforced. This is an important part of the treatment. And the fact that so many varied ailments are cured by a course of these mineral waters with enforced dietetic regulations only shows the prevalence of gastro-duodenal catarrhs and their relation to a great variety of human ailments. To a certain extent the potassio-tartrate of sodium and other saline laxatives may take the place of these waters if perseveringly used and taken in the same way. In feebler subjects minute doses of strychnia or some of the simple vegetable bitters may be used in conjunction with the laxative salines.

In chronic inflammatory conditions of the gastric mucous membrane, which frequently follow acute attacks, the protracted use of hot water is often followed by excellent results. There can be no doubt of the value {478} of hot water in subacute inflammation of mucous membranes in any locality; and it is specially valuable in gastro-intestinal catarrh associated with lithæmia. Hot water, laxative salines, combined with restricted diet and healthful regimen, accomplish much in correcting morbid conditions of primary assimilation; and by accomplishing this many secondary ailments promptly disappear. A pint of water, hot as the patient can drink it, should be taken on an empty stomach on first rising in the morning, and it may be repeated again an hour before each meal and at bedtime. A few grains of the bicarbonate of sodium and a little table-salt may be added. In some cases three or four drops of tincture of nux vomica or some of the simple bitters may be taken at the same time with benefit. Alkaline bitters are natural to the upper portion of the digestive track. No food should be taken for a half hour or an hour after the hot water. This treatment, to be effective, must be persevered in for a length of time. A most rigid system of dietetics suited to individual cases should be enforced at the same time. This is an important part of the treatment.

In irritable and morbidly sensitive conditions of the mucous membrane the sedative plan of treatment is not unfrequently followed by good results; and of remedies belonging to this class bismuth is the most effective. It is specially indicated in the more irritable forms of gastric disturbance in which there is a sense of uneasiness and pain at the epigastrium after taking food. If there is much acidity present, it may be combined with magnesia or a few grains of finely-pulverized animal charcoal.

Chronic cases of long-continued inflammatory action, with intestinal complication, are often much benefited by the use of mercurials in small doses. The one-fifth of a grain of calomel, combined with bismuth or the bicarbonate of sodium, may be given for weeks without danger of salivation. Excellent results sometimes follow this treatment. In small doses calomel is undoubtedly sedative to the mucous membrane of the upper portion of the digestive track. In cases of long standing that have resisted other modes of treatment the more direct astringents have been found of great value. Of these, nitrate of silver is to be preferred, alike for its sedative, astringent, and alterative properties. It may be given in pill form in from one-quarter to one-grain doses, combined with opium, a half hour before each meal. The writer of this article can speak from much experience of the value of this drug. It proves in many cases a valuable addition to the hot-water and dietetic course already alluded to.

If large quantities of mucus are vomited from time to time, especially in the morning, we may resort with benefit to the use of other astringents, such as bismuth, oxalate of cerium, kino, and opium; and if we have reason to suspect stricture of the pylorus in connection with a catarrhal condition of the mucous membrane, the stomach-pump gives the patient great relief. It should be used about three hours after a meal, injecting tepid water, and then reversing the syringe until the water comes out perfectly clear. Niemeyer speaks highly of it in such cases. He says: "Even the first application of the pump generally gives the patients such relief that, so far from dreading a repetition of this by no means pleasant operation, they clamorously beg for it."

The gastric catarrh of phthisis is difficult to relieve. Artificial digestives may be tried, with dilute muriatic acid, as already indicated; and {479} for the relief of pain and irritation there is no remedy so efficacious as hydrocyanic acid, which may be combined with bismuth and opium in case there is diarrhoea. Hot water may be also tried, with restricted animal food.

Habitual constipation must be overcome by suitable laxatives and by enemata. Castor oil is mild and efficient in these cases, or in cases of unusual torpor of the muscular coat of the bowels small doses of aloes and strychnia may be tried. The free use of diluents toward the close of digestion favors free action of the bowels. All harsh and irritating cathartics are to be carefully avoided.

When there is much tenderness of the epigastrium, benefit may be derived from counter-irritation, and nothing is so effectual as the repeated application of small blisters.

General hygienic measures are in all cases to be insisted upon. In morbid conditions of the liver and the upper portion of the digestive track the free supply of oxygen to the lungs is a remedy of much power. Hence patients should live as much as possible in the open air. They should be warmly clad, and, if not too feeble, frequent cold baths should be resorted to.

After local irritation has been subdued by appropriate treatment, tonics may be tried to counteract the enfeebled state of the stomach. They are such as are appropriate for functional diseases of the stomach. But they should be used with caution and judgment in irritable and inflammatory forms of dyspepsia. If we attempt to force an appetite by their use, and to crowd upon the stomach more food than it has capacity to digest, we may intensify the trouble and thereby add to the patient's general debility. Food and tonics fail to impart strength because the stomach is not in a condition to digest them.

One thing should be mentioned, in conclusion, as an important item in the treatment--namely, patience. Chronic gastric catarrh, it should be remembered, is essentially a chronic disease, and time becomes an important element in its cure.

{480}

SIMPLE ULCER OF THE STOMACH.

BY W. H. WELCH, M.D.

DEFINITION.--Simple ulcer of the stomach is usually round or oval. When of recent formation it has smooth, clean-cut, or rounded borders, without evidence of acute inflammation in its floor or in its borders. When of long duration it usually has thickened and indurated margins. The formation of the ulcer is usually attributed, in part at least, to a disturbance in nutrition and to a subsequent solution by the gastric juice of a circumscribed part of the wall of the stomach. The ulcer may be latent in its course, but it is generally characterized by one or more of the following symptoms: pain, vomiting, dyspepsia, hemorrhage from the stomach, and loss of flesh and strength. It ends frequently in recovery, but it may end in death by perforation of the stomach, by hemorrhage, or by gradual exhaustion.

SYNONYMS.--The following epithets have been employed to designate this form of ulcer: simple, chronic, round, perforating, corrosive, digestive, peptic; ulcus ventriculi simplex, s. chronicum, s. rotundum, s. perforans, s. corrosivum, s. ex digestione, s. pepticum.

HISTORY.--It is only since the description of gastric ulcer by Cruveilhier in the year 1830 that especial attention has been paid to this disease.

In the writings of the ancients only vague and doubtful references to ulcer of the stomach are found (Galen, Celsus). It is probable that cases of this disease were described under such names as passio cardiaca, gastrodynia, hæmatemesis, and melæna.

After the revival of medicine in the sixteenth century, as post-mortem examination of human bodies was made with greater frequency, the existence of ulcers and of cicatrices in the stomach could not escape attention. But only isolated and curious observations of gastric ulcer are recorded up to near the end of the eighteenth century. One of the earliest recorded unmistakable cases of perforating ulcer was observed by John Bauhin, and is described in the Sepulchretum of Bonetus, published in 1679. Other cases belonging to this period were described by Donatus, Courtial, Littré, Schenck, and Margagni.[1]

[Footnote 1: References to these and to other cases may be found in Lebert's Krankheiten des Magens, Tübingen, 1878, p. 180 et seq.]

To Matthew Baillie unquestionably belongs the credit of having first accurately described, in 1793, the anatomical peculiarities of simple gastric ulcer.[2] At a later date he published three good engravings of {481} this disease.[3] Baillie's concise and admirable description of the morbid anatomy of gastric ulcer was unaccompanied by clinical data, and seems to have had little or no influence in directing increased attention to this disease.

[Footnote 2: The Morbid Anatomy of Some of the Most Important Parts of the Human Body, London, 1793, p. 87.]

[Footnote 3: A Series of Engravings, accompanied with Explanations, etc., London, 1799.]

A valuable account of the symptoms of gastric ulcer was given by John Abercrombie in 1824.[4] Nearly all of the symptoms now recognized as belonging to this affection may be found in his article. He knew the latent causes of the disease, the great diversity of symptoms in different cases, and the modes of death by hemorrhage, by perforation, and by asthenia. He regarded ulcer simply as a localized chronic inflammation of the stomach, and did not distinguish carefully between simple and cancerous ulceration.

[Footnote 4: "Contributions to the Pathology of the Stomach, the Pancreas, and the Spleen," Edinburgh Med. and Surg. Journ., vol. xxi. p. 1, Jan. 1, 1824. See also, by the same author, Pathological and Practical Researches on Diseases of the Stomach, etc.--an excellent work which passed through several editions.]

Cruveilhier,[5] in the first volume of his great work on Pathological Anatomy, published between the years 1829 and 1835, for the first time clearly distinguished ulcer of the stomach from cancer of the stomach and from ordinary gastritis. He gave an authoritative and full description of gastric ulcer from the anatomical, the clinical, and the therapeutical points of view.

[Footnote 5: J. Cruveilhier, Anatomie pathologique du Corps humain, tome i., Paris, 1829-35, livr. x. and livr. xx.; and tome ii., Paris, 1835-42, livr. xxx. and livr. xxxi.]

Next to Cruveilhier, Rokitansky has had the greatest influence upon the modern conception of gastric ulcer. In 1839 this pathologist gave a description of the disease based upon an analysis of 79 cases.[6] The anatomical part of his description has served as the model for all subsequent writers upon this subject.

[Footnote 6: Rokitansky, Oesterreich. med. Jahrb., 1839, Bd. xviii. (abstract in Schmidt's Jahrb., Bd. 25, p. 40).]

Since the ushering in by Cruveilhier and by Rokitansky of the modern era in the history of gastric ulcer, medical literature abounds in articles upon this disease. But it cannot be said that the importance of these works is at all commensurate with their number or that they have added very materially to the classical descriptions given by Cruveilhier and by Rokitansky. Perhaps most worthy of mention of the works of this later era are the article by Jaksch relating to symptomatology and diagnosis, that of Virchow pertaining to etiology, the statistical analyses by Brinton, and the contributions to the treatment of the disease by Ziemssen and by Leube.[7] In 1860, Ludwig Müller published an extensive monograph upon gastric ulcer.[8]

[Footnote 7: Jaksch, Prager Vierteljahrschr., Bd. 3, 1844; Virchow, Arch. f. path. Anat., Bd. v. p. 362, 1853, and A. Beer, "Aus dem path. anatom., Curse des Prof. R. Virchow in Berlin, Das einfache duodenische (corrosive) Magengeschwür," Wiener med. Wochenschr., Nos. 26, 27, 1857; Brinton, On the Pathology, Symptoms, and Treatment of Ulcer of the Stomach, London, 1857; V. Ziemssen, Volkmann's Samml. klin. Vorträge, No. 15, 1871; Leube, Ziemssen's Handb. d. spec. Path. u. Therap., Bd. vii., Leipzig, 1878.]

[Footnote 8: Das corrosive Geschwür im Magen und Darmkanal, Erlangen, 1860. Good descriptions of gastric ulcer are to be found in the well-known works on diseases of the stomach by the English writers, Budd, Chambers, Brinton, Habershon, Fenwick, and Wilson Fox.]

ETIOLOGY.--We have no means of determining accurately the average frequency of simple gastric ulcer. The method usually adopted is to observe the number of cases in which open ulcers and cicatrices are found {482} in the stomach in a large number of autopsies. But this method is open to two objections. The first objection is, that scars in the stomach, particularly if they are small, are liable to be overlooked or not to be noted in the record of the autopsy unless special attention is directed to their search. The second objection is, that it is not proven that all of the cicatrices found in the stomach are the scars of healed simple ulcers, and that, in fact, it is probable that many are not. In consequence of these defects (and others might be mentioned) this method is of very limited value, although it is perhaps the best which we have at our disposal.

In 32,052 autopsies made in Prague, Berlin, Dresden, Erlangen, and Kiel,[9] there were found 1522 cases of open ulcer or of cicatrix in the stomach. If all the scars be reckoned as healed ulcers, according to these statistics gastric ulcer, either cicatrized or open, is found in about 5 per cent. of persons dying from all causes.

[Footnote 9: The Prague statistics embrace 11,888 autopsies, compiled from the following sources: 1, Jaksch, Prager Vierteljahrschr., vol. iii.; 2, Dittrich, ibid., vols. vii., viii., ix., x., xii., xiv.; 3, Willigk, ibid., vol. li.; 4, Eppinger, ibid., vol. cxvi.

The Berlin statistics are to be found in dissertations by Plange (abstract in Virchow's Archiv, vol. xviii.), by Steiner, and by Wollmann (abstracts in Virchow und Hirsch's Jahresbericht, 1868), and by Berthold (1883).

The Dresden statistics are in a dissertation by Stachelhausen (Würzburg, 1874), referred to by Birch-Hirschfeld, Lehrb. d. path. Anat., Bd. ii. p. 837, Leipzig, 1877.

The Erlangen statistics are reported by Ziemssen in Volkmann's Samml. klin. Vorträge, No. 15.

The Kiel report is in an inaugural dissertation by Greiss (Kiel, 1879), referred to in the Deutsche med. Wochenschr., Feb. 4, 1882, p. 79.

So far as possible, duodenal ulcers have been excluded. Only those reports have been admitted which include both open ulcers and cicatrices.]

It is important to note the relative frequency of open ulcers as compared with that of cicatrices. In 11,888 bodies examined in Prague, there were found 164, or 1.4 per cent., with open ulcers, and 373, or 3.1 per cent., with cicatrices. Here scars were found about two and one-fourth times as frequently as open ulcers. The observations of Grünfeld in Copenhagen show that when especial attention is given to searching for cicatrices in the stomach, they are found much more frequently than the figures here given would indicate.[10] It would be a moderate estimate to place the ratio of cicatrices to open ulcers at 3 to 1.

[Footnote 10: Grünfeld (abstract in Schmidt's Jahrb., Bd. 198, p. 141, 1883) in 1150 autopsies found 124 cicatrices in the stomach, or 11 per cent., but in only 450 of these cases was his attention especially directed to their search, and in these he found 92 cases, or 20 per cent., with scars. Grünfeld's statistics relate only to persons over fifty years of age. Gastric ulcer, moreover, is extraordinarily common in Copenhagen.

The inexact nature of the ordinary statistics relating to cicatrices is also evident from the fact that in the four collections of cases which comprise the Prague statistics the percentage of open ulcers varies only between 0.81 and 2.44, while the percentage of cicatrices varies between 0.89 and 5.42.]

The statistics concerning the average frequency of open ulcers are much more exact and trustworthy than those relating to cicatrices. It may be considered reasonably certain that, at least in Europe, open gastric ulcers are found on the average in from 1 to 2 per cent. of persons dying from all causes.[11]

[Footnote 11: If in this estimate were included infants dying during the first days of life, the percentage would be much smaller.]

It is manifestly impossible to form an accurate estimate of the frequency of gastric ulcer from the number of cases diagnosed as such {483} during life, because the diagnosis is in many cases uncertain. Nevertheless, estimates upon this basis have practical clinical value. In 41,688 cases constituting the clinical material of Lebert[12] in Zurich and in Breslau between the years 1853 and 1873, the diagnosis of gastric ulcer was made in 252 cases, or about 2/3 per cent.

