DEFINITION.—Inflammation of the interior of the mouth, usually unilateral, eventuating in multiple ulcerations of the mucous membrane.
SYNONYMS.—Fetid stomatitis, Phlegmonous stomatitis, Putrid sore mouth, Stomacace, are synonymous terms for idiopathic ulcerous stomatitis. Ulcero-membranous stomatitis, Mercurial stomatitis (Vogel), are synonymous terms for the deuteropathic variety of the disease.
ETIOLOGY.—The principal predisposing cause of the disease is to be found in ochlesis; the contaminating atmosphere of crowded dwellings and apartments insufficiently ventilated; uncleanliness; insufficiency of proper clothing; unhealthy food, and the like. It prevails epidemically in crowded tenements, schools, prisons, asylums, and hospitals; in garrisons and in camps; in transports and men-of-war. It is often propagated by contagion, but whether by infection or actual inoculation seems undetermined. Measles is an active predisposing cause. Feeble individuals are the most liable to the disease. It occurs at all ages. In civil life it is most frequent between the ages of four and ten years. Sometimes more girls are affected than boys (Meigs), and sometimes it is the more prevalent among boys (Squarrey). Autumn is the season of greatest prevalence.
Carious teeth, fracture and necrosis of the jaw (Meigs), and protracted catarrhal stomatitis are among the chief exciting causes. Irregular dentition is sometimes the exciting cause; and this may occur at the first and second dentition or at the period of eruption of the last molars.
PATHOLOGY.—The anatomical lesion is the destructive inflammation of portions of the mucous membrane of the mouth, leaving ulceration on detachment of the eschars. It usually commences as a gingivitis. At two periods of life—namely, from the fourth to the eighth year of life, and from the eighteenth to the twenty-fifth year—it is apt to be ulcero-membranous, a condition asserted to be altogether exceptional at other periods (Chauffard).
A diffuse fibro-purulent infiltration of the lymph-spaces of the mucosa is regarded as the first step in the pathological process. This infiltration is sufficiently abundant to compress the capillary vessels of the tissues, and thus arrest the circulation (Cornil et Ranvier). All those localized portions of mucous membrane from which the circulation is cut off perish and are discharged in fragments. The ulcers thus left are grayish, granular, and sanious, with thin, irregularly dentated borders a little undermined, through which pus can be expressed on pressure. The usual cryptogams of the oral cavity, in various stages of development, are in great abundance in the grayish detritus, which likewise contains altered red and white blood-corpuscles.
According to some observers (Caffort, Bergeron), the first evidence of the disease is an intensely congested erythematous patch, upon which one or more pustules present, point, and rupture promptly, leaving the characteristic ulcerations.
For some indeterminate reason, the ulcerations are mostly unilateral, and occur much the more frequently on the left side. The principal primal points of ulceration are upon the external borders of the gums, more frequently those of the lower jaw, and upon the corresponding surface of the cheek and lip—the cheek much oftener than the lip. Thence ulceration may extend to the tongue, less frequently to the palate. The ulcerative process follows the outline of the gums, baring the bases of the teeth to a variable extent, so that they seem elongated. On the cheek the patch of inflammation is generally oval, the longest diameter being antero-posterior, and the most frequent position is opposite to the last molar.
Each ulcer is surrounded by an intensely red areola, beyond which the tissues are succulent and tumid from collateral inflammatory oedema, often giving the ulcers an appearance of great depth; but when the detritus is discharged they are seen to have been superficial. Detachment of the necrosed segments of mucous membrane takes place by gradual exfoliation from periphery to centre. Sometimes detachment occurs in mass, usually in consequence of friction or suction. The ulcers, gingival and buccal, bleed easily when disturbed. They may remain separate, or may coalesce by confluence of interposing ulcerations extending across the furrow between gum and cheek or lip. The adjoining side of the tongue sometimes undergoes similar ulceration from behind forward, inoculated, most likely, by contact with adjoining ulceration. In rare instances, neglected cases most probably, the ulceration may extend to the palatine folds, the tonsils, and the soft palate.
