Diseases of the paranasal sinuses: causes, symptoms, diagnosis, treatment

Diseases of the paranasal sinuses of the nose are more than one-third of all pathological conditions of the ENT organs. If we consider that most of these diseases are accompanied by nasal diseases, which either precede the diseases of the paranasal sinuses of the nose and are their cause, or are their consequence, their number is significantly increased. The anatomical position of the paranasal sinuses of the nose is itself a significant risk factor for possible complications in diseases of the paranasal sinuses of the nose from the side of the brain, eye, ear and other areas of the body.

In the pathological conditions of the paranasal sinuses of the nose, violations of the various links of the anatomo-functional system under consideration play an important role not only in ensuring its regional homeostasis, but also in maintaining the normal state of vital functions of the central nervous system, such as hemodynamics, liquorodynamics, etc., and through them - non-alternative sentences of mental, motor and autonomic functions of nerve centers. From what has been said, it follows that any pathological conditions of the paranasal sinuses of the nose should be attributed to systemic diseases that cause corresponding disorders not only in the craniofacial region and upper respiratory tract, but also in the whole body.

A systematic approach to the treatment of the pathogenesis of diseases of the paranasal sinuses of the nose finds justification in the variety of various functions that the PNS implements. Here we dwell only on their brief exposition with respect to this section.

Barrier function of the nasal mucosa and paranasal sinuses of the nose. The barrier function is understood as a special physiological mechanism that protects the body from the effects of the environment, preventing the penetration of bacteria, viruses and harmful substances into it, and also contributing to the preservation of the permanent composition and properties of blood, lymph, and tissue fluid. The mucous membrane of the nose and paranasal sinuses belong to the so-called external barriers, through which the inhaled air is cleared of dust and harmful substances in the atmosphere, mainly by means of the epithelium lining the mucous membrane of the respiratory tract and having a specific structure. Internal barriers between blood and tissues are called histohematic. They play an important role in hindering the spread of infection in tissues and organs by hematogenous way, in particular, the onset of hematogenous sinusitis, on the one hand, and sinusogenic intracranial complications, on the other. In the latter case, the crucial role belongs to the BBB. A similar barrier exists between the blood and intralubirintic fluids of the inner ear. This barrier was called hematolabyrinth. As GI Kassel believes (1989), GGB are highly adaptable to the composition and properties of the internal environment of the body. This is important for maintaining the constancy of the limits of the physiological and biochemical parameters of the organism, preserving the organ or system of organs within the physiological response and in the active and effective counteraction to pathogenic factors.

The barrier function is under constant influence and systemic control by the ANS and closely related endocrine system. Such risk factors as nervous fatigue, alimentary depletion, avitaminosis, chronic intoxication, allergens, etc., violate the barrier function, which leads to an increase in the effect of these factors and to the emergence of a vicious circle, defined by us as a functional pathological system with a predominant effect of positive feedback.

The introduction of an infection against this background, a decrease in the activity of tissue immunity under the influence of certain risk factors, leading to increased cellulence, causes the development of appropriate diseases, which is largely inherent in the PNS. Firstly, the function of the mucous glands is disrupted and the biochemical composition of their secretion changes, the immune properties of the cellular elements of the blood are weakened and the bactericidal properties of substances such as lysozyme, neoplastic processes progress, local tissue pathological processes occur, leading to trophic disturbances, with consequent consequences characteristic of each specific nosological form.

Violation of the barrier function and local immunity with weakness of the central mechanisms of regulation of humoral homeostasis leads to disruption of the physiological functions of such structures of the nasal mucosa, as a mucociliary apparatus, interstitial tissue, tissue fluid, etc., which, in turn, potentiates the underlying pathological process, new perverse cycles with the involvement of new organs and systems in them.

These pathogenetic processes significantly affect the PNS receptors, causing the appearance of pathological viscorocortico-visceral and viscurohypothalamo-visceral reflexes that disharmonize the adaptation mechanisms that oppose the pathological process, reduce their effect on the repair processes to a minimum, which leads to decompensation of adaptive responses to this disease and progressive development of the latter.

