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Alveolitis is a diffuse inflammatory lesion of the alveolar and interstitial lung tissue, which can occur in isolation or develop against the background of other diseases.

The pulmonary alveoli take part in the act of breathing, providing gas exchange with the pulmonary capillaries, and are the end part of the respiratory apparatus. Total alveoli reaches 600–700 million in both lungs.

Causes and risk factors

Exogenous allergic alveolitis develops against the background of allergic reactions (often allergens are plant and house dust, medications, pet hair, components of microscopic fungi, industrial irritants, etc.). The entry of an allergen into the body causes the formation of IgG. Immune complexes (antigen-antibody) settle on the surface of the alveoli, which causes damage to the cell membrane, the release of a significant amount of biologically active substances with the development of the inflammatory process. In the development of this form of alveolitis, repeated entry of the allergen into the body plays an important role.

Secondary alveolitis occurs against the background of other pathological processes. Most often these are sarcoidosis, tuberculosis, and diffuse connective tissue diseases.

Risk factors include:

genetic predisposition;
collagen metabolism disorders.

Forms of the disease

Depending on the etiological factor, as well as the characteristics of the course of the disease, the following are distinguished:

idiopathic fibrosing alveolitis;
toxic fibrosing alveolitis;
exogenous allergic alveolitis.

Alveolitis can be primary and secondary, as well as acute, subacute and chronic.

Idiopathic fibrosing alveolitis is prone to gradual progression with the development of complications. Due to increasing irreversible changes in the alveolar-capillary system of the lungs, the risk of death is high.

Stages of the disease

Depending on the histological picture, there are five stages of idiopathic fibrosing alveolitis:

Infiltration and thickening of the septa of the pulmonary alveoli.
Filling of the pulmonary alveoli with cellular composition and exudate.
Destruction of pulmonary alveoli.
Changes in the structure of lung tissue.
Formation of cystic cavities.

Symptoms of alveolitis

Symptoms of alveolitis vary depending on the form of the disease, but there are a number of manifestations that are common to all forms of pulmonary alveolitis. The main symptom is shortness of breath, which initial stage The disease occurs after physical activity, but as the pathological process progresses, it begins to appear at rest. In addition, patients complain of a dry, unproductive cough, fatigue, and soreness in the muscles and joints. In the later stages of the disease, weight loss, cyanosis of the skin, as well as changes in the shape of the fingers (“drumsticks”) and nails (“watch glasses”) are observed.

The first symptoms of acute exogenous allergic alveolitis may appear within a few hours after contact with the allergen. In this case, the general symptoms of the disease resemble the clinical picture of influenza. Patients experience increased body temperature, chills, headache, then cough and shortness of breath, heaviness and pain in the chest. In children with certain allergic diseases, initial stages Exogenous allergic alveolitis causes asthmatic-type shortness of breath, and sometimes attacks of suffocation. On auscultation, fine moist rales are heard over almost the entire surface of the lungs. After eliminating contact with the allergen that caused the development of the disease, the symptoms disappear within several days, but return upon subsequent contact with the causative allergen. In this case, general weakness, as well as shortness of breath, which is aggravated by physical exertion, may persist in the patient for several more weeks.

The chronic form of exogenous allergic alveolitis can occur with repeated episodes of acute or infraspinatus alveolitis or independently. This form The disease is manifested by inspiratory shortness of breath, persistent cough, weight loss, and deterioration of the patient’s general condition.

Complications of alveolitis can include chronic bronchitis, pulmonary hypertension, cor pulmonale, right ventricular heart failure, interstitial fibrosis, pulmonary emphysema, respiratory failure, and pulmonary edema.

Idiopathic fibrosing alveolitis develops gradually, while the patient experiences irreversible changes in the pulmonary alveoli, which is expressed in increasing shortness of breath. In addition to severe shortness of breath, patients complain of pain under the shoulder blades, which interferes with deep breathing, and fever. With the progression of the pathological process, hypoxemia (decreased oxygen content in the blood), right ventricular failure, and pulmonary hypertension increases. The terminal stage of the disease is characterized by pronounced signs of respiratory failure, enlargement and expansion of the right chambers of the heart (pulmonary heart).

The main signs of toxic fibrosing alveolitis are shortness of breath and dry cough. During auscultation of the lungs, gentle crepitus is heard in patients.

Diagnostics

The diagnosis is determined on the basis of data obtained from the collection of complaints and anamnesis, physical diagnosis, examination of external respiratory function, and chest radiography.

An X-ray examination of exogenous allergic alveolitis reveals a decrease in the transparency of the lung tissue with the formation of a large number of small focal shadows. To confirm the diagnosis, laboratory immunological diagnostics, provocative inhalation tests, and computed tomography of the lungs are performed. In diagnostically difficult cases, a biopsy of lung tissue is resorted to, followed by histological examination of the obtained material.

Exogenous allergic alveolitis is differentiated from bronchial asthma, atypical pneumonia, tuberculosis, sarcoidosis, and other forms of pulmonary alveolitis.

In the case of idiopathic fibrosing alveolitis, a radiograph of the lungs on both sides reveals small focal diffuse changes, more pronounced in the lower parts. In the later stages of the disease, secondary cystic changes are detected in the lung tissue. Computed tomography data of the lungs allows you to determine the area of altered lung tissue for subsequent biopsy. Electrocardiogram results indicate the presence of hypertrophy and overload of the right heart.

Differential diagnosis of this form of alveolitis is carried out with pneumonia, granulomatosis, pneumoconiosis, diffuse forms of amyloidosis and lung neoplasms.

X-ray changes in acute toxic fibrosing alveolitis may be absent. Subsequently, deformation and diffuse strengthening of the pulmonary pattern, as well as diffuse fibrosis, are determined.

