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 {341} 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 {342} 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
{343} 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]
[Footnote 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 {344} 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.
Toxic Stomatitis.
DEFINITION.--An inflammation of the interior of the mouth due to
poisoning, especially by drugs, and chiefly by mercury, copper, and
phosphorus.
Mercurial Stomatitis.
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
published[14] in which fatal results have ensued, after prolonged
suffering, from the incautious administration of a single moderate dose
of a mercurial drug.
[Footnote 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 {345} 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.
[Footnote 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
{346} 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 {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.