The depicted picture of pathogenetic mechanisms of paranasal sinus infections is only a part of those grandiose systemic processes that are played out in the PNS and which often go beyond its limits. Each of these processes has its own specific features that determine the disease nosology, but they all have common features that characterize the pathological process with such pathoanatomical concepts as inflammation, dystrophy, atrophy, hyperplasia, fibrosis, metaplasia, necrosis, etc., and pathophysiological concepts - dysfunction, areactivity, decompensation, parabiosis, death, etc. It should be borne in mind that the development of any pathological state is accompanied by a process directed to the diametrically opposite side, i.e., in the direction of recovery, even without external therapeutic intervention. The components of this process are determined by the essence of the pathological state itself, which, figuratively speaking, "provokes fire" and precisely the "caliber" of those "tools" and the quality of those "shells" that are disastrous for him. Bright examples of this are immunity, inflammation, reparative tissue processes, not to mention the numerous humoral phenomena that are the basic mechanisms of any adaptive-adaptive and reparative processes.

The variety of pathogenetic forms of PNS diseases is most demonstratively reflected in the principles or criteria for classifying inflammatory processes in this system.

Criteria for the classification of inflammatory diseases of the paranasal sinuses of the nose

1. Topografoanatomichesky criterion:
   1. sinusitis craniofacial, or anterior:
      1. sinusitis of the maxillary;
      2. sinusitis rhinoemoid;
      3. sinusitis frontal.
   2. sinusitis craniobasal, or posterior:
      1. sinusitis sphenoidal;
      2. sinusitis is etmoid-sphenoidal.
2. . Quantitative criterion:
   1. monosynusitis (inflammation of only one paranasal sinus of the nose);
   2. polysynusitis:
      1. geminolisinusit (one-sided inflammation of two or more paranasal sinuses);
      2. pansinusit (simultaneous inflammation of all paranasal sinuses of the nose.
3. Anatomico-clinical criteria:
   1. acute sinusitis of all localizations, reflected in points 1 and 2;
   2. subacute sinusitis of all localizations, reflected in points 1 and 2;
   3. chronic sinusitis of all localizations, reflected in points 1 and 2.
4. Pathological criteria:
   1. sinusitis exudative:
      1. sinusitis catarrhal serous;
      2. sinusitis is purulent;
   2. sinusitis proliferative:
      1. hypertrophic;
      2. hyperplastic;
   3. Associated forms:
      1. simple serous-purulent sinusitis;
      2. polypozno-purulent sinusitis;
      3. ulcerative-necrotic fungal-pyogenic etiology;
      4. osteomyelitic sinusitis.
5. Etiological criteria:
   1. mono- and polymicrobial nonspecific sinusitis (pneumococcus, streptococcus, staphylococcus, etc.);
   2. specific microbial sinusitis (syphilis, tuberculosis, etc.);
   3. anaerobic sinusitis;
   4. viral sinusitis.
6. Pathogenetic criterion:
   1. primary sinusitis:
      1. hematogenous;
      2. lymphogenous;
   2. secondary:
      1. rhinogenic sinusitis (the vast majority of inflammatory diseases of the paranasal sinuses of the nose, according to the figurative expression of the outstanding French otorhinolaryngologist Terracol, "Every sinusitis is born, lives and dies simultaneously with the rhinitis that gave birth to it");
      2. odontogenous sinusitis;
      3. sinusitis in general infectious and specific diseases;
      4. traumatic sinusitis;
      5. allergic sinusitis;
      6. metabolic sinusitis;
      7. secondary tumor sinusitis (congestive sinusitis).
7. Age criterion:
   1. sinusitis of childhood;
   2. sinusitis of adulthood;
   3. sinusitis of senile age.
8. Treatment criterion:
   1. sinusitis nonoperative treatment;
   2. sinusitis of surgical treatment;
   3. sinusitis combined treatment.

These classification criteria do not pretend to be an exhaustive classification of inflammatory diseases of the paranasal sinuses of the nose, but only inform the reader of the variety of causes, forms, clinical course, treatment methods, etc. Of these diseases. Below, the main criteria for the classification of inflammatory diseases of the paranasal sinuses are discussed in more detail.