[Footnote 12: Lebert, op. cit., p. 196.]

Of 1699 cases of gastric ulcer collected from various hospital statistics[13] and examined post-mortem, 692, or 40 per cent., were in males, and 1007, or 60 per cent., were in females. The result of this analysis makes the ratio 2 males to 3 females.

[Footnote 13: These statistics include the previously-cited Prague, Berlin, Dresden, and Erlangen cases so far as the sex is given, and in addition the returns of Rokitansky, op. cit.; Starcke (Jena), Deutsche Klinik, 1870, Nos. 26-29; Lebert, op. cit.; Chambers, London Journ. of Med., July, 1852; Habershon, Dis. of the Abdomen, 3d ed.; Moore, Trans. of London Path. Soc., 1880; and the Munich Hospital, Annalen d. städt. Allg. Krankenh. zu München, vols. i. and ii.

Only series of cases from the post-examinations of a number of years have been admitted. It is an error to include isolated cases from journals, as Brinton has done, because an undue number of these are cases of perforation, which is a more common event in females than in males. Thus, of 43 cases of gastric ulcer presented to the London Pathological Society since its foundation up to 1882, 19, or 44 per cent., were cases of perforation. In my cases are included a few duodenal ulcers not easily separated from the gastric ulcers in the compilation.]

In order to determine from post-mortem records the age at which gastric ulcer most frequently occurs, all cases in which only cicatrices are found should be excluded, because a cicatrix gives no evidence as to the age at which the ulcer existed.

The following table gives the age in 607 cases of open ulcer collected from hospital statistics[14] (post-mortem material):

Age. | No. of cases. | Totals. ----------+---------------+-------- 1-10. | 1 | 10-20. | 32 | 33 ----------+---------------+-------- 20-30. | 119 | 30-40. | 107 | 226 ----------+---------------+-------- 40-50. | 114 | 50-60. | 108 | 222 ----------+---------------+-------- 60-70. | 84 | 70-80. | 35 | 119 ----------+---------------+-------- 80-90. | 6 | 90-100. | ... | Over 100. | 1 | 7 ----------+---------------+--------

From this table it is apparent that three-fourths of the cases are found between the ages of twenty and sixty, and that the cases are distributed with tolerable uniformity between these four decades. The largest number of cases is found between twenty and thirty. The frequency of gastric ulcer after sixty years diminishes, although it remains quite considerable, especially in view of the comparatively small number of those living after that period.

[Footnote 14: The sources of these statistics are the same as those of the statistics relating to sex in the preceding foot-note. The age in the Erlangen cases of open ulcer is given by Hauser (Das chronische Magengeschwür, p. 191, Leipzig, 1883). It is evident that only about two-fifths of the cases could be utilized, partly because in some the age was not stated, but mainly on account of the necessity of excluding scars--a self-evident precaution which Brinton did not take.]

The probability that many cases of ulcer included in the above table existed for several years before death makes it desirable that estimates as to the occurrence of the disease at different ages should be made also from cases carefully diagnosed during life, although the diagnosis must necessarily be less certain than that in the post-mortem records. The best {484} statistics of this character which we possess are those of Lebert, from whose work the following table has been compiled:

Age in 252 Cases of Gastric Ulcer diagnosed during Life by Lebert.[15]

Age. | No. of cases. | Totals. | Per cent. ----------+---------------+---------+---------- 5-10. | 1 | | 11-20. | 24 | 25 | 9.92 ----------+---------------+---------+---------- 21-30. | 87 | | 31-40. | 84 | 171 | 67.85 ----------+---------------+---------+---------- 41-50. | 34 | | 51-60. | 17 | 51 | 20.24 ----------+---------------+---------+---------- 61-70. | 5 | 5 | 1.99 ----------+---------------+---------+----------

Of these cases, nearly seven-tenths were between twenty and forty years of age--a preponderance sufficiently great to be of diagnostic value.[16]

[Footnote 15: Op. cit., p. 199. Of these cases, 19 were fatal, and the diagnosis was confirmed after death. All of the cases were studied by Lebert in hospitals in Zurich and Breslau.]

[Footnote 16: In my opinion, clinical experience is more valuable than are post-mortem records in determining the age at which gastric ulcer most frequently develops. In support of this opinion are the following facts: In many cases no positive conclusions as to the age of the ulcer can be drawn from the post-mortem appearances, and sufficient clinical history is often wanting; a considerable proportion of the cases of gastric ulcer do not terminate fatally with the first attack, but are subject to relapses which may prove fatal in advanced life; in most general hospitals the number of patients in advanced life is relatively in excess of those in youth and middle age. By his faulty method of investigating this question, Brinton came to the erroneous conclusion that the liability to gastric ulcer is greatest in old age--a conclusion which is opposed to clinical experience.]

The oldest case on record is the one mentioned by Eppinger,[17] of an old beggar whose age is stated at one hundred and twenty years.

[Footnote 17: Prager Vierteljahrschrift, Bd. 116.]

The occurrence of simple ulcer of the stomach under ten years of age is extremely rare. Rokitansky, with his enormous experience, said that he had never seen a case under fourteen years.[18] There are recorded, however, a number of cases of gastric ulcer in infancy and childhood, but there is doubt as to how many of these are genuine examples of simple ulcer. Rehn in 1874 analyzed a number, although by no means all, of the reputed cases, and found only six, or at the most seven, which would stand criticism.[19] The age in these seven cases varied between seven days and thirteen years. In one case (Donné) a cicatrix was found in the stomach of a child three years old. Since the publication of Rehn's article at least four apparently genuine cases have been reported--namely, one by Reimer in a child three and a half years old; one by Goodhart in an infant thirty hours after birth; one by Eröss in a girl twelve years old suffering from acute miliary tuberculosis, in whom the ulcer perforated into the omental sac; and one by Malinowski in a girl ten years of age.[20]

[Footnote 18: Communication to Von Gunz in Jahrbuch d. Kinderheilkunde, Bd. 5, p. 161, 1862.]

[Footnote 19: Jahrb. d. Kinderheilk., N. F., Bd. 7, p. 19, 1874.]

[Footnote 20: Reimer, ibid., Bd. x. p. 289, 1876; Goodhart, Trans. London Path. Soc., vol. xxxii. p. 79, 1881; Eröss, Jahrb. f. Kinderheilk., Bd. xix. p. 331, 1883; Malinowski, Index Medicus, vol. v. p. 575, New York, 1883.

Rehn does not mention Buzzard's case of perforating ulcer in a girl nine years old (Trans. London Path. Soc., vol. xii. p. 84, 1861). See also Chvostek's case of round ulcer in a boy (Arch. f. Kinderheilk., 1881-82) and Wertheimber's case of recovery from gastric ulcer in a girl ten years old (Jahrb. f. Kinderheilk., Bd. xix. p. 79).]

The mean age at which gastric ulcer develops is somewhat higher in {485} the male than in the female. This is apparent from the following collection of 332 cases of open ulcer in which both age and sex are given:[21]

Age. | Males. | Females. ----------+--------+--------- 10-20. | 9 | 13 20-30. | 33 | 35 30-40. | 44 | 25 40-50. | 39 | 25 50-60. | 37 | 18 60-70. | 20 | 18 70-80. | 5 | 9 80-90. | 1 | ... 90-100. | ... | ... Over 100. | 1 | ... ----------+--------+--------- Total. | 189 | 143 ----------+--------+---------

In males the largest number of cases is found between thirty and forty years, and in females between twenty and thirty. In males 54½ per cent. of the cases occur after forty years of age, and in females 48.9 per cent.

[Footnote 21: These cases are obtained from the same sources as those of the first table (page 483).]

The relation between age and perforation of gastric ulcer will be discussed in connection with this symptom.

The conclusions concerning the age of occurrence of gastric ulcer may be recapitulated as follows: Simple ulcer of the stomach most frequently develops in the female between twenty and thirty, and in the male between thirty and forty. At the post-mortem table it is found with almost equal frequency in the four decades between twenty and sixty, but clinically it appears with greatly diminished frequency after forty years of age. In infancy and early childhood simple ulcer of the stomach is a curiosity.

We have no positive information as to the influence of climate upon the production of gastric ulcer. The disease seems to be somewhat unequal in its geographical distribution, but the data bearing upon this point are altogether insufficient.

According to the returns of Dahlerup and of Grünfeld, gastric ulcer is unusually common in Copenhagen.[22] According to Starcke's report[23]--which, however, is not based upon a large number of cases--the percentage is also unusually high in Jena. Sperk says that gastric ulcer is very common in Eastern Siberia.[24] Palgrave gives a high percentage of its occurrence in Arabia.[25] The disease is less common in France than in England or in Germany,[26] and in general appears to be more common in northern than in southern countries. The statement of DaCosta[27] coincides with my own impression that gastric ulcer is less common in this country than in England or in Germany. I have found 6 cases of open ulcer of the stomach in about 800 autopsies made by me in New York.

[Footnote 22: Dahlerup in Copenhagen (abstract in Canstatt's Jahresbericht, 1842) found 26 cases in 200 autopsies (13 per cent.) made in the course of a year and a half. Grünfeld (loc. cit.) found 124 cicatrices in 1150 autopsies (11 per cent.).]

[Footnote 23: Starke (loc. cit.) found 39 cases in 384 autopsies (10 per cent.); cf. also Müller, Jenaische Zeitschr., v. 1870.]

[Footnote 24: Deutsche Klinik, 1867.]

[Footnote 25: Narrative of a Year's Journey through Central and Eastern Arabia, London, 1865.]

[Footnote 26: Laveran and Teissier, Nouveaux Éléments de Path. et de Clin. méd., t. ii. p. 1060, Paris, 1879; and Godin, Essai sur l'Ulcère de l'Estomac, Thèse, Paris, 1877, p. 8.]

[Footnote 27: Medical Diagnosis, 5th ed., Philada., 1881. Keating expresses the same opinion in the Proc. of Path. Soc. of Philadelphia, vol. i. p. 142.

In 444,564 deaths in New York City from 1868 to 1882, inclusive, ulcer of the stomach was assigned as the cause of death only in 410 cases. Little value can be assigned to these statistics as regards a disease so difficult of diagnosis.]

{486} Gastric ulcer is more common among the poor than among the rich. Anxiety, mental depression, scanty food, damp dwellings, insufficient exercise, and exposure to extreme cold are among the depressing influences which have been assigned as predisposing causes of gastric ulcer, but without sufficient proof.

The comparative frequency of gastric ulcer among needlewomen, maidservants, and female cooks has attracted the attention of all who have had large opportunity for clinical observation.

Pressure upon the pit of the stomach, either by wearing tight belts or in the pursuit of certain occupations, such as those of shoemaking, of tailoring, and of weaving, is thought by Habershon and others to predispose to ulcer of the stomach.[28]

[Footnote 28: Bernutz found gastric ulcer in a turner in porcelain, and learned that other workmen in the same factory had vomited blood. He thinks that in this and in similar occupations heavy particles of dust collecting in the mouth and throat may be swallowed with the saliva, and by their irritation cause gastric ulcer (Gaz. des Hôpitaux, June 18, 1881).]

Vomiting of blood has been known in several instances to affect a number of members of the same family, but beyond this unsatisfactory evidence there is nothing to show hereditary influence in the origin of gastric ulcer.

In a few cases injury of the region of the stomach, as by a fall or a blow, has been assigned as the cause of ulcer. The efficacy of this cause has been accepted by Gerhardt,[29] Lebert, Ziemssen, and others. In many of the cases in which this cause has been assigned the symptoms of ulcer appeared so long after the injury that it is doubtful whether there was any connection between the two.

[Footnote 29: "Zur Aetiologie u. Therapie d. runden Magengeschwürz," Wiener med. Presse, No. 1, 1868.]

That loss of substance in the mucous membrane of the stomach may be the result of injury directly or indirectly applied to this organ cannot admit of question. But it is characteristic of these traumatic ulcers that they rapidly heal unless the injury is so severe as to prove speedily fatal. Thus, Duplay[30] relates three cases in which pain, vomiting, repeated vomiting of blood, and dyspepsia followed contusions of the region of the stomach. But these traumatic cases, which for a time gave the symptoms of gastric ulcer, recovered in from two weeks to two months, whereas the persistence of the symptoms is a characteristic of simple ulcer.[31]

[Footnote 30: "Contusions de l'Estomac," Arch. gén. de Méd., Sept., 1881.]

[Footnote 31: In a case reported by Potain, however, the symptoms of ulcer appeared immediately after injury to the stomach, and continued up to the time of death (Gaz. hebdom., Sept. 12, 1856).]

In the same way, ulcers of the stomach produced by corrosive poisons as a rule soon cicatrize, unless death follows after a short time the action of the poison. That corrosive ulcers may, however, be closely allied to simple ulcers is shown by an interesting case reported by Wilson Fox,[32] in which the immediate effects of swallowing hydrochloric acid were recovered from in about four days, but death resulted from vomiting of blood two weeks after. At the autopsy the source of the hemorrhage was found in an ulcer of the pyloric region of the stomach. An equally striking case is reported by Williams.[33] A boy who suffered severely for three or four days after drinking some strong mineral acid recovered, so that he {487} ate and drank as usual. Two months afterward he died suddenly from perforation of a gastric ulcer.

[Footnote 32: Trans. of the Path. Soc., vol. xix. p. 239, London, 1868.]

[Footnote 33: The Lancet, April 9, 1842.]

While, then, it would be a great error to identify traumatic and corrosive ulcers of the stomach with simple ulcer, it is possible that either may become chronic if associated with those conditions of the stomach or of the constitution, for the most part unknown to us, which prevent the ready healing of simple ulcer.

Gastric ulcer is often associated with other diseases, but it occurs also uncomplicated in a large number of cases. Most of the diseases with which it has been found associated are to be regarded simply as coincident or complicating affections; but as some of them have been thought to cause the ulcer, they demand consideration in this connection.

The large share taken by pulmonary phthisis in deaths from all causes renders this disease a frequent associate of gastric ulcer. It is probable that the lowered vitality of phthisical patients increases somewhat their liability to gastric ulcer. Moreover, it would not be strange if gastric ulcer, as well as other exhausting diseases, such as diabetes and cancer, diminished the power of resisting tuberculous infection. Genuine tuberculous ulcers occur rarely in the stomach, but they are not to be identified with simple ulcer.

There is no proof that amenorrhoea or other disorders of menstruation exert any direct influence in the production of gastric ulcer, although Crisp went so far as to designate certain cases of gastric ulcer as the menstrual ulcer.[34] Nevertheless, amenorrhoea is a very common symptom or associated condition in the gastric ulcer of females between sixteen and thirty years of age.

[Footnote 34: The Lancet, Aug. 5, 1843.]

