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

Diseases of the paranasal sinuses account for more than 1/3 of all pathological conditions of the ENT organs. If we consider that most of these diseases are accompanied by diseases of the nose, which either precede diseases of the paranasal sinuses and serve as their cause, or are their consequence, then their number increases significantly. The anatomical position of the paranasal sinuses in itself is a significant risk factor for possible complications in diseases of the paranasal sinuses on the part of the brain, organ of vision, ear and other areas of the body.

In pathological conditions of the paranasal sinuses, disorders of various links of the considered anatomical and functional system occur, playing 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, cerebrospinal fluid dynamics, etc., and through them - the uncontested sending of mental, motor and vegetative functions of the nerve centers. From the above it follows that any pathological conditions of the paranasal sinuses should be attributed to systemic diseases causing corresponding disorders not only in the craniofacial region and upper respiratory tract, but also in the whole organism.

A systemic approach to interpreting the pathogenesis of paranasal sinus diseases is justified by the diversity of functions implemented by the paranasal sinus. Here we will only briefly outline them in relation to this section.

Barrier function of the mucous membrane of the nose and paranasal sinuses. The barrier function is understood as special physiological mechanisms that protect the body from environmental influences, preventing the penetration of bacteria, viruses and harmful substances, and helping to maintain a constant composition and properties of blood, lymph, and tissue fluid. The mucous membrane of the nose and paranasal sinuses are the so-called external barriers, due to which the inhaled air is cleared of dust and harmful substances in the atmosphere, mainly with the help of the epithelium lining the mucous membrane of the respiratory tract and having a specific structure. Internal barriers located between the blood and tissues are called histohematic. They play an important role in preventing the spread of infection to tissues and organs by hematogenous means, in particular, the occurrence of hematogenous sinusitis, on the one hand, and sinusogenic intracranial complications, on the other. In the latter case, the decisive role belongs to the BBB. A similar barrier exists between the blood and the intralabyrinthine fluids of the inner ear. This barrier is called the hematolabyrinthine barrier. According to G.I. Kassel (1989), the hematolabyrinthine barrier is 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 body, preserving an organ or organ system within the limits of physiological response and in a state of active and effective counteraction to pathogenic factors.

The barrier function is under constant influence and systemic control by the autonomic nervous system and the endocrine system closely associated with it. Risk factors such as nervous exhaustion, alimentary exhaustion, vitamin deficiency, chronic intoxication, allergens, etc., disrupt the barrier function, which leads to an increase in the effect of these factors and to the emergence of a vicious circle, which we define as a functional pathological system with a predominant effect of positive feedback.

The introduction of infection against this background, the decrease in the activity of tissue immunity under the influence of certain risk factors, leading to increased cellular oncogenesis, causes the development of corresponding diseases, which is largely inherent in the PNS. First of all, 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 and the bactericidal properties of such substances as lysozyme are weakened, neoplastic processes progress, local tissue pathological processes arise, leading to a violation of trophism with the ensuing 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 the mucociliary apparatus, interstitial tissue, tissue fluid, etc., which, in turn, potentiates the basic pathological process, causing new vicious cycles in it with the involvement of new organs and systems.

The above pathogenetic processes significantly affect the receptors of the PNS, causing the occurrence of pathological viscerocortico-visceral and viscerohypothalamic-visceral reflexes, which disharmonize the adaptive mechanisms that resist the pathological process, reduce their influence on reparative processes to a minimum, which leads to decompensation of adaptive reactions to this disease and the progressive development of the latter.

The depicted picture of the pathogenetic mechanisms of diseases of the paranasal sinuses is only a part of those grandiose systemic processes that are played out in the PNS and that often go beyond its limits. Each of these processes has its own specific features that determine the nosology of the disease, but they all have common features that characterize the pathological process with such pathological 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 condition is accompanied by a process directed in a diametrically opposite direction, i.e., towards recovery, even without external therapeutic intervention. The components of this process are determined by the essence of the pathological condition itself, which, figuratively speaking, "calls fire upon itself" and precisely by the "caliber" of those "weapons" and the quality of those "shells" that are fatal to it. Vivid examples of this are immunity, inflammation, reparative tissue processes, not to mention numerous humoral phenomena that are the basic mechanisms of any adaptive-adaptive and reparative processes.