SYMPTOMATOLOGY.—The affection usually begins without any constitutional symptoms. Young infants sometimes present slight febrile symptoms, with impairment of appetite and general languor. Fetid breath, salivation, and difficulty in deglutition are usually the first manifestations of the disease to attract attention. The mouth will be found to be hot, painful, and sensitive to the contact of food. Infants often refuse food altogether, though usually they can be coaxed to take liquid aliment. Larger children and adults complain of scalding sensations. They find mastication painful, and cannot chew at all on the affected side. The salivation is excessive, the saliva bloody and often extremely fetid. When swallowed, this fetid saliva causes diarrhoea. The cheeks sometimes become swollen, and the submaxillary connective tissue oedematous. Adenitis takes place in the submaxillary, retro-maxillary, and sublingual glands of the affected side. Sometimes the other side becomes affected likewise, but to a less extent. The glands do not suppurate, but the adenitis may remain as a chronic manifestation in scrofulous subjects.
The disease, left to itself, will often continue for a number of weeks, or even months as may be, unmodified even by intercurrent maladies (Bergeron). Long continuance may result in partial or complete disruption of the teeth, or in local gangrene, or even in necrosis of the alveoli (Damaschino). Properly managed, the ulcers become cleansed of their detritus, and within a few days heal by granulation, their position long remaining marked by delicate red cicatrices upon a hard and thickened substratum. Repeated recurrences are sometimes observed.
DIAGNOSIS.—The appearances of the gums and adjoining structures described under the head of Pathology establish the diagnosis. The usually unilateral manifestation and the peculiar fetid odor distinguish it from severe forms of catarrhal stomatitis. From cancrum oris it is distinguished by the absence of induration of the skin of the cheek over the swollen membrane, and by the succulence and diffuseness of the tumefaction. From mercurial stomatitis it is discriminated by the history, and by the absence of the peculiar manifestations to be discussed under the head of that disease.
PROGNOSIS.—The prognosis is good, the disease being susceptible of cure in from eight to ten days in ordinary cases. When due nutrition is prevented by the pain in mastication and deglutition, and in much-reduced subjects, the disease may continue for several weeks. It is in these cases that detachment of the teeth takes place, with periostitis and necrosis of the alveoli. Protracted suppuration and failure in nutrition may lead to a fatal result, but such a termination is uncommon.
TREATMENT.—Fresh air, unirritating and easily digestible food, the best hygienic surroundings practicable, attention to secretions from skin and bowels by moderate and judicious use of ablutions, diaphoretics, and laxatives, with the internal administration of cinchona or its derivatives, with iron and cod-liver oil, comprise the indications for constitutional treatment.
Locally, demulcent mouth-washes are called for, containing astringents, detergents, or antiseptics. Acidulated washes are more agreeable in some instances. For antiseptic purposes, however, sprays and douches may be used of solutions of potassium permanganate, boric acid, carbolic acid, or salicylic acid. Gargles of potassium chlorate, ten or twenty grains to the ounce, are highly recommended, as well as the internal administration of the same salt in doses of from two to five grains three times a day for children, and of ten to twenty grains for adults.
If the sores are slow to heal, the ulcerated surfaces may be touched once or twice daily with some astringent, such as solution of silver nitrate (ten grains to the ounce), or, if that be objectionable, with alum, tincture of iodine, or iodoform.
Prompt extraction of loose teeth and of loose fragments of necrosed bone is requisite.
DEFINITION.—A non-contagious, deuteropathic inflammation of the interior of the mouth, almost invariably unilateral, and characterized by a peculiar gangrenous destruction of all the tissues of the cheek from within outward.
