there is usually pain in a particular spot, and often general
feverishness, in addition to all the symptoms before mentioned,
according to the seat of the oedema. Sometimes the suffering in
laryngeal abscess at its height is very intense. Perforation into the
pharynx, oesophagus, or even externally, may take place, but usually
the pus points into the larynx. When the pus is evacuated either
spontaneously or by incision, violent choking, coughing, and hawking
may occur, but after it is evacuated all dangerous symptoms usually
rapidly subside.
In sanguineous infiltration the symptoms do not differ from serous or
purulent oedema under the same circumstances. Hemorrhagic infusion is
usually {115} sudden, and the resulting stenosis often fatal. Muscular
spasm or paralysis sometimes coexists with laryngeal oedema, and
greatly adds to the interference with respiration.
PATHOLOGY AND MORBID ANATOMY.--The seat of the morbid process being the
connective tissue, those localities of the larynx in which this tissue
is most abundantly interposed between the mucous membrane and the
cartilage are most liable to infiltration. I must say from my own
experience that the epiglottis--particularly the glosso-epiglottic
region--is most frequently affected,[3] next the ary-epiglottic folds,
then the arytenoid region, and then the ventricular folds. The
ventricles and the vocal bands are very rarely involved. Infraglottic
oedema is still more rare, and is never an extension of the
supraglottic. The disease is never a primary one, and, though seated in
the submucous connective tissue, it may have started with inflammation
of either the overlying mucous membrane or the underlying
perichondrium. Effusion of blood is generally limited to traumatic
cases, but has ensued from mercurialization, small-pox, and typhus;
purulent infiltration and abscess formation is the result of
phlegmonous inflammation and breaking down of the tissue, occurring
especially in the cushion of the epiglottis and in the ventricular and
ary-epiglottic folds; but as a rule the effusion in laryngeal oedema is
of a serous or sero-purulent character.[4] In infraglottic oedema it is
said to be fibrinous.
[Footnote 3: According to Sestier, the ary-epiglottic folds are
affected in nearly every case, either alone or together with other
parts.]
[Footnote 4: In 90 cases Sestier found the infiltration serous 60
times, sero-gelatinous 6, sero-purulent 9, sero-purulent with plastic
lymph 4, purulent 8 times, sero-sanguineous twice, and sanguineous
once.]
The mucous membrane covering the oedematous structures is tense and
discolored; except in very inflammatory conditions it is yellowish,
shimmering, and pallid. On cutting into the diseased parts often but
little exudation takes place, and sometimes even squeezing between the
fingers does not suffice to cause disgorgement.[5] After the fluid is
evacuated the parts collapse and the mucous membrane is left wrinkled
and folded.
[Footnote 5: In 23 autopsies Sestier found that incisions into the
oedematous structures made the liquid run out either without any or
with slight pressure 10 times; with repeated pressure, with difficulty
and only in small quantity, 6 times; and not at all, in spite of
repeated incisions and pressure, 7 times.]
DIAGNOSIS.--With the laryngoscope, the spatula, and the finger the
seat, the degree, and often the nature of the infiltration can be
determined. A successful laryngoscopical examination may sometimes
require in such cases more than ordinary skill, and there is often so
much tumefaction that the parts are not easily recognizable. The
epiglottis may appear as a thick roundish tumor, or be of a more or
less indistinct horse-shoe shape, overhanging the laryngeal aperture;
the ary-epiglottic folds may be converted into large lateral cushions
pressing against the arytenoid bodies, or be merged with the latter
into huge, irregularly pear-shaped, oval, or globular masses; and the
ventricular folds may be immensely tumefied, or else, by means of the
swelling and the being pushed into a horizontal position of the whole
lateral lining of the upper laryngeal cavity, may be obliterated
altogether. Glottic oedema never occurs except with supraglottic, and
the upper surface of the vocal bands may look elevated, arched, and
bladder-like, even if only the thyro-arytenoid muscles are infiltrated.