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

Criteria for the classification of inflammatory diseases of the paranasal sinuses

1. Topographical anatomical criterion:
   1. craniofacial or anterior sinusitis:
      1. maxillary sinusitis;
      2. rhinoethmoid sinusitis;
      3. frontal sinusitis.
   2. craniobasal or posterior sinusitis:
      1. sphenoidal sinusitis;
      2. ethmoid-sphenoid sinusitis.
2. . Quantitative criterion:
   1. monosinusitis (inflammation of only one paranasal sinus);
   2. polysinusitis:
      1. geminosinusitis (unilateral inflammation of two or more paranasal sinuses);
      2. pansinusitis (simultaneous inflammation of all paranasal sinuses.
3. Anatomical and clinical criterion:
   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 criterion:
   1. exudative sinusitis:
      1. catarrhal serous sinusitis;
      2. purulent sinusitis;
   2. proliferative sinusitis:
      1. hypertrophic;
      2. hyperplastic;
   3. associated forms:
      1. simple serous-purulent sinusitis;
      2. polypous-purulent sinusitis;
      3. ulcerative-necrotic fungal-pyogenic etiology;
      4. osteomyelitic sinusitis.
5. Etiological criterion:
   1. mono- and polymicrobial non-specific 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; in the figurative expression of the outstanding French otolaryngologist Terracola, “Every sinusitis is born, lives and dies simultaneously with the rhinitis that gave birth to it”);
      2. odontogenic 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 in children;
   2. sinusitis in adulthood;
   3. sinusitis in old age.
8. Treatment criterion:
   1. sinusitis non-surgical treatment;
   2. sinusitis surgical treatment;
   3. sinusitis combination treatment.

The classification criteria specified do not claim to be an exhaustive classification of inflammatory diseases of the paranasal sinuses, but merely inform the reader of the diversity of causes, forms, clinical course, treatment methods, etc. of these diseases. Below, the main criteria for classifying inflammatory diseases of the paranasal sinuses are considered in more detail.

Cause of inflammatory diseases of the paranasal sinuses. Repeated bacterial seeding of the nasal mucosa caused by inhalation of atmospheric air is the reason for the presence of polymorphic apathogenic microbiota (saprophytes) in the nasal cavities. The apathogenicity of the microbiota is ensured by the presence of specific enzymes in the nasal secretion that have bacteriostatic and bactericidal properties. These include a group of lysozymes - protein substances capable of causing lysis of some microorganisms by depolymerization and hydrolysis of microorganisms' mucopolysaccharides. In addition, as Z.V. Ermolieva (1938) proved, lysozymes have the ability to stimulate tissue regeneration processes. When acute rhinitis occurs, especially of viral etiology, the bactericidal properties of lysozyme are sharply reduced, as a result of which the saprophyte acquires pathogenic properties. At the same time, the barrier functions of the connective tissue layer of the nasal mucosa are reduced, and microorganisms freely penetrate into its deep sections. In addition to lysozyme, there are a number of other substances in the nasal mucosa (collagen, basic and amorphous substance, chemical substances of a glucidic nature, polysaccharides, hyaluronic acid, etc.), which regulate diffusion processes in cellular membranes and provide protection against the penetration of microorganisms into the deep layers of the nasal mucosa and even beyond them. However, pathogenic microorganisms also have their own means of protection in the form of the enzyme hyaluronidase produced by them, which hydrolyzes hyaluronic acid and increases the virulence of microorganisms and their penetrating ability.

In acute purulent inflammatory diseases of the paranasal sinuses, the most common are streptococcus, pneumococcus, Staphylococcus aureus, Pfeiffer's coccobacillus, Friedlander's klebsiella, rhinoviruses, adenoviruses and some others. In some cases, when the sinus contents are cultured in the usual way, these contents are sterile. Indirectly, this indicates either a viral or anaerobic etiology of sinusitis. For chronic purulent inflammatory diseases of the paranasal sinuses, gram-negative microorganisms are more typical, such as pseudodiphtheria Pseudomonas aeruginosa, E. coli, etc., and for odontogenic sinusitis - anaerobes. As A.S. Kiselev (2000) notes, in recent years mycoses of the paranasal sinuses caused by irrational use of antibiotics and dysbacteriosis have become relevant. The role of influenza and parainfluenza infection in the occurrence of acute inflammatory diseases of the paranasal sinuses has not been fully clarified. Currently, the dominant hypothesis is that the virus plays the role of an allergen causing an exudative process, after which inflammation develops as a result of superinfection with banal microbiota.