Secondary alveolitis occurs against the background of other pathological processes. Most often these are sarcoidosis, tuberculosis, and diffuse connective tissue diseases.

Treatment of alveolitis

Treatment tactics for alveolitis depend on the form of the disease. In some cases, the patient may need to be hospitalized in a hospital.

The effectiveness of treatment for idiopathic fibrosing alveolitis decreases as the pathological process progresses, so it is important to start it at an early stage. Drug therapy for this form of the disease consists of the use of glucocorticoids; if this is not enough, immunosuppressants and bronchodilators are prescribed. As the disease progresses, plasmapheresis provides a therapeutic effect. Surgical treatment of this form of the disease involves lung transplantation. Indications for it are dyspnea, severe hypoxemia, and decreased diffusion capacity of the lungs.

For alveolitis of allergic and toxic etiology, in addition to the main treatment, it is necessary to eliminate or maximally limit the patient’s exposure to allergic or toxic agents, contact with which caused the development of the disease. In mild forms of alveolitis, this is usually sufficient for the disappearance of all clinical signs; the need for drug treatment may not arise.

In the treatment of severe forms of exogenous allergic alveolitis, glucocorticoids, inhaled bronchodilators, bronchodilators, and oxygen therapy are used.

For toxic fibrosing alveolitis, mucolytics and glucocorticoids are prescribed (orally or inhaled).

For all forms of alveolitis, in addition to the main treatment, taking vitamin complexes, potassium supplements, as well as performing breathing exercises(therapeutic breathing exercises).

Possible complications of alveolitis and consequences

Complications of alveolitis can include chronic bronchitis, pulmonary hypertension, cor pulmonale, right ventricular heart failure, interstitial fibrosis, pulmonary emphysema, respiratory failure, pulmonary edema.

Forecast

With timely and adequate treatment of acute exogenous allergic, as well as toxic fibrosing alveolitis, the prognosis is usually favorable. As the disease becomes chronic, the prognosis worsens.

Idiopathic fibrosing alveolitis is prone to gradual progression with the development of complications. Due to increasing irreversible changes in the alveolar-capillary system of the lungs, the risk of death is high. The five-year survival rate after surgical treatment reaches 50-60%.

Prevention

In order to prevent the development of alveolitis, it is recommended to promptly and adequately treat infectious diseases, limit contact with potentially dangerous allergens, eliminate household and professional factors that may cause the development of the pathological process, observe occupational hygiene rules, and also give up bad habits.

Persons at risk for alveolitis should undergo regular preventive medical examinations.

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It's probably no secret that not only children, but also some adults are afraid of dentists. Therefore, for many people, deciding to have a tooth removed is enough. difficult decision. And it’s good if the process goes smoothly and the wound heals in 7-10 days. But if the jaw socket continues to hurt and become inflamed, it is alveolitis. In this case, treatment should begin immediately, after consulting with your dentist.

What is the disease?

In dentistry, alveolitis is the inflammatory process of the jaw socket after surgical tooth extraction. Pathogenic microorganisms constantly enter an open wound with food, which, in case of weakened immunity or non-compliance elementary rules hygiene increase their colonies in a comfortable environment. As a result, we have a fairly strong pain syndrome.

Three percent of patients require treatment, a statistic that rises to 20% if we're talking about about wisdom tooth extraction.

Causes of the disease

Even the most experienced dentist cannot guarantee a quick gum healing process after tooth extraction. This is explained by the fact that the disease can develop not only if the advice of a specialist is ignored, but also become a consequence of many other reasons. The most common of them are:

The patient's weakened immune system;

A complicated operation involving the removal of not only a tooth, but also part of the bone tissue;

During the operation, various tooth fragments fall into the bottom of the socket;

Poor postoperative wound treatment;

Ignoring the rules of antiseptics during surgery;

Poor blood clotting, which prevents the formation of a clot;

To avoid the need for treatment of alveolitis after tooth extraction, you should be responsible for your own health and strictly follow the doctor’s advice. This will reduce the risk of developing the disease and will contribute to the rapid healing process of the wound.

Clinical picture

The inflammatory process usually begins quickly. However, already at the first symptoms, such as hyperemia and mild pain, it is better to consult a dentist. After examination, the specialist will tell you whether alveolitis is developing. The doctor will prescribe treatment in any case to relieve pain and speed up the healing of the jaw socket.

Ignoring the primary symptoms of the disease leads to the fact that the very next day the inflammatory process extends beyond the wound. In this case, the patient experiences severe pain in the area where the tooth was recently located and around it. In addition to hyperemia and swelling, a grayish coating with a specific unpleasant odor appears on the inflamed part of the gums. Self-administration of medications when the disease is in such an acute phase can be not only useless, but also extremely dangerous.

The advanced stage of alveolitis is characterized by purulent discharge from the wound, a strong bad breath and severe pain. Often this inflammatory process is accompanied by high body temperature, enlarged submandibular lymph nodes and general malaise.

Seeing a dentist if you experience primary symptoms of the disease will help prevent further development inflammatory process, as well as avoid dangerous consequences.

Types of disease: serous alveolitis

The clinical manifestations of the disease largely depend not only on its stage, but also on the type. In dentistry, the disease is divided into three main types. The first is serous alveolitis, the treatment of which will take no more than 3-5 days. The disease is characterized by a continuous mild pain syndrome, which intensifies during drinking and eating. At the same time, patients do not notice a deterioration in their health, enlarged lymph nodes or hyperthermia. Lack of therapy within a week leads to the development of a purulent process in the jaw socket.

Purulent form of the disease

The second type of disease is purulent alveolitis of the tooth. Treatment at home using traditional methods in this case can lead to widespread spread of infection. Characterized by this type illness with severe pain in the wound area and around it. With palpation, the pain intensifies and can radiate to the temporal area or ear.