SYNONYMS.—Gangrenous stomatitis; Gangrena oris; Grangrenopsis; Cancrum oris; Stomato-necrosis; Necrosis infantilis; Gangrene of the mouth; Gangrenous erosion of the cheek; Noma; Buccal anthrax; Aquatic cancer; Water cancer; Scorbutic cancer; Sloughing phagedæna of the mouth.
HISTORY.—The most important work upon the subject was published in 1828, from the pen of Dr. A. L. Richter,10 whose accurate historical account of the disease was in great part reproduced, with additions thereto, by Barthez and Rilliet in their Treatise on the Diseases of Infants, Paris, 1843, and quoted by nearly all subsequent writers on the theme. From these records it appears that the first accurate description of the affection was given in 1620 by Dr. Battus, a Dutch physician, in his Manual of Surgery. The term aquatic cancer, water-kanker, bestowed on it by van de Voorde, has been generally followed by the physicians of Holland, although van Swieten (1699) properly designated it as gangrene. J. van Lil termed it noma, as well as stomacace and water-kanker, and cited a number of Dutch physicians who had observed its epidemic prevalence. The majority of more recent observers, however, deny its epidemic character.
10 Der Wasserkrebs der Kinder, Berlin, 1828; further, Beiträg zur Lehre vom Wasserkrebs, Berlin, 1832; Bemerkungen über den Brand der Kinder, Berlin, 1834.
Of Swedish writers, Lund described it as gangrene of the mouth; Leutin, under the name of ulocace. In England, Boot was the first to write of gangrene of the mouth, and was followed by Underwood, Symmonds, Pearson, S. Cooper, West, and others.
In France it has received great attention. Berthe11 described it as gangrenous scorbutis of the gums; Sauvages (1816) as necrosis infantilis. Baron in 1816 published12 a short but excellent account of a gangrenous affection of the mouth peculiar to children; and Isnard presented in 1818 his inaugural thesis on a gangrenous affection peculiar to children, in which he described, simultaneously, gangrene of the mouth and gangrene of the vulva. Then followed Rey, Destrees (1821), Billard (1833), Murdoch, Taupin (1839), and others, until we reach the admirable description by Barthez et Rilliet, from which the present historical record has been chiefly abstracted.
11 Mémoires de l'Académie royale de Chirurgie, Paris, 1774, t. v. p. 381.
12 Bullétins de la Faculté de Médecine de Paris, 1816, t. v. p. 161.
German physicians likewise have largely studied the subject. De Hilden, A. G. Richter, C. F. Fischer, Seibert, and many others preceded A. L. Richter, whose important contribution to the literature and description of the disease has been so highly extolled by Barthez and Rilliet.
In America the disease has been best described by Coates, Gerhard, and Meigs and Pepper, all of Philadelphia.
(For extensive bibliographies the following sources should be consulted in addition to those cited: J. Tourdes, Du Noma ou du Sphacèle de la Bouche chez les Enfants, Thèse, Strasbourg, 1848: A. Le Dentu, Nouveau Dictionnaire de Médecine et de Chirurgie pratique, article "Face," Paris, 1871.)
ETIOLOGY.—Almost exclusively a disease of childhood, gangrenous stomatitis is exceedingly rare in private practice, and very infrequent at the present day even in hospital and dispensary practice. Lack of hygienic essentials of various kinds, impoverishment, long illnesses, and debilitating maladies in general are the predisposing causes. It is sometimes endemic in hospitals and public institutions, but rarely, if at all, epidemic. It is not generally deemed contagious, though so considered by some writers. It appears to have been more frequent in Holland than elsewhere, to be more frequent in Europe generally than in the United States, and now much less frequent in the United States than formerly. To recognition of the predisposing causes and to their abolition and avoidance may probably be attributed its diminished frequency all over the world. Though attacking children only as a rule, it has been observed in adults (Barthez et Rilliet, Tourdes, Vogel). Nurslings are not liable to the disease. Though occurring occasionally earlier in life, the greatest period of prevalence is from the third to the fifth or sixth year of age, and thence, with diminishing frequency, to the twelfth and thirteenth years. It is probably equally frequent in the two sexes, though the majority of authors have described it as more frequent in females.