In infraglottic oedema there is usually neither epiglottic nor
supraglottic oedema; pads are seen underneath the vocal bands, either
ring-shaped or projecting from side to side toward the middle line, and
fill up to a greater or less degree the rima glottidis. The oedematous
parts have sometimes a pinkish, but usually a yellowish, translucent or
semi-translucent aspect. Accumulation of pus lessens the translucency
and sometimes makes the yellow more marked. Sanguineous {116}
infiltration shows a bluish-red or livid discoloration. In chronic
oedema the color is lighter, sometimes a dirty gray.
I have already explained the proper method of using the spatula. It
reveals in all cases, sometimes best during retching, the epiglottis,
and in many cases the ary-epiglottic folds. With the finger these parts
can be touched, and all the more easily when they are swollen; but
great care must be exercised to avoid provoking by digital examination
a suffocative paroxysm. When felt by the finger the peculiar elasticity
or fluctuation present is unmistakable.
PROGNOSIS.--Laryngeal oedema is always a very dangerous condition--in a
chronic case less so than in an acute one. The prognosis depends
largely upon the causative or accompanying disease. The more local the
oedema and the more promptly medical, and in most instances surgical,
aid can be had, the more favorable is the prognosis, though uncertain
even then. Sometimes a rapidly fatal attack supervenes in a mild,
chronic, or apparently convalescing case. In abscess formation it is
generally favorable unless the underlying disease makes it the reverse.
TREATMENT.--Antiphlogistic treatment of every sort has been recommended
against this dread disease. Its frequently rapid course usually
necessitates primarily topical measures. Even fifty years ago, when
bleeding and tartar emetic were in vogue, Ryland entirely
discountenanced these, and said: "Our chief reliance must be placed on
the local detraction of blood by means of a large number of leeches
applied in the vicinity of the larynx; on the use of blisters, which
should never be put on the front of the neck, as their operation will
interfere with the subsequent performance of tracheotomy should such a
step be necessary, but on the back of the neck or the upper part of the
chest; and on the internal administration of large doses of calomel,
which, either by their purgative effect or by their specific action on
the general system, tend to check the inflammation in the glottis and
to promote the absorption of the effused fluids. These remedies can
only be of use during the early stages of the disease, and experience
shows but too plainly that even then we have far more reason to
anticipate failure than success."
Many years ago it was proposed to catheterize the trachea for the
purpose of allowing air to reach the lungs in this and other diseases
in which the larynx is obstructed; and more recently Hack has shown the
great benefit of using, under sight by means of the laryngoscopic
mirror, Schrötter's dilating hard-rubber tubes in acute as well as
chronic laryngeal oedema. According to him, they do good not only
symptomatically, but also curatively.
Furthermore, we can employ, under the guidance of the mirror or of the
finger, scarifications of the infiltrated structures by means of the
laryngeal lancet, or in its absence of a long bent, sharp-pointed
bistoury covered, except for a quarter of an inch or so from its point,
with adhesive plaster. (For the epiglottis the ordinary gum lancet will
often do.) An abscess is opened in the same way. When the bleeding
following scarification is excessive we use ice internally or
externally, or both; when bleeding is insufficient, steam inhalation,
hot fomentations, etc. To promote absorption we make topical
applications, either before or certainly after the scarification, of a
saturated solution of iodoform in sulphuric ether (drachm ij ad ounce
j), or of a strong watery solution of silver nitrate (scruple ij-drachm
j ad ounce j). Astringents, especially tannin and alum, applied in the
form of spray to parts that cannot otherwise be reached, are advisable;
and antispasmodics and narcotics (potassium bromide and morphine)
should not be omitted in cases complicated with muscular spasm, etc.