When examining the inflamed area, acute hyperemia and swelling of the tissues, a gray coating on the jaw socket and adjacent areas, as well as a sharp putrid odor from the mouth are noted. In this case, the patient complains of general malaise, fever, enlargement and tenderness of the lymph nodes in the neck and under the jaw.

Hypertrophic alveolitis

This form of the disease develops when the purulent process becomes chronic. Many patients note a decrease in pain, improved well-being and the disappearance of other general symptoms of the inflammatory process. The disease no longer causes much discomfort, so patients believe that it has receded. However, such an opinion has nothing to do with the truth. moving from the acute stage to the chronic stage, it continues to destroy healthy tissue.

Hypertrophic alveolitis is characterized by a wide area of soft tissue infection. During examination, the leakage of purulent fluid from the wound is recorded, as well as hyperemia, swelling and even cyanosis of the areas adjacent to the hole. Palpation reveals the presence of hollow spaces and areas of dead gum tissue.

The disease is most severe in patients with diabetes mellitus. This is explained by the fact that the two diseases significantly aggravate each other.

Alveolitis of the lungs

In addition to dental alveolitis, there is a lung disease of the same name. This disease involves the development of an inflammatory process in the alveoli of the lungs, the etiology is different. Modern medicine classifies the disease into three main types: allergic, toxic and idiopathic. And if the reasons for the first two are interaction with the allergen and intoxication, then scientists have not yet figured out why the latter occurs.

Treatment of pulmonary alveolitis is carried out under the strict supervision of a doctor at home; hospital therapy is indicated only for severe forms of the disease.

Why is dental alveolitis dangerous?

The rate of development of the inflammatory process in the jaw socket largely depends on the state of the immune system. And if the body’s defense system is weakened, then within a couple of hours after the first symptoms appear, the disease can enter the acute phase. Lack of timely treatment and ignoring clinical manifestations for a long period can be very dangerous. After all, the consequence of such carelessness can be the penetration of infection into the deep layers of soft and bone tissue. As a result, periostitis, phlegmon, abscess, osteomyelitis and even blood poisoning develop.

Treatment of the disease at an early stage

If the doctor diagnoses alveolitis after dental treatment, he will definitely determine the cause of the disease. To do this, the patient must undergo radiography. From the resulting image, the specialist will be able to determine the presence of foreign bodies in the socket and begin to remove them.

Initially, the patient is given an injection of lidocaine or another pain reliever. When the anesthetic medicine begins to act, the doctor will treat the hole with an antiseptic solution. For this, medications such as Furacilin or Chlorhyxedine are most often used. Next, the dentist will use instruments to remove the foreign body and re-treat the wound.

An antiseptic bandage is applied to the hole that has been dried with a gauze swab, and the patient is prescribed systemic painkillers. In some cases, if the patient has alveolitis, treatment may include a course of antibacterial therapy. However, make a decision on this issue should only be done by a doctor.

Treatment of advanced forms of alveolitis

If purulent or hypertrophic alveolitis is diagnosed, the doctor will begin treatment with pain relief. To do this, the patient is given an anesthetic blockade, the hole is cleaned of pus and foreign bodies are removed. Then a tampon with antibacterial drugs is inserted into the wound, which is changed every 24 hours. Such alveolitis is expected to be treated at home after tooth extraction, but daily visits to the dentist are mandatory.

For soft tissue necrosis, doctors use protiolytic enzymes to stop the inflammatory process and also remove dead tissue. After the acute stage the illness will pass, treatment is supplemented with physiotherapeutic procedures that help improve the process of tissue regeneration. In this case, the patient may be prescribed infrared laser or ultraviolet radiation.

Pulmonary alveolitis is a pathological process in which damage to the alveoli occurs with subsequent fibrosis. With this disorder, the tissue of the organ becomes thicker and does not allow the lungs to work fully, which often causes oxygen deficiency. The rest of the organs also lack oxygen, hence the metabolic disorder.

Description of the disease

Pulmonary alveolitis is an inflammatory pathology characterized by damage to the alveoli with subsequent growth of connective tissue in it. The disease can appear independently or occur with other disorders:

chronic hepatitis;
arthritis;
AIDS;
Schanger syndrome;
scleroderma;
lupus erythematosus, etc.

The disease can develop in acute (signs appear within 4-12 hours) and chronic forms. The second is the most dangerous, since the symptoms are characterized gradually and often do not allow themselves to be recognized in the early stages, but are noticed only when an irreversible process has appeared in the lungs.

Alveolitis is more often observed in people over 50 years of age and in the male half of the population, as well as in smokers. Treatment involves relieving the inflammatory process and normalizing blood circulation. This can be done with special medications and herbal medicine prescribed by a doctor.

Kinds

Alveolitis that forms independently is called primary, and if it appears against the background of other pathologies, it is called secondary.

There are 3 forms of the disease:

Exogenous allergic – caused by various pathogens through the respiratory organs. Often observed in people who have pets.
Idiopathic fibrosing - appears hereditarily.
Toxic – provoked by the penetration of toxic and chemical substances and medications into the respiratory system. This form is curable quite simply; you need to avoid contact with the agent being called.

Idiopathic fibrosing is not common, but is the most dangerous. This form is associated with hypertension, increasing pneumofibrosis, and respiratory failure.

Sometimes the toxic form is combined with an allergic one and is very difficult, and treatment of alveolitis takes a long time.