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

Local causes are divided into determining and contributing. The former determine the nature and extent of the inflammatory process and play the role of its cause. Infectious rhinitis in the overwhelming majority of cases is the primary cause of inflammatory diseases of the paranasal sinuses. Contributing risk factors are many circumstances, including professional and domestic hazards, unfavorable climatic conditions and many other factors that directly affect the mucous membrane of the nose and its receptor apparatus.

One of the important risk factors is the unfavorable anatomical structure of the paranasal sinuses and nasal cavity. These include, for example, a high position of the internal opening of the excretory duct of the maxillary sinus, or an excessively narrow and long frontonasal 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 occurrence of their inflammation. Obstruction of these ducts, as a rule, leads to a violation of ventilation of the cavities, dissolution of gases in the fluids of the mucous membrane, the formation of negative pressure and, as a consequence, to the appearance of transudate or cyst-like formations (mucous blisters). Transudate can remain sterile for a long time (amber-colored translucent opalescent liquid), but penetration of infection to it leads to its suppuration and the development of acute purulent sinusitis. Often, the paranasal sinuses partially or all communicate with each other, especially the frontal, maxillary sinuses and the cells of the ethmoid labyrinth. And then the inflammation of any one sinus leads to a chain inflammatory reaction that can affect two, three or even all the air cavities of the facial skull.

Of great pathogenic importance in the occurrence of inflammatory diseases of the paranasal sinuses is the fact that all, without exception, ventilation and drainage openings of the paranasal sinuses are in the path of the air stream, which carries microorganisms, protein and plant antigens, aggressive substances, and temperature fluctuations in the air that go beyond the limits of physiological tolerance, which together cause significant stress on the protective functions of the mucous membrane of the nose and paranasal sinuses.

Another anatomical risk factor is the presence of bony septa in the sinuses (developmental anomalies), which are often observed in the maxillary, frontal and sphenoid sinuses, as well as the presence of bays 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 inflammatory diseases of the paranasal sinuses begin.

The same risk factors include developmental defects of the nasal cavity (atresia, narrow and curved nasal passages, deformations of the nasal vestibule, curvature of the nasal septum, etc.).

Local causes of inflammatory diseases of the paranasal sinuses also include numerous diseases of the internal nose, described above.

Traumatic factors can cause the development of not only inflammatory diseases of the paranasal sinuses, but also various types of extra- and intracranial purulent complications. Particularly dangerous are injuries to the paranasal sinuses, accompanied by fractures of their bone walls (ethmoid plate, orbital walls of the maxillary and frontal sinuses). In these cases, hematomas that arise both in the sinuses and outside them most often become infected. Gunshot foreign bodies pose a significant danger in terms of the development of abscesses and phlegmons, in which the infectious process develops not only in the immediate vicinity of foreign bodies, but also far beyond it along the wound channel as a result of a hydrodynamic impact, causing damage to the surrounding tissues. The resistance of these tissues to infection becomes minimal, many of them undergo necrosis and secondary infection with the development of extensive phlegmons of the face.

Traumatic lesions with possible subsequent development of inflammatory processes also include barotrauma of the paranasal sinuses, which occurs during sudden decompression during caisson work, significant changes in altitude during an airplane dive, during rapid diving to great depths, etc. A certain danger of infection of the paranasal sinuses is posed by household foreign bodies in the nose, rhinoliths, and various tumor processes.