Chlorosis and anæmia, especially in young women, favor the development of gastric ulcer, but that there is no necessary relation between the two is shown by the occurrence of ulcer in those previously robust. Moreover, it is probable that in some cases in which the anæmia has been thought to precede the ulcer it has, in fact, been a result rather than a cause of the ulcer.

Especial interest attaches to the relation between gastric ulcer and diseases of the heart and of the blood-vessels, because to disturbances in the circulation in the stomach the largest share in the pathenogenesis of ulcer has been assigned by Virchow. As might be expected, valvular lesions of the heart and atheroma of the arteries are not infrequently found in elderly people who are the subjects of gastric ulcer. A small proportion of cases of ulcer has been associated also with other diseases in which the arteries are often abnormal, such as with chronic diffuse nephritis, syphilis, amyloid degeneration, and endarteritis obliterans. But, after making the most generous allowance for the influence of these diseases in the causation of ulcer of the stomach, there remains a large number of cases of ulcer in which no disease of the heart or of the arteries has been found.[35] Gastric ulcer develops most frequently between fifteen and forty years of age, a period when arterial diseases are not common. Changes in the {488} blood-vessels of the stomach will be described in connection with the morbid anatomy of gastric ulcer.

[Footnote 35: From Berlin are reported the largest number of cases of gastric ulcer associated with diseases of the circulatory apparatus; thus, by Berthold 170 out of 294 cases, and by Steiner 71 out of 110 cases of ulcer. Endocarditis and arterial atheroma (present in one-third of Berthold's cases of ulcer) form the largest proportion of these diseases.]

Chronic passive congestion of the stomach in cases of cirrhosis of the liver, direct injury to the mucous membrane of the stomach by parasites in trichinosis, hemorrhage into the coats of the stomach in scorbutus and in dementia paralytica, persistent vomiting in pregnancy, and anæmia induced by prolonged lactation, have each been assigned as causes in a few cases of gastric ulcer, but they are not associated with gastric ulcer in enough cases to make their causative influence at all certain.

Galliard assigns diabetes mellitus as the cause in one case of gastric ulcer.[36]

[Footnote 36: Clin. méd. de la Pitié, Paris, 1877, p. 77.]

Rokitansky attributed some cases of gastric ulcer to intermittent fever.

Those who believe in the inflammatory origin of ulcer of the stomach think that chronic gastritis is an important predisposing cause.

The abuse of alcohol is admitted as an indirect cause of gastric ulcer by the majority of writers.

Lastly, burns of the skin, which are an important factor in the etiology of duodenal ulcers, have been followed only in a very few instances by ulcer of the stomach.

The direct causes of ulcer of the stomach, concerning which our positive knowledge is very limited, will be considered under the pathenogenesis of the disease.

SYMPTOMATOLOGY.--The following classes of cases of gastric ulcer may be distinguished:

First: Gastric ulcer may give rise to no symptoms pointing to its existence, and be found accidentally at the autopsy when death has occurred from some other disease. This latent course is most frequent with gastric ulcers complicating chronic wasting diseases, such as tuberculosis, and with gastric ulcers in elderly people.

Second: Gastric ulcer may give rise to no marked symptoms before profuse hemorrhage from the stomach or perforation of the stomach, resulting speedily in death, occurs. Acute ulcers in anæmic females from fifteen to thirty years of age are those most liable to perforate without previous symptoms.

Third: Gastric ulcer may occasion only the symptoms of chronic gastritis, or of functional dyspepsia, or of purely nervous gastralgia, so that its diagnosis is impossible. In this class of cases after a time characteristic symptoms may develop. Here, too, sudden death may occur from hemorrhage or from perforation.

Fourth: In typical cases characteristic symptoms are present, so that the diagnosis can be made more or less positively. These symptoms are pain, and hemorrhage from the stomach, associated usually with vomiting and disturbances of digestion.

The different symptoms of gastric ulcer will now be described.

Of all the symptoms, pain is the most constant and is often the first to attract attention. It is absent throughout the disease only in exceptional cases. In different cases, and often in the same case at different times, the pain varies in its quality, its intensity, its situation, its duration, and in other characteristics.

The kind of pain which is most characteristic of gastric ulcer is severe {489} paroxysmal pain strictly localized in a circumscribed spot in the epigastrium, coming on soon after eating, and disappearing as soon as the stomach is relieved of its contents.

More common, although less characteristic, than the strictly localized pain are paroxysms of severe pain, usually called cardialgic[37] or gastralgic, diffused over the epigastrium and often spreading into the surrounding regions. This is like the neuralgic pain of nervous gastralgia, which is not infrequent in chlorotic and hysterical females. The pain may be so intense as to induce syncope, or even convulsions, in very sensitive patients.

[Footnote 37: There is much confusion as to the meaning of the term cardialgia. With most English and American writers it signifies heartburn, while continental writers understand by cardialgia the severe paroxysms of epigastric pain which we more frequently call gastralgia.]

The strictly localized pain is probably caused by direct irritation confined to the nerves in the floor of the ulcer. In the diffuse gastralgic attacks the irritation radiates or is reflected to the neighboring nerves, and sometimes to those at a distance.

In most cases of gastric ulcer localized epigastric pain and diffuse gastralgic paroxysms are combined.

The painful sense of oppression and fulness in the epigastrium which is felt in many cases of gastric ulcer after eating is simply a dyspeptic symptom, and is probably referable to an associated chronic catarrhal gastritis. This dyspeptic pain is of little value in diagnosis.

Most subjects of gastric ulcer feel in the intervals between the paroxysms a more or less constant dull pain, or it may be only a sense of uneasiness, in the epigastrium. When sharp epigastric pain is felt continuously, it is usually inferred that the ulcer has extended to the peritoneum and has caused a circumscribed peritonitis, but this inference is not altogether trustworthy.

The quality of the pain caused by gastric ulcer is described variously as burning, gnawing, boring, less frequently as lancinating.

More important than the quality is the situation of the pain. The situation of the localized pain is usually at or a little below the ensiform cartilage. It may, however, be felt as low as the umbilicus or it may deviate to the hypochondria. In addition to pain in the epigastrium (point épigastrique), Cruveilhier called attention to the frequent presence of pain in the dorsal region (point rachidien). The dorsal pain, which may be more severe than the epigastric, is sometimes interscapular, and sometimes corresponds to the lowest dorsal or to the upper lumbar vertebræ. It is usually a little to the left of the spine. The pain is often described as extending from the pit of the stomach through to the back.

According to Brinton, the situation of the localized pain gives a clue to the situation of the ulcer, pain near the left border of the ensiform cartilage indicating ulcer near the cardiac orifice, pain in the median line and to the right of this indicating ulcer of the pyloric region, and pain in the left hypochondrium indicating ulcer of the fundus. It does not often happen that the pain remains so sharply localized as to make possible this diagnosis, even if the situation of the pain were a safe guide.

Of the various circumstances which influence the severity of the pain in gastric ulcer, the most important is the effect of food. Pain usually {490} comes on within a few minutes to half an hour after taking food, although it may appear immediately after ingestion or be delayed for an hour or more. The pain continues until the stomach is relieved of its contents by vomiting or by their passage into the duodenum. It is unsafe to attempt to diagnose the position of the ulcer merely from the length of time which elapses between the ingestion of food and the onset of pain. It has sometimes been noticed that as improvement progresses pain comes on later and later after eating. As might naturally be expected, coarse, indigestible, imperfectly-masticated food, sour and spirituous liquids, and hot substances are more irritating than bland articles of diet. In some exceptional cases the ingestion of even coarse food, instead of aggravating, has had no effect upon the pain, or at least for the time being has even relieved it.

External pressure usually increases the intensity of the pain of gastric ulcer; in rare instances pressure relieves the pain.

Rest and the recumbent posture as a rule alleviate the pain of ulcer of the stomach. The position of the patient may affect the severity of the pain in a more striking way. It may naturally be supposed that that posture is most agreeable which removes from the ulcer the weight of the food during digestion. Hence it was claimed by Osborne[38] that the site of the ulcer could often be inferred from the effect of posture on the pain. Thus, relief in the prone position would indicate ulcer of the posterior wall; relief in the supine position, ulcer of the anterior wall; relief on the left or on the right side, ulcer of the pyloric or of the cardiac region respectively. As ulcer of the posterior wall is the most frequent, relief should be obtained oftener by bending forward or by lying on the face than in the supine position. Experience has shown that the influence of posture on the pain is not a safe guide in diagnosing the location of the ulcer.

[Footnote 38: Jonathan Osborne, Dublin Journal of Medical Science, vol. xxvii. p. 357, 1845.]

Mental emotions--particularly anxiety and anger--fatigue, even moderate exercise, exposure to cold, and the menstrual molimen may each cause exacerbations of pain in some cases of gastric ulcer.

Tenderness on pressure is a common symptom of gastric ulcer. A localized point of tenderness may be discovered even when the subjective pain is not localized. Pain sometimes follows pressure not immediately, but after a brief interval. A fixed point of tenderness can often be determined when the stomach is empty more accurately than when it is full. The tender spot can sometimes be covered by the finger's end. In searching for a point of tenderness it should be remembered that many persons are very sensitive to pressure in the epigastrium, and also that pressure is not without danger to those who are the subjects of gastric ulcer. Not only may pressure induce paroxysms of pain, but it may cause even rupture of the ulcerated walls of the stomach.[39] Hence pressure should be cautiously employed and should not be often repeated.

[Footnote 39: Dalton has reported a case in which perforation of a gastric ulcer occurred while the patient was subjected in a water-cure establishment to kneading of the abdomen to relieve his flatulence (Trans. N.Y. Path. Soc., vol. i. p. 263.)]

In some cases of gastric ulcer pain is felt in regions at a distance from the stomach. The most frequent of these so-called radiation neuralgias are--neuralgia of the lower intercostal spaces, combined sometimes with {491} hyperæsthesia or with analgesia of the affected region, pain in the right shoulder (perhaps due to adhesions between the stomach and the liver or the diaphragm), pain in the left shoulder, and pain in the loins. In a case of ulcer reported by Traube terminating in perforation the sole complaint, besides loss of appetite and retching, had been difficulty in breathing and oppression in the chest. These symptoms, which may be combined with gastralgic paroxysms, are referred by Traube to transference of the irritation from the gastric to the pulmonary filaments of the pneumogastric nerve.[40]

[Footnote 40: Deutsche Klinik, 1861, No. 10. These symptoms evidently correspond to the vagus neurosis described by Rosenbach, in which, as the result of reflex irritation of the pneumogastric nerve in the stomach, occur difficulty in breathing, oppression in the chest, palpitation, arhythmical action of the heart, and epigastric pulsation (Deutsche med. Wochenschr., 1879, Nos. 42, 43).]

Sometimes the pain of gastric ulcer intermits for days or even weeks. When the intermission is of considerable duration it is probable that cicatrization has been in progress. It should, however, be remembered that gastralgic attacks may continue even after cicatrization of the ulcer is completed, probably in consequence of compression of nerve-filaments by the cicatricial tissue. Once in a while the pain exhibits a marked periodicity in its appearance. Thus in a case of ulcer ending fatally from hemorrhage the pain came on but once a day, and that with considerable regularity at the same hour. In this case the pain was relieved by taking food.[41] The pain of gastric ulcer may be temporarily relieved by hemorrhage from the stomach, and perhaps by division of the irritated nerve by sloughing (Habershon).

[Footnote 41: Case reported by Peacock, Rep. of Proceedings of London Path. Soc., vol. i. p. 253, 1847.]

The causes of the pain of gastric ulcer are not far to seek. Foremost is the irritation of nerve-filaments exposed by the ulcerative process. The irritation may be by mechanical, chemical, or thermic agencies. With our present imperfect knowledge it is profitless to discuss whether the pneumogastric or the sympathetic nerves are the chief carriers of the abnormal sensations.[42] In the next place, we may have radiation of the irritation from these nerves to neighboring and even to remote nerves. Furthermore, the extension of the inflammation to the peritoneum and the surrounding parts, and the formation of adhesions, are additional factors in some cases in causing pain. Finally, the great differences in susceptibility to pain manifested by different individuals is to be borne in mind.

[Footnote 42: Leven, without sufficient reason, distinguishes two kinds of gastralgic attacks--the one having its point of departure in the pneumogastric, the other in the sympathetic nerve; in the former the pain is associated with dyspnoea and palpitation of the heart; in the latter the pain is deeper, and is accompanied by vaso-motor (?) troubles on one side of the body.]

Next to pain, vomiting is the most frequent symptom of gastric ulcer. There is, however, little which is characteristic of ulcer in this symptom, unless the vomited material contains blood. In some cases of gastric ulcer vomiting is the most marked and most distressing symptom of the disease. It may, however, be absent during the whole course of gastric ulcer.

Vomiting occurs most frequently after taking food, and is greatly aggravated by an unregulated diet. Sometimes nearly everything which is taken into the stomach is vomited. The vomiting of mucus or of a {492} thin fluid unmixed with food is indicative only of chronic catarrhal gastritis. Alimentary vomiting, which is more indicative of gastric ulcer, usually occurs not immediately after taking food, but at the acme of a gastralgic attack caused by the food. Soon after the stomach is emptied by one or more acts of vomiting the pain is relieved. The act of vomiting is usually easy, and at times is hardly more than regurgitation of the food. Sometimes the patient experiences an excessively sour taste from the vomit.

Vomiting exhausts the patient by withdrawing nutriment, and when persistent may even cause death from inanition. But in some cases of gastric ulcer, especially in women, the vomiting seems to be mainly a nervous symptom, and even when long continued may be attended by little or no loss of flesh. Evidently, more food is retained in these cases than might be supposed.

There are two evident causes of vomiting in gastric ulcer--namely, chronic catarrhal gastritis, which is a frequent complication, and direct irritation of the nerves in the ulcer. Vomiting due to dilatation of the stomach is oftener a sequel than an immediate symptom of gastric ulcer.

For the diagnosis of gastric ulcer hemorrhage from the stomach is the most important symptom.

The frequency of only the larger hemorrhages can be determined with any degree of exactness. If the blood be effused in small quantity or slowly, it may be discharged solely with the stools and escape detection. Such slight hemorrhages doubtless occur in most cases of gastric ulcer. It is probable that easily-recognized hemorrhages from the stomach occur in about one-third of the cases of gastric ulcer.[43] Hemorrhage is absent as a rule in the acute perforating ulcer of the stomach.

[Footnote 43: In consequence of the uncertainty of the diagnosis in cases of gastric ulcer which recover without hemorrhage, the estimates of the frequency of this symptom have a very limited value, and will vary with different observers according to their standard of diagnosis of this disease. Lebert observed gastric hemorrhage in four-fifths of his carefully-studied cases, and in three-fifths of his cases there was profuse hæmatemesis. Brinton estimates that the larger hemorrhages occur in about one-third of the cases. Müller found them in one-fourth of the cases which he analyzed.]