Causes

To date, the causes of alveolitis have not yet been fully studied. Some indicate genetic factors, others suggest that a virus is involved in the development of the disease. Regardless of the type of pathology, the reasons may be the following:

contact with harmful substances;
presence of hepatitis C;
use of certain medications;
some food products;
bronchial asthma (in childhood);
weak immune system;
bacterial, fungal infections;
prolonged exposure to a polluted atmosphere;
external irritants (plant pollen, animal hair, sawdust, hay);
inflammation of the esophageal mucosa;
smoking;
experienced radioactive radiation in the chest area.

Damage to the alveoli in the lungs occurs during regular interaction with an irritant.. Due to its natural basis, it contributes to allergic diseases, and in case of poisoning – toxic pathologies.

It is worth noting that alveolitis is completely non-contagious, because in the essence of the inflammatory process there is a disorder, as a result of which immune complexes appear that affect neutrophils.

Symptoms

Since there is an acute and chronic form, the symptoms of pulmonary alveolitis will differ markedly. Acute disease is characterized by:

strong increase in temperature;
sudden development of shortness of breath;
intense wet cough, runny nose.

Such symptoms are similar to other respiratory tract pathologies, for example, pneumonia. But with any such manifestations, you should definitely consult a specialist. The chronic form is expressed as follows:

difficult painful breathing;
shortness of breath that occurs gradually;
unbearable dry cough;
expectoration with blood particles.

If treatment is not started in a timely manner, shortness of breath will become increasingly worse. As a result, there will be an increase in pressure, followed by respiratory failure. All this can lead to death. Diagnosis becomes difficult because the main symptoms are similar to a cold, because of this the patient may not visit the doctor for a long time, which aggravates the situation. In addition, there are other symptoms that occur with both forms of alveolitis:

malaise, fatigue;
weight loss;
chest tightness;
swelling;
increased sweating;
pain in the joints, chest, hoarseness observed when listening;
protrusion of the nail plate, thinning of the ends of the fingers;
muscle weakness;
goosebumps, pale skin.

Alveolitis of the lungs in a child is expressed by growth retardation. All these signs require a diagnosis and treatment.

Diagnostics

Since the symptoms are similar to other diseases, diagnostic measures are based on different actions. The doctor carefully listens to the patient’s complaints, establishes the period of development of symptoms, goes through the person’s clinical picture, looks for acceptable causes, based on the patient’s work and living conditions. The main manipulation is a blood test and examination of sputum produced during coughing.

Diagnostics implies:

chest x-ray;
bronchoscopy;
careful examination of changes in the respiratory organ;
spirometry;
biopsy.

In addition to the above measures, you may need to consult a therapist. Having completed the diagnosis and established the cause of alveolitis, the pulmonologist prescribes a treatment regimen individually in each order.

Treatment

Therapy for alveolitis can be traditional and carried out using folk recipes. Elimination tactics depend on the type of disease. Treatment takes place in a hospital under the supervision of a doctor. The basis is the elimination of the pathology itself and preventing the transformation of lung tissue into connective tissue.

In case of toxic, allergic alveolitis, it is important to avoid contact with the allergen, the toxin that causes the disease. For treatment, the doctor prescribes glucocorticoid hormones in the form of inhalations. As internal use mucolytics are prescribed. At an advanced stage, cytostatics are used, they are aimed at suppressing the spread of cells.

The idiopathic form is treated with glucocorticoid hormonal agents, also in the form of inhalations. If treatment does not produce results, cytostatics are used.

Any form of alveolitis requires the use of the following medications:

Medicines that help thin mucus and cough up.
Drugs that suppress symptoms.
Hormonal agents (Prednisolone) – prevent the occurrence of inflammation. Used in small proportions over a long period.
Immunosuppressants - prescribed in case of idiopathic type.
Vitamin and mineral complexes.
Antibiotics (Penicillin) – kill pathogenic microorganisms.

It is possible to use traditional methods. They involve inhalations with various medicinal herbs, a diet, and you will also need special breathing exercises for pulmonary alveolitis, which will help normalize the patient’s health.

Traditional methods

Herbal infusions quickly calm the irritated respiratory system, have an expectorant effect, eliminate coughing attacks, and remove inflammation.

Treatment of alveolitis at home using traditional methods is used as an additional treatment. Decoctions, infusions, and inhalations are used.

To prepare folk recipes use:

chamomile, motherwort;
oregano;
mint, eucalyptus;
nettles, ground pepper;
hawthorn, etc.

To achieve the best results, it is good to follow a simple diet:

drink at least 2 liters of water per day;
eat boiled, steamed, baked food;
eat more vegetables and dried fruits;
eat low-fat broths;
there are fermented milk products.

By following a simple diet, the positive effect will not be long in coming.

Respiratory exercise therapy for lung pathology is aimed at normalizing the human condition - eliminating respiratory disorders, shortness of breath. Gymnastics is aimed at:

strengthening the muscles that take part in the respiratory movement;
prevention of oxygen starvation;
restoration of breathing control;
normalization of gas exchange in the lungs;
improving the psycho-emotional state of the patient.

A specialist will help you create a set of breathing exercises. Each execution will take no more than 20 minutes.

Complications

If left untreated, lung disease leads to complications. Swelling of the organ, pulmonary heart disease, and difficult and inadequate breathing may appear. Blood penetrates into the tissue of the organ, leading to disruption of gas exchange. In this case, the person will need urgent medical attention to avoid death. Edema may be:

acute – expressed over a period of time and causes death;
subacute – occurs alternately, then an increase and then a weakening of the signs of the disease;
protracted – the most common form, lasts for 12-24 hours;
fulminant – develops very quickly, the state of health suddenly deteriorates, and death is possible.

As alveolar lungs progress, they can cause increased pressure, chronic bronchitis, and heart failure.

The prognosis for treatment of alveolitis will be unfavorable only if the disease is detected on last stage development. Usually, the idiopathic form of the disease is considered fatal. When a disorder in the lungs is detected in time, it is quite possible to cope with it, although it will take a lot of time.

