Lymphadenitis
Historical document, translated for reference. It reflects medical knowledge of the 1920s–30s and is not medical advice.
Summary
Lymphadenitis is the inflammation of lymph nodes, which can be caused by various infectious or non-infectious agents. The article describes different forms of lymphadenitis, including catarrhal, purulent, and hemorrhagic types, as well as their clinical manifestations and outcomes.
Encyclopedia article (1928–1936)
LYMPHADENITIS (lymphadenitis), inflammation of the lymph glands. Adenitis (see) is a less correct and less frequently used designation for the same condition; bubo (see) is the general name for L. of the inguinal region; bronchoadenitis (see) is for L. of the mediastinum. These terms are contrasted with adenosis (see) and lymphadenosis—systemic diseases of the lymph glands of a non-inflammatory nature. The broadest concept, adenopathy (see), encompasses the most varied conditions of the lymph glands. Since the function of the lymph glands consists in retaining all sorts of often harmful substances coming with the lymph, and partly with the blood, it is natural that regional lymph glands, acting as filters, come into a state of irritation whenever the lymph passing through them carries any harmful substances. Therefore, swelling of the lymph glands is constantly observed with all sorts of diseases or injuries of both the skin and the mucous membranes and parenchyma of various organs. Such L. are called lymphogenous. In rarer cases, the infectious agent penetrates the lymph gland through the bloodstream (hematogenous L., for example, in sepsis); finally, the inflammatory process can involve the gland, spreading to it from adjacent tissue. Inflammation can occur in the lymph glands in the same forms as in other places. The mildest form is simple L. (1. simplex hyperplastica), so-called catarrhal L. (1. catarrhalis). The term is not entirely correct, since the concept of catarrh is usually applied to inflammation of mucous membranes. The gland slightly swells, becomes somewhat sensitive to pressure, its vessels fill with blood, and the tissue becomes increasingly red and juicy. Microscopically, one finds intense capillary hyperemia and dilation of the lymph sinuses and lymphatic channels; in them are found individual polymorphonuclear leukocytes, partly brought here by the lymph flow from the periphery, partly emigrated from the blood vessels of the gland itself. But mainly the sinuses contain swollen, detached from the walls and reticular stroma reticulo-endothelial cells (so-called sinusitis, desquamative catarrh of the sinuses, or Sinus-katarrh of German authors), elements larger than neutrophils, with bubble-like round or oval nuclei and a large protoplasmic body. These cells exhibit phagocytic properties, capturing from the lymph various particles: microbes, erythrocytes, pigment and other grains, etc. Along with the reaction of the reticulo-endothelium, an intensification of the proliferative activity of the lymph follicle multiplication centers—hyperplasia of adenoid tissue—is also observed. In various cases of this L., either changes in the sinuses or hyperplasia of the lymphadenoid tissue may predominate; cases of the latter kind some authors single out as a special form—hyperplastic L. Usually, catarrhal lymphadenitis ends favorably as soon as the cause that produced it on the periphery disappears; hyperemia and swelling pass, the sinuses are cleared of the cells and particles that filled them, and restitutio ad integrum occurs. In other cases, with intensification of the inflammation in the tissue of the lymph gland, necroses develop, and subsequently suppuration; thus catarrhal L. can pass into purulent (see below). In those cases when the irritant remains in the lymph gland for a long time, the inflammation takes a prolonged course, and foreign particles are deposited in the reticular stroma. This occurs, for example, in lymph glands receiving lymph from disintegrating tumors or chronic ulcers or from lungs contaminated with dusty air. The sinuses and lymphatic channels in such glands remain filled with both reticulo-endothelial phagocytes and particles of foreign substances, and sometimes phenomena of xanthomatosis develop. The crossbars of the reticular network in chronic L. coarsen, turn into collagenous crossbars, and then the stroma undergoes hyaline degeneration, scleroses. Little by little the lymph gland becomes dense, indurated; acute adenitis passes into chronic. Such an outcome is constantly observed in enlarged lymph glands under the influence of coal deposition (so-called anthracosis) and in primary tuberculosis of them. As further contamination occurs, soot particles are not only captured by the reticulo-endothelium of the lymph sinuses, but also by the reticular cells of the follicles, so that the deposition of coal, initially limited to areas where lymph flows, subsequently captures more or less the entire gland; its stroma coarsens, gradually