In most cases hemorrhage from gastric ulcer is preceded by pain, vomiting, and disturbances of digestion. Antecedent symptoms may, however, be absent, or may be so obscure that no suspicion of ulcer exists until the hemorrhage occurs.

The hemorrhage may be slight, moderate, or excessive in amount (Cruveilhier). The larger hemorrhages are those which are most distinctive of gastric ulcer.

The blood may be vomited, or voided with the stools, or retained in the stomach and the intestines.

As has been remarked, when the hemorrhage is scanty all the blood may escape by the bowel. Sometimes, although much less frequently, blood effused in large quantity is entirely evacuated with the stools. After hæmatemesis more or less blood is discharged by the bowel, sometimes for several days after the vomiting of blood has ceased. Blood which has traversed the whole length of the intestinal canal acquires a tarry consistence and a black or brownish color in consequence of the production of dark-brown hæmatin by the action of the digestive juices {493} upon the hæmoglobin, and in consequence of the formation of black sulphide of iron by the union of hydrogen sulphide in the lower part of the intestine with the iron of the hæmatin. The passage of these black viscid stools is called melæna. Inasmuch as we cannot presume gastric hemorrhage to be absent simply because no blood has been vomited, it is evidently important to examine the stools for blood when the diagnosis of gastric ulcer is obscure, and also in cases of gastric ulcer where there are symptoms of internal hemorrhage not accounted for by blood vomited. It should be remembered that certain drugs, particularly iron and bismuth, may blacken the feces.

In very exceptional cases of gastric ulcer the effusion of a large volume of blood causes sudden death before any of the blood has been vomited. The autopsy shows the stomach and more or less of the small intestine distended with coagulated blood.

Hemorrhage from gastric ulcer is usually made manifest by the vomiting of blood. The quantity of the vomited blood varies from mere traces to several pounds. The color and the consistence of the blood depend upon the quantity effused and the length of time that the blood has remained in the stomach. Blood which has been acted upon by the gastric juice is coagulated, has a grumous consistence, and acquires by the formation of hæmatin out of hæmoglobin a dark-brown color, often compared to that of coffee-grounds. Blood effused in small quantity is usually vomited only with the food, and has usually the coffee-grounds appearance. The patient's condition is not appreciably influenced by this slight loss of blood. A little blood expelled after repeated acts of vomiting has no diagnostic importance. Vomiting usually occurs soon after a large gastric hemorrhage. It is the mechanical distension of the stomach rather than any irritating quality of the blood which causes the vomiting. Blood which is rejected immediately after a large gastric hemorrhage is alkaline, fluid, and of an arterial (rarely of a venous) hue. Often, however, even with large hemorrhages, the blood remains sufficiently long in the stomach to be partly coagulated and to be darkened in color. Ulcer more frequently than any other disease of the stomach causes the vomiting of unaltered blood in large quantity. But this kind of hæmatemesis is not peculiar to simple ulcer. It may occur in other diseases, such as gastric cancer, and coffee-ground vomiting may be associated with ulcer.

Copious hæmatemesis in cases of gastric ulcer appears usually without premonition, or it may be preceded for a day or two by increased pain. Its occurrence is somewhat more common during the digestion of food than in the intervals, but there have been cases of ulcer where the bleeding was favored by an empty stomach and was checked by the distension of the organ with food. The free use of stimulants and violent physical or mental exertion may excite hemorrhage. With the onset of the hemorrhage the patient experiences a sense of warmth and of oppression at the epigastrium, followed by faintness, nausea, and the vomiting of a large quantity of blood. An attack of syncope often causes, at least temporarily, cessation of the hemorrhage. But the thrombus which closes the eroded vessel may easily be washed away, so that the hemorrhage often recurs and continues at intervals for several days, thereby greatly increasing the danger to the patient. Thus, the tendency is for {494} the hemorrhage from gastric ulcer to appear in phases or periods occupying several days.

A single hemorrhage is rarely so profuse as to cause immediate death. More frequently the patient dies after successive hemorrhages. In the majority of cases the hemorrhage is not immediately dangerous to life, but is followed by symptoms of anæmia, more or less profound according to the strength of the patient and the amount of blood lost. Prostration and pallor follow the larger hemorrhages. Dizziness, ringing in the ears, and dimness of vision appear when the patient attempts to leave the recumbent posture. Thirst is often a marked symptom. The pulse is feeble and more frequent than normal. There is often a moderate elevation of temperature (anæmic fever) after profuse hemorrhage. The urine is pale, abundant, and sometimes contains albumen (Quincke). After a few days anæmic cardiac murmurs can often be heard. Under favorable circumstances these symptoms of anæmia disappear in the course of a few weeks.

The other symptoms of ulcer, particularly the pain, are sometimes notably relieved, and may even disappear, after an abundant hemorrhage. They usually, however, return sooner or later. After a variable interval one attack of hæmatemesis is likely to be followed by others. There is much diversity in different cases as regards the frequency of these attacks and the character of the symptoms in the intervals. In a few cases recovery follows a single attack of gastric hemorrhage; in other cases the hemorrhage recurs frequently after intervals of only a few days, weeks, or months; in still other cases hemorrhage recurs only after long intervals, perhaps of years, although other symptoms of ulcer continue. Sometimes the disappearance of symptoms indicates only an apparent cure, and later the patient dies suddenly while in apparent health by a profuse gastric hemorrhage. In the rare cases of this last variety Cruveilhier has found sometimes that the ulcer has cicatrized except just over the eroded blood-vessel.

The sources of the hemorrhage in gastric ulcer will be described in connection with the morbid anatomy.

The symptoms of gastric indigestion are commonly, although not constantly, present in gastric ulcer. They may constitute the sole symptoms, in which case the diagnosis of the lesion is impossible. The most important local symptoms of gastric dyspepsia are diminution, less frequently perversion or increase, of the appetite; increased thirst; during digestion, and sometimes independent of digestion, a feeling of discomfort merely or of painful oppression, or even of sharp pain, in the epigastrium; nausea; vomiting of undigested food, of mucus, and of bile; regurgitation of thin fluids; often acid, sometimes neutral or alkaline, flatulence, with belching of gas, and constipation. In many cases of gastric ulcer the appetite is not disturbed, but the patient refrains from eating on account of the pain caused by taking food. Among the so-called sympathetic symptoms of dyspepsia are headache, dizziness, depression of spirits, oppression in the chest, and irregularity of the heart's action. Dyspepsia contributes its share to the production of the anæmia and of the loss of flesh and strength which are present in some degree in most cases of chronic gastric ulcer.

{495} In many cases of acute perforating ulcer, as well as in some cases of chronic ulcer, the symptoms are either absent or they are but slightly marked. It has been demonstrated that in many cases of gastric ulcer the resorptive power of the mucous membrane of the stomach is unimpaired.[44]

[Footnote 44: This is shown by the experiments of Pentzoldt and Faber, who determined the length of time which elapsed between swallowing gelatin capsules containing iodide of potassium and the appearance of the iodide in the saliva (Berl. klin. Wochenschr., No. 21, 1882). Quetsch observed rapid absorption from the stomach in two cases of gastric ulcer (ibid., 1884, No. 23). It is believed that also the duration of the digestive process in the stomach is often within normal limits in cases of gastric ulcer, although exact experiments upon this point, as they require the use of the stomach-pump, have not been made in this disease (Leube).]

The most common cause of dyspepsia in gastric ulcer is the chronic catarrhal gastritis which usually accompanies this disease. It is probable that the movements of the stomach may be seriously interfered with by destruction of the muscular coat of the stomach when the ulcer is of considerable size and is seated in the pyloric region. Adhesions of the stomach to surrounding parts may likewise impair the normal movements of the stomach. It is possible that ulcers, especially those which are very painful, may cause reflex disturbance of the peristaltic movements of the stomach and alterations in the quality or the quantity of the gastric juice. The serious digestive disturbances which are caused by distortions and dilatation of the stomach resulting from cicatricial contraction of gastric ulcer are not considered in this article.

Although Niemeyer emphasized the frequency in gastric ulcer of a strikingly red tongue with smooth or furrowed surface, it does not appear that any especial importance is to be attached to this or to any other condition of the tongue as a symptom of the disease.

Increased flow of saliva is a rare symptom, which, when it occurs, is usually associated with dyspepsia.

Constipation is the rule in gastric ulcer. The most important of the various circumstances which combine to produce this condition is the small amount of solid food taken and retained by the patient. The restraint caused by gastric ulcer and gastric catarrh in the normal movements of the stomach may diminish by reflex action the peristalsis of the intestines (Traube and Radziejewski). The passage of large quantities of blood along the intestinal canal is often associated with colicky pains and diarrhoea.

Amenorrhoea is a symptom which was formerly thought to be characteristic of gastric ulcer, although there was much discussion as to whether it was the cause or the result of the ulcer. Amenorrhoea is indeed common in the gastric ulcer of young women, but there is nothing strange in this when one considers the frequency of amenorrhoea in general, and its causation by various debilitating and depressing influences such as are to be found in gastric ulcer. Notwithstanding a few striking cases which have been recorded, it has not been demonstrated that hemorrhages vicarious of menstruation take place from gastric ulcer.

Gastric ulcer is not a febrile disease. Temporary elevation of temperature may follow profuse gastrorrhagia and may attend various complications, of which the most important are gastritis and peritonitis. It has been recently claimed by Peter that the surface-temperature of the {496} epigastrium is elevated in gastric ulcer, but the observations upon this point are as yet too few for any positive conclusions.[45]

[Footnote 45: According to Peter, the normal surface-temperature of the epigastrium is from 95½° to 96° F. (35.3° to 35.5° C.), while in gastric ulcer the temperature may equal or even exceed by one or two degrees the axillary temperature. It is said to register the highest during attacks of pain and of vomiting and after hemorrhages (Gaz. des Hôpitaux, June 23 and 30, 1883). See also Beaurieux (Essai sur la Pseudo-gastralgie, etc., Thèse, Paris, 1879).]

The general health of the patient remains sometimes surprisingly good, even in cases of gastric ulcer with symptoms sufficiently marked to establish the diagnosis. But in most cases of chronic gastric ulcer the general nutrition sooner or later becomes impaired. This cannot well be otherwise when dyspepsia, vomiting, paroxysms of severe pain, and hemorrhage are present, separately or in combination, for any great length of time. In proportion to the severity and the continuance of these symptoms the patient becomes pale, weak, and emaciated. The face, thin, anxious, of a grayish-white color, and marked with sharp lines of suffering, presents the appearance which the older writers called facies abdominalis, to which even so recent an author as Brinton attaches exaggerated diagnostic importance. A little cachectic dropsy may appear about the ankles. While it is true that the general nutrition is less rapidly, less continuously, and, as a rule, less deeply, impaired in gastric ulcer than in gastric cancer, nevertheless sometimes a cachexia develops in the former which is not to be distinguished from that of cancer. Litten[46] relates a case of gastric ulcer which simulated for a time pernicious anæmia. In this case the profound anæmia could not be explained by vomiting, hemorrhage, or other symptoms of ulcer.

[Footnote 46: Berliner klin. Wochenschrift, Dec. 6, 1880.]

Beyond determining the existence of a fixed point of epigastric tenderness, physical examination of the region of the stomach is usually only of negative value in the diagnosis of gastric ulcer. In some cases of ulcer of the stomach epigastric pulsation is very marked, and sometimes most marked during gastralgic attacks. In these cases there may be dilatation of the aorta from paralysis of vaso-motor nerves analogous to the dilatation of the carotid and temporal arteries in certain forms of migraine (Rosenbach). When the diagnosis lies between gastric ulcer and gastric cancer, the presence of epigastric tumor is justly considered to weigh against ulcer; but it is important to know that tumor may be associated with ulcer. Thickening of the tissues around old ulcers and the presence of adhesions may give rise to a tumor. A thickened portion of omentum which had become adherent over an old gastric ulcer produced a tumor which led to a mistake in the diagnosis.[47] Rosenbach[48] calls attention to the occasional production of false tumors by spasm of the muscular coat of the stomach around a gastric ulcer. These tumors disappear spontaneously or yield to the artificial distension of the stomach by Seidlitz powders--a procedure which one would not venture to adopt if he suspected gastric ulcer. Fenwick thinks that in some cases of gastric ulcer fixation of the stomach by adhesions can be made out by physical exploration.

[Footnote 47: A. Beer, Wiener med. Wochenschrift, No. 26, 1857.]

[Footnote 48: Deutsche med. Wochenschrift, 1882, p. 22.]

The gravest symptom which can occur in gastric ulcer is the perforation of the ulcer into the general peritoneal cavity.

{497} Only rough estimates can be made of the frequency of this symptom. These estimates vary from 2 to 25 per cent. From the data which I have collected I infer that perforation into the general peritoneal cavity occurs in about 6½ per cent. of all cases of gastric ulcer.[49]

[Footnote 49: Miquel (Schmidt's Jahrb., Bd. 125, p. 65, 1864) reckons the frequency of perforation at 2 per cent. Brinton's estimate of 13½ per cent. is the one generally accepted. He found 69 cases of perforation in 257 open ulcers collected from various sources. He doubles the number of open ulcers, as he considers cicatrized ulcers twice as frequent as the open. The statistics of some of the authors to whom he refers should not be used in this computation, either because they do not give accurately the number of cases of perforation, or because they include under perforation all cases of ulcer which have penetrated all of the coats of the stomach, whereas of course only perforation into the general peritoneal cavity should be here included. Valuable and laborious as are Brinton's researches, his statistics upon this point, as upon many others, are inaccurate.

In 249 fatal cases of open ulcer taken from the statistics of Jaksch, Dittrich, Willigk, Wrany (Prager Vierteljahr., vols. xcv. and xcix.), Eppinger, Starcke, Chambers, Moore, and Lebert (loc. cit.), I find 50 cases of perforation into the peritoneal cavity. This makes the percentage of perforations 6½ if the open ulcers be multiplied by 3, the number of cicatrized ulcers being taken as three times that of open ulcers (p. 482). This method of computation, which is adopted by Brinton, is defective on account of the uncertainty as to the proper proportion between cicatrized and open ulcers.

Lebert observed 9 cases of perforation with fatal peritonitis in his 252 cases studied clinically. He places the frequency of perforation with peritonitis at 3 to 5 per cent., which corresponds to Engel's estimate of 5½ per cent. (Prager Vierteljahrschrift, 1853, ii.).]

As regards sex, perforation occurs two to three times oftener in the female than in the male. This increased liability is referable mainly to the preponderance of the acute perforating ulcer in young women.[50]

[Footnote 50: The liability to perforation in females seems to be not only absolutely, but also relatively, to the number of ulcers greater than in males, although, on the contrary, Brinton holds that the excess of perforations in females is not greater than that of ulcers. Berthold found perforation in 3.1 per cent. of the cases of gastric ulcer in males, and in 9.7 per cent. of the cases in females (op. cit., p. 28).]

