Rhinitis( runny nose) symptoms

Runny nose( rhinitis) is a general term for a group of weak and highly contagious viral diseases that cause inflammation of the mucous membranes of the nose and throat. Symptoms usually appear two to three days after a virus encounter;the runny nose remains contagious in the first two to three days after the onset of symptoms. There are no cures for the common cold;for a full recovery takes from a week to 10 days. Coryza is more common in winter than in summer and more common in children than in adults, as resistance to many viruses develops with age. Runny nose can cause serious complications in patients suffering from chronic respiratory illnesses. That advises folk medicine at this disease look here.

The diagnosis can be made on the observed symptoms without the involvement of a physician.

Acute rhinitis is a nonspecific inflammation of the nasal mucosa, at which characteristic symptoms are observed: nasal congestion, rhinorrhea, sneezing and itching in the nose. The diagnosis is made with one or more symptoms. The disease refers to the most frequent in both children and adults. Rhinitis can also occur as an independent disease - nonspecific inflammation, and as a concomitant process with various infectious diseases - specific rhinitis.

The clinic distinguishes:

Etiology and pathogenesis of .The causative agents of acute infectious rhinitis can be viruses, microbes and their associations. Primarily, the nasal mucosa is affected primarily by rhinoviruses, adenoviruses, influenza viruses, parainfluenza, etc.

Any virus that has a tropism to the epithelium of the nasal mucosa can cause respiratory infection and acute rhinitis. The virus creates conditions for activating the microbial flora, and then various microorganisms - pneumococci, hemophilic rod, streptococci, staphylococcus, moraxella, etc., can trigger pathogens of acute infectious rhinitis.

In violation of acute rhinitis, disruption of local and general immune defense of the organism is important. Usually this occurs with general or local hypothermia of the body and develops more rapidly in individuals with reduced resistance( especially in the presence of chronic diseases) or weakened by acute diseases. In addition, predisposing factors for the development of acute rhinitis can be various injuries of the mucosa, foreign bodies and condition after surgery in the nasal cavity. In some cases, the cause of acute rhinitis can be a production factor - mechanical and chemical stimuli of stone-woodworking, chemical and other industries( exposure to smoke, gas, dust, etc.).

Morphological changes in the nasal mucosa are characterized by the development of typical stages of inflammation: hyperemia is replaced by serous effusion, edema. The cilia of the ciliated epithelium slow down, and in the future, and ceases movement of cilia, which promotes the adhesion of pathogens on the mucous membrane of the nasal cavity. Epithelium and submucosal layer gradually become inflamed, desquamation of the epithelium and erosion of the mucous membrane develop.

Clinic. In a typical clinic of acute rhinitis, three stages of flow are distinguished:

The disease is characterized by an acute onset and lesion of both halves of the nose. The main symptoms are a disorder of the general condition, discharge from the nose and difficulty in nasal breathing. These symptoms can be expressed in varying degrees depending on the stage of the disease.

The first stage of ( dry irritation stage) usually lasts several hours, rarely lasts for 1-2 days. The patient is concerned about dryness in the nose and nasopharynx, sensations of tickling, scraping, burning. At the same time, malaise, scroach, heaviness and pain in the head appear. Often there is an increase in body temperature to 37 ° C or higher. With anterior rhinoscopy, hyperemia and injection of the vessels of the mucosa, its dryness, and the absence of a discharge are noted.

This period is characterized by intense aggression of the virus, its replication in the epithelial cells of the nasal mucosa. The virus is actively resisted by nonspecific factors of local defense: the role of mucociliary epithelium present in the mucus of secretory immunoglobulins, immunocompetent cells and other factors of immune defense is great.

The second stage of ( the stage of serous discharge) is characterized by an increase in inflammation, a large amount of transparent watery fluid swirls out of the vessels( transudate).Simultaneously, the function of goblet cells and mucous glands increases, so that the discharge in the nose becomes serous and mucous. In the transudate contains sodium chloride( table salt) and ammonia, which causes its irritating effect on the skin of the vestibule of the nose, especially in children.

The sensation of burning and dryness in this stage of the disease decreases, but the disturbance of breathing through the nose increases, and, due to the transition of the process to the tear ducts and the auditory tube, conjunctivitis, lacrimation, feeling of stuffiness and tinnitus often develop.