fibroses, and coal deposits are found already among bundles of collagenous tissue. Fibrosis of the gland occurs. The same picture is observed in the bronchial glands of stonecutters, in which, besides coal, particles of silica (chalicosis) are deposited. Thus, transition to induration is a frequent consequence of chronic contamination of lymph glands with insoluble particles. Induration of lymph glands sometimes causes the spread of the fibrous process beyond the capsule of the gland to the surrounding cellular tissue; this process is called chronic periadenitis. It leads to a dense adhesion of the gland to adjacent organs. Acute purulent L. (lymphadenitis acuta purulenta) usually accompanies acute purulent processes on the periphery. Pyogenic microbes brought by the lymph flow and detained in the glands first cause destructive changes (necroses), followed by acute purulent inflammation with exudation from the vessels and massive emigration of polymorphonuclear leukocytes. As a result, the glands quickly and strongly swell, become markedly painful on palpation, and a more or less severe edema of the surrounding cellular tissue appears around them. The matter goes either to the formation of abscesses in the gland itself, or to necrosis of it and suppuration of the surrounding cellular tissue. If the process in the gland stops, abscesses in it can gradually resorb, leaving behind only small scarred areas or general induration of the gland; or the purulent bodies undergo fatty degeneration, disintegrate into a focus of detritus, around which a fibrous capsule forms. The focus of detritus can later become impregnated with lime, petrify. In more severe cases, suppuration involves the capsule, spreads to the surrounding tissues, and forms an abscess, in the pus of which one can sometimes distinguish remnants of necrotic gland tissue (sequestrum). Such abscesses (purulent L., phlegmonous L.) require surgical intervention, as they open up spontaneously too slowly and can cause pyemia. The death or induration of a group of lymph glands from suppuration can subsequently create difficulties for the outflow of lymph from the periphery and cause chronic edema, for example, of the extremities, ch dilation of the lymph vessels (lymphangiectasia) and even hypertrophy of the connective tissue in them (pachydermia, elephantiasis). The acute L. described above are local, regional lesions of the lymph glands. In some cases of L., especially those forms that proceed with necroses and destruction, hemorrhage into the gland tissue occurs (hemorrhagic L.). Hemorrhagic L. are particularly characteristic of plague (see) and anthrax (see). But besides these L., acute simultaneous swelling of many lymph glands of the body is observed, for which there is no cause in some local inflammation on the periphery. Then one must assume some general cause in the form of an infectious or toxic agent entering the glands with the bloodstream, or in the form of the action on the lymph glands of some abnormal products of disturbed metabolism. Such L. belong to the hematogenous type. They are incomparably rarer than lymphogenous. Examples can be glandular fever (Drüsenfieber), scarlatinal L., L. in tuberculous bacteriemias, in secondary syphilis, etc. f. Chistovich. Clinic of L. Lymphadenitis is more often observed in persons engaged in heavy physical labor who inflict numerous injuries to the skin cover; for example, in workers of chemical production coming into contact with strong solutions of acids and alkalis, sharp changes in the skin of the hands develop in the form of abrasions, cracks, ulcers, consequently they often suffer from chronic L., both because there are many portals of entry for infection, and because inflammation of the glands can also be caused by chemical agents. The same is noted in persons of other professions subjected to frequent injuries to the fingers of the hands (weavers, cooks, surgeons, housewives, etc.).- In general, the reaction of the glands to the introduction of infection proceeds violently due to the rich blood supply of the lymphoid tissue. The clinical picture changes depending on the irritant, the intensity and duration of its action, on the state of the adenoid tissue of a given individual and on the position of the glands. The course of the disease and prognosis noticeably worsen in persons engaged in heavy physical labor if, at the very beginning of the disease, movements of the limb that contribute to the further spread of infection are not stopped. Acute L. is more often observed in the axillary fossa and in the groin. Under the skin, enlarged, indurated, painful glands of various sizes are visible and palpable. Clearly defined and movable in relation to the skin and the underlying tissues, they then, increasing in volume, form immobile masses; the contours of individual glands disappear behind the edema and infiltrate of the tissue. The skin covering them slightly reddens and adheres to the still non-fluctuating tumor.