In the female the liability to perforation of gastric ulcer is greatest between fourteen and thirty years of age. In the male there seems to be no greater liability to perforation at one age than at another.[51]

[Footnote 51: Of 139 cases of perforated ulcer in females, Brinton found that four-fifths occurred before the age of thirty-five. He calculates the average age at which perforation occurs in the female as twenty-seven, and in the male as forty-two. He thinks that the average liability to perforation in both sexes decreases as life advances, although he holds that the liability to ulcer itself constantly increases with age.]

As will be explained in considering the morbid anatomy, ulcers of the anterior wall of the stomach perforate more frequently than those in other situations.

As regards the symptoms which may have preceded perforation three groups of cases can be distinguished:

In the first there has been no complaint of gastric disturbance. In the midst of apparent health perforation may occur and cause death within a few hours. This is the ulcère foudroyante of French writers. It is met with more commonly in chlorotic young women than in any other class.

In the second group of cases, which are more frequent, gastric symptoms have been present for a longer or shorter time, but have been so ambiguous that the diagnosis of gastric ulcer is not clear until perforation occurs. Then, unfortunately, the diagnosis is of little more than retrospective interest.

In the third group of cases perforation takes place in the course of gastric ulcer, the existence of which has been made evident by characteristic symptoms, such as localized pain and profuse hemorrhage.

{498} The immediate cause of perforation of gastric ulcer is often some agency which produces mechanical tension of the stomach, such as distension of the organ with food or with gas, vomiting, straining at stool, coughing, sneezing, pressure on the epigastrium, violent exertion, and jolting of the body.

With the escape of the solid, the fluid, and the gaseous contents of the stomach into the peritoneal cavity at the moment of perforation, an agonizing pain is felt, beginning in the epigastrium and extending rapidly over the abdomen, which becomes very sensitive to pressure. The pain sometimes radiates to the shoulders. Symptoms of collapse often appear immediately or they may develop gradually. The pulse becomes small, rapid, and feeble. The face is pale, anxious, and drawn (facies hippocratica). The surface of the body, particularly of the extremities, is cold and covered with clammy sweat. The internal temperature may be subnormal, normal, or elevated; after the development of peritonitis it is usually, but not always, elevated. Consciousness is usually retained to the last, although the patient is apathetic. Vomiting is sometimes absent--a circumstance which may be of value in diagnosis, and which Traube attributes to the readiness with which the contents of the stomach can be discharged through the abnormal opening into the peritoneal cavity. There is usually constipation. The respirations become more and more frequent and costal in type. Thirst is often urgent. Suppression of urine is not an uncommon symptom, although there may be frequent and painful attempts at micturition. Albumen and casts may appear temporarily in the urine. Retraction of one testicle, like that in renal colic, has been observed (Blomfield). The patient usually lies on his back with the knees drawn up. The abdomen is often at first hard and retracted from spasmodic contraction of the abdominal muscles, but later it usually becomes tympanitic, sometimes to an extreme degree. The presence of tympanitic resonance replacing hepatic dulness in front is usually considered the most important physical sign of gas free in the peritoneal cavity, but this sign is equivocal. On the one hand, the presence of adhesions over the anterior surface of the liver may prevent the gas from getting between the liver and the diaphragm;[52] and on the other hand, in cases of meteorism coils of intestine may make their way between the liver and the diaphragm, or the liver may be pushed upward and backward, so that its anterior surface becomes superior and the hepatic dulness in front disappears. Physical examination may reveal in the dependent parts of the peritoneal cavity an accumulation of fluid partly escaped from the stomach and partly an inflammatory exudate.[53] For humane reasons one should not submit the patient to the pain of movement in order to elicit a succussion sound or to determine change in the position of the fluid upon changing the position of the patient.[54] There is sometimes relief from pain for some hours before death.

[Footnote 52: Even without these adhesions liver dulness may persist after perforation of the stomach, as in a case of Nothnägel's in which for twenty-four hours after a large perforation from gastric ulcer the abdomen was retracted and hepatic dulness was well marked (Garmise, Ulcus Ventriculi cum peritonitide perforativa, Inaug. Diss., Jena, 1879).]

[Footnote 53: In a case of peritonitis resulting from perforation of a latent ulcer of the duodenum, Concato found in the acid fluid withdrawn by aspiration from the peritoneal cavity Sarcina ventriculi (Giorn. internaz. delle Scienze Med., 1879, No. 9).]

[Footnote 54: Other symptoms which have been thought to be diagnostic of pneumo-peritoneum in {499} distinction from meteorism, but the value of which is doubtful, are these: In pneumo-peritoneum the respiratory murmur can be heard by auscultation over the entire abdomen, while in meteorism it does not extend beyond the region of the stomach (Cantani); in the former amphoric sounds synchronous with respiration can sometimes be heard over the abdomen (Larghi); borborygmi are heard, if at all, distantly and feebly; the percussion note of gas free over the liver is different from that of tympanitic intestine (Traube); the percussion note is of the same character over the whole anterior wall of the abdomen; the epigastric region is more elastic to the feel than in tympanites; the distension of the abdomen is more uniform than in tympanites; and coils of distended intestine, sometimes showing peristaltic movement, cannot be seen or felt as in some cases of meteorism (Howitz).]

There are exceptional cases of perforation in which some of the most important of the enumerated symptoms, such as pain, tenderness of the abdomen on pressure, tympanites, and the symptoms of collapse, are absent.

Death sometimes occurs from shock within six or eight hours after perforation. More frequently life is prolonged from eighteen to thirty-six hours, it may be even for three or four days, and, very rarely, even longer.[55] When life is prolonged more than twelve hours an acute diffuse peritonitis is usually but not always developed.

[Footnote 55: In the Descriptive Catalogue of the Warren Anatomical Museum, by Dr. J. B. S. Jackson, p. 448, Boston, 1870, is described a case of gastric ulcer in which, so far as can be judged by the symptoms and the post-mortem appearances, the patient lived nineteen days after perforation.]

The contents of the stomach, instead of being diffused throughout the peritoneal cavity, may be confined by a rapidly-developed circumscribed peritonitis to a space near the stomach, or perforation may occur into a space previously shut off from the general peritoneal sac by adhesions. In this way circumscribed peritoneal abscesses form in the neighborhood of the stomach. Diffuse peritonitis may be caused either by an extension of the inflammation or by the rupture of these abscesses into the general peritoneal cavity. The cases of circumscribed peritonitis following perforation of gastric ulcer, with escape of the contents of the stomach, although more protracted than those in which the whole peritoneal surface is at once involved, generally terminate fatally sooner or later. The symptoms are often very obscure.

The most interesting of these peritoneal abscesses is the variety to which Leyden has given the name of pyo-pneumothorax subphrenicus (false pneumothorax of Cossy), the diagnostic features of which first were recognized by G. W. Barlow and Wilks in 1845.[56] Here there is a cavity, circumscribed by adhesions, just beneath the diaphragm, containing pus and gas and communicating with either the stomach or the intestine. By the encroachment of this cavity upon the thoracic space the symptoms and signs of pyo-pneumothorax are simulated. Barlow and Leyden have diagnosed during life this affection when resulting from perforated gastric ulcer. The points in diagnosis from genuine pyo-pneumothorax are the presence of respiratory murmur from the clavicle to the third rib, the extension of the respiratory murmur downward by deep inspiration, history of preceding gastric disturbance with circumscribed peritonitis, absence of preceding pulmonary symptoms, rapid variations in the limits of dulness with changes in the position of the body, absence or only slight evidence of increased intrapleural pressure (such as bulging of the {500} thorax as a whole, and of the intercostal spaces), displacement of the heart, displacement of the liver downward, and, if necessary, the determination by means of a manometer that the pressure in the abscess cavity rises during inspiration and falls during expiration, the reverse being true in genuine pneumothorax.[57]

[Footnote 56: Barlow and Wilks, London Med. Gazette, May, 1845; Leyden, Zeitschr. f. klin. Med., i. Heft 2; Cossy, Arch. gén. de Méd., Nov., 1879; Tillmanns, Arch. f. klin. Chirurg., Bd. 27, p. 103, 1881.]

[Footnote 57: Schreiber has shown that this last diagnostic point, which was given by Leyden, is not without exceptions, for the pressure in the peritoneal cavity may sink during inspiration and rise during expiration (as in the pleural cavity), especially when the diaphragm takes little or no part in respiration ("Ueber Pleural- und Peritonealdruck," Deutsches Arch. f. klin. Med., July 31, 1883).]

Through the medium of subphrenic abscess, or directly through adhesions between the stomach and the diaphragm, gastric ulcer may perforate into one of the pleural cavities (generally the left) and cause empyema or pneumo-pyothorax. Adhesions may form between the diaphragm and the pulmonary pleura, so that the ulcer perforates directly into the lung; in which case pulmonary gangrene or pulmonary abscess is usually developed. The diagnosis of the perforation into the lung has been made by recognizing a sour odor and sour reaction of the expectoration, and by finding in the sputum particles of food derived from the stomach. Sudden death from suffocation has followed perforation of the stomach into the lung.[58]

[Footnote 58: Tillmanns (loc. cit.) has collected 12 cases of communication between the stomach and the thoracic cavity from perforation of gastric ulcer; all proved fatal. In Sturges's case of recovery from pneumothorax supposed to be produced by perforation of a gastric ulcer the diagnosis of the cause of the pneumothorax was very doubtful (The Lancet, Feb. 7, 1874).]

Perforation of gastric ulcer into the transverse colon has been followed by the vomiting of formed feces and by the passage of undigested food by the bowel (Abercrombie). Enemata may be vomited, so that, as suggested by Murchison, the introduction of colored enemata may aid in the diagnosis.

Gastro-cutaneous fistulæ are among the rare results of perforation of gastric ulcer. In these cases food, sometimes only in liquid form, escapes through the fistula.

The opening of gastric ulcer into the pericardium is one of the rare causes of pneumo-pericardium.

Other varieties of perforation which are of pathological rather than of clinical interest will be mentioned under the morbid anatomy of gastric ulcer.

COURSE.--Few diseases are more variable in their course and duration than is simple gastric ulcer. It is customary to distinguish between acute and chronic forms of gastric ulcer, but this is a distinction which cannot be sharply drawn. Those cases are called acute in which, with absence or short duration of antecedent gastric symptoms, perforation or gastrorrhagia suddenly causes death. But in some of these cases the thickened and indurated margins of the ulcer found at the autopsy show that the disease has been of much longer duration than the clinical history would indicate. Still, there is reason to believe that within the course of a few days ulcers may form and perforate all of the coats of the stomach.

In the great majority of cases of gastric ulcer the tendency is to assume a chronic course, so that the often-used term chronic gastric ulcer is generally applicable.

{501} The great diversity of the symptoms in different cases makes it impossible to give a generally applicable description of the course of gastric ulcer. It is, however, useful to designate the main clinical forms of the disease. Thus we may distinguish--

1. Latent ulcers, with entire absence of symptoms, and revealed as open ulcers or as cicatrices at the autopsy.

2. Acute perforating ulcers. With or without a period of brief gastric disturbance perforation occurs and causes speedy death.

3. Acute hemorrhagic form of gastric ulcer. After a latent or a brief course of the ulcer profuse gastrorrhagia occurs, which may terminate fatally or may be followed by the symptoms of chronic ulcer.

4. Gastralgic-dyspeptic form. In this, which is the most common form of gastric ulcer gastralgia, dyspepsia and vomiting are the symptoms. Sometimes one of the symptoms predominates greatly over the others, so that Lebert distinguishes separately a gastralgic, a dyspeptic, and a vomitive variety. Gastralgia is the most frequent symptom.

5. Chronic hemorrhagic form. Gastrorrhagia is a marked symptom, and occurs usually in combination with the symptoms just mentioned.

6. Cachectic form. This usually corresponds only to the final stage of one of the preceding forms, but the cachexia may develop so rapidly and become so marked that the course of the disease closely resembles that of gastric cancer.

7. Recurrent form. In this the symptoms of gastric ulcer disappear, and then follow intervals, often of considerable duration, in which there is apparent cure, but the symptoms return, especially after some indiscretion in the mode of living. This intermittent course may continue for many years. In these cases it is probable either that fresh ulcers form or that the cicatrix of an old ulcer becomes ulcerated.

8. Stenotic form. By the formation of cicatricial tissue in and around the ulcer the pyloric orifice becomes obstructed and the symptoms of dilatation of the stomach develop.

DURATION.--The average duration of gastric ulcer may be said to be from three to five years, but this estimate is not of great value, on account of the absence of any regularity in the course and duration of the disease. In cases of very protracted duration, such as forty years in a case of Habershon's and thirty-five in one of Brinton's, it is uncertain whether the symptoms are referable to the persistence of one ulcer or to the formation of new ulcers, or to sequels resulting from cicatrization.

In 110 cases (44 fatal) analyzed by Lebert[59] the course was latent until the occurrence of perforation or of profuse hemorrhage in 15 per cent., the duration was less than one year in 18 per cent., from one to six years in 46½ per cent., from six to twenty years in 18 per cent., from twenty to thirty-five years in 2½ per cent.

[Footnote 59: Op. cit., p. 235.]

TERMINATIONS.--In the majority of cases gastric ulcer terminates in recovery. The recovery is often complete. Various gastric disturbances may, however, follow the cicatrization of gastric ulcer, especially if the ulcer was large and of long duration. These sequential disturbances are due to the contraction of the cicatrix, to adhesions between the stomach and surrounding parts, to deformity of the stomach, and especially to dilatation of the stomach by cicatricial stenosis of the pylorus. Hence, {502} gastralgia, dyspepsia, and vomiting may continue after the ulcer has healed, so that anatomical cure of the ulcer is not always recovery in the clinical sense. Relapses may occur after recovery, as those who have once had gastric ulcer are more prone to the disease than are others. Not infrequently the patient recovers so far as to be able to attend to the active duties of life, but to avoid renewed attacks he is always obliged to be very careful as regards his mode of living.

How often gastric ulcer ends in death it is impossible to say. It is certain that Brinton under-estimates the number of recoveries when he computes that only one-half of the ulcers cicatrize. Lebert reckons the mortality from gastric ulcer as 10 per cent., which appears to be too low an estimate. Perhaps 15 per cent. would be a more correct estimate of the mortality.

The causes of death are perforation, hemorrhage, exhaustion, and complicating diseases.

About 6½ per cent. of the cases of gastric ulcer terminate fatally by perforation into the peritoneal cavity. Although this estimate can be considered only approximative, there is little doubt but that the much larger percentages given by most writers are excessive, and are referable to the undue frequency with which cases of perforation of gastric ulcer have been published. Such cases naturally make a strong impression upon the observer, and are more likely to be published than those which terminate in other ways.