From the point of view of pathomorphology in the second stage, the microcirculatory bed of the nasal mucosa is involved in the inflammatory process of the endothelium. Its permeability is increased, active involvement of immunocompetent cells from the vascular bed into the inflammatory focus begins.

The third stage of ( stage of mucopurulent discharge) occurs on the 4th-5th day after the onset of the disease. The leading role at this time is acquired by virus-microbial associations. To viruses that damage the cells of the epithelium, a microbial flora is added, colonizing the nasal mucosa.

Clinical disease at this stage is characterized by the appearance of a thick lean mucopurulent yellowish-greenish discharge, which is due to the presence in it of the formed elements of blood( inflammatory cells) - sweating leukocytes, lymphocytes, detached epithelium. Swelling of the nasal concha in this period is moderate, the mucous membrane is hyperemic, with a cyanotic shade.

In the following days the amount of discharge decreases, the swelling of the mucous membrane disappears, nasal breathing is restored, the general condition improves.

After 8 to 12 days from the onset of the disease, an acute cold stops.

The duration of acute rhinitis depends on the immunobiological state of the body and the mucous membrane of the nasal cavity. With good reactivity of the body, as well as with adequate treatment, rhinitis can abortively occur within 2 to 3 days;with a weakening of protective forces - can last up to 3-4 weeks, which indicates the possibility of its transition to a chronic form.

Treatment of acute infectious rhinitis is outpatient and is conducted in accordance with the stages of the process.

In the initial stage of the common cold, sweatshops and distractions are recommended. Assign a hot foot, general or manual bath with a duration of 10 - 15 minutes, which can be combined with mustard plaits on the calf muscles or on the sole of the feet;immediately after such a procedure the patient drinks hot tea with raspberries. In addition, it is advisable to use UHF and UFO on the nose.

Medical treatment:

In the third stage of acute rhinitis, astringent and antimicrobial medications can be recommended - 3 -5% solution of collargol or protargol, 20% solution of albucid, IRS-19 spray;continue physiotherapy, appoint multivitamins, amixin inward, normal human immunoglobulin( 3 ml per muscle once).

In the complex therapy of rhinitis / rhinosinusigs in the presence of thick detachable, the use of mucolytic and mucoregulatory medications is also effective. Good results were noted on the background of the use of the drug Fljuditik( carbocysteine).The drug effectively dilutes the secret and simultaneously stimulates the activity of villi of the ciliated epithelium, restores the viscosity and elasticity of mucus, promotes mucosal regeneration, restores its structure, improves mucociliary clearance, activates the activity of ciliary epithelium, restores the synthesis of secretory immunoglobulin A.

It should be remembered that infusion into the noseany drops, injection of powders, administration of inhalations and other therapeutic measures should be limited to 8-10 days. Longer use of drugs leads to the development of pathological processes: disruption of the function of the ciliated epithelium, vasomotor function of the nasal mucosa, etc. The patient needs to be warned that it is necessary to note the contents from the nose gently, without much effort and only alternately through each half of the nose,to be ajar.

Classification of chronic rhinitis is as follows.

Etiology and pathogenesis. The causes of chronic rhinitis are diverse. Often the disease develops as a relapse of acute rhinitis, especially if the paranasal sinuses are involved in the process. Another reason is the constant influence of unfavorable environmental factors: hypothermia, dust, gases, various allergens. An important role is played by the presence of local changes in the nasal cavity and pharynx: deformation of the septum of the nose and other intranasal structures, diseases of the paranasal sinuses, adenoids, chronic tonsillitis, etc. Stagnant changes in the nasal cavity leading to the development of chronic rhinitis may result from various somatic diseasesor functional changes in the endocrine and autonomic nervous systems.

Different forms of chronic rhinitis differ in clinical manifestations, the therapeutic approaches applied to them differ substantially.

Chronic catarrhal rhinitis is characterized by persistent disruption of nasal breathing and the periodic appearance of discharge of mucous or mucocutaneous purulent discharge from the nose. Disturbance of nasal breathing increases in the cold. In the "lying on the side" position, the nasal congestion is more pronounced in that half of the nose, which is lower, which is explained by the filling of the cavernous cavities of the underlying shells with blood. Sometimes there is a violation of smell( hyposmia) and / or the transition of the inflammatory process to the mucous membrane of the auditory tube( tubo-otitis).