The internal administration of fluid extract of jaborandi in drachm
doses or the hypodermic injection of pilocarpine is highly lauded as
promoting absorption; also diaphoretics, purgatives (salines and croton
oil), {117} etc. From the beginning the patient's general functions
must be regulated and his strength supported by tonics and nutritives,
and any underlying disease amenable to treatment must of course be
attended to. The slow swallowing of pieces of ice is often of great
benefit. In every case that does not visibly improve by the vigorous
carrying out of the treatment hitherto detailed, especially the
catheterization by means of Schrötter's tubular dilators, the ultima
ratio--viz. tracheotomy, particularly inter-crico-thyroid
laryngotomy--must be resorted to without waiting until the patient has
lost much ground by the impediment to respiration. One of the lessons
taught us by pathological investigation is that epiglottic,
supraglottic, and glottic oedema does not extend beyond the upper
surface of the vocal bands: therefore, while in infraglottic oedema,
and when the two conditions supraglottic oedema and infraglottic
coexist, tracheotomy should be performed, in the other cases the
air-passage should be opened by introducing a tube through the
inter-crico-thyroid membrane. This operation is, especially for the
general medical practitioner, much easier, safer, and quicker of
performance, and answers in those cases all purposes. This important
lesson is not heeded by any of the recent authors on the subject.
Indeed, Cohen expressly says: "The trachea is to be opened in
preference to the larynx, as being at a greater distance from the seat
of the disease and less liable to involvement, as well as for the
reason that the disease occasioning the oedema may be extending low
down in the larynx, and therefore exist at the very point usually
selected for laryngotomy." Supraglottic oedema does not extend to the
region of the inter-thyro-cricoid membrane, and the tube may therefore
safely be there introduced.
Perichondritis and Chondritis of the Larynx.
DEFINITION.--Inflammation of the laryngeal perichondrium and cartilage.
SYNONYMS.--Phthisis laryngea of the older authors, Laryngitis affecting
the cartilages, Deep-seated ulcerative laryngitis, Caries cartilaginum
laryngis, Vomica laryngis, Perichondric laryngeal abscess, Necrosis
laryngis. (Some of these names refer to the product or terminal stage
of the disease.)
ETIOLOGY.--Laryngeal perichondritis and chondritis occur either as
idiopathic or as symptomatic or secondary affections. Even the former,
caused by so-called catching cold or exposure to cold and wet while the
system is in a state of lowered vitality, may have a septicæmic basis;
it is much more rare than the secondary. Rühle has remarked that
arytenoid perichondritis may probably sometimes start in the
crico-arytenoid articulation, and in an instance which has come under
my observation this certainly seemed to have been the case. Authors
state that occasionally the inflammation commences in the cartilaginous
tissue itself, instead of in its investment; this is hardly
conceivable. Perichondritis must always precede chondritis, but it
always causes the cartilage to become involved in the morbid process.
Quite often perichondritis and chondritis constitute an extension of a
particular ulcerative disease of the mucous and elastic membranes. In
the great majority of cases the causes are tuberculosis, syphilis,
diphtheria, cancer, lupus, typhus and typhoid fever, small-pox, or else
traumatic occurrences, especially suicidal throat-cutting, decubitus or
other pressure upon the part--as, for instance, the frequent
introduction in an aged subject of the oesophageal sound observed by
Ziemssen, and overstrain of the voice alleged by Flormann. At least
three cases are reported (viz. by Porter, Lawrence, and Eppinger) in
which the disease has been ascribed to the administration of mercury,
and Graves and Stokes remark that in broken-down constitutions, {118}
where large quantities of mercury have been used, chronic laryngitis is
very apt to terminate in ulceration of the cartilages.
The disease occurs oftener in men than in women, and oftener between
the twentieth and fortieth years than at any other age.
SYMPTOMATOLOGY.--I distinguish three stages of laryngeal perichondritis
and chondritis--viz. the inflammatory, suppurative, and necrotic. The
symptoms of the first stage are obscure: the main one is pain, usually
of a boring, burning character, localized according to the precise
cartilage affected, which is increased by functional or other movement
of the part and by pressure from the outside. To the pain there are
gradually added--also depending somewhat upon the precise seat of the
inflammation--cough, dysphonia, and dysphagia. In cricoid
perichondritis--especially when, as is generally the case, the
posterior surface of the plate of the cricoid cartilage is
affected--there is sometimes inflammatory reddening of the pharyngeal
mucous membrane which may extend upward to the palate. Inflammatory
swelling of some part of the cartilaginous framework may be
recognizable in the first stage of the disease by means of the
laryngoscope.