Death from hemorrhage occurs probably in from 3 to 5 per cent. of the cases of gastric ulcer.[60] In many more cases hemorrhage is an indirect cause of death by inducing anæmia. Unlike perforation, fatal hemorrhage from gastric ulcer is more common in males than in females--more common after than before forty years of age. The average age at which fatal hemorrhage occurs is given by Brinton as forty-three and a half years both for males and females.

[Footnote 60: In 270 fatal cases of open ulcer from the statistics of Jaksch, Dittrich, Eppinger, Starcke, Chambers, Habershon, Moore, and Lebert, I find 27 deaths by hemorrhage. Reckoning three cicatrices to one ulcer, this would give a percentage of 3-1/3.]

In a considerable proportion of the fatal cases exhaustion is the cause of death. According to Lebert, death from exhaustion occurs in about 4 per cent. of the cases of gastric ulcer. The causes of exhaustion are the pain, hemorrhage, dyspepsia, and vomiting which constitute the leading symptoms of the disease.

Finally, death may be due to some of the complications or sequels of gastric ulcer.

COMPLICATIONS.--Some of the complications of gastric ulcer are directly referable to the ulcer, others are only remotely related to it, and others are merely accidental.

Pylephlebitis is among the most important of the complications directly referable to the ulcer. This pylephlebitis is usually of the infectious variety, and leads to abscesses in the liver, sometimes to abscesses in the spleen and other organs.

As has already been mentioned, chronic catarrhal gastritis stands in close relationship to gastric ulcer. Chronic peritonitis is a rare complication of gastric ulcer (Moore, Vierordt). Chronic interstitial gastritis, with contraction of the stomach and thickening of its walls, was {503} associated with ulcer in a case under my observation. In a case of ulcer under the care of Owen Rees[61] this condition of the stomach was associated with chronic deforming peritonitis (thickening, induration, and contraction of the peritoneum) and ascites, so that the symptoms during life and the gross appearances after death resembled cancerous diseases of the peritoneum. Simple ulcer and cancer may occur together in the same stomach, or cancer may develop in an ulcer or its cicatrix. Glässer reports a case of phlegmonous gastritis with gastric ulcer.[62] Extension of inflammation to the pleura without perforation of the diaphragm sometimes occurs. Fatty degeneration of the heart may be the result of profound anæmia induced by gastric ulcer.[63] Embolic pneumonia and broncho-pneumonia are occasional complications. A moderate degree of cachectic dropsy is not very infrequent in the late stages of gastric ulcer.

[Footnote 61: Med. Times and Gaz., April 24, 1869.]

[Footnote 62: Berlin. klin. Wochenschrift, 1883, No. 51.]

[Footnote 63: Shattuck, Boston Med. and Surg. Journ., June, 1880, vol. ciii.]

Other complications, such as pulmonary tuberculosis, valvular disease of the heart, general atheroma of the arteries, cirrhosis of the liver, syphilis, chronic Bright's disease, waxy degenerations, and malaria, have been considered under the Etiology, and some of them will be referred to again in connection with the Pathology, of gastric ulcer. In most instances when ulcer is associated with these diseases the ulcer is secondary.

SEQUELÆ.--The most important sequelæ of gastric ulcer are changes in the form of the stomach in consequence of adhesions and in consequence of the formation and contraction of cicatrices. These lesions are most conveniently described under the Morbid Anatomy. The symptoms of the most important of these sequels--namely, stenosis of the pylorus with dilatation of the stomach--will be described in another article.

MORBID ANATOMY.--As regards number, simple ulcer of the stomach is usually single, but occasionally two or more ulcers are present. It is not uncommon to meet in the same stomach open ulcers and the scars of healed ulcers. According to Brinton, multiple ulcers are found in about one-fifth of the cases. In one case O'Rorke found six ulcers on the anterior wall of the stomach.[64] Berthold mentions a case in which thirty-four ulcers were found in the same stomach.[65]

[Footnote 64: Trans. of the New York Path. Soc., vol. i. p. 241. Wollmann mentions the occurrence of over eight simple ulcers in the same stomach (Virchow und Hirsch's Jahresb., 1868, Bd. ii. p. 126).]

[Footnote 65: Op. cit., p. 21. It is expressly stated that these were not hemorrhagic erosions, but deep corrosive ulcers.]

The usual position of simple gastric ulcer is the posterior wall of the pyloric portion of the stomach on or near the lesser curvature. Ulcers of the anterior wall are rare, but they carry a special danger from their liability to perforate without protective adhesions. The least frequent seats of ulcer are the greater curvature and the fundus.

The table on page 504 gives the situation of 793 ulcers recorded in hospital statistics:[66] {504}

Lesser curvature 288 (36.3 per cent.) Posterior wall 235 (29.6 " ) Pylorus 95 (12 " ) Anterior wall 69 ( 8.7 " ) Cardia 50 ( 6.3 " ) Fundus 29 ( 3.7 " ) Greater curvature 27 ( 3.4 " )

From this table it is apparent that ulcers occupy the lesser curvature, the posterior wall, and the pyloric region three and a half times more frequently than they do the remaining larger segment of the stomach.

[Footnote 66: These statistics are collected from the previously-cited works of Rokitansky, Jaksch, Wrany, Eppinger, Chambers, Habershon, Steiner, Wollmann, Berthold, Starcke, Lebert, and Moore. They represent 566 cases. So far as noted, most of the ulcers on the posterior wall were nearer to the lesser curvature than to the greater; those on the lesser curvature extended more frequently to the posterior than to the anterior wall. Although not apparent from the table, most of the ulcers of the lesser curvature and of the posterior wall were in the pyloric region. So far as possible, cicatrices were excluded. Pylorus and cardia in the table indicate on or near those parts.]

Occasionally two ulcers are seated directly opposite to each other, the one on the anterior, the other on the posterior, wall of the stomach. The most plausible explanation of this is that the ulcers are caused by a simultaneous affection of corresponding branches which are given off symmetrically from the same arterial trunk as it runs along one of the curvatures of the stomach (Virchow).[67]

[Footnote 67: A. Beer, "Aus dem path. Anatom. Curse et. Prof. R. Virchow, etc.," Wiener med. Wochenschr., Nos. 26, 27, 1857.]

The ordinary size of the ulcer varies from a half inch to two inches in diameter. The ulcer may be very minute, as in two cases reported by Murchison, in each of which a pore-like hole was found leading into a perforated artery from which fatal hemorrhage had occurred.[68] On the other hand, the ulcer may attain an enormous size, extending sometimes from the cardiac to the pyloric orifice and measuring five or six inches in diameter.[69]

[Footnote 68: Murchison, Trans. of the Path. Soc., vol. xxi. p. 162, London, 1870.]

[Footnote 69: In one of Cruveilhier's cases the ulcer was 6½ inches long and 3-1/3 inches wide. Law describes an ulcer measuring 6 inches by 3 inches (Dublin Hosp. Gaz., ii. p. 51).]

The ulcer is usually round or oval in shape. The outline of the ulcer may become irregular by unequal extension in the periphery, or by the coalescence of two or more ulcers, or by partial cicatrization. Simple ulcers, especially when seated near the lesser curvature, have a tendency to extend transversely to the long axis of the stomach, thus following the course of the blood-vessels. By this mode of extension, or more frequently by the coalescence of several ulcers, are formed girdle ulcers, which more or less completely surround the circumference of the stomach, oftener in the pyloric region than elsewhere.

As the ulcer extends in depth it often destroys each successive layer of the stomach in less extent than the preceding one, so that the form of the ulcer is conical or funnel-shaped, with a terrace-like appearance in its sloping edges. The apex of the truncated cone, which is directed toward the peritoneum, is often not directly opposite to the centre of the base or superior surface which occupies the mucous membrane, so that one side of the cone may be vertical and the other sloping. In the half of the stomach nearer the lesser curvature the cone slopes upward, and in the lower half of the stomach it slopes downward. The usual explanation of its conical shape is that the ulcer exactly corresponds to the territory supplied by an artery with its branches. Virchow finds an explanation for the oblique direction of the funnel in the arrangement of the arteries of the stomach. These, coming from different sources, run along the curvatures of the stomach, and there give off symmetrically branches which run obliquely toward the mucous membrane, so that one of these {505} branches with its distributive twigs (arterial tree) would supply a part shaped like an oblique funnel. One of the chief supports of the theory which refers the origin of simple gastric ulcer to an arrest of the circulation is this correspondence in shape of the ulcer to the area of distribution of the branches of the arteries supplying the stomach.

All ulcers do not present the conical form and terraced edges which have been described. These appearances are far from constant in fresh ulcers, and they are usually absent in those of long duration.

The most characteristic anatomical feature of simple ulcer of the stomach is the appearance of the edges and of the floor of the ulcer. The edges of recently-formed ulcers (acute ulcers) are clean-cut, smooth, and not swollen. To use Rokitansky's well-known comparison, the hole in the mucous coat looks as if it had been punched out by an instrument. The floor of the ulcer may be smooth and firm or soft and pulpy. The floor and edges of fresh ulcers are often infiltrated with blood, but they may be of a pale-grayish color. Usually no granulations and no pus are to be seen on the surface of the ulcer.[70] In ulcers of longer duration the margins become thickened, indurated, and abrupt; the floor acquires a dense fibrous structure.

[Footnote 70: In rare instances granulations may be present, as in a case of W. Müller's, in which their presence rendered difficult the diagnosis of simple ulcer from carcinoma (Jenaische Zeitschrift, v., 1870). The microscope may also be required to distinguish the irregularly thickened margins of old ulcers from scirrhous cancer.]

The floor of the ulcer may be the submucous, the muscular, or the serous coat, or, if the whole thickness of the stomach be perforated, it may be some adjacent organ to which the stomach has become adherent, this organ being usually the pancreas or the left lobe of the liver or neighboring lymphatic glands.

The microscopic examination of recently-formed ulcers shows that the tissue immediately surrounding the ulcer is composed of granular material, disintegrated red blood-corpuscles, pale and swollen fragments of connective-tissue fibres, and cells unaffected by nuclear-staining dyes. The red blood-corpuscles are sometimes broken into fragments of various sizes in about the same way as by the action of heat. The gastric tubules are separated from each other and compressed by infiltrated blood, and contain cells which do not stain. Around this margin of molecular disintegration, which has evidently been produced by the action of the gastric juice, there is often, although not constantly, a zone of infiltration with small round cells, probably emigrated white blood-corpuscles. These cells are most abundant near the muscularis mucosæ and in the submucosa. Extravasated red blood-corpuscles extend a variable distance around the ulcer, farthest as a rule in the submucous coat. Many of the blood-vessels in the immediate neighborhood of the ulcer appear normal; others, particularly the arterioles and the capillaries, may be filled with hyaline thrombi. Clumps of hyaline material may also be seen in the meshes of the tissue around the ulcer. Fine fatty granules may be seen in the tissue near the ulcer. The interstices of the loose submucous tissue and the lymphatic vessels are often filled with fibrillated fibrin and scattered blood-corpuscles for a considerable distance around the ulcer.

In the margins of old gastric ulcers there is also a zone of molecular necrosis. The induration and the thickening of the edges of these ulcers {506} are caused by a new growth of fibrillated connective tissue, which blends together all of the coats invaded by the ulcer. This new tissue is usually rich in lymphoid cells, which are often most abundant in the lymphatic channels. In the fibrous edges and base of old ulcers are arteries which are the seat of an obliterating endarteritis, and which may be completely obliterated by this process. An interstitial neuritis may affect the nerve-trunks involved in the fibrous growth. Blood-pigment may be present as an evidence of an old hemorrhagic infiltration.[71]

[Footnote 71: The histological changes here described are based upon the examination of typical specimens both of recent and of old gastric ulcers which have come under my observation.]

Cicatrization is accomplished by the development of fibrous tissue in the floor and borders of the ulcer. By the contraction of this new-formed tissue the edges of the mucous membrane are united to the floor of the ulcer, and may be drawn together so as to close completely the defect in the mucous membrane. The result is a white stellate cicatrix, which is usually somewhat depressed and surrounded by puckered mucous membrane. It is probable that small, superficial ulcers may be closed so that the scar cannot be detected. The mucous membrane which has been drawn over the cicatrix is intimately blended with the fibrous substratum, and is usually itself invaded by fibrous tissue which compresses and distorts the gastric tubules. Hauser[72] has shown that the tubular glands grow down into the cicatricial tissue, where they may branch in all directions. These new-formed tubules are lined by clear cylindrical or cutical epithelial cells, and may undergo cystic dilatation. Very irregular cicatrices may result from the healing of large and irregular ulcers. When the ulcer is large and deep and the stomach is adherent to surrounding parts, the edges of the mucous membrane making the border of the ulcer cannot be united by the contraction of the fibrous tissue in the floor of the ulcer. The cicatrix of such ulcers consists of fibrous tissue uncovered by mucous membrane. The closure of the ulcer is incomplete. Such cicatrices are liable to be the seat of renewed ulceration.

[Footnote 72: Das chronische Magengeschwür, etc., Leipzig, 1883. In the rare instances of carcinoma developing in the borders or in the cicatrix of gastric ulcer, Hauser believes that the cancerous growth starts from these glandular growths, which in general have only the significance of Friedländer's atypical proliferation of epithelial cells.]

The formation and contraction of the cicatrix may cause various deformities of the stomach. The character of these deformities depends upon the situation, the size, and the depth of the ulcer which is cicatrized. Among the most important of these distortions are stenosis of the pyloric orifice, followed by dilatation of the stomach, more rarely stenosis of the cardiac orifice, with contraction of the stomach, approximation of the cardiac and of the pyloric orifices by the healing of ulcers on the lesser curvature, and an hour-glass form of the stomach, produced by the cicatrization of girdle ulcers or of a series of ulcers extending around the stomach. These abnormalities in form of the stomach, particularly the constriction of the orifices, may be attended by more serious symptoms than the original ulcer.

As the ulcer extends in depth a circumscribed peritonitis, resulting in the formation of adhesions between the stomach and surrounding parts, is usually excited before the serous coat is perforated, so that the gravest of all possible accidents in the course of gastric ulcer--namely, perforation {507} into the peritoneal sac--is permanently or temporarily averted. It has been estimated that adhesions form in about two-fifths of all cases of gastric ulcer (Jaksch). On account of the usual position of the ulcer on the lesser curvature or on the posterior wall of the stomach, the adhesions are most frequently with the pancreas (in about one-half of all cases of adhesion); next in frequency with the left lobe of the liver; rarely with other parts, such as the lymphatic glands, the diaphragm, the spleen, the kidney, the suprarenal capsule, the omentum, the colon, and other parts of the intestine, the gall-bladder, the sternum, and the anterior abdominal wall. Adhesions cannot readily form between the anterior surface of the stomach and the anterior abdominal wall, on account of the constant movement of these parts, so that ulcers of the anterior gastric wall are those most liable to perforate into the peritoneal cavity.