Healthy children are not attacked. Even in delicate children it is so rarely idiopathic that this character is utterly denied it by many observers. The disease which it follows, or with which it becomes associated, may be acute or chronic. According to most writers, it occurs with greatest frequency after measles. It follows scarlatina and variola much less often. It is observed likewise after whooping cough, typhus fever, malarial fever, entero-colitis, pneumonitis, and tuberculosis. Excessive administration of mercury has been recognized as an exciting cause, some cases of mercurial stomatitis progressing to gangrene.
According to Barthez et Rilliet, acute pulmonary diseases, and especially pneumonia, are the most frequent concomitant affections, and are usually consecutive.
SYMPTOMATOLOGY, COURSE, DURATION, TERMINATIONS, COMPLICATIONS, AND SEQUELÆ.—The disease usually becoming manifested during other disease, acute or chronic, or during convalescence therefrom, there are no special constitutional symptoms indicating its onset. Hence considerable progress may be made before its detection. The earliest local characteristic symptom distinguishing gangrenous stomatitis is a tense tumefaction of one cheek, usually in proximity to the mouth. The lower lip is generally involved, thus rendering it a matter of difficulty to open the mouth. This tumefaction in some instances progresses over the entire side of the face up to the nose, the lower eyelid, and even out to the ear in one direction, and down to the chin, and even to the neck, in the other. Before the parts become swollen externally, ulceration will have taken place to some extent in the mucous membrane, but usually without having attracted special attention, the subjective symptoms having been slight. A gangrenous odor from the mouth, however, is almost always constant. Its presence, therefore, should lead to careful investigation as to its seat and cause. The gums opposite the internal ulcer become similarly affected in most instances, and undergo destruction, so that the teeth may become denuded and loosened, and even detached, exposing their alveoli. The bodies of the maxillary bones suffer in addition in some instances, and undergo partial necrosis and exfoliation.
It is maintained (Löschner, Henoch) that in some instances there is no involvement of the mucous membrane until the ulcerative process has reached it from the exterior.
The tumefied portions of the check and lip are pale, hard, unctuous, and glistening. They are rarely very painful, and often painless. On palpation a hard and rounded nodule one or two centimeters in diameter can be detected deep in the central portion of the swollen cheek.
From the third to the sixth day a small, black, dry eschar, circular or oval, becomes formed at the most prominent and most livid portion of the swelling, whether cheek or lip. This gradually extends in circumference for a few days or for a fortnight, sometimes taking in almost the entire side of the face or even extending down to the neck. As it enlarges the tissues around become circumscribed with a zone intensely red. The internal eschar extends equally with the external one. Eventually, the eschar separates, in part or in whole, and becomes detached, leaving a hole in the cheek through which are seen the loosened teeth and their denuded and blackened sockets.
During this time the patient's strength remains tolerably well maintained, as a rule, until the gangrene has become well advanced. Intelligence usually remains good. Many children sit up in bed and manifest interest in their surroundings. Others lie indifferent to efforts made for their amusement. Some exhibit insomnia and delirium. The pulse is small and moderately frequent, rarely exceeding 120 beats to the minute until near the fatal close, when it often becomes imperceptible. Appetite is often well preserved, unless pneumonia or other complications supervene, but thirst is often intense, even though the tongue remain moist. The desire for food sometimes continues until within a few hours of death. Toward the last the skin becomes dry and cold, diarrhoea sets in, emaciation proceeds rapidly, collapse ensues and death.
Death usually occurs during the second week, often before the complete detachment of the eschar—in many instances by pneumonia, pulmonary gangrene, or entero-colitis. Some die in collapse, which is sometimes preceded by convulsions. When the eschars have become detached, suppuration exhausts the forces of the patient, and death takes place by asthenia.