With forward rhinoscopy, congestive congestion and swelling of the nasal mucosa( mainly in the area of ​​the inferior and middle nasal concha) are determined, pastoznost, often with a cyanotic shade, a mild detached discharge.

Treatment for chronic catarrhal rhinitis includes the elimination of exogenous( production, climatic) and endogenous( curvature of the septum of the nose, adenoid vegetations) factors.

For local therapy apply:

Chronic hypertrophic rhinitis is characterized by the presence of hypertrophied areas of the mucous membrane, which develop more often on the surface of the lower and middle nasal concha. The surface of such areas can be smooth, bumpy or coarse, have a wide base and reach considerable dimensions. The disease is characterized by a prolonged course, the presence of persistent disruption of nasal breathing, often the weakening or lack of smell.

The rhinoscope picture in catarrhal and hypertrophic rhinitis is similar in many respects. To differentiate these two forms of chronic rhinitis, an anemia test is performed. Lubricate the mucosa with a vasoconstrictor( 0.1% solution of adrenaline, galazolin, etc.);the resulting significant decrease in the volume of the inferior nasal concha shows that there is no true hypertrophy. If their reduction is not significant or absent, it indicates a hypertrophic process.

Treatment for hypertrophic rhinitis surgical. The criterion for choosing a method of treatment in each specific case is the degree of hypertrophy of nasal conchae or other parts of the nasal mucosa, as well as the degree of disturbance of nasal breathing.

In case of mild hypertrophy, when mucous membrane is moderately reduced after anemia( lubrication with vasoconstrictor) and nasal breathing improves, the most sparing surgical interventions are used: cauterization with chemical substances( 30-50% solution of silver nitrate, tri-chloroacetic and chromic acids), galvanic caustics, ultrasonic disintegration of the inferior nasal cavity, laserogenesis, submucosal vasotomy.

On an outpatient basis, ultrasonic disintegration of the inferior nasal concha( UZDG) can be performed. For its implementation, an ultrasound generator is used with a set of special waveguides. After the preliminary application and infiltration anesthesia of the mucous membrane of the inferior nasal concha, the included waveguide is introduced into its thickness, carried to the posterior third of the shell and slowly withdrawn. The exposure exposure is determined individually.

Scarring of moderately hypertrophic areas can be achieved by submucosal vasotomy of the inferior nasal cavity. After local anesthesia, a small incision is made at the anterior end of the inferior nasal cavity through which the soft tissue is removed by the rasper from the surface of the bone skeleton of the shell, forming a narrow canal from the anterior end to the posterior end.

This can be done on the bottom surface of the bow sink. Subsequent scarring of cavernous tissue reduces the volume of the shell and consequently increases the lumen of the nasal passages, improving breathing.

With more pronounced fibrous hypertrophy of the mucous membrane and bone base of the nasal concha, accompanied by a significant disturbance of breathing through the nose, as a rule:

These operations are recommended to combine with the displacement of the nasal conchae lateral to the lateral wall of the nose - lateroconchopexy.

Gentle lower cochomatomy is performed in a hospital after an outpatient examination of the patient. In the lying position, the patient is given a local infiltration anesthesia of the mucous membrane of the inferior nasal concha. For the entire length of the shell, a clamp is applied for 1 minute to reduce bleeding. After removing the clamp, special, angled scissors cut off the hypertrophied part of the shell. The hyperplasticized posterior end of the shell is easily removed with a nasal loop. Conchotomy should be done sparingly, especially trying to keep the front end of the shell, since its complete removal is unacceptable and can lead to atrophy of the mucous membrane of the nasal cavity.

With the introduction of optical systems( endoscopes, microscopes) into medical practice, the effectiveness of intranasal operations has significantly increased. Endoscopes allow under constant visual control to perform all stages of intranasal operations, including in the intractable posterior parts of the nasal cavity. To remove hypertrophic areas of nasal conchaes, the use of various microdebriders( shavers) is effective. These tools are a rotary microfreshe attached to the suction, which allows the removal of hypertrophied tissues with high accuracy without damaging the healthy mucosa.

Depending on the causes that cause it, chronic atrophic rhinitis is primary, or genuine( zhena), and secondary. In addition, the dystrophic process can be local( as with dry dry rhinitis) or diffuse, extending to the entire nasal cavity. Primary atrophic rhinitis( ozena) has a diffuse character and can be a manifestation of a systemic disease. The cause of secondary atrophic rhinitis is the impact of adverse industrial or climatic factors - dust, gases, vapor, etc.