Pulmonary alveolitis is an inflammatory process belonging to the group of diffuse ones, the course of which occurs in the lungs (in the respiratory section). In alveolitis, the alveoli (vesicles of the lungs) are affected.

This disease can be either independent or a consequence of other diseases (chronic hepatitis, sarcoidosis, thyroiditis, Sjögren's syndrome, diffuse connective tissue disease, AIDS).

There are 3 forms of pulmonary alveolitis:

toxic– occurs due to toxins entering the lungs (through medications, chemical substances);
allergic– allergens of various origins are inhaled through the nose and enter the lungs (most often found in adults and children who love animals and aquarium fish);
indopathy fibrosing– the rarest form of the disease, the disease is mainly transmitted genetically.

Symptoms:

1 allergic alveolitis: similar to ARVI, pneumonia, bronchitis;
2 indopathy fibrosing alveolitis: dry cough, shortness of breath begins at the slightest physical exertion, excessive fatigue, pale (sometimes bluish) skin due to pulmonary heart failure that occurs during the course of the disease, a sharp decrease in body weight, nails change shape, the nail plate becomes convex, fingertips thicken (become like drumsticks);
3 toxic alveolitis: there are no particular obvious signs, the symptoms are similar to those listed above, treatment consists of getting rid of toxic substances and cleansing the lungs of them.

General signs of pulmonary alveolitis:

increased body temperature;
increased sweating;
“goosebumps” run throughout the body and head;
shortness of breath with a very rapid rate of increase;
either a dry or wet cough without obvious reasons;
feeling of tightness in the chest;
when taking laboratory tests, in very frequent cases the level of ESR is increased;
wheezing in the sternum;
chest pain.

Useful foods for pulmonary alveolitis

Before you start following a diet, you need to cleanse your stomach. If you have a fever, you need to drink water with lemon or cranberry juice. Also, you should not force him to eat, it will only harm your health. Food should be light and aimed at increasing immunity.

With alveolitis of the lungs you need to eat:

broth cooked with lean meats and fish;
milk, kefir, low-fat sour cream;
semolina porridge and any milk porridge in general;
more fresh vegetables and fruits (but in order not to weaken the body by loss of chewing strength, it is better to give them in the form of purees);
freshly squeezed juices from carrots, beets, fruits and berries (especially cranberries, apples, citrus fruits);
raisins, dried apricots, prunes, rosehip, currant, and sea buckthorn compotes.

All food should be boiled or steamed; stewed dishes can be given from time to time.

Traditional medicine for pulmonary alveolitis:

1 Pumpkin juice. You need to drink half a liter of it per day. It relieves swelling of the lungs and alveoli very well.
2 An infusion of lingonberry leaves will be a good antiseptic. To prepare it, you need to add 10-15 grams of dry, crushed lingonberry leaves to 250 milliliters of water. You need to boil for 15 minutes. Let cool. Filter. This is a daily portion, you need to drink it in several doses.
3 An effective remedy for pulmonary alveolitis, infusions of birch buds or leaves are used. To prepare this healing infusion, you will need half a liter of hot boiled water and 40 grams of birch leaves or buds (you can take half of both). Leave for 50-60 minutes, then filter. Divide into 4 doses. Consume 20 minutes before meals.
4 In case of severe suffocation, it is necessary to take a decoction prepared from pharmaceutical chamomile, hawthorn (it is better to take the bright red color), motherwort, and marsh cudweed. Take all these herbs in equal portions. For a glass of boiling water you need 20 grams of this mixture. Boil for a few minutes. Leave with the lid closed for a quarter of an hour. Filter. Drink 75 milliliters after meals.
5 If fluid has accumulated in the lungs, you need to take the following medicine: take 2 tablespoons of flax seeds, place them in a saucepan, add a liter of water, bring to a boil, leave for 50 minutes. Filter. To improve the taste, you can add a little lemon juice and take half a glass warm every 3 hours (the number of doses per day should not exceed 6 times).
6 Also, infusions from

Alveolitis of the lungs refers to diffuse parenchymal lung diseases. This is a non-bacterial inflammation of interstitial tissue. Large group parenchymal diseases (alveolitis) are united by a similar x-ray picture; in the clinic they predominate progressive (V in this case difficulty breathing) and there are functional disorders (mainly of the restrictive type).

Breathing disorders are based on changes in the elasticity of the lung tissue and limitation of their expansion during inhalation. About half of alveolitis are diseases of unknown etiology.

Interstitium in this disease is the target of damage. This is the anatomical part of the lungs, their actual connective tissue frame and skeleton, in which there is a dense network of vessels, bronchi and bronchioles, and alveoli. The interstitium is strong because it supports the shape of the airways, small vessels and air-containing spaces. On the other hand, it is thin and elastic, so it does not interfere with the processes gas exchange . The intralobular interstitium is especially thin and elastic, which maintains the shape of the alveoli and thin capillaries involved in gas exchange.

The bronchi, as they branch into the lung tissue, decrease in diameter and the smallest alveolar bronchioles end in pulmonary alveoli (vesicles). Their totality forms, in fact, the tissue of the lungs. These are spaces containing air, separated by the thinnest partitions. Each septum is simultaneously the wall of two alveoli, through which gas exchange occurs - oxygen enters and carbon dioxide is removed. It has collagen and elastic fibers, which impart elasticity so that the alveoli easily change volume during inhalation and exhalation. The surface area of the alveoli is much greater than the volume, which is important for high-quality gas exchange. The walls are lined with surfactant and liquid in which gases dissolve. Oxygen from the environment enters the alveoli, then into and is transferred to the cells of the body.