The cause of inflammatory diseases of the paranasal sinuses of the nose. Repeated bacterial contamination of the nasal mucosa due to inhalation of atmospheric air is the reason for the presence of polymorphic apatogenic microbiota (saprophytes) in the nasal cavities. Apathogenicity of the microbiota is ensured by the presence in the nasal secret of unique enzymes that possess bacteriostatic and bactericidal properties. These include a group of lysozymes - protein substances that can cause lysis of certain microorganisms by depolymerization and hydrolysis of mucopolysaccharides of microorganisms. In addition, as ZV Ermol'eva (1938) has shown, lysozymes have the ability to stimulate tissue regeneration processes. When there is an acute rhinitis, especially a viral etiology, the bactericidal properties of lysozyme are sharply reduced, resulting in saprophyte acquiring pathogenic properties. At the same time, the barrier functions of the connective tissue layer of the nasal mucosa decrease, and microorganisms freely penetrate into its deep sections. In addition to lysozyme, a number of other substances exist in the nasal mucosa (collagen, basic and amorphous substance, chemical substances of glutzid nature, polysaccharides, hyaluronic acid, etc.), which regulate the diffusion processes in cellular "membranes and provide protection against the penetration of microorganisms into deep layers of the nasal mucosa and even beyond. However, pathogenic microorganisms have their own protection in the form of their hyaluronidase enzyme, which hydrolyzes hyaluronic acid and increases the virulence of microorganisms and their penetrating ability.

In acute purulent inflammatory diseases of the paranasal sinuses of the nose, streptococcus, pneumococcus, Staphylococcus aureus, Pfeiffer's coccobacillus, Friedlander's Klebsiella, rhinoviruses, adenoviruses and several others are most common. In some cases, when sowing the contents of the sinus, carried out in the usual way, this content is sterile. Indirectly, this indicates either a viral or anaerobic etiology of sinusitis. For chronic purulent inflammatory diseases of the paranasal sinuses of the nose, gram-negative microorganisms, such as the pseudodipteria Pseudomonas aeruginosa, E. Coli, etc., are more typical, and for the odontogenic genyantritis - anaerobes. As AS Kiselev (2000) notes, in recent years mycoses of paranasal sinuses caused by irrational use of antibiotics and dysbacteriosis are becoming topical. The role of influenza and parainfluenza infection in the occurrence of acute inflammatory diseases of the paranasal sinuses of the nose has not been fully clarified. At the present time, the hypothesis that the virus plays the role of an allergen that causes an exudative process dominates, after which, as a result of superinfection of the banal microbiota, inflammation develops.

The pathogenesis of inflammatory diseases of the paranasal sinuses of the nose is directly dependent on four categories of the causes of this disease: 1) local; 2) anatomically close; 3) anatomically distant; 4) common.

Local causes are divided into determinative and contributing factors. The first determine the nature and extent of the inflammatory process and play the role of its cause. Infectious colds in the vast majority of cases are the primary cause of inflammatory diseases of the paranasal sinuses of the nose. Promoting risk factors are a variety of circumstances, including occupational and domestic hazards, unfavorable climatic conditions and many other factors that directly affect the mucosa and its receptor apparatus.

One of the important risk factors is the unfavorable anatomical structure of the paranasal sinuses and the nasal cavity. These, for example, include the high location of the inner opening of the excretory duct of the maxillary sinus or an excessively narrow and long frontal-nasal canal, or excessively large paranasal sinuses. According to many authors, it is the functional state of the excretory ducts of the paranasal sinuses that plays a decisive role in the onset of their inflammation. Obstruction of these ducts, as a rule, leads to a violation of the ventilation of the cavities, the dissolution of gases in the fluids of the mucous membrane, the formation of negative pressure and, as a consequence, the appearance of transudate or cyst-like formations (mucous membranes). The transudate can remain sterile for a long time (amber color translucent opalescent liquid), however penetration to it leads to its suppuration and development of acute purulent sinusitis. Often, the paranasal sinuses, in part or in whole, communicate with each other, especially in the frontal, maxillary sinuses and cells of the latticed labyrinth. And then the inflammation of any sinus leads to a chain inflammatory reaction, which can affect two, three or even all airway cavities of the facial skull.

A great pathogenic role in the onset of inflammatory diseases of the paranasal sinuses of the nose is the fact that, without exception, all the ventilation and drainage openings of the paranasal sinuses are in the path of an air stream that pesoes itself and microorganisms, and protein and vegetable antigens, and aggressive substances, limits of physiological tolerance, temperature fluctuations of air, which together cause a significant strain of the protective functions of the nasal mucosa and paranasal grooves x.

Another anatomical risk factor is the presence of bone septa (anomalies of development) in sinuses, which are often observed in the maxillary, frontal and sphenoid sinuses, as well as the presence of coils and additional cavities that extend into the thickness of the facial skeleton. Their conditioning is extremely difficult, and therefore it is often with them that the inflammatory disease of the paranasal sinuses of the nose begins.