Histological picture. Chronic atrophic rhinitis is accompanied by:

As already mentioned, chronic atrophic rhinitis is divided into simple and fetid( ozena).

With simple atrophic rhinitis, nonspecific changes in the mucous membrane of the nasal cavity develop, which are based not on the inflammatory but dystrophic process.

Its development is often promoted by trauma and extensive surgical interventions in the nasal cavity, such as radical conchotomy, tumor removal, etc. Endocrine and hormonal disorders and frequent inflammatory diseases of the nasal cavity play an important role, leading to an increase in trophic changes in the mucosa.

Clinic. The clinical picture of simple atrophic rhinitis includes complaints of dryness in the nose, the formation of crusts, difficulty in nasal breathing, a decrease in smell. Cracks in the nose often cause itching, so the patient tries to remove them with a finger, which leads to damage to the mucous membrane, periodic bleeding, ulceration, and this, in turn, accelerates the appearance of perforation of the septum, usually in the area of ​​the Kisselbach zone.

With forward rhinoscopy, wide nasal passages( due to atrophy of the nasal concha) are visible and the posterior wall of the nasopharynx can be seen. In the general nasal passage there is a dense yellow-green discharge, it dries up with the formation of crusts, which are removed at a certain effort by large pieces and in the form of casts. In the anterior part of the nasal septum, the mucosa is especially thinned, sometimes perforation is visible here.

Treatment of simple atrophic rhinitis conservative - general and local conservative therapy. To remove the crust, the nasal cavity is systematically( 1-2 times a day) irrigated or washed with an isotonic sodium chloride solution( physiological solution) with the addition of iodine( 200 ml of a solution of 6-8 drops of 10% iodine tincture).Apply an oily solution of vitamins A and E( aevit) in the form of drops in the nose and local irritating therapy - lubrication of the nasal mucosa with iodine-glycerin( once a day for 10 days).Iodine preparations intensify the activity of glands of the mucous membrane, increasing their secretory function.

Alkaline and oil inhalations in the nose, irrigation and inhalation of the nasal cavity with 2 -3% solutions of sea salt are useful. Stimulating and improving the trophism of the mucous membrane of the nasal cavity has an endo-nasal application of a helium-neon laser( 7-10 procedures for 5-10 min).

From the general effect, biogenic stimulants( aloe, FIBS, humisol) are administered subcutaneously or intramuscularly, vitamin therapy, iodine and iron preparations( ferrumlec).

This is a severe form of atrophic process in the nasal cavity and paranasal sinuses that spreads both to the mucous membrane and to the bony walls of the nasal cavity and nasal concha with the production of a rapidly drying off with a specific unpleasant odor. There are social, anatomical, inflammatory, focal, infectious, neurodystrophic and endocrine theories of the onset of this disease. The most common are infectious and neurodystrophic theories.

According to the infectious theory, the leading role in this pathology is assigned to Klebsiella ozena( Klebsiella ozaenae), which is often( in 80% of cases) sown from the nasal mucosa in patients with ozona.

Neurodystrophic theory of the emergence of the ozona plays a major role in disturbing the state of the vegetative and endocrine systems or sympathetic innervation, which cause the development of dystrophic processes in the nasal cavity. Trophic disorders lead subsequently to osteomalacia, bone resorption and metaplasia of the epithelium. The destruction of tissue proteins is accompanied by the formation of indole, scatol and hydrogen sulphide, which cause a fetid odor from the nose.

In the lake there is an atrophy of all tissues of the walls of the nasal cavity, thinning of the mucous membrane, vessels. Cavernous tissue empties, the cylindrical epithelium degenerates into a flat, cylindrical ciliated epithelium completely absent, the osseous layer of the nasal concha contains a large number of osteoclasts - cells that dissolve bone.

Clinical manifestations of the lake are very characteristic. These are complaints of pronounced dryness and the formation of a large number of crusts in the nose;presence of an unpleasant, fetid smell from the nose, which patients usually do not feel;difficulty in nasal breathing and lack of smell.

The fetid smell from the nose is so pronounced that the surrounding avoid the presence of the patient, which affects his mental state. Often, women are ill more often, the disease lasts a lifetime;During menstruation there is an exacerbation, but during pregnancy and after childbirth the symptoms of the ozona are noticeably softened.