The complication most frequent is pneumonia, and the next entero-colitis. Gangrene of the lungs, of the palate, pharynx, or oesophagus, of the anus, and of the vulva, may supervene. Hemorrhage from the facial artery or its branches has been noted as an exceptional mode of death (Hueber), the rule being that the arteries in the gangrenous area become plugged by thrombi, and thus prevent hemorrhage.
Recovery may take place before the local disease has penetrated the cheek—indeed, while the mucous membrane alone is involved. In recent instances, however, the disease does not subside until after the loss of considerable portions of the cheek, and the child recovers with great deformity, not only from loss of tissue in the cheek and nose, but from adhesions between the jaws and the cheek.
PATHOLOGY AND MORBID ANATOMY.—Gangrenous stomatitis always involves the cheek, almost always that portion in proximity to the mouth. It is almost invariably unilateral. Either side seems to be equally liable. Both sides suffer only, it is contended, when the gangrene is limited in extent, confined to the mucous membrane, and occupies the sides of the frenums of the lips (Barthez et Rilliet). It usually if not invariably begins in the mucous membrane, as a phlyctenular inflammation, which undergoes ulceration, followed by gangrene, immediately or not for several days, and then becomes covered with a more or less brownish-gray eschar. The ulceration of the mucous membrane is occasionally preceded by an oedematous condition of the cheek externally, similar to that sometimes observed in ordinary ulcerous stomatitis; but this is not the characteristic circumscribed, tense infiltration observed later. This ulceration is situated most frequently opposite the junction of the upper and lower teeth. Sometimes it proceeds from the gingivo-buccal sulcus of the lower jaw, sometimes from the alveolar border of the gums. It extends in all directions, and often reaches the lower lip. From three to sixteen days may be consumed in these extensions. The surrounding mucous membrane becomes oedematous. The ulceration soon becomes followed by gangrene, sometimes within twenty-four hours, sometimes not for two or three days, and exceptionally not for several days. The ulcerated surfaces bleed readily, change from gray to black, and become covered with a semi-liquid or liquid putrescent detritus. They are sometimes surrounded by a projecting livid areola, which soon becomes gangrenous in its turn. The shreds of mortified membrane, though clinging a while to the sound tissues, are easily detached, and often drop spontaneously into the mouth. Meanwhile, there is abundant salivation, the products of which pour from the mouth, at first sanguinolent, and subsequently dark and putrescent and mixed with detritus of the tissues. Large portions of the gums, and even of the mucous membrane of the palate, may undergo destruction within a few (three to six) days. The gangrenous destruction of the gums soon exposes the teeth, which become loose and are sometimes spontaneously detached. Thence the periosteum and bone become implicated and undergo partial denudation and necrosis, and portions of necrosed bone become detached if the patient survives. The characteristic implication of the exterior of the cheek becomes manifest from the first to the third day, but occasionally not until a day or two later. A hard, circumscribed swelling of the cheek or cheek and lip occurs, sometimes preceded, as already intimated, by general oedematous infiltration. The surface is tense and unctuous, often discolored. In its central portion is an especially hard nucleus, one to two centimeters or more in diameter. Gangrene often takes place at this point from within outward at a period varying from the third to the seventh day or later. The skin becomes livid, then black; a pustule is formed at the summit of the swelling, which bursts and discloses a blackened gangrenous eschar from less than a line in thickness to the entire thickness of the cheek beneath. The area of gangrene gradually extends. The dead tissues become detached, and a perforation is left right through the cheek, through which are discharged saliva and detritus. Meanwhile, the submaxillary glands become swollen and the surrounding connective tissue becomes oedematous. In some instances, however, no change is noticeable in these glands.
Examinations after death have shown that thrombosis exists for some distance around the gangrenous mass. Hence the rarity of hemorrhage during the detachment of the eschar.