A special role in the breathing process is given to surfactant - a fat-like substance that lines the alveoli. It reduces the tension force of moisture in the alveoli and resists the collapse of the alveoli during deep exhalation. Without it, surface tension would be 10 times higher than normal, and the alveoli would stick together after exhalation and require more effort to expand during inhalation. When you inhale, this substance is distributed less densely, so the lungs stretch well. In addition to participating in the act of inhalation and exhalation, surfactant dissolves oxygen and carbon dioxide (facilitates their diffusion), regulates water exchange and microcirculation in the lungs. It also helps neutralize bacteria that have entered the alveoli. Surfactant is produced in utero and its production is continuously maintained throughout a person’s life.

Various lesions of the lung tissue in one way or another cause thickening of the interstitium, changes in the alveoli and the quality of surfactant. Some changes go away after treatment, others become chronic and incurable.

In general, these diseases are initially severe and progressive - they develop rapidly in the interstitial tissue scar changes (fibrosis) . If speak about idiopathic fibrosing alveolitis , then it is very rare, with the highest prevalence among men (1.9:1 in women) aged 40-70 years. Prevalence exogenous allergic alveolitis behind last years has increased. The incidence rate is 42 per 100 thousand population.

Pathogenesis

To date, the causative factor that triggers the characteristic idiopathic fibrosing alveolitis (IFA) changes in lung tissue. Many authors consider fibrosing alveolitis. This theory is supported by the presence of circulating immune complexes, hypergammaglobulinemia and rheumatoid factor.

Role being discussed adenoviruses , And Epstein-Barr . Indeed, viral proteins can increase chronic inflammation and activate collagen production.

The step-by-step process in lung tissue looks like this:

thickening and inflammatory infiltration of the alveolar wall;
filling the lumens of the alveoli with secretions and various cells;
their loss of normal structure;
violation of the architectonics of the lung tissue when the bronchi and blood vessels are involved in the process;
development of cystic cavities.

In the later stages, normal parenchyma is replaced by connective tissue, into which dilated cystic alveoli are embedded, lined with hyperplastic epithelium that does not perform its function. The lungs appear compacted and wrinkled in appearance.

The main place in pathogenesis is alveolar macrophage is a cellular barrier to the penetration of components from the inhaled air. These cells are involved in the capture of foreign inhaled particles and the formation of an inflammatory response. The response can be minimal or very active - up to damage to the lung tissue.

Under the influence of immune complexes with an antigen (it is not known by ELISA), the macrophage is activated and releases mediators. Some stimulate neutrophils and lymphocytes and cause their increased migration from capillaries to the alveoli (edema forms inside the alveoli).

Exudate with desquamated cells of the alveoli appears in the lumen of the air cavities. This stage corresponds inflammation (alveolitis). The inflammatory process is limited at first, but can then spread. Inside the alveoli is also found mucin , protein, crystals cholesterol , and also , and . The walls of blood vessels in the area affected by the inflammatory process also thicken, but in unaffected tissue they may be normal.

This disease is characterized by changes in the composition and amount of surfactant. When its quantity decreases or is destroyed, the ability of the lungs to stretch during inhalation is significantly reduced. Therefore, the depth of the patient’s breaths decreases, and the breathing frequency increases. Outwardly, this manifests itself as superficial and.

If alveolitis does not resolve on its own or with treatment, inflammatory infiltration invades the interalveolar septa and fibrosis develops under the influence of another group of mediators that cause the growth of fibroblasts and smooth muscle cells. First, the structure of small bronchioles and the interstitium surrounding them changes. Fibrotic processes also extend to the vessels (they collapse, causing deformation of the alveoli). When the walls of the alveoli rupture and merge with the bronchioles, smooth-walled cavities appear. As a result of such changes, the architectonics are completely disrupted - cystic cavities appear in the lungs, which are described on X-ray examination and CT as “ cellular lung ».

It should be noted that the process fibrosis very intense, therefore the primary role in the pathogenesis of the disease is assigned to fibrosis without a pronounced inflammatory process. In the processes of fibrosis formation, mast cells are also given importance, the number of which is sharply increased in areas of fibrosis. There is also an increase histamine And tryptase (these are products of mast cells). In patients, as fibrosis and respiratory failure progress, chronic cor pulmonale occurs.

Condition for development exogenous allergic alveolitis (EAA) is the inhalation of any antigenic material in a sufficient dose and for a certain time. If the antigen is up to 5 microns in size, it settles in the alveoli and bronchioles, giving impetus to the development of the disease. Larger particles are fixed in bronchi of larger caliber, and if the allergen is soluble, then when it dissolves it causes the same effect. Most people do not get the disease, which may be due to genetic factors and the immune response.

Undoubtedly, allergic alveolitis is an immunopathological disease, since allergic reactions (types 3 and 4) play a major role in its occurrence. Non-immune inflammation also plays a role. The third type is associated with the formation of immune complexes, which play a role in the early stages of the disease. When antigen and IgG interact, immune complexes are formed in the interstitium, which have a damaging effect on the interstitium and alveoli. As a result of increased capillary permeability, neutrophils rush into the zone.

Immune complexes activate alveolar macrophages. Active neutrophils and macrophages, in addition to releasing pro-inflammatory agents, also produce toxic products ( cytokines And oxygen radicals ). These in turn cause further damage to the interstitium and increase the inflammatory response. In addition, they attract lymphocytes and monocytes to the area of inflammation, which support delayed allergic reactions.

