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 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 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.
DIAGNOSIS.—The inflammatory stage may be suspected, rather than positively recognized, from the peculiar pain if the laryngoscope (or, in the rare case of thyroid perichondritis, palpation) reveals enlargement of a part of the cartilaginous structure without much injection of the mucous membrane. The presence of other symptoms mentioned, and in the case of cricoid perichondritis the localized pharyngeal reddening, make the diagnosis more probable. During the suppurating and necrotic stages the diagnosis becomes certain from the symptoms I have described, especially expectoration of fragments of necrosed cartilage, together with direct examination. The laryngoscope may show the abscess; sometimes the finger or a probe can detect fluctuation, and frequently through an opening the probe detects the necrosis. The movement of one or both vocal bands may be affected either mechanically from purulent accumulation, or from articular ankylosis, or from interference with muscular attachments or action, or with innervation. In my hand, and in that of others, a probe introduced through an external fistula has been seen in the larynx; others have been able to inject colored fluid and find it in the interior.