The same risk factors include defects in the development of the nasal cavity (atresia, narrow and curved nasal passages, deformities of the vestibule of the nose, curvature of the septum of the nose, etc.).

To the local causes of inflammatory diseases of the paranasal sinuses of the nose are numerous internal nose diseases, described above.

Traumatic factors can cause the development of not only inflammatory diseases of the paranasal sinuses of the nose, but also various extra- and intracranial purulent complications. Especially dangerous are traumas of the paranasal sinuses, accompanied by fractures of their bone walls (trellis plate, orbital walls of the maxillary and frontal sinuses). In these cases, the most common are the hematomas that arise both in the sinuses and beyond. Significant danger with regard to the occurrence of abscesses and phlegmon are fire foreign bodies, in which the infectious process develops not only in the immediate vicinity of foreign bodies, but also far beyond its limits along the course of the wound channel as a result of a hydrodynamic shock that causes damage to surrounding tissues. Resistance to infection of these tissues becomes minimal, many of them are subjected to necrosis and secondary infection with the emergence of extensive face phlegmon.

To traumatic lesions with possible subsequent occurrence of inflammatory processes is the barotrauma of the paranasal sinuses that occurs when sudden decompression during caisson works, significant altitude differences during the dive of the airplane, with a rapid immersion to a greater depth, etc. A certain danger of infection of the paranasal sinuses is the domestic foreign bodies of the nose , rhinolites, various tumor processes.

Foci of infection in neighboring organs and tissues play no small role in provoking inflammatory diseases of the paranasal sinuses of the nose. In childhood, these foci, localized primarily in the nasopharyngeal (acute and chronic adenoiditis) and palatine tonsils, often serve as a source of infection of the paranasal sinuses. It should not be forgotten that many inflammatory diseases of the paranasal sinuses of adults begin in childhood. Often, the rhinologist must meet with the so-called odontogenic genyantritis arising from a dental disease (second premolar, I and II molars), whose roots are affected by apical granuloma or pericornic abscess or periodontitis. Often the apical parts of the roots of these teeth are placed directly in the alveolar bay of the maxillary sinus, from which only the mucous membrane of the latter separates them. Removal of such teeth leads to the formation of a fistula of the maxillary sinus, and in the presence of odontogenic sinusitis, drainage through the sinus loop can lead to spontaneous recovery.

Diseases of internal organs and the endocrine system can also contribute to the onset of inflammatory diseases of the paranasal sinuses of the nose, especially when interacting with local risk factors and general adverse weather and climate conditions. According to M. Lazian, alimentary dystrophy, hypoavitaminosis, hypercholesterolemia, hyperuricemia, general obesity, hypocalcaemia, protein metabolism disorders, diabetes, anemia, rheumatism may serve as factors contributing to the development of upper respiratory tract diseases and, in particular, inflammatory diseases of the paranasal sinuses of the nose. And many other forms of lesions of internal organs. A major role in the onset of inflammatory diseases of the paranasal sinuses of the nose is played by vegetative-vascular and trophic disorders, which reduce the natural adaptive and adaptive functions of the PNS. Great importance in the pathogenesis of inflammatory diseases of the paranasal sinuses, as their trigger mechanism and the factor of chronic inflammation, belongs to allergies. According to the Romanian authors, in 10% of cases of all diseases of the ENT organs, the role of allergy has been established. According to different authors, stated at the VII International Congress of Otorhinolaryngologists, allergy in inflammatory diseases of the paranasal sinuses of the nose, depending on the country and the continent, is found in 12.5-70% of cases.

Pathological anatomy. The basis of pathoanatomical changes in inflammatory diseases of the paranasal sinuses of the nose is inflammation as a fundamental biological category in which two opposing processes are dialectically connected - destructive and creative, reflected in terms of alteration and reparation.

From the point of view of pathology, inflammation is a local multi-vector vascular-tissue and humoral process that arises in response to the action of a variety of pathogenic factors, playing the role of a protective-adaptive reaction aimed at destroying damaging agents and protecting them, removing non-viable tissues and toxic substances, morphological and functional restoration of viable structures. Therefore, considering the phenomenon of inflammation as a pathological process, it is always necessary to remember that due to this process the organism is released from the disease or, at least, struggles with it to return to its normal state. It is also important to know that excessive or prolonged inflammation, as well as inflammation that develops in vital organs and systems and disrupts their functions, can be dangerous for the body, often ending with his death.

Inflammation, depending on the prevalence of a particular process in the outbreak, is divided into the following forms.