The suppurative stage is attended with more swelling of the part
affected, due to accumulation of pus and to collateral oedema. Pain,
dysphagia, or dysphonia, and sometimes irritative, harsh cough may be
much augmented; but, above all, dyspnoea now appears, which sometimes
so rapidly increases that the patient dies asphyxiated unless
tracheotomy is performed.
During the necrotic stage the symptoms of laryngeal stenosis sometimes
persist, and sometimes cease with the expectoration of quantities of
pus containing possibly a part, and occasionally the altered whole, of
the affected cartilage: with continued purulent expectoration the
patient's strength fails, the breath becomes very fetid, and hectic
fever and death may supervene.
Swelling of cervical lymphatic glands, though by no means always
present, has been observed in the early and sometimes only in the later
stages of the disease.
The course of the disease, whether idiopathic or secondary, is either
acute or chronic. It tends either toward abscess-formation, which
predominates, or toward new growth of tissue; for a time sometimes the
one, sometimes the other occurs, and, as a rule, during the former the
process is more acute, and during the latter more chronic: the
proliferated tissue, after being produced, may break down and increase
the amount of pus. When acute, the three stages of the disease follow
each other rapidly, if, indeed, the third be not cut off by the death
of the patient. When chronic, the pus collected is very apt to burrow
and to make fistulous passages and openings internally and externally.
At various points also perichondric hypertrophies, ecchondroses, and
exostoses are apt to occur.
The inflammatory stage can terminate by more or less complete
resolution, though usually some enlargement of the cartilages
permanently remains; recovery can also take place in the later stages,
and leave deformities and produce cicatricial contractions.
PATHOLOGY AND MORBID ANATOMY.--The perichondrium of the larynx is
diseased comparatively oftener than that of any other region of the
body; which, aside from other causes, is partly due to the fact that
the laryngeal cartilages become with increasing age normally vascular
and ossified. The morbid process never affects at one time the whole of
the cartilaginous framework of the larynx, and usually only one
cartilage, or even only a limited portion of one cartilage, except in
the case of the cricoid and arytenoid, which are sometimes together
implicated. Perichondritis does not spread easily. The cricoid is most
frequently affected, next the arytenoid, far less often the thyroid,
and exceedingly rarely the epiglottis.
As already remarked, the inflammation of cartilage and perichondrium
{119} has a great tendency to suppuration--occasionally, though rarely,
proliferation and hypertrophy; or, on the other hand, and more
frequently if the inflammation is a slowly progressing one, the
processes leading to ossification take place. The suppurative stage
follows the inflammatory quickly unless the latter has been
comparatively very slight. A great abundance of pus collects between
the cartilage and its investing membrane. As the former is thereby
denuded and separated from its nutritive vessels, it must become
necrotic. Exfoliated pieces of cartilage are generally found in the
abscess. Caries of adjacent tissues is apt to take place, and oedema of
the surrounding connective tissue, and sometimes far-reaching
destruction, before the perichondrium bursts or becomes destroyed over
a large extent. In cricoid perichondritis, the plate mainly being
affected, the abscess projects mostly toward the oesophagus and the
trachea, or it points outwardly when the narrow portion is involved;
the opening when the abscess has burst is frequently large, and shows a
portion of the necrosed cartilage; sometimes there are a number of
perforations. In arytenoid perichondritis the abscess bulges either
into the interior of the larynx or into the adjacent pyriform sinus;
bursting usually occurs at the posterior portions of the ventricular
folds or near the posterior vocal process, and the undermined edges may
disclose the dead cartilage. In thyroid perichondritis either the
interior of the larynx, the pyriform sinus, or the outside of the neck
is encroached upon.