The odor disorder( hyposmia, and then very quickly anosmia) at the onset of the disease is due to the crusts covering the olfactory area, and is subsequently associated with atrophy of the olfactory receptors.

With forward rhinoscopy, brownish or yellow-green crusts are visible in both halves of the nose, filling the entire nasal cavity and extending into the nasopharynx and underlying airways. After the removal of the crusts, the nasal cavity becomes so wide that the back wall of the nasopharynx, the mouth and even the cushions of the auditory tubes are seen in the rhinoscopy. Patients often observe iron deficiency anemia.

In the diagnosis take into account the characteristic complaints of the patient, the presence of sharp atrophy of the mucous membrane of the nasal cavity, abundant crusts, fetid odor, loss of smell. On the x-ray of the paranasal sinuses, their bone walls are sharply thinned. The distinction of the lake from tuberculosis and syphilis is the absence of ulcers and infiltrative formations of the mucous membrane characteristic for these diseases.

Treatment of the oceana complex;it is carried out by courses and uses both pathogenetic and symptomatic means.

Pathogenetic therapy includes the use of antimicrobial agents, iron therapy and immunocorrection.

Symptomatic treatment is aimed at eliminating severe manifestations of the ozen - crusts and fetid smell. It includes:

Surgical treatment is performed with the purpose of artificial narrowing of the nasal passages, for which various grafts are introduced into the mucous tissue of the septum and the bottom of the nasal cavity [autochondria, polyphosphazene, polyurethane, etc.].

Vasomotor rhinitis is characterized by a triad of symptoms:

There are two forms of vasomotor rhinitis( according to LB Dainiak):

Etiology. Patients with vasomotor rhinitis, as a rule, are diagnosed with disorders of the neural-reflex mechanisms that cause normal functioning of the nasal mucosa, as a result of which the usual irritants cause hyperergic reactions. In this case, the cause of allergic rhinitis is an allergen - a substance to which there is an increased sensitivity of the organism. The development of the neurovegetative form is based on organic and functional changes of the nervous system and endocrine dysfunctions;in the history of the disease and in a special allergological study, they do not reveal any causally significant allergens.

Rhinoscopic signs in both forms of vasomotor rhinitis are similar, they include puffiness and pallor of the mucosa, as well as bluish( cyanotic) or white spots on it.

This is one of the variants of the immune pathology - the painful reaction of the mucous membrane of the nasal cavity to external stimuli. There is a division into seasonal( pollinosis) and all-the-year-round( permanent) forms of allergic rhinitis.

The seasonal form of the disease is associated with exposure to pollen of various plants and is repeated yearly at the same time during the flowering period of one or more plant species. Allergen can be pollen grass( ambrosia, wormwood, quinoa, timothy, etc.) or trees( birch, alder, poplar, hazel, etc.).Among urban residents is more common sensitization to pollen trees, in rural - to the pollen of weeds and cultivated grass. Less commonly observed monosensibilization( allergy to pollen of one plant), more often - multiple - to several pollen allergens.

The intensity of an allergic reaction depends on the type of stimulus, the duration of its effect and the way the allergen enters the body, and also on the state of the immune system of the individual. A certain value in the pathogenesis of allergic rhinitis has genetic factors - the risk of allergy development is significantly increased if both parents of the patient suffer from allergic diseases.

Seasonal allergic rhinitis is more common in residents of large industrial cities. This is due to the depletion of factors of local immune defense due to prolonged antigenic load inhaled with air products of industrial or infectious origin.

The pathogenetic basis of allergic rhinitis is the hyperproduction of antibodies - IgE.When IgE interacts with mast cells and basophils on the membrane of these cells, the mediators of the allergic reaction are released: histamine, serotonin, etc. Mediators act on histamine H, and H2 receptors, resulting in a contraction of the smooth muscle of the endothelium and cells of the postcapillary division of the microcirculatory bedthe nasal mucosa. In the end, this leads to increased vascular permeability, the development of edema and allergic inflammation.

To form allergic reactions due to IgE antibodies, two phases are characteristic that determine the clinical manifestations of seasonal allergic rhinitis.

The early phase associated with the release of mast cells of histamine is characterized by itching, sneezing, and the release of watery mucus. There is an increase in the permeability of the vascular wall, hypersecretion of the mucus, narrowing of the lumen of the nasal passages. This phase manifests itself 5-30 minutes after exposure to the allergen.