Subsequently, the infiltrate softens; fluctuation appears in the center; the skin, which had previously reddened, turns blue and thins. The abscess ruptures spontaneously or is surgically opened; the abscess cavity, after the sloughing of dead tissues, is filled with granulations and scars; in individual cases, fistulas may persist for a long time. General symptoms (fever, malaise) subside from the moment the abscess is opened. The process can stop at any stage and undergo regression. As a result of acute inflammation or due to prolonged repeated minor irritations, chronic L. may develop. This is possible with poorly treated, neglected wounds, cracks, ulcers, carious teeth, etc. Chronic L. is manifested by moderate enlargement, hardening, and slight tenderness of the gland. Such chronic L. is rarely accompanied by general symptoms. - Complications of L. Besides abscesses and phlegmons, other complications of L. are possible - the development of thrombophlebitis in neighboring veins, formation of pulmonary infarcts, abscesses, and finally general infection. The diagnosis of simple, superficial, acute L. presents no difficulties, as individual or 'a whole bundle of painful glands' can be palpated; superficial, suppurative L. may be confused with a simple abscess, but based on the localization in relation to one or another group of lymph glands, the primary focus of suppuration can be relatively easily established; deep, suppurative L. sometimes presents great difficulties, may be confused with phlegmon, osteomyelitis, and is often diagnosed only on the basis of localization; in chronic L., it is sometimes necessary to differentiate from tuberculosis, syphilis, malignant tumor, and lymphadenosis. - Prevention requires the strictest observance of the rules of sanitation and hygiene: 1) removal from the body surface of sweat, sebum, all secretions from natural openings (leucorrhea, urine), dirt - especially in persons engaged in heavy physical labor, 2) introduction of widespread use of special clothing (gloves in chemical production, masks in dusty environments), 3) a series of appropriate sanitary measures to disinfect the workplace, 4) timely consultation with a doctor in case of fresh injury or onset of inflammatory disease. By applying an aseptic or antiseptic dressing and providing rest for a fresh injury to an extremity, it is often possible to prevent the development of lymphadenitis. Treatment. If L. is present, attention should first be directed to the portal of entry of infection. It is necessary to stop the influx of septic material by opening purulent cavities, expanding fistulous tracts, packing, and drainage. Then conditions of maximum rest and best blood supply must be created. This is achieved by placing the patient at rest in bed, splint bandages, elevating the affected extremity, moist and dry heat (wet dressings with hypertonic solutions of alkalis, compresses, baths, hot-water bottles, photo- and radiotherapy). In suppurative L., an incision must be made to provide drainage for the pus. If it is possible to eliminate the retraction of the edges, tampons can be dispensed with. In deep L. - wide packing and drainage. Treatment of chronic L. consists in eliminating the portal of entry followed by resorption therapy. Abortive treatment with inconsistent success is applied in the suppurative form of venereal buboes. Complete excision of a group of glands should be approached with caution due to their protective role for the body, as well as because of the danger of intractable edema with excessive radicalism.
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“Lymphadenitis.” Soviet Medical Encyclopedia. English translation of Bolshaya Meditsinskaya Entsiklopediya, 1st ed. (Moscow, 1928–1936), ed. N. A. Semashko. https://sovietmedicalencyclopedia.pages.dev/article/lymphadenitis/