It is difficult to include in any description all of the various and complicated lesions which may result from perforation by gastric ulcer of all of the coats of the stomach. The consequences of perforation may be conveniently classified as follows:

1. Some solid organ, usually the pancreas, the liver, or the lymphatic glands, may close the hole in the stomach.

2. An intra-peritoneal sac shut in by adhesions may communicate through the ulcer with the cavity of the stomach.

3. A fistulous communication may form either between the stomach and the exterior (external gastric fistula) or between the stomach and some hollow viscus (internal gastric fistula).

4. The ulcer may perforate into the general peritoneal cavity.

These lesions may be variously combined with each other. It is to be noted that in the first three varieties protective adhesions are present, and that in the last these adhesions are either absent or ruptured.

When the pancreas, the liver, or the spleen form the floor of the ulcer, they may be protected from extension of the ulcerative process by a new growth of fibrous tissue extending from the floor of the ulcer a variable depth into these organs. Sometimes, however, the ulcerative process, aided doubtless by the corroding action of the gastric juice, eats out large excavations in these organs. These excavations communicate with the cavity of the stomach, and are usually filled with ichorous pus. The pancreas, unlike the spleen and the liver, possesses comparative immunity against this invasion by the ulcerative process.

The situation, the form, and the extent of circumscribed peritoneal abscesses resulting from perforation of gastric ulcer depend upon the parts with which the stomach has contracted adhesions. Should an ulcer on the posterior wall of the stomach perforate before the formation of adhesions, the perforation would of course be directly into the lesser peritoneal cavity. An interesting example of this rare occurrence has been communicated by Chiari.[73] In this case, the foramen of Winslow being closed by adhesions, the lesser peritoneal cavity which communicated with a gastric ulcer was filled with ichorous pus, and in this floated the pancreas, which had necrosed in mass and had separated as a sequestrum. That form of intra-peritoneal abscess known as subphrenic pneumo-pyothorax has been already described under Symptomatology. Peritoneal abscesses communicating with the stomach may open into various places, {508} as into the general peritoneal cavity, into the pleural cavity, into the retro-peritoneal tissue, through the abdominal or thoracic walls, etc.

[Footnote 73: Wiener med. Wochenschr., 1876, No. 13.]

Gastro-cutaneous fistulæ are a rare result of the perforation of gastric ulcer.[74] The external opening is most frequently in the umbilical region, but it may be in the epigastric or in the left hypochondriac region or between the ribs. Fistulous communications resulting from the perforation of gastric ulcer have been formed between the stomach and one or more of the following hollow viscera or cavities: the colon, the duodenum and other parts of the small intestine, the gall-bladder, the common bile-duct, the pancreatic duct, the pleura, the lung, the left bronchus, the pericardium, and the left ventricle. Gastro-colic fistulæ, in contrast to gastro-cutaneous fistulæ, are more frequently produced by cancer than by ulcer of the stomach.[75] In rare instances the peritoneum over ulcers of the lesser curvature has contracted adhesions with the pyloric portion of the stomach or with the first part of the duodenum. To accomplish this it is necessary that a sharp bend in the lesser curvature should take place. By extension of the ulcerative process abnormal communication is established between the left and the right half of the stomach or between the stomach and the duodenum. In either case the right half of the stomach is often converted into a large blind diverticulum, the digested food passing through the abnormal opening.[76] Gastro-duodenal fistulæ are more frequently with the third than with the first part of the duodenum. In one of Starcke's cases the stomach communicated with the colon and through the medium of a subphrenic abscess with the left lung.[77]

[Footnote 74: Of the 25 cases of gastro-cutaneous fistula collected by Murchison, 18 were the result of disease. In 12 of these cases the probable cause was simple gastric ulcer (Med.-Chir. Trans., vol. xli. p. 11, London, 1858). Middeldorpf says that among the internal causes of the 47 cases of external gastric fistula which he tabulated, simple ulcer of the stomach played an important rôle (Wiener med. Wochenschr., 1860).]

[Footnote 75: Of 33 cases of gastro-colic fistula collected by Murchison, 21 were from gastric cancer and 9 or 10 probably from simple ulcer. On the other hand, gastro-cutaneous fistulæ are twice as frequently the result of simple ulcer as of cancer (Edinb. Med. Journ., vol. iii. 1857).]

[Footnote 76: Thierfelder has made the best study of the complicated relations existing in these cases (Deutsches Arch. f. klin. Med., Bd. iv. p. 33, 1868).]

[Footnote 77: Deutsche Klinik, 1870, No. 39. Habershon also reports a case in which a subphrenic abscess communicated with the lung, the stomach, and the colon, but he believes that the ulceration was primary in the colon (Guy's Hosp. Rep., Ser. 3, vol. i. p. 109).]

Four cases of perforation of gastric ulcer into the pericardium,[78] with the production of pneumo-pericardium, have been reported, and two cases of perforation into the left ventricle.[79] Müller found lumbricoid worms in a pleural cavity which had been perforated by gastric ulcer.[80] Diaphragmatic hernia may result from perforation of the pleural cavity by gastric ulcer.[81] In one instance the greater part of the small intestines {509} passed through a hole in the transverse meso-colon which had been caused by a gastric ulcer.

[Footnote 78: Hallin, Schmidt's Jahrb., cxix. S. 37; Säxinger, Prager med. Wochenschr., 1865; Guttmann, Berl. klin. Wochenschr., 1880, No. 23. Murchison mentions a specimen in the museum of King's College, London, of a simple gastric ulcer opening into the pericardium (Edinb. Med. Journ., vol. iii. p. 6). In a case reported by Graves a liver abscess burst into the stomach and into the pericardium (Clin. Lect., ii. p. 237, Dublin, 1848).]

[Footnote 79: Oser, Wiener med. Blätter, 1880, No. 52; Brenner, Wiener med. Wochenschr., 1881, No. 47.]

[Footnote 80: Müller, Memorabilien, xvii., Oct., 1872.]

[Footnote 81: Needon, Wiener med. Presse, 1869, No. 42. In a case of Günsburg's the hole in the diaphragm was as large as the hand, and the left pleural cavity contained the upper half of the stomach and the spleen (Arch. f. phys. Heilk., xi. 3, 1852).]

The various fistulæ which have been mentioned may be either direct or through the medium of an abscess. While some of them are only pathological curiosities, others, particularly the communications of the stomach with the pleural cavity and with the lung, are sufficiently frequent to be of practical clinical interest.

As has already been explained, ulcers of the anterior wall are the ones most liable to perforate into the general peritoneal cavity,[82] but on account of their comparative infrequency perforation occurs oftener in other situations, particularly in the lesser curvature and near the pylorus. Except on the anterior wall the perforation is often brought about by the rupture of adhesions which for a time had prevented this accident. In a considerable number of cases, particularly of ulcers on the anterior wall, the ulcer looks as if recently formed (acute perforating ulcer); in other cases its thickened and indurated margins indicate long duration. Chiari[83] describes a case in which rupture into the peritoneal cavity took place through the cicatrix of an old ulcer, probably in consequence of the distension of the stomach with gas. The hole in the peritoneum is usually circular, smaller than the inner surface of the ulcer, and has sharp, well-defined edges. Less frequently the edges are ragged. Post-mortem digestion may, however, so change the borders of the opening as to make it difficult or impossible to tell from their post-mortem appearances alone whether perforation has occurred before or after death. The peritoneal cavity after death from perforation is found to contain gas and substances from the stomach. Usually within a few hours after perforation septic peritonitis is excited, but in exceptional cases no inflammation of the peritoneum has occurred even when life has been prolonged twenty-four hours after perforation.

[Footnote 82: According to Brinton, "the proportion of perforations to ulcers is such that of every 100 ulcers in each of the following situations, the numbers which perforate are--on the posterior surface, about 2; the pyloric sac, 10; the middle of the organ, 13; the lesser curvature, 18; the anterior and posterior surface at once, 28; the cardiac extremity, 40; and the anterior surface, 85."]

[Footnote 83: Wiener med. Blätter, 1881, No. 3.]

Emphysema of the subcutaneous, subperitoneal, and other loose areolar tissue of the body is a rare but remarkable result of the perforation of gastric ulcer. The emphysema is sometimes observed shortly before death, but it attains its maximum development after death, when it may spread rapidly over the greater part of the body. The gas consists in part of hydrogen, as it burns with a blue flame. It is generated, at least in great part, by fermentation of the contents of the stomach. The gas may enter the subserous tissue at the edges of the ulcer and thence spread, or, after perforation of the stomach, it may make its way from the peritoneal cavity into the loose subserous connective tissue through some place in the parietal peritoneum which has been macerated, perhaps by the digestive action of the gastric juice.[84]

[Footnote 84: Roger (Arch. gén. de Méd., 1862) and Demarquay (Essai de Pneumatologie médicale, Paris, 1866) deserve the credit of first calling general attention to the occurrence of subcutaneous emphysema after rupture of the digestive tract. The following writers have each reported a case of emphysema following the perforation of gastric ulcers: Cruveilhier, Anat. Path., t. i. livr. xx.; Bell, Edinb. Med. Journ., vol. vi. p. 783; Thierfelder, Deutsches Arch. f. klin. Med., iv., 1868, p. 33; Newman, The Lancet, 1868, vol. ii. p. 728; Poensgen, Das subcutane Emphysem nach continuitätstrennungen des Digestionstractus, etc., Inaug. Diss., Strassburg, 1879, p. 40; Korach, Deutsche med. Wochenschr., 1880 p. 275; {510} Jürgensen, Deutsches Arch. f. klin. Med., Bd. 31, p. 441, 1882. Doubtful cases are reported by Lefèvre, W. Mayer, and Burggraeve. The fullest consideration of the subject is to be found in the dissertation of Poensgen.]

In two cases of sudden death from gastric ulcer Jürgensen found gas in the veins and arteries of various parts of the body. He believes that this gas, which certainly was not the result of putrefaction after death, was derived from the stomach, and that it entered during life the circulation through vessels exposed in the borders of the ulcer, thus causing death. In one of the cases a profuse hemorrhage preceded death, and in the other the ulcer had perforated into the peritoneal cavity.[85]

[Footnote 85: Jürgensen does not consider whether this gas may not have made its way into the blood-vessels after death in a manner similar to its extension through the cellular tissue of the body in the cases of emphysema just mentioned. In the case which he has reported in full interstitial and subserous emphysema could be traced from the ulcer ("Luft im Blute," Deutsches Arch. f. klin. Med., Bd. 31, p. 441, 1882).]

The source of hemorrhage from gastric ulcer is from blood-vessels either in the stomach itself or in the neighborhood of the stomach. Hemorrhages slight or of moderate severity occur from the capillaries and small arteries and veins in the mucous and submucous coats. Sometimes profuse and even fatal hemorrhage comes from arteries or from veins in the submucous coat, especially when these vessels are dilated. Quickly-fatal hemorrhages take place from the large vessels between the muscular and the serous coats, particularly from the main trunks on the curvatures. After the formation of adhesions, followed by the perforation of all of the coats of the stomach, profuse bleeding may proceed from the erosion of large vessels near the stomach, such as the splenic, the hepatic, the pancreatico-duodenal arteries, the portal and the splenic veins, and the mesenteric vessels. Bleeding may also occur from vessels in the parenchyma of organs invaded by the ulcer. The most common source of fatal hemorrhage is from the splenic artery, which from its position is peculiarly exposed to invasion by ulcers of the posterior wall of the stomach. The hemorrhage is usually arterial in origin. It may come from miliary aneurisms of the gastric arteries or from varicose veins in the wall of the stomach. As Cruveilhier has pointed out, an ulcer may cicatrize except over one spot corresponding to an artery from which fatal hemorrhage may occur. Ulcers which give rise to large hemorrhages are usually chronic in their course. Those seated on the middle of the anterior wall, although peculiarly liable to perforate, are comparatively exempt from hemorrhage on account of the small size of the blood-vessels there.

Changes in the blood-vessels of the stomach have been seen in a considerable number of cases of gastric ulcer. Instances have been recorded of the association with gastric ulcer of most of the diseases to which blood-vessels are subject. An example in all respects convincing of embolism of the artery supplying the ulcerated region of the stomach has not been published. Probably the best case belonging here is one of perforating ulcer of the stomach with hemorrhagic infiltration in its walls, presented by Janeway to the New York Pathological Society in 1871.[86] In this case there was in the gastro-epiploic artery an ante-mortem fibrinous plug which was continued into the nutrient artery of the ulcerated piece of the stomach. No source for an embolus could be found. In one case Merkel found an embolus in a small artery leading to an ulcer {511} of the duodenum.[87] The arch of the aorta was atheromatous and contained a thrombus. Patches of hemorrhagic infiltration existed in the stomach.

[Footnote 86: Trans. of the N.Y. Path. Soc., vol. ii. p. 1.]

[Footnote 87: Wiener med. Presse, vii. p. 30, 1866.]

In many cases thrombosis of the arteries, and especially of the veins involved in the diseased tissue around an ulcer, has been observed, and in some the thrombus was prolonged in the vessels for a considerable distance from the ulcer. It is probable that in most of these cases the thrombus was secondary to the ulcer. Hyaline thrombosis of the capillaries near the ulcer is also to be mentioned.

In a certain, but not large, number of cases atheroma with calcification or with fatty degeneration of the arteries of the stomach has been found associated with gastric ulcer.[88] Reference has already been made to the occurrence of obliterating endarteritis in the thickened edges and floor of gastric ulcer, where it is doubtless secondary. In one case of gastric ulcer I found a widespread obliterating endarteritis affecting small and medium-sized arteries in many parts of the body, including the stomach.[89]

[Footnote 88: For cases in point see Norman Moore, Trans. of the Path. Soc. of London, vol. xxxiv. p. 94.]

[Footnote 89: On the posterior wall of the stomach, midway between the greater and the lesser curvature and five inches to the right of the cardiac orifice, was a round ulcer half an inch in diameter, with smooth, sharp edges. In the floor of the ulcer, which extended to the muscular coat, was a small perforated aneurism of a branch of the coronary artery. In addition there were small, granular kidneys, hypertrophied heart without valvular lesion, and chronic interstitial splenitis. Small and medium-sized arteries in the kidneys, spleen, heart, lymphatic glands, and stomach were the seat of a typical endarteritis obliterans, resulting in some instances in complete closure of the lumen of the vessel. The patient, who was attended by Sassdorf, was seized during the night with vomiting of blood, which continued at intervals for twenty-four hours until his death. The patient was a man about fifty years of age, without previous history of gastric ulcer or of syphilis.]

In one case Powell[90] found a small aneurism of the coronary artery in an ulcer of the lesser curvature of the stomach. Hauser[91] found an aneurismal dilatation of an atheromatous and thrombosed arterial twig in the floor of a recent ulcer. In my case of obliterating endarteritis just referred to there was a small aneurism in the floor of the ulcer. These miliary aneurisms in the floor of gastric ulcers seem to be analogous to those in the walls of phthisical cavities. Miliary aneurisms occur in the stomach independently of gastric ulcer, and may give rise to fatal hæmatemesis, as in four cases reported by Galliard.[92]

[Footnote 90: Trans. of the Path. Soc. of London, vol. xxix.]