Infection foci in adjacent organs and tissues play a significant role in provoking inflammatory diseases of the paranasal sinuses. In childhood, these foci, localized primarily in the nasopharyngeal (acute and chronic adenoiditis) and palatine tonsil, often serve as a source of infection of the paranasal sinuses. It should not be forgotten that many inflammatory diseases of the paranasal sinuses in adults begin in childhood. Often, a rhinologist has to deal with so-called odontogenic sinusitis, which occurs as a result of dental disease (second premolar, first and second molars), the roots of which are affected by apical granuloma or periradicular abscess or periodontitis. Often, the apical parts of the roots of these teeth are located directly in the alveolar bay of the maxillary sinus, from which they are separated only by the mucous membrane of the latter. Removal of such teeth leads to the formation of a lunar fistula of the maxillary sinus, and in the presence of odontogenic sinusitis, drainage through the sinus lumen can lead to spontaneous recovery.

Diseases of the internal organs and endocrine system can also contribute to the development of inflammatory diseases of the paranasal sinuses, especially when interacting with local risk factors and general unfavorable atmospheric and climatic conditions. According to M. Lazyan, factors contributing to the development of diseases of the upper respiratory tract and, in particular, inflammatory diseases of the paranasal sinuses can be alimentary dystrophy, hypovitaminosis, hypercholesterolemia, hyperuricemia, general obesity, hypocalcemia, protein metabolism disorders, diabetes, anemia, rheumatism and many other forms of damage to internal organs. Vegetative-vascular and trophic disorders, which reduce the natural adaptive and adaptive functions of the PNS, play a major role in the development of inflammatory diseases of the paranasal sinuses. Allergy plays a major role in the pathogenesis of inflammatory diseases of the paranasal sinuses, as their trigger and factor in the chronicity of the inflammatory process. According to Romanian authors, allergy plays a role in 10% of all ENT diseases. According to data from various authors presented at the VII International Congress of Otorhinolaryngologists, allergy in inflammatory diseases of the paranasal sinuses, depending on the country and continent, is found in 12.5-70% of cases.

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

From the pathological point of view, inflammation is a local multi-vector vascular-tissue and humoral process that occurs in response to the action of various pathogenic factors, playing the role of a protective-adaptive reaction aimed at destroying damaging agents and protecting against them, removing non-viable tissues and toxic substances from the body, and morphological and functional restoration of viable structures. Therefore, when considering the phenomenon of inflammation as a pathological process, it is always necessary to remember that thanks to this process, the body is freed from the disease or, at least, fights it in order to return to a normal state. It is also important to know that excessively pronounced or prolonged inflammation, as well as inflammation developing in vital organs and systems and disrupting their functions, can be dangerous for the body, often ending in its death.

Depending on the prevalence of one or another process in the focus, inflammation is divided into the following forms.

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

Exudative inflammation is manifested by increased permeability of cell membranes by abundant leakage of the liquid part of the blood with proteins dissolved in it and transition of formed elements of the blood into tissues. Depending on the nature of the formed inflammatory exudate 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 (i.e., the liquid part of the blood with proteins dissolved in it), in which leukocytes, erythrocytes, and deflated cells of the surrounding tissue are suspended in small quantities.

In fibrinous inflammation, the exudate contains a lot of fibrin. When it leaves the vessel, the blood fibrinogen coagulates and turns into fibrin, which covers the mucous membrane in the form of a plaque (film). If fibrinous inflammation is combined with deep tissue necrosis, the films are tightly fused with the underlying surface and are difficult to separate from it. This inflammation is called fibrinous-necrotic, or diphtheritic (not to be confused with diphtheria). Fibrinous exudate can be absorbed, grow into connective tissue, forming adhesions, sfarts, synechiae, etc., or be rejected together with necrotic tissue.

In purulent inflammation, the exudate consists mainly of leukocytes, a significant portion 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 they contain are capable of melting non-viable (necrotic) tissues, which is essentially a suppurative process. Suppuration that is not clearly delimited from the surrounding tissues and diffusely spreads into 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 cavity or one of the paranasal sinuses, is called empyema. If the exudate contains a large number of erythrocytes, for example, in influenza pneumonia or influenza sinusitis, the inflammation is called hemorrhagic.

In catarrhal inflammation, the mucous membranes (respiratory tract, gastrointestinal tract, etc.) are affected. Exudate (serous, purulent, etc.) is released, flows onto the surface of the mucous membrane and in some cases is excreted, as, for example, in catarrhal inflammation of the paranasal sinuses. Mucus secreted by the mucous glands is mixed with the exudate, as a result of which it becomes viscous.

