Perichondritis

By M. Skvortsov · Pathology, Otorhinolaryngology, Infectious Diseases

Also known as: Perichondritis inflammation, Cartilage inflammation

Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.

Summary

Perichondritis is inflammation of the perichondrium, the membrane covering cartilage. Unlike periosteum, the perichondrium lacks significant regenerative capacity, leading to cartilage death when damaged. This condition primarily affects the larynx and trachea, often resulting from infections like tuberculosis or syphilis.

Encyclopedia article (1928–1936)

PERICHONDRITIS (perichondritis) (from the Greek chondros-grain, cartilage), inflammation of the perichondrium, i.e., the membrane that covers cartilage and is in no way analogous to the periosteum. However, the pathology of the two is far from identical, just as the consequences of their diseases for cartilage and bone tissues are different. This is due to the fact that 1) blood vessels penetrate the bone, while in cartilage they do not go beyond the perichondrium; 2) bone is nourished not only from the periosteum but also from the bone marrow, whereas cartilage has nothing analogous to the latter; due to this, when the perichondrium is detached or dies, the corresponding part of the cartilage inevitably and completely dies; 3) the periosteum possesses enormous proliferative and plastic potential, which is especially evident in the formation of callus at the site of a fracture and thanks to which it responds to many irritations by producing bone substance. On the contrary, the perichondrium has both of these abilities to a small extent, for which reason perichondritis with a markedly productive character or significant cartilage neoplasm is never encountered. Thus, pathology knows only alterative-exudative forms of perichondritis inflammation, among which the main and almost the only form of significance is the suppurative type. This occurs because in the larynx and trachea, where perichondritis is mainly observed, lesions of the perichondrium are always associated with the formation of ulcers, which either develop primarily and serve as the cause of perichondritis (e.g., in tuberculosis, in measles necrosis, in bedsores caused by intubation), or in the case of hematogenous infection (e.g., syphilitic) are formed secondarily very quickly due to the delicacy of the mucous membrane, which is easily involved in the process during the development and disintegration of the main pathological focus. Thus, if suppurative infection does not arise as such from the very beginning, it quickly joins any lesion of the perichondrium due to the almost constant presence of the corresponding causative agents on the mucous membrane of the pharynx and upper respiratory tract. In this case, regardless of whether pus-forming microbes are carried into the perichondrium by the bloodstream or penetrate it through lymphatic spaces from any ulcerative defects of the mucous membrane, in both cases the suppurative process usually begins from the deepest parts of the perichondrium, bordering the cartilage. Accumulating here, the pus detaches the perichondrium, the corresponding area of cartilage dies, and then gradually undergoes fibrous disintegration and melting or separates from the healthy parts, forming one or several sequestra suspended in the pus. A abscess formed in this way usually opens after a short period of time; if it concerns the laryngeal cartilages, it most often opens into the laryngeal cavity, less often into one of the so-called recessus pharyngo-laryngei. In the case of the presence of cartilaginous sequestra in the pus, they can at this time enter the respiratory tract and cause a symptom complex of a foreign body. Occasionally, with rapidly penetrating ulcers, the destruction of the perichondrium may begin from the superficial layers, which leads to the gradual exposure of the cartilage, after which death of the cartilage results in a more or less widely open suppurative cavity. The localization of perichondritis depends entirely on the primary disease. In decubital ulcers, which often occur in intubated children from pressure of the tube, the cricoid cartilage is most frequently affected, corresponding to the favorite localization of these ulcers. In measles necrosis, located mainly in the area of the vocal cords, the arytenoid cartilages are first in frequency of affection. They also give the highest percentage of perichondritis developing on the basis of tuberculous ulcers of the larynx. The epiglottis is the predominant site for the formation of syphilitic infiltrates and gummas, which, when ulcerated, give rise to the development of perichondritis precisely in this area. In catarrhal (or catarrhal-necrotic) processes in the pharynx and upper part of the larynx, almost always accompanying the acute period of typhoid fever, decubital ulcers often form on the free edges of the epiglottis due to their tight adhesion to the swollen mucous membrane of the root of the tongue, for which reason the affection of the perichondrium of the epiglottis in this disease is rather typical. In addition, typhoid fever can give rise to the formation of ulcers in the larynx due to the occasionally observed specific brain-like swelling of the mucous follicles with their subsequent necrosis and ulceration. Such specific typhoid ulcers are located on the posterior surface of the epiglottis and in the area of the Morgagni ventricles, accordingly, the perichondritis developing on their basis affects the epiglottis, as well as the thyroid and arytenoid cartilages. As for hematogenous perichondritis, they occur significantly less frequently, namely, in primary and secondary pyemias of various origins, especially those that complicate the course of typhoid, typhus, sometimes relapsing fever and smallpox. In these cases, pus accumulation can occur on both the inner and outer surfaces of the laryngeal cartilages, without any particular preference for either of them. The breakthrough of pus in external perichondritis still more often occurs into the larynx, pharynx or esophagus, less often onto the skin surface. Hematogenous perichondritis of the same type can also develop on the cartilages of the ribs, usually with subsequent exit of pus outward through the skin cover, or in more rare cases with the spread of the process to the pleura, pericardium, mediastinum.-The extent of the process in suppurative perichondritis varies within very wide limits and, like localization, is largely dependent on the primary disease. Perichondritis arising in the larynx on the basis of limited ulcerative or necrotic damage to the mucous membrane usually affects only the part of the cartilage closest to the site of damage. An entire cartilage is rarely affected, especially a small one (e.g., the arytenoid). However, with widespread syphilitic or extensive disintegrating cancerous ulcers, it can lead to the death and sequestration of almost all laryngeal cartilages, as a result of which the walls of the larynx become soft and collapse, causing sudden death. The course of perichondritis is very prolonged, and the chances of restoration of normal structure are extremely poor. Due to the negligible regenerative and plastic capacity of cartilage and perichondrium, the resulting defects are filled with granulation tissue extremely slowly and with great difficulty. As a result, a significant number of patients die from sepsis or complicating pneumonia. The most favorable outcome of the process is always associated with the formation of a scar, which causes a greater or lesser deformation of the organ and narrowing of its lumen depending on its volume. If the process occurs near the vocal cords, the voice is very often affected, and large scarred erosions of the edges of the laryngeal inlet can cause difficulty in swallowing due to frequent entry of food particles into the respiratory tract. Clinical picture and treatment-see Chondritis.

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“Perichondritis.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/perichondritis/