DIAGNOSIS.—In the early stage of the disease the main point of differential diagnosis rests in the locality of the primitive lesion, the mucous membrane of the inside of one cheek. Subsequently there is the gangrenous odor from the mouth; the rapid peripheric extension of the local lesion, which acquires a peculiar grayish-black color; its rapid extension toward the exterior of the cheek or lip; the tumefaction of the cheek, discolored, greasy, hard, surrounded by oedematous infiltration, and presenting a central nodule of especial hardness; then the profuse salivation, soon sanguinolent, subsequently purulent and mingled with detritus of the mortified tissues. Finally, the eschar on the exterior of the swollen cheek or lip leaves no doubt as to the character of the lesion. From malignant pustule it is distinguished by not beginning on the exterior, as that lesion always does (Baron).
PROGNOSIS.—The prognosis is bad unless the lesion be quite limited and complications absent. At least three-fourths of those attacked perish; according to some authorities fully five-sixths die. The objective symptoms of the local disease are much more important in estimating the prognosis than are the constitutional manifestations, the vigor of the patient, and the hygienic surroundings, although, as a matter of course, the better these latter the more favorable the prognosis. Prognosis would be more favorable in private practice than in hospital or asylum service.
TREATMENT.—Active treatment is required, both locally and constitutionally. Local treatment is of paramount importance, and alone capable of arresting the extension of the process of mortification. The topical measure in greatest repute is energetic cauterization with the most powerful agents, chemical and mechanical—hydrochloric acid, nitric acid, acid solution of mercuric nitrate, and the actual cautery, whether hot iron, thermo-, or electric cautery. The application of acids is usually made with a firm wad or piece of sponge upon a stick or quill, care being taken to protect the healthy tissues as far as practicable with a spoon or spatula. After the application the mouth is to be thoroughly syringed with water to remove or dilute the superfluous acid. Hydrochloric acid has been preferred by most observers.
As these cauterizations must be energetic to prove effective, anæsthesia ought to be induced. Should ether be employed for this purpose, hydrochloric acid or the acid solution of mercuric nitrate would be selected of course.
In the early stages these agents are to be applied to the inside of the cheek, so as to destroy all the tissue diseased, if practicable, and expose a healthy surface for granulation. Should the exterior of the cheek become implicated before cauterization has been performed or in spite of it, it is customary to destroy the tissues from the exterior, including a zone of apparently healthy surrounding tissue. As the gangrene extends, the cauterization is to be repeated twice daily or even more frequently. After cauterization the parts are dressed with antiseptic lotions, and antiseptic injections or douches are to be used frequently during day and night to wash out the mouth and keep it as clear as possible from detritus.
Meigs and Pepper report beneficial results from the topical use of undiluted carbolic acid, followed by a solution of the same, one part in fifty of water, frequently employed as a mouth-wash. The progress of the sloughing was checked and the putridity of the unseparated dead tissue completely destroyed in the two cases mentioned by them, one of which recovered quickly without perforation of the cheek. Gerhard preferred undiluted tincture of the chloride of iron; Condie, cupric sulphate, thirty grains to the ounce. Bismuth subnitrate has recently been lauded as a topical remedial agent.13
13 Maguire, Medical Record N.Y., Feb. 3, 1883.
The mouth should be frequently cleansed by syringing, douching, spraying, or washing with disinfectant solutions, such as chlorinated soda liquor, one part to ten; carbolic acid, one to twenty. Lemon-juice is sometimes an agreeable application, as in some other varieties of stomatitis. Constitutionally, tonic and supporting treatment is demanded, even in those instances where the appetite is well maintained and the general health apparently well conserved. Soups, milk, semi-solid food, egg-nog, egg and wine, wine whey, milk punch, finely-minced meat, should be administered as freely as the state of the digestive functions will permit. If necessary, resort should be had to nutritive enemata. Quinia and tincture of chloride of iron are the medicines indicated. When sufficient alcohol cannot be given with the food, it should be freely exhibited in the most available form by the mouth or by the rectum. The apartment should be well ventilated, the linen frequently changed, the discharges promptly removed.