Alterative inflammation is characterized by the most pronounced damage (alteration) of the affected substrate, its essence is in various dystrophic and necrotic processes.

Exudative inflammation is manifested by increasing the permeability of cell membranes by the abundant leakage of the liquid part of the blood with the proteins dissolved in it and the transfer to the tissues of the blood elements. Depending on the nature of the inflammatory exudate formed and the further development of inflammation, serous, fibrinous, purulent and hemorrhagic and catarrhal exudative inflammation are distinguished.

In serous inflammation, the exudate consists of serous fluid (ie, from the liquid part of the blood with proteins dissolved in it) in which leukocytes, erythrocytes, deflated cells of the surrounding tissue are suspended in a small amount.

With fibrinous inflammation, there is a lot of fibrin in the exudate. Upon exiting the vessel, the fibrinogen of blood coagulates and turns into fibrin, which covers the mucous membrane in the form of a film (film). If fibrinous inflammation is combined with deep necrosis of the tissue, the films are densely soldered to the underlying surface and are hardly separated from it. Such inflammation is called fibrinous-necrotic, or diphtheria (not to be confused with diphtheria). Fibrinous exudate can resolve, germinate with a connective tissue, forming spikes, Shphards, synechia, etc., or tearing away with necrotic tissues.

With purulent inflammation, the exudate consists mainly of leukocytes, a significant part of which are in a state of decay. Leukocytes released into the tissue due to increased vascular permeability perform a phagocytic function. In addition, the various proteolytic enzymes contained in them are capable of melting non-viable (necrotic) tissues, which, in essence, is a suppuration process. Suppuration, unclearly delimited from surrounding tissues and diffusely spreading in them, is called phlegmon, in contrast to an abscess, in which the inflammatory process is delimited from the surrounding tissues by a pyogenic membrane. The accumulation of pus in any anatomical cavity, for example the pleural or in one of the paranasal sinuses, is called empyema. If the content in the exudate of a large number of red blood cells, for example in case of influenza pneumonia or influenza genyantritis, inflammation is called hemorrhagic.

With catarrhal inflammation, mucous membranes are affected (respiratory tract, gastrointestinal tract, etc.). Exudate (serous, purulent, etc.) is excreted, drains to the surface of the mucous membrane and in some cases is excreted, as, for example, with catarrhal inflammation of the paranasal sinuses. To the exudate mucus, excreted by the mucous glands, is mixed, so that it becomes viscous.

A productive, or proliferative, inflammation is characterized by the multiplication of cells in the area of inflammation. Usually these are cells of connective tissue, histiocytes, which are part of the granulation tissue. As a result of productive inflammation, scar tissue forms, which leads to wrinkling and disfigurement of the affected organ (for example, scars and adhesions in the tympanic cavity that bind the chain of auditory ossicles, - thymiasclerosis, or synechiae in the nasal cavity). If this type of inflammation occurs in the parenchymal organs, for example in the liver, this process is called inflammatory sclerosis or cirrhosis.

Inflammation can occur acutely or chronically. Its outcomes depend on a variety of direct and indirect factors, for example, the type of pathogen, the nature of the inflammation, the volume of the affected tissue, the nature of the lesion itself (burn, injury, etc.), the reactivity of the organism,

The inflammatory process in the paranasal sinuses, which develops for one reason or another, is characterized by several successive stages of pathomorphological changes in the mucous membrane, knowledge of the nature and dynamics of which is of great importance for determining the mode of treatment and increasing its effectiveness. The essence of this provision is that at certain pathomorphological stages, complete morphological and functional restoration of the mucous membrane and its elements is possible, which is characterized as recovery. With deeper lesions of the mucous membrane, reparative processes occur only on its limited surfaces, which under favorable conditions serve as initial regeneration centers for all or most of the surface of the mucous membrane of the paranasal sinuses. In far-reaching cases, with pronounced purulent-necrotic processes affecting the periosteum or even causing osteomyelitis, the process of recovery passes through the rejection of the affected tissues and scarring of the cavities of the paranasal sinuses.

In the initial phase of acute rhinosinusitis, the biochemical changes occur in the mucous membrane, leading to a change in the pH of the liquid media, the viscosity of the mucus segregated by the glandular apparatus, and the disappearance of the semiliquid film, which is the "habitat" of the ciliated cilia. These changes lead to hypofunction of goblet cells, segregating nasal and intraspidular mucus and slowing the movement of cilia. The cessation of their movement is revealed by biomicroscopy of the nasal mucosa and is expressed in smoothing the lower surface of the mucous layer covering the mucous membrane.

