Toxic-allergic lesions of the larynx: causes, symptoms, diagnosis, treatment

Toxic-allergic lesions of the larynx cover a huge layer of pathological conditions of the larynx, many of which have not been studied in sufficient depth in relation to both etiology and pathogenesis.

The combination of toxic and allergic causes in one category may seem artificial only at first glance, however, both have much in common, since they are directly related to a number of the most important biological functions of the body - the permeability and filtration capacity of biological membranes, electrolyte and protein metabolism, mechanisms for regulating the acid-base balance of tissue fluid and blood plasma, various biochemical processes that ensure the state of homeostasis of both individual organs and tissues, and the body as a whole, and finally, to regulatory neuroendocrine systems.

The diversity of the above significantly complicates the problem of toxic-allergic diseases of the body and its individual organs and systems. To a large extent, this situation also concerns the upper respiratory tract, in particular the larynx - an organ that is extremely sensitive to various toxic-allergic factors of both endogenous and exogenous origin. These factors may include both allergies themselves, the manifestations of which are mostly caused by the reactive pre-preparedness of the body for an inadequate or hyperreactive response of the body to the introduction of foreign substances into it from the outside, and products of internal origin formed as a result of disruption of metabolic and endocrine processes or the occurrence of inflammatory diseases and some other pathological conditions ( diseases of the cardiovascular and excretory systems, dysfunctions of the liver and small intestine, "slagging" of the body with under-oxidized metabolic products, toxicosis of pregnant women, etc.). All of the above factors and conditions primarily disrupt the function of cell membranes, mucous membranes, connective tissue and vascular endothelium of the larynx, which causes one of the most basic toxic-allergic manifestations - edema and associated obstructive processes in the respiratory tract.

What causes toxic-allergic lesions of the larynx?

Edema of the larynx in toxic-allergic laryngitis is related to membranogenic edemas, which can occur with local and general effects of a wide variety of factors (infection, heat, cold, various substances, radiant energy, etc.). Increased capillary permeability, which underlies the pathogenesis of edema of an inflammatory and toxic nature, is carried out with the participation of a number of substances (histamine, active globulins, etc.), released or formed in the tissue when an irritant (pathogenic factor) acts on it. Thus, the toxigenic action of the agent provokes the manifestation of humoral mechanisms of allergy, which potentiate the action of the former and begin to play their own role in the occurrence of edema.

Allergic and anaphylactic laryngeal edema are closely related to membranogenic edema. In typical allergic manifestations (serum sickness, urticaria, Quincke's angioedema, bronchial asthma, etc.), edema of the skin and mucous membranes also develops due to impaired permeability of the capillary walls, which occurs as a result of the antigen-antibody reaction.

Bites of stinging insects, especially bees and wasps, in the area of the face, and sometimes the mucous membrane of the mouth and pharynx, often cause severe swelling of the laryngopharynx and larynx.

A number of diseases of the kidneys, heart, and such as toxicosis of pregnancy, accompanied by anasarca, can lead to swelling of the larynx.

Drug-induced laryngeal edema is most often observed in cases of intoxication with iodine-containing drugs, salicylates, belladonna preparations, as well as products of plant and animal origin (eggplants, mushrooms, strawberries, cheeses, seafood, etc.); these edemas develop more slowly than allergic ones, but last longer. In recent years, laryngeal edema has been noted that occurs during antibiotic therapy, especially when these drugs are prescribed in the form of inhalations and aerosols.

Impaired permeability of capillary walls in allergic edema is explained by the release of histamine from mast cells, as well as the activation of proteolytic enzymes that occurs during the antigen-antibody reaction, and the effects of macromolecular irritants.

Pathological anatomy of toxic-allergic lesion of the larynx

Edema is a general or local disturbance of water metabolism, characterized by excessive accumulation of water, proteins and electrolytes in the extracellular tissue space or serous cavities of the body. Edema fluid originates from the blood.

The transition of fluid from the blood into tissues through the capillary membrane is facilitated by the hydrodynamic pressure of the blood, determined by the magnitude of blood pressure and the speed of blood flow in the capillaries, and the oncotic (colloid-osmotic) pressure of the proteins of the fluid.

The latter counteracts the exit of fluid from the capillary bed, since the capillary wall functions as a semipermeable membrane through which proteins pass with great difficulty, while water and crystalloids (microelements dissolved in it) pass easily. When the capillary membrane permeability mechanism is disrupted, both crystalloids and proteins penetrate from the blood into the tissue, which leads to tissue or cavity (ascites, hydrothorax, effusion into the joint capsule) edema.

During edema, cells and fibers move apart due to the accumulation of edema fluid, which liquefies the interstitial substance. Connective tissue fibers are broken down into fibrils.

With prolonged edema, the fibrils swell and disappear (dissolve in the “edematous-intermediate” substance).

In cases of severe edema, cells (connective tissue, epithelium, muscles) move away from the interstitial tissue, swell, and vacuolate, which leads to metabolic disorders in the tissue, leading to degenerative and necrobiotic processes in its cells.

Macroscopically, with mucosal edema, they become translucent and gelatinous. In some cases, prolonged edema leads to the development of proliferation and sclerosis of connective tissue, which is of particular importance in the pathogenesis of the development of respiratory failure of the upper respiratory tract.

The occurrence of toxic-allergic edema of the larynx is facilitated by the presence of fibrous hydrophilic tissue in its submucosal layer, which is especially developed on the lingual surface of the epiglottis, in the aryepiglottic folds, in the post-fold space and, to a lesser extent, in the folds of the vestibule.

Symptoms of toxic-allergic damage to the larynx

Laryngeal edema can occur acutely, subacutely, or develop chronically.

Allergy most often causes such manifestations either during generalized urticaria or, more often, during Quincke's edema.

Cases of familial allergic laryngeal edema with recurring crises that can become life-threatening have been described.

According to observations by Romanian authors, in some cases there is a family predisposition to periodically occurring laryngeal edema; cases of fatal outcomes have been observed in individuals in several generations of the same family. During a crisis, in addition to laryngeal edema, corresponding changes also occur on the face, in the oral cavity and pharynx.

In people with allergies, laryngeal edema may occur suddenly during the day or night and lead to severe respiratory failure, sometimes life-threatening. Laryngeal edema is characterized by a foreign body sensation, dysphagia, dysphonia and aphonia, and dyspnea. Laryngoscopy reveals a massive gelatinous edema occupying almost the entire vestibule of the larynx and blocking the respiratory (vocal) gap.

Treatment of toxic-allergic lesions of the larynx

Treatment of toxic-allergic damage to the larynx involves eliminating contact of the body with agents that cause toxic and allergic swelling of the larynx and prescribing antihistamines, decongestants and sedatives.

How are toxic-allergic lesions of the larynx prevented?

To prevent drug-induced laryngeal edema, it is advisable to prescribe intralaryngeal administration of antibiotics mixed with hydrocortisone against the background of antihistamine prophylaxis. Antibiotic intolerance is manifested by the development of enanthem of the oral mucosa, pharynx and larynx, as well as significant edema of the indicated anatomical areas.

With prolonged use of antibiotics without observing antifungal measures (for example, simultaneous administration of nystatin), patients, in addition to laryngeal edema, may develop candidiasis of the upper respiratory tract.