Type 4 immune reactions are associated with T-lymphocytes and determine delayed-type reactions. These reactions develop two days after inhalation of the antigen. Cytokines, which are released at the first stage of damage, significantly increases the influx of lymphocytes and monocytes into the lesion. CD4+ lymphocytes secrete interferon gamma, which activates macrophages. Thus, delayed-type reactions are constantly maintained, and this causes the formation of granulomas, activates fibroblasts, and excessive collagen synthesis, which ultimately leads to interstitial fibrosis. The presence of T-lymphocytes (in the patient’s blood and lungs), histological confirmation of granulomas and interstitial fibrosis are evidence of the presence of type 4 reactions in the patient’s body.

Classification

All interstitial lung diseases can be divided into diseases of unknown nature, known and secondary (for example, with systemic diseases, hepatitis , biliary cirrhosis , Crohn's disease , Hashimoto's thyroiditis ).

The classification of interstitial lung diseases (1984) distinguishes the following types of alveolitis:

allergic alveolitis of the lungs ;
idiopathic fibrosing alveolitis ;
.

From the title (EAA) it follows that the disease has a clearly established allergic nature and develops under the influence of substances entering the body from the outside. Exogenous allergic alveolitis can be caused by more than 200 allergens, long-term inhalation of which causes immune inflammation in the lungs and activates the development of fibrosis. Thus, there are known diseases that are caused by inhalation of dust with animal and plant proteins (syndromes: “ farmer's lung », « cheesemaker's lung », « poultry farmer's lung »).

The list of these factors is constantly expanding, which is associated with the emergence of new medications, industrial development and constant pollution. environment. Therefore, today they distinguish toxic alveolitis associated with inhalation of heavy metal vapors or taking certain medications (mainly chemotherapy And busulfan , and ).

In this regard, there is another classification of interstitial lung diseases, which is based on the etiological principle (based on the causes of the disease). Identifies diseases associated with the hazards and effects of medications:

exogenous allergic alveolitis ;
toxic fibrosing alveolitis ;
pneumoconiosis ;
interstitial fibrosis caused by radiation injuries.

The summarized data in the tables will help you understand this in more detail.

Thus, exogenous allergic alveolitis (synonym - hypersensitivity pneumonitis ) is a group of related diseases that combine diffuse changes in the parenchyma and bronchioles that arise in response to repeated inhalation of various antigens. The description of the first cases of the disease in farmers who worked with moldy hay dates back to 1932, and in 1965 the disease was described in hobbyists who raised pigeons. A common cause of acute and recurrent forms of the disease in adults are molds and yeast-like fungi, subacute - animal proteins, and chronic - dust (library or construction).

In this regard, allergic alveolitis has a different course and prognosis. In some cases, the disease is completely reversible, while in others, irreversible damage to the lung tissue occurs. This depends on many factors: exposure to the antigen, the person's immune response, the nature of the inhaled allergen.

Since the clinical picture and course are varied, in most cases this group of diseases is not diagnosed in a timely manner, which ultimately leads to progression of the disease. Most researchers conclude that 5-15% of individuals exposed to high concentrations of the agent develop EAA. The prevalence of the disease when inhaling low concentrations of the allergen has not been established.

Fibrosing alveolitis has a different origin. Term idiopathic fibrosing alveolitis (ELISA) means, first of all, the unknown nature of the occurrence of this pathology and the rapid development of fibrosis characteristic of it - the progressive replacement of normal lung tissue with connective tissue. This process is accompanied by impaired gas exchange, rapidly progressing respiratory failure and rapid death of the patient. Since existing theories of viral and autoimmune origin have not received the necessary evidence, treating this disease presents certain difficulties. Currently, the synonym for ELISA is “ usual interstitial pneumonia».

Causes

As mentioned above, nature idiopathic fibrosing alveolitis not completely clear. Provoking factors play a certain role, of which we can indicate:

smoking;
environmental aggression (ozone, chlorine, sulfur oxide, industrial and automobile exhaust);
genetic factors;
occupational hazards.

According to one theory, the causes include occupational factors: contact with metal (brass, lead, nickel, steel) and wood dust (for carpenters). The role of asbestos, silicate and silicon dust cannot be excluded. The presence of familial forms of the disease supports the genetic theory.

The etiology of exogenous alveolitis is associated with antigens , which a person constantly encounters due to the nature of his professional activity. The most important in agriculture are antigens of birds and actinomycetes (bacteria with the properties of fungi). The latter are found in soil, water and compost. They actively reproduce during rotting and in the water of heating systems (the optimal temperature for this is 50-60 0 C). It is actinomycetes that cause the development of “farmer's lung” in those who grow mushrooms, work with sugar cane and in people who use air conditioners.

Avian antigens are proteins gamma globulin and albumin, which are contained in the secretions of the glands and excrement of pigeons, turkeys, parrots, canaries and others. More common among fungal antigens Aspergillus spp. calling " malt brewer's lung », « cheese makers », « farmer », suberosis (when working with balsa wood) and disease in persons staying in damp and unventilated areas.

Symptoms of pulmonary alveolitis

Ideopathic fibrosing alveolitis (IFA)

Symptoms of alveolitis are nonspecific and at first do not allow a correct diagnosis. The onset of the disease is imperceptible and the main symptom is not very pronounced at first and does not bother the patient. There may be an occasional cough without sputum. Exactly like this clinical picture characteristic of a subacute course. As the disease worsens and progresses, shortness of breath increases, and a periodic increase in temperature is noted.

In some cases, ELISA begins with acute symptoms, like a viral infection. Increasing shortness of breath, cough and fever force the patient to see a doctor, but he is given a diagnosis pneumonia of bacterial origin and treatment does not bring results. The condition is improving somewhat, but without proper treatment the disease progresses.

When listening to the lungs, a characteristic phenomenon is determined - crepitus , similar to " cellophane crackle" It is heard most often in the posterior lower parts, but in 1/5 of patients crepitus also appears in the upper parts. Unlike crepitus in other pulmonary cases, in this case it is not loud and is heard at the height of inspiration.