The late phase occurs in 8-24 hours. The release of mediators from eosinophils, polymorphonuclear leukocytes and mast cells gives a clinical picture in the form of persistent disruption of nasal breathing.

Detailed finding out the anamnesis of the disease and conducting a special allergological examination, it is usually possible to establish which plant is the cause of the disease. Long and multiple exacerbations of rhinitis with violation of the vasomotor mechanisms of the nasal mucosa can facilitate the transition of the seasonal form of the disease into a permanent one.

The year-round form of allergic rhinitis develops as a result of constant contact of a person with a causally significant allergen - home and paper dust contained in them with mites. Animal wool that contains epidermal allergens, aquarium fish feed, lower mushrooms, food, medicines and some other substances are also active allergens.

Complaints about sneezing attacks, rhinorrhea and shortness of nasal breathing in the year-round form of the disease from the outset are permanent. However, in contrast to what can be observed with seasonal allergic rhinitis, sneezing attacks are much less common, the itch in the nose is often absent, the discharge is not watery, but more dense, mucous. The leading symptom is a permanent nasal congestion. Along with rhinological symptoms, skin itching, conjunctival hyperemia, lacrimation, headache, fatigue, decreased sense of smell, sleep disturbance are often observed in patients.

Treatment of allergic rhinitis should be comprehensive and include the following components:

During the flowering season of causative plants, the patient may be recommended to change the climate or geographic region. When sensitizing to domestic allergens( house dust, animal hair), when it is difficult to eliminate the causative factor, it is recommended to use special filters, air cleaners, respirators, etc. It is necessary to exclude pets staying in an apartment, the presence of aquariums, remove carpets and soft toys,cleaning of rooms, frequent washing of linen, etc.

Elimination of allergens reduces the severity of clinical manifestations, however, it is often impossible to completely eliminate contact with an allergen. With the year-round form of the disease, the effect of elimination can only be manifested in weeks and months. Therefore, in the treatment of various forms of allergic rhinitis, the role of the use of medicines is great.

For the treatment of allergic rhinitis, the following main groups of medicines are used:

In the initial stages of the disease and with mild forms of rhinitis, it is justified to prescribe the drugs of the first group - the stabilizers of the membranes of mast cells. They include cromons as a local intranasal action( intal, cromolyn sodium, nedocromil sodium, croup, taileed mint), and systemic( ketotifen, zaditen).The effectiveness of these drugs is lower than that of other drugs.

The effect of taking antihistamines is related to their effect on H, -receptors. They reduce sneezing, itchy nose, rhinorrhoea, but have little effect on nasal congestion. The use of antihistamines of the first generation( dimedrol, suprastin, etc.) is limited by their sedative effect and a short period of excretion from the body. Antihistamines of the second generation - astemizole, claritine( loratadine), terfenadine, telfast( fexofenadine), zirtek( cetirazine), kestin( ebastin) and others act quickly, as early as 15 minutes, and the sedative effect is much less pronounced. However, side effects are known and in the drugs of this group, in particular cardiotoxic, - in terfenadine.

The drug of the new generation, which immediately has a triple action - antihistaminic, anti-allergic and anti-inflammatory, is desloratadine( erius).It selectively blocks H, -receptors, providing a fast( 30 minutes after administration) and a prolonged( up to 27 h) effect. It reduces nasal congestion, itching, sneezing, rhinorrhea, lacrimation and choking in the throat.

For mild forms of the disease, antihistamines of local( topical) action - allergodyl( azelastine) and histamet( levocabastine) may be recommended. These drugs, available in the form of drops in the nose and nose spray, have an effect comparable to oral antihistamine drugs, but they only work at the injection site.

Corticosteroids are highly effective in the treatment of patients with moderate and severe forms of allergic rhinitis. Currently, topical corticosteroids are widely used. They have a pronounced anti-inflammatory effect and, penetrating through the cell membrane, suppress the synthesis of histamine from mast cells and reduce the permeability of the vascular walls.