Productive, or proliferative, inflammation is characterized by the proliferation of cells in the inflammation zone. These are usually connective tissue cells, histiocytes, which are part of the granulation tissue. Productive inflammation results in the formation of scar tissue, which leads to the wrinkling and disfigurement of the affected organ (for example, scars and adhesions in the tympanic cavity, which bind the chain of auditory ossicles - thymian sclerosis, or synechiae in the nasal cavity). When this type of inflammation occurs in parenchymatous organs, such as the liver, this process is called inflammatory sclerosis or cirrhosis.

Inflammation can be acute or chronic. Its outcome depends on many direct and indirect factors, such as the type of pathogen, the nature of the inflammation, the volume of affected tissue, the nature of the lesion itself (burn, injury, etc.), the reactivity of the body, etc.

The inflammatory process in the paranasal sinuses, developing 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 method 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 centers of regeneration for the entire or most of the surface of the mucous membrane of the paranasal sinuses. In advanced cases, with pronounced purulent-necrotic processes affecting the periosteum or even causing osteomyelitis, the recovery process occurs through the rejection of affected tissues and scarring of the cavities of the paranasal sinuses.

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

The 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 shorten, agglomerate into small clusters and disappear. However, if islands of normally functioning ciliated epithelium are preserved and the disease progresses favorably, the process can be reversible.

Histological studies have shown that even with the disappearance of the ciliated epithelium on large areas of the inner surface of the paranasal sinuses and with the preservation of small areas capable of reparative processes, there remains a real possibility of restoring the functions of the mucous membrane almost in full. 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 that the epithelium of the mucous membrane of the nose and paranasal sinuses undergoes concerns the number and distribution of goblet cells. The same factors that cause hyperemia and edema of the mucous membrane of the nose also cause an increase in the number of these cells, which increases their secretory function tens of times. Many researchers consider the fact of an increase in the number of goblet cells to be a primary adaptive reaction that promotes an increase in the amount of lysozyme, washing out of the sinuses and nasal cavity of multiplying microorganisms and the products of their vital activity, replacing the function of the disappearing cilia. However, at the same time, polypoid edema of the mucous membrane develops, which not only disrupts nasal breathing, but also completely stops ventilation of the paranasal sinuses due to obstruction of their excretory ducts. The rarefaction developing in the sinuses causes the appearance of transudate in their cavities and polypoid changes in the mucous membrane.

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

In the depth of the above ulcerations, granulation tissue appears, the exudate of which covers the ulcer bottom with fibrin, which in a certain way also modifies the basal layer of the mucous membrane. It thickens due to the increase in the number of argyrophilic precollagen fibers, impregnated with hyaline and forming a barrier on the path of catabolites of the inflammatory process developing in the mucous membrane. This process should also be considered as one of the last stages of 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 leads to compression of the finest nerve fibers penetrating the epithelial layer, which disrupts the neurotrophic function of the VNS in relation to the mucous membrane.

Polypoid formations of the mucous membrane differ in their structure and shape. Their occurrence is caused by increased activity of the glandular apparatus of the mucous membrane, which occurs in conditions when the excretory ducts of the mucous and serous glands are compressed by edema of the interstitial tissue or the resulting hyalinosis of the basement 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 and anatomical form of sinusitis and indicates a deep pathomorphological restructuring of the mucous membrane, leaving no hope for a non-surgical cure for the patient.

Clinical manifestations of inflammatory diseases of the paranasal sinuses are characterized by general and local symptoms. In acute inflammatory processes, general symptoms are manifested by an increase in body temperature, general weakness, malaise, loss of appetite, inflammatory changes in the blood picture. Local symptoms include hyperemia in the frontal-facial region corresponding to the site of inflammation, swelling in the projection of the frontal or maxillary sinuses, general and localized headache. Serous, serous and purulent discharge from the nose is often observed. In chronic inflammatory processes, nasal discharge is purulent with an unpleasant putrid odor, periodic exacerbations of the inflammatory process are possible, pain is more diffuse, and during exacerbations it is localized in the above-mentioned zones and at the exit points of the branches of the trigeminal nerve. General symptoms during exacerbations are the same as in acute processes.

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