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

Toxico-allergic lesions of the larynx cover a huge layer of pathological conditions of the larynx, many of which have not been thoroughly studied with respect to both etiology and pathogenesis.

Unification of toxic and allergic causes into one heading can only seem artificial at first glance, but both have much in common, since they are directly related to a number of the most important biological functions of the organism-the permeability and filtration capacity of biological membranes, electrolyte and protein metabolism , the mechanisms of regulation of the CBS tissue fluid and blood plasma, a variety of biochemical processes, providing a state of homeostasis as separate organs and tissues, and the body as a whole, nak end, - to regulatory neuroendocrine systems.

The variety 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 applies to the upper respiratory tract, in particular, the larynx, an organ that is extremely sensitive to various toxic and allergic factors of both endogenous and exogenous origin. These factors can include both the actual allergy, the manifestations of which are largely due to 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 outside, as well as products of internal origin that are formed as a result of metabolic and endocrine disruption or the onset of inflammatory diseases and other pathological conditions ( diseases of the circulatory and excretory systems, liver dysfunction small intestine, "slagging" of the body of unoxidized products of metabolism, toxemia of pregnancy, and many others. Al.). All the above factors and conditions primarily affect the function of cell membranes, mucous membrane, 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 airways.

What causes toxic-allergic lesions of the larynx?

Laryngeal edema in toxic-allergic laryngitis refers to membranogenic swelling, which can occur with local and general effects of a wide variety of factors (infection, heat, cold, various substances, radiant energy, etc.). The increase in capillary permeability, which is the basis of the pathogenesis of inflammatory and toxic edema, is carried out with the participation of a number of substances (histamine, active globulins, etc.) that are released or formed in the tissue when the stimulus (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 an own role in the onset of edema.

Allergic and anaphylactic swelling of the larynx is closely related to membranous edema. In typical allergic manifestations (serum sickness, urticaria, angioedema Quincke, bronchial asthma, etc.), the swelling of the skin and mucous membranes also develops due to a violation of the permeability of the capillary walls resulting from the antigen-antibody reaction.

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

A number of diseases of the kidneys, the heart and such as the toxicosis of pregnant women, accompanied by an anasarka, can lead to swelling of the larynx.

Medicamentous edema of the larynx is most often observed with intoxications with iodine-containing drugs, salicylates, belladonna preparations, as well as products of plant and animal origin (eggplant, mushrooms, strawberries, cheese, seafood, etc.); these swelling develops more slowly than allergic ones, however they last longer. In recent years, laryngeal edema has been noted in the course of antibiotic therapy, especially with the administration of these drugs in the form of inhalations and aerosols.

Infringements of permeability of walls of capillaries at an allergic edema is explained by release from mast cells of histamine, and also by activation of proteolytic enzymes arising at reaction antigen-antibody, and influence 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 body cavities. The edema fluid comes from the blood.

Transition of fluid from the blood to the tissues through the capillary membrane is facilitated by hydrodynamic blood pressure, determined by the value of blood pressure and blood flow velocity in the capillaries, and the oncotic (colloid-osmotic) pressure of the fluid proteins.

The latter counteracts the escape of liquid from the capillary bed, since the wall of the capillary functions as a semipermeable membrane, through which proteins pass with great difficulty, while water and crystalloids (dissolved in trace elements) are easy. When the mechanism of permeability of the membranes of the copillaries breaks from the blood in the tissue, both crystalloids and proteins penetrate, which leads to tissue or cavity (ascites, hydrothorax, effusion to the joint bag) edema.

When swelling, cells and fibers move apart due to the accumulation of edematous fluid, which dilutes the interstitial substance. The connective tissue fibers are split into fibrils.

With prolonged swelling, fibrils swell and disappear (dissolve in the "edematous" substance).

With pronounced swelling, cells (connective tissue, epithelium, muscles) move away from the interstitial tissue, swell and vacuolize, which leads to a disruption of metabolism 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 sclerosis and connective tissue, which is of particular importance in the pathogenesis of respiratory failure in the upper respiratory tract.

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

Symptoms of toxic-allergic lesions of the larynx

Laryngeal edema can occur acutely, subacute or develop chronically.

Allergy causes most often such manifestations either during generalized urticaria, or, more often, during the angioedema.

Cases of family allergic edema of the larynx with recurring crises are described, which can acquire a threatening character.

According to the observations of Romanian authors, in some cases there is a family predisposition to periodically developing edema of the larynx; There were deaths in individuals in several generations of the same family. During the crisis, in addition to the laryngeal edema, there are corresponding changes on the face, in the mouth and throat.

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

Treatment of toxic-allergic lesions of the larynx

Treatment of toxic-allergic damage to the larynx is to exclude contact of the body with agents that cause toxic and allergic edema of the larynx and the appointment of antihistamines, decongestants and sedatives.

How are toxico-allergic lesions of the larynx prevented?

To prevent drug laryngeal edema, it is advisable to administer intralaryngeal administration of antibiotics in a mixture with hydrocortisone against antihistamine prophylaxis. Intolerance to antibiotics is manifested by the emergence of the enanthema of the mucous membrane of the oral cavity, pharynx and larynx, as well as a significant edema of these anatomical regions.

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