DEFINITION.—An inflammation of the interior of the mouth due to poisoning, especially by drugs, and chiefly by mercury, copper, and phosphorus.
DEFINITION.—An inflammation of the mucous membrane of the mouth, eventually ulcerating, the result of systemic poisoning by the absorption of mercury.
SYNONYMS.—Stomatitis mercurialis; Mercurial ptyalism, Ptyalismus mercurialis; Mercurial salivation, Salivatio mercurialis.
ETIOLOGY—Predisposing and Exciting Causes.—Special vulnerability to the toxic influence of mercury, and special proclivity to inflammatory affections of the mouth and the organs contained therein, are the predisposing causes of mercurial stomatitis. The exciting cause is the absorption of mercury into the tissues of the organism. The susceptibility of healthy adults is much greater than that of healthy children. The susceptibility of adults varies very greatly. Constitutions deteriorated by prolonged disease, undue exposure, and the like are much more promptly influenced in consequence. Tuberculous subjects do not bear mercury well.
Idiosyncratic susceptibility to toxæmia by mercurial preparations is now and then encountered in practice, and instances have been published14 in which fatal results have ensued, after prolonged suffering, from the incautious administration of a single moderate dose of a mercurial drug.
14 For example, see in Watson's Practice of Physic a case of furious salivation following one administration of two grains of calomel as a purgative, the patient dying at the end of two years, worn out by the effects of the mercury and having lost portions of the jaw-bone by necrosis.
Until comparatively recent years the most common cause of mercurial poisoning was the excessive employment of mercurial medicines, whether by ingestion, inunction, or vapor bath. Topical cauterization with acid solution of mercuric nitrate is likewise an infrequent, and usually an accidental, cause of the affection. Elimination of the mercury by way of the mucous glands of mouth and the salivary glands proper excites the stomatitis in these instances. An entirely different series of cases occur in artisans exposed to handling the metal and its preparations or to breathing its vapor or its dust. In these instances the poison may gain entrance into the absorbent system by the skin, the mucous membranes of the nose, mouth, and throat, the stomach, or the lungs. No matter what care may be exercised in cleansing the hands, it is often impossible to prevent occasional transference of the noxious material from fingers to throat, or to thoroughly free the finger-tips under the nails. The avocations entailing the risks of mercurial stomatitis comprise quicksilver-mining, ore-separating, barometer- and thermometer-making, gilding, hat-making, manufacturing of chemicals, and exhausting the globes employed in certain forms of electric illumination.15 The slow absorption of mercury into the bodies of artisans induces in addition serious constitutional nervous disturbances—tremors, palsy, etc.
15 Med. and Surg. Reporter, Philada., Dec. 30, 1883, p. 734.
SYMPTOMATOLOGY, COURSE, DURATION, TERMINATIONS, COMPLICATIONS, AND SEQUELÆ.—The principal subjective symptoms of mercurial stomatitis are—characteristic fetor of the breath, sore gums and mouth, continuous nauseous metallic brassy or coppery taste, and profuse salivation.