In the course of the necrotic stage of the disease the laryngeal
framework may cave in, and a stenosis be produced which may quickly put
an end to the patient's life unless tubage--as explained under the head
Oedema--or tracheotomy be performed. A loose piece of dead cartilage
getting into the rima can produce the same fatal effect. Smaller or
larger pieces of necrosed cartilage, sometimes partially or wholly
ossified, have been expectorated, or, post-mortem, found lying in the
respiratory passage, looking dirty-yellowish or blackish. Fistulous
openings may take place in the larynx, pharynx, and in the skin
covering these parts. Gaucher has reported an extraordinary case in
which a perichondritic abscess of the thyroid cartilage had opened into
the vertebral canal, as well as externally by the side of the
sterno-cleido-mastoid muscle. If the perichondritis has followed
deep-going ulcerative destruction of the mucous membrane, the
perichondritic abscess bursts more easily, and less burrowing of the
pus usually takes place.
In the rare termination of healing of the necrotic stage of
perichondritis the loss of cartilage-substance is supplied by
connective-tissue granulation emanating from the perichondrium. Cohen
has reported a case in which there was apparently a reproduction of the
whole cricoid cartilage, the necrosed original one remaining in the
interior of the larynx as a foreign body.
Just as laryngeal stenosis is the grave danger during the continuance
of the disease before the perichondritic abscess has opened from its
protrusion into the laryngeal cavity, together with the accompanying
oedema, and from the undermining of soft parts by burrowing pus, and
after the abscess has opened from exfoliated pieces of cartilage
blocking the interior, or, when eliminated, from caving in of the
laryngeal framework, so laryngeal stenosis is the grave consequence of
the disease from remaining deformity, cicatricial contraction,
ankylosis of the crico-arytenoid articulation, etc. An open
perichondritic abscess may also lead to extensive gangrenous
destruction, and occasionally to subcutaneous emphysema.
Under the microscope the first stage of perichondritis is marked by the
appearance in the fibrous basis-substance of the perichondrium of more
or less coarsely granular corpuscles, the so-called inflammatory
corpuscles. As to their origin, it is well known that Virchow taught
that they are produced by the enlargement, division, and subdivision of
the connective-tissue corpuscles, while Cohnheim claimed that they are
nothing but emigrated {120} colorless blood-corpuscles: in point of
fact, most of them arise from the liberation of the living matter
contained in the basis-substance, by the liquefaction or melting out of
the non-living ingredient, and the increase and division of this matter
into medullary or inflammatory corpuscles which constitute the
so-called inflammatory infiltration. So long as the corpuscles remain
connected by filaments of living matter, the inflammatory process may
terminate by a new formation of basis-substance in hyperplasia--_i.e._
in the new formation of connective tissue. When, on the contrary, the
inflammatory corpuscles are torn apart and become suspended in a liquid
exudate, they constitute pus, and then the termination of the
inflammatory process is in suppuration; that is to say, usually in an
abscess.
The perichondrium and cartilage are normally so closely connected that
the one tissue passes gradually into the other without definite
boundary-line, and the cartilage participates in the inflammatory
process by a liquefaction of its basis-substance, reappearance of the
living matter therein contained, and the formation of more inflammatory
corpuscles. So long as the inflamed perichondrium remains in living
connection with the cartilage, both tissues may participate in the new
formation of a dense connective tissue, and hyperplasia be the result
of the perichondritis and chondritis. Should, on account of suppuration
at the boundary of the cartilage, the vascularized portion of the
perichondrium become detached, the cartilage, being itself devoid of
blood-vessels, will become dead. Its corpuscles will shrivel, and
together with the lifeless basis-substance become disintegrated. Pieces
of necrotic cartilage may be found lying in the surrounding pus, and,
though usually chondritis has preceded the necrosis, the latter may
ensue without previous change of the cartilage tissue, especially if
the perichondritis runs its course to suppuration rapidly; but in every
case suppurative perichondritis precedes necrosis of the cartilage.
After the elimination of necrosed portions cartilage is as a rule
replaced by newly-formed dense fibrous connective tissue. Some
clinically-observed cases, aside from the remarkable case of Cohen
already mentioned, indicate, however, that, exceptionally, new
formation of cartilage may occur from hyperplastic perichondrium, in
the same manner as new bone is sometimes formed from hyperplastic
periosteum after osseous necrosis.