New intranasal corticosteroids do not have a systemic effect and can be used as first-choice drugs. Among them, flixonase( fluticasone), aldecin( baconase, beclomethasone), nazonex( mometasone), budesonide, etc. They release these drugs in the form of nasal sprays, prescribe 2-4 injections in the nose 1-2 times a day. When the clinical effect is achieved, the dose is reduced. These drugs are characterized by a relatively slow onset of action( 12-18 hours), moreover, the maximum effect from the admission develops only after a few days or weeks, so they need to be used for a long time - 4-6 months.

Drug kits used for seasonal and allergic rhinitis all year round are different. So, with the year-round form of the disease, antihistamines and decongestants( vasoconstrictors) for topical application are moderately effective;more pronounced result of the application of kromonov in the form of a spray on the nasal mucosa( intal, tayled mint, kropoz) and through the mouth( ketotifen, zaditen);very effective topical corticosteroids( baconase, aldecin, fliksonase, nazoneks).

Nasonex is an intranasal spray, which begins to function as early as 7-12 hours after use, and can be used as a prophylactic for seasonal allergic rhinitis. Due to low bioavailability( only 0.1% of the drug is absorbed into the blood through the mucous membrane), nazonex is safe for long-term( up to 12 months) use.

Specific immunotherapy( SIT) is indicated in those cases when the causative allergen is accurately determined in the conditions of the allergological cabinet or hospital. The method is based on the introduction into the body of a minimum amount of a causally significant allergen in a gradually increasing dose, usually subcutaneously. This introduction of an allergen allows the body to develop protective antibodies to it, which leads to a reduction or complete disappearance of the symptoms of allergic rhinitis. Conduct SIT during the remission of the disease. To achieve a stable clinical effect, at least 3 courses of such therapy are recommended. However, SIT is much less effective in polyallergies, with allergic rhinitis started and generally not applicable in cases where it is not possible to identify the causative allergen.

The stepwise approach is recommended for the treatment of allergic rhinitis. For mild symptoms, intranasal cromons and oral antihistamines are prescribed;with moderate or frequent symptoms - intranasal corticosteroids and oral antihistamines;In severe allergic rhinitis, prednisolone is administered orally( 30 mg in the morning) in a short course.

Indications for surgical intervention for allergic rhinitis occur in the following cases:

If you prefer to perform the procedure while sitting, then the head should be thrown back and turning it to the side into which the dripping drops. In this situation, the medication falls into the middle nasal passage, which contributes to a better outflow of the contents of the maxillary sinus.

Danish professor of medicine Johan Beckmann investigated the causes of susceptibility to influenza and other colds. The results of his observations were stunning. It turned out that the infection most often affects people with a bad temper!

Here are the features of nature that are leading in the list of Professor Beckmann:

After consulting a doctor, you can use one of these recipes to facilitate or get rid of symptoms of rhinitis in a short time.

In the initial stage of the disease, such a remedy is good. Attach the mustard plasters to the heels, cover them with flannel, put on woolen socks and keep the mustard plaster so much;how much will you bear( usually 1-2 hours).Remove the mustard plasters and quickly walk around for a few minutes. Then go to bed. Runny nose will stop in the morning.

Finely chop the garlic, warm with butter and inhale alternately one or the other nostrils.

Several times a day, rinse your nose with salted warm water( enough 1/2 teaspoon of salt to a glass of water).

Clean several potatoes, put the cook. When the potatoes boil well, throw in a pan 2 tbsp.spoons of dry leaves of eucalyptus. Remove from heat, bend over the pan, cover with a towel and breathe broth for 10-15 minutes. Repeat the procedure 2 times a day: half an hour after lunch and at night.

For inhalation, a decoction of 3 tbsp.spoons of pine buds.

Because the viruses that cause ARVI and ARI, "do not like" the alkaline environment, drink more mineral water.

After every 2 hours, bury aloe juice in your nose.

Add a small piece of butter to the glass of hot boiled milk, a dessert spoon of honey, half orange juice, 50 ml of quality liquor. Take 2 times a day: morning and night.

Before going to bed, spread the heels with iodine, put on warm woolen socks, do not remove them until morning.

Make an evening for the feet a very hot bath with soda, salt and with mustard, put on warm socks and so go to bed.

Every half an hour sniff ammonia alcohol alternately with each nostril: one close, another sniff, then vice versa.

Juice freshly beetroot mixed with an equal amount of honey. Take 1/2 cup 3-4 times a day.

Smell the grated horseradish. He, wrapped in several layers of gauze, attach for 30 minutes to the back of the head.