At first the mouth feels parched and painful, the gums tender, the teeth, the lower incisors especially, set on edge. Soon the gums become swollen, and when touched with the tongue seem to have receded from the necks of the teeth, which thereby appear to be longer than usual. The gums feel quite sore when pressed upon with the finger or when put on the stretch by clashing the rows of teeth against each other. This sort of soreness is often watched for in the therapeutic administration of mercurials purposely given to "touch the gums," as an indication that the system is under the influence of the drug. It is, therefore, one of the earliest indications of mercurial poisoning, but if not sought for it may elude attention until after the mouth has become sore a little later. The pain in the mouth is augmented by efforts of mastication and expectoration, and may be associated with pains at the angle of the lower jaw or extending along the domain of the third or of the third and second divisions of the distribution of the fifth cerebral nerve. Mastication of solid food is often unendurable. Constitutional manifestations become evident about this time in increased heat of skin, acceleration of pulse, furred tongue, dry mouth, great thirst, and loss of appetite. The dryness of the mouth does not last long, but is soon followed by hypersalivation, one of the characteristic phenomena of the disorder. The saliva secreted, often acid in reaction, varies greatly in quantity, which is usually proportionate to the severity of the case. It is secreted night and day, sometimes to the amount of several pints in the twenty-four hours—in moderately severe cases to the amount of from one to two pints in that space of time. It is limpid or grayish, mawkish or somewhat fetid, and reacts readily to the simplest tests for mercury. The salivation is almost continuous, sometimes quite so. The patient soon becomes unable to endure the fatigue of constant expectoration, and the fluid then dribbles from his mouth or runs off in an unimpeded slobber. When excessive, the patient's strength becomes rapidly exhausted—in part by impoverishment of the fluids, in great measure from the lack of refreshing sleep.
Meanwhile, the local inflammatory process extends from the gums to the floor of the mouth and to the lips, and thence to the tongue and the cheeks. The salivary glands are in a state of inflammation likewise, but rather in consequence of direct irritation in the elimination of the poison through their channels than by extension of the stomatitis along their ducts. The lymphatic glands of the lower jaw become engorged and tender. Mastication, deglutition, and articulation all become impeded mechanically by tumefaction of the tissues.
In some instances the glossitis is so great that the tongue protrudes, thereby impeding respiration and even threatening suffocation. In some cases oedema of the larynx has been noted, threatening suffocation from that cause. Should the inflammatory process extend along the pharynx to the Eustachian tubes, deafness and pains in the ears will become additional symptoms.
The subsequent progress of unarrested mercurial stomatitis is that of ulcerous stomatitis.
Should gangrene of the mucous membrane take place, there will be great fetor from the mouth, and some danger of hemorrhage on detachment of the sloughs should the process be taking place in the direction of vessels of some calibre. Necrosis of the inferior maxilla entails continuance of the disagreeable local symptoms until the discharge in fragments or in mass of the dead portions of bone.
In the earlier stages of the attack the constitutional symptoms may be sthenic. Fever, cephalalgia, and the usual concomitants of pyrexia, however, soon give way to the opposite condition of asthenia. Exhausted by the excessive salivation, and unable to repair waste by eating or sleeping, the sufferer soon passes into a condition of hopeless cachexia. Those who survive remain cachectic and feeble for a long time—some of them disfigured for life by various cicatrices between cheeks and jaw, by loss of teeth or of portions of the jaw-bone.
The duration of mercurial stomatitis varies with the susceptibility of the patient, the intensity of the toxæmia, and the character of the treatment. Mild cases may get well in a week or two; severe cases may continue for weeks, and even months; extreme cases have persisted for years. Even moderate cases occasionally resist treatment for weeks.
Under the improved therapeutics of the present day mercurial stomatitis almost always terminates in recovery, especially if it receive early and prompt attention. Neglected or improperly managed, it may terminate in serious losses of tissue in gums, cheeks, teeth, and bone, leaving the parts much deformed and the patient in a permanently enfeebled condition.
Erysipelas, metastatic abscesses, inflammations, pyæmia, or colliquative diarrhoea may be mentioned as complications which may prove sufficiently serious to produce death, independently of the virulence of the primary stomatitis.
PATHOLOGY AND MORBID ANATOMY.—Mercurial stomatitis is an ulcerative process attended with an excessive flow of saliva containing mercury. It has a tendency to terminate in destruction and exfoliation of the mucous membrane of the gums and other tissues attacked, and eventually in necrosis of the jaw-bone. The detritus is found, microscopically, to consist of granular masses of broken-down tissue, swarming with bacteria and micrococci, and containing some blood-cells and many pus-cells. In some instances micrococci have been detected in the blood.
The disease usually begins in the gums of the lower incisors, and 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 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.