Further development of the pathomorphological process in the ciliated epithelium is that with the disappearance of the "habitat" of the cilia, they undergo a number of changes: they are shortened, agglomerated into small clusters and disappear. However, if the islets of normally functioning ciliated epithelium are preserved and the disease flows favorably, the process can be reversible.

Histological studies showed that even with the disappearance of ciliated epithelium on the vast areas of the inner surface of the paranasal sinuses and with the preservation of small areas capable of reparative processes, the real possibility of recovering the functions of the mucosa almost in full is preserved. This circumstance proves the inconsistency of the method of radical scraping of the mucous membrane of the paranasal sinuses during surgical interventions on them.

Another change, which undergoes the epithelium of the nasal mucosa and paranasal sinuses, concerns the number and distribution of goblet cells. The same factors that cause hyperemia and edema of the nasal mucosa, also cause an increase in the number of these cells, which in tens of times increases their secretory function. Many researchers consider the fact of an increase in the number of goblet cells as a primary adaptive reaction, which contributes to an increase in the amount of lysozyme, the washing out of the sinuses and the nasal cavity of reproducing microorganisms and the products of their vital functions, which is replaced by the function of vanishing cilia. However, at the same time, polypoid edema of the mucous membrane develops, which disrupts not only the nasal breathing, but also completely stops the ventilation of the paranasal sinuses due to obstruction of their excretory ducts. Developed in the sinuses, rarefaction causes the appearance in their cavities of the transudate and polypoid changes in the mucous membrane.

Progression of the pathological process in the paranasal sinuses leads to destructive phenomena in the mucous membrane, which consists in the complete disappearance of cilia, atrophy and disappearance of goblet cells, disruption of the biochemical composition of the tissue fluid and metabolism in the surviving cells, reduction of the barrier function of cell membranes and reduction in the amount of nasal mucus. All these factors lead to metaplasia of the cylindrical ciliated epithelium into a flat keratinizing epithelium with its desquamation, first islet, then subtotal. Desquamation of the epithelium leads to erosion of the mucous membrane, up to the violation of the integrity of its basal layer. However, even with this far-reaching phase of inflammation of the mucosa, the islets of the viable epithelium almost always remain.

In the depth of the above ulcers, a granulation tissue appears, the exudate of which covers the bottom of the ulcer with fibrin, which in a certain way modify the basal layer of the mucous membrane. It thickens due to the increase in the number of argyrophilic precollagenic fibers impregnated with hyaline and forming a barrier to the catabolites of the inflammatory process developing in the mucosa. This process should also be considered as one of the last stages of the local adaptation of the macroorganism to local inflammation. However, impregnation of the basal membrane with hyaline and an increase in the number of collagen fibers in it lead to compression of the finest nerve fibers penetrating the epithelial layer, which disrupts the neurotrophic function of the VNS with respect to the mucosa.

Polypoid formations of the mucous membrane differ in their structure and form. Their occurrence is due to increased activity of the glandular apparatus of the mucous membrane, which occurs when the excretory ducts of the mucous and serous glands are compressed by the swelling of the interstitial tissue or the emerging hyaline of the basal membrane. Violation of the excretory function of the glandular apparatus leads to the formation of retention cysts, the size of which can vary from fractions of a millimeter to 1 cm or more. The presence of these cysts determines the clinical-anatomical form of sinusitis and indicates a profound pathomorphological reconstruction of the mucous membrane, leaving no hope for a non-operative cure of the patient.

Clinical manifestations of inflammatory diseases of the paranasal sinuses of the nose are characterized by general and local symptoms. In acute inflammatory processes, general symptoms are manifested by increased body temperature, general weakness, malaise, loss of appetite, inflammatory changes in the blood picture. Local symptoms include hyperemia in the fronto-facial area corresponding to the inflammation focus, swelling in the projection of the frontal or maxillary sinuses, general and localized headache. Often, there are patches, serous and purulent discharge from the nose. In chronic inflammatory processes, nasal discharge is purulent in nature with an unpleasant putrefactive odor, periodic exacerbations of the inflammatory process are possible, pains are more diffuse, and with exacerbations are localized in the zones noted above and at the exit sites of the branches of the trigeminal nerve. Common symptoms with exacerbations are the same as in acute processes.

[1], [2], [3], [4], [5], [6], [7]