[Footnote 91: Das chronische Magengeschwür, etc., p. 11, Leipzig, 1883.]

[Footnote 92: L'Union méd., Feb. 26, 1884. Curtis reported a case of fatal hæmatemesis from an aneurism, not larger than a small pea, seated in the cicatrix of an old ulcer (Med. Annals of Albany, Aug., 1880).]

Gastric ulcer is occasionally associated with waxy degeneration of the arteries of the stomach.[93] In most of these cases there were multiple shallow ulcers. Hæmatemesis is generally absent in gastric ulcer resulting from waxy disease of the gastric blood-vessels. As is well known, the amyloid material itself resists the action of the gastric juice.

[Footnote 93: Hauser (op. cit.) alludes to a case in which, with waxy degeneration of the stomach, over one hundred small ulcers were found in different stages of development, from hemorrhagic infiltrations to complete ulcers. Cases belonging here are reported by Fehr, Ueber die Amyloide Degeneration, Inaug. Diss., Bern, 1866; Merkel, Wiener med. Presse, 1869; Edinger, Deutsches Arch. f. klin. Med., Bd. 29, p. 568; Marchiafava, Atti del Accad. Med. di Roma, iii. p. 114; and Mattei, Deutsche med. Zeitung, July 5, 1883.]

Finally, varicosities of the veins of the stomach have been once in a {512} while found with gastric ulcer. In a large number, probably in the majority, of cases of gastric ulcer no changes have been found in the blood-vessels of the stomach except such as were manifestly secondary to the ulcer.

That gastric ulcer is frequently complicated with chronic catarrhal gastritis has been repeatedly mentioned in the course of this article.

PATHOGENESIS.--Without doubt, the most obscure chapter in the history of gastric ulcer is that relating to its origin and to its persistence. Notwithstanding a vast amount of investigation and of discussion, unanimity of opinion upon these subjects has not been reached. In view of this uncertainty it is desirable in this article to do little more than to summarize the leading theories as to the development of gastric ulcer.

Most observers are agreed that the digestive action of the gastric juice has some share in the development and the progress of the ulcer, but as to the first cause of the ulcer there are various hypotheses.

The earliest theory refers the origin of simple ulcer of the stomach to inflammation. Since its advocacy by Abercrombie and by Cruveilhier this theory has always had its adherents, particularly among French writers. It is true that in stomachs which are the seat of simple ulcer evidences of inflammation can often be found both in the neighborhood of the ulcer and elsewhere. In recent times the supporters of the inflammatory origin of gastric ulcer lay especial stress upon the presence of foci of infiltration with small round cells in the mucous and the submucous coats.[94] But it is difficult to explain by the inflammatory theory the usually solitary occurrence and the funnel-like shape of gastric ulcer.

[Footnote 94: Laveran, Arch. de Phys. norm. et path., 1876, p. 443; Galliard, Essai sur la Pathogenie de l'Ulcère simple de l'Estomac, Thèse de Paris, 1882; Colombo, Annali univ. di Med., 1877.]

The theory that gastric ulcer is of neurotic origin has also been advocated. Some refer the origin to the secretion of an excessively acid gastric juice under abnormal nervous influence (Günsburg), others to vaso-motor disturbances, and others to trophic disturbances. Wilks and Moxon compare simple gastric ulcer to ulcers of the cornea resulting from paralysis of the trigeminus. The neurotic theory of the origin of gastric ulcer is altogether speculative and has never gained wide acceptance.[95]

[Footnote 95: The first to attribute gastric ulcer to nervous influence was Siebert (Casper's Wochenschr. f. d. Heilk., 1842, No. 29, and Deutsche Klinik, 1852). Cf. also Günsburg, Arch. f. phys. Heilk., xi., 1852; Wilks and Moxon, Lect. on Path. Anat., 2d ed., Philada., 1875, p. 386. Osborne in 1845 attributed gastric ulcer to the secretion of an abnormally acid juice by a circular group of the gastric glands (Dublin Journ. of Med. Sci., vol. xxvii. p. 357).]

The view which has met with the greatest favor is that which attributes the origin of gastric ulcer to impairment or arrest of the circulation in a circumscribed part of the wall of the stomach, and to a subsequent solution by the gastric juice of the part thus affected. Rokitansky first suggested this view by assigning hemorrhagic necrosis of the mucous membrane as the first step in the formation of the ulcer; but it is Virchow who has most fully developed this view and has given it its main support. The first cause of gastric ulcer, according to Virchow, is a hemorrhagic infiltration of the coats of the stomach induced by local disturbances in the circulation. The part the nutrition of which is thus impaired or destroyed is dissolved by the gastric juice.

{513} The affections of the gastric blood-vessels to which importance has been attached are (a) embolism and thrombosis; (b) diseases of the coats of the vessels, as atheroma, obliterating endarteritis, fatty degeneration, amyloid degeneration, and aneurismal and varicose dilatations; (c) compression of the veins by spasm of the muscular coats of the stomach in vomiting and in gastralgia; (d) passive congestion of the stomach by obstruction in the portal circulation.

In support of this view are urged the following facts: First, it has been proven by the experiments of Pavy that parts of the gastric wall from which the circulation has been shut off undergo digestion; second, hemorrhagic infarctions have been observed in the stomach, both alone (Von Recklinghausen, Hedenius) and associated with gastric ulcer (Key, Rindfleisch); third, the hemorrhagic infiltration in the walls of recently-formed ulcers indicates a hemorrhagic origin; fourth, the funnel-like shape of the ulcer resembles the funnel-shaped area of distribution of an artery; fifth, gastric ulcers have been experimentally produced by injecting emboli into the gastric arteries (Panum, Cohnheim).[96]

[Footnote 96: Pavy, Philosoph. Trans., 1763, p. 161; V. Recklinghausen, Virchow's Archiv, Bd. 30, p. 368; Axel Key, Virchow und Hirsch's Jahresb., 1870, Bd. ii. p. 155; Rindfleisch, Lehrb. d. path. Gewebelehre, 5te Aufl., Leipzig, 1878; Panum, Virchow's Archiv, Bd. 25, p. 491; Cohnheim, Vorles. über allgem. Path., Bd. ii. p. 53, Berlin, 1880.]

The main objections to this view are the infrequency with which the assumed changes in the blood-vessels have been demonstrated, the common occurrence of gastric ulcer at an age earlier than that at which diseases of the blood-vessels are usually present, and the absence of gastric ulcer in the vast majority of cases of heart disease, with widespread embolism of different organs of the body. To meet some of these objections, Klebs[97] presupposes in many cases a local spasmodic contraction of the gastric arteries, causing temporary interruption of the circulation; Rindfleisch and Axel Key, compression of the gastric veins, with resulting hemorrhagic infiltration by spasm of the muscular coat of the stomach in vomiting and in gastralgic attacks. But these are pure hypotheses.

[Footnote 97: Handb. d. path. Anat., Bd. i. p. 185, Berlin, 1869.]

What is actually known concerning diseases of the gastric blood-vessels in ulcer of the stomach has already been stated under the morbid anatomy. From this it may be inferred that the origin of gastric ulcer in diseased conditions of the blood-vessels has been established only for a comparatively small group of cases.

Böttcher's[98] view that gastric ulcer is of mycotic origin, being produced by micrococci, has thus far met with no confirmation.

[Footnote 98: Dorpater med. Zeitschr., Bd. v. p. 148, 1874.]

There are those who hold an eclectic view concerning the origin of gastric ulcer. They believe that ulcer of the stomach may be produced by a variety of causes, such as inflammation, circulatory disturbances, irritating substances introduced into the stomach, traumatism, etc. The peculiarities of the ulcer are due not to any specific cause, but to the solvent action of the gastric juice, which keeps clean the floor and the sides of the ulcer. These clean edges and floor, which are incident to all ulcers of the stomach, justify no conclusion as to the cause of the ulcer. Engel[99] over thirty years ago held that gastric ulcer might {514} originate in various ways--that there was nothing specific about it. Brinton was also of similar opinion.

[Footnote 99: Prager Vierteljahrschr., 1853, ii.]

Gastric ulcers have been produced experimentally in animals in a variety of ways, but these experiments have not materially elucidated the pathenogenesis of ulcer in man. Schiff by lesions of various parts of the brain, and later Ebstein by lesions of many parts of the central and peripheral nervous system by injections of strychnine--in fact, apparently by any means which greatly increased the blood-pressure--produced in the stomachs of animals ecchymoses and ulcers. Müller by ligation of the portal vein, Pavy by ligation of arteries supplying the stomach, likewise produced hemorrhages and ulcers. The results of Pavy could not be confirmed by Roth and others. Panum, and afterward Cohnheim, produced gastric ulcers by introducing multiple emboli into the gastric arteries. Daettwyler under Quincke's direction caused, in dogs with gastric fistulæ, ulcers of the stomach by various mechanical, chemical, and thermic irritants applied to the inner surface of the stomach. Aufrecht observed hemorrhages and ulcers in the stomachs of rabbits after subcutaneous injections of cantharidin.[100]

[Footnote 100: Schiff, De vi motorea baseos encephali, 1845, p. 41; Ebstein, Arch f. exp. Path. u. Pharm., 1874, p. 183; Müller, Das corrosive Geschwür im Magen, etc., p. 273, Erlangen, 1860; Pavy, Guy's Hosp. Rep., vol. xiii., 1867; Roth, Virchow's Archiv, Bd. 45, p. 300, 1869; Panum, loc. cit.; Cohnheim, op. cit.; Daettwyler, Quincke, Deutsche med. Wochenschr., 1882, p. 79; Aufrecht, Centralbl. f. d. med. Wiss., 1882, No. 31.]

The most interesting of these experiments are those of Cohnheim and of Daettwyler, who demonstrated that in one essential point all of these experimental ulcers differ from simple gastric ulcer in man--namely, in the readiness with which they heal. To this ready healing the gastric juice, much as it has been accused of causing the spread of gastric ulcers in man, seems to have offered no obstacle. We know that similar losses of substance in the human stomach heal equally well.[101] Hence it has been maintained throughout this article that it is unjustifiable to regard all of the scars found in the human stomach as the result of simple ulcer.

[Footnote 101: Portions of the mucous membrane of the stomach, sometimes with some of the submucous coat, have been in several instances removed with the stomach-pump, but thus far no bad effects have followed.]

It appears from these experiments, as well as from observations on man, that it is more difficult to explain why ulcers in the stomach do not heal than it is to understand how they may be produced. From this point of view the observation of Daettwyler is of interest, that in dogs which had been rendered anæmic by repeated abstraction of blood not only did slighter irritants suffice to produce ulcers of the stomach, but the ulcers healed much more slowly. Practically, it is important to learn what are the obstacles to the repair of gastric ulcers, but our positive knowledge of these is slight. It is probable that such obstacles are to be found in constitutional causes, such as anæmia and chlorosis, in abnormal states of the blood-vessels around the ulcer, in catarrhal affections of the stomach, in irritating articles of food, in improper modes of living, and in increased acidity of the gastric juice.

DIAGNOSIS.--In many cases the diagnosis of gastric ulcer can be made with reasonable certainty; in other cases the diagnosis amounts only to a suspicion more or less strong, and in still other cases the diagnosis is impossible.

{515} The diagnostic symptoms are epigastric pain, vomiting, and gastric hemorrhage. The characteristics of the pain which aid in the diagnosis are its fixation in one spot in the epigastric region, its onset soon after eating, its dependence upon the quantity and the quality of the food, its relief upon the complete expulsion of the contents of the stomach, its alleviation by changes in posture, and its increase by pressure. That the pain of gastric ulcer has not always these characteristics has been mentioned under the Symptomatology. Vomiting without hæmatemesis is the least characteristic of these symptoms. It aids in the diagnosis when it occurs after eating at the acme of a gastralgic attack and is followed by the relief of pain. Hæmatemesis is the most valuable symptom in diagnosis. The more profuse the hemorrhage and the younger the individual in whom it occurs, the greater is the probability of gastric ulcer. It should not be forgotten that the blood is sometimes discharged solely by the stools.

The simultaneous occurrence of all these symptoms renders the diagnosis of gastric ulcer easy.[102] In all cases in which gastrorrhagia is absent the diagnosis is uncertain; but gastric ulcer should be suspected whenever the ingestion of food is followed persistently by severe epigastric pain and other causes of the pain have not been positively determined. When the course of the ulcer is latent and when the symptoms are only those of dyspepsia, the diagnosis is of course impossible. In cases previously obscure a diagnosis in extremis is sometimes made possible by the occurrence of perforation of the stomach.

[Footnote 102: That even under the most favorable circumstances absolute certainty in the diagnosis of gastric ulcer is not reached is illustrated by a case reported with great precision and fulness by Banti: A female servant, twenty-one years old, had every symptom of gastric ulcer, including repeated hæmatemesis and the characteristic epigastric pain. She was nourished by enemata. She died from an ulcerative proctitis four days after the last hemorrhage from the stomach. Only a slight catarrhal inflammation of the stomach was found at the autopsy, without trace of ulcer, cicatrix, or ecchymosis ("Di un Caso d'Ematemesi," La Sperimentale, Feb., 1880, p. 168). It would seem as if there must have been an ulcer which had healed so completely as to leave no recognizable scar.]

In making a differential diagnosis of gastric ulcer, as well as of any disease, reliance should be placed more upon the whole complexion of the case than upon any fancied pathognomonic symptoms.

The diseases which are most difficult to distinguish from gastric ulcer are nervous affections of the stomach. Like gastric ulcer, most of these are more common in women than in men, and especially in chlorotic women with disordered menstruation and with hysterical manifestations. These nervous affections are manifold and their leading characteristics are not yet well defined. The most important of these affections are nervous dyspepsia, nervous vomiting, nervous gastralgia, and gastric crises.

The leading symptoms of nervous dyspepsia, as described by Leube,[103] are the ordinary symptoms of dyspepsia without evidence of anatomical alteration of the stomach, and with the proof by washing out the stomach that the process of digestion is not delayed. Nervous dyspepsia is often associated with other nervous affections, and is caused especially by influences which depress the nervous system. Epigastric pain, and especially tenderness on pressure over the stomach, are not common symptoms in nervous dyspepsia. Only those rare cases of gastric ulcer in which hemorrhage from the stomach is absent and epigastric pain is not prominent {516} are likely to be confounded with nervous dyspepsia. In such cases, although the diagnosis of nervous dyspepsia is by far the most probable, the patient may be confined to bed and put upon the strict regimen for gastric ulcer. If in the course of ten days or two weeks essential relief is not obtained, ulcer may be excluded, and the proper treatment for nervous dyspepsia with tonics and electricity may be adopted (Leube).

[Footnote 103: Deutches Arch. f. klin. Med., Dec. 18, 1878.]

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