When working with chemical compounds (plastics, polyurethane dyes, resins), this disease can also occur. In Moscow, the leading causes of allergic alveolitis are avian and fungal antigens.

In a chronic course, the condition gradually worsens, and the patient adapts to shortness of breath by reducing activity and may long time do not consult a doctor. Most at the time of treatment and examination have had a disease experience of 6 months to a year. With sudden progression, which is associated, for example, with a viral infection or accession pneumonia , the condition worsens significantly: due to shortness of breath, the patient cannot walk or even talk, let alone care for himself, and the temperature may rise. 50% of patients have tachyptic (rapid shallow breathing), which requires less energy expenditure.

Fibrosing alveolitis in the later stages is characterized by the development emphysematous bullae , which burst and a spontaneous pneumothorax . This emergency also requires you to see a doctor.

Other symptoms are weakness, pain in joints and muscles, weight loss, changes in the phalanges of the nails (“ Drumsticks", this symptom predominates in men). The patient has a symptom drumsticks“is combined with a more severe prognosis.

The terminal stage of fibrosing alveolitis is characterized by severe respiratory failure and the development of cor pulmonale. The patient has swelling and swelling of the neck veins.

Cyanosis in pulmonary failure is caused by poor blood saturation in the lungs. Its intensity increases, it is diffuse in nature, but is more pronounced at the tips of the ears, nose and fingers. Swelling of the neck veins is the result of increased venous pressure in big circle blood circulation and indicates a decompensated pulmonary heart.

Edema occurs with right ventricular failure in conditions of severe hypercapnia . In this case, increased sodium reabsorption occurs in the kidneys, which leads to fluid retention. Swelling appears first on the feet and legs, and then spreads to the upper parts of the body. In the morning, swelling is less, and in the evening it increases.

At this stage, squeezing and pressing pain appears in the heart area, which is associated with:

metabolic disorders in the myocardium due to hypoxia;
an undeveloped network of collaterals in hypertrophied heart tissue;
myocardial overload due to increased pressure in the pulmonary artery;
narrowing of the coronary vessels ( pulmonary coronary reflex ).

Exogenous allergic alveolitis (EAA)

It occurs in acute, subacute and chronic forms. Acute occurs when there is a massive intake of antigen at work or at home. In this case, clinical manifestations develop quickly - after 4-12 hours. This may include chills, cough, weakness, heaviness in the chest, shortness of breath, muscle and joint pain. Sputum is rare or scanty. A common symptom is.

All manifestations resolve within a day or three, while shortness of breath on exertion and lethargy persist for several weeks. The clinic repeats again after repeated contact with the antigen. This form is rarely diagnosed, since it is assumed that pneumonia viral or fungal nature.

Subacute form occurs with constant, but not intense exposure to antigens (usually at home). For example, in contact with birds. The patient experiences shortness of breath on exertion, fatigue, and cough with sputum. Fever appears at the onset of the disease.
Chronic form develops with prolonged inhalation of a low dose of antigen. Also, the untreated subacute form has a risk of becoming chronic. The onset of the disease is imperceptible. A characteristic symptom is progressive shortness of breath, lack of appetite and weight loss. At the end of the disease, fibrosis and cor pulmonale with heart failure develop.

Upon examination, it is revealed cyanosis and changes in the phalanges of the fingers (“ watch glasses" And " Drumsticks"). Symptom " drumsticks“- a common sign and is a harbinger of an unfavorable outcome. When listening to the patient, crepitus is detected, expressed in the lower parts; wheezing can be heard (with additional bronchial obstruction), but this is not a characteristic sign.

Tests and diagnostics

The main problem is the early diagnosis of this disease and solving it will improve the quality of life and increase its duration.

Laboratory research

In the diagnosis of allergic alveolitis, importance is attached to the identification of specific antigens. Of particular importance is the determination of precipitating antibodies to the antigen using methods immunoelectrophoresis and immunoenzyme. Precipitating antibodies are detected during the acute course, and are found in the serum for another 1-3 years after cessation of contact with the antigen. In chronic cases, antibodies are not detected. False-positive test results also occur. In EAA, antibody levels are not associated with disease activity. Thus, the presence of antibodies does not confirm the diagnosis in all cases; their absence does not exclude its presence.

Laboratory tests for the idiopathic form are not of great significance, since in all cases there is an increase, CECs (immune complexes) and an increase in the level of immunoglobulins are detected. A promising marker is the level of surfactant proteins A and D. Due to the increased permeability of the alveolar membrane, there is an increase in surfactant proteins, which reflect the activity of the process. Determination in blood mucinantigens also allows you to assess the activity of alveolitis.

Instrumental methods

X-ray of the lungs

It is nonspecific, especially in the early stages, and does not make it possible to reliably distinguish ELISA from other diffuse lung diseases. The radiograph shows a symmetrical increase in the pulmonary pattern, and then its deformation, which is more pronounced in the lower sections. In the early stages, a decrease in the volume of lung fields and a decrease in their transparency may be detected (the “phenomenon” frosted glass"). Characteristic development bullous emphysema , which may appear earlier than other changes in the pulmonary pattern. Involvement of the pleura, enlarged lymph nodes, and local compactions in the parenchyma are not typical. With this disease, the lung tissue is uniformly affected.

It is important to study dynamics when, as the pulmonary pattern progresses, it becomes rough, and cysts measuring 1-2 cm reflect the mesh type of structure of the lung parenchyma. This indicates the development of " cellular lung"(light as a honeycomb): thickened septa between the alveoli cover swollen lobules and acini. In the later stages, a displacement of the trachea to the right and its enlargement are detected. However, in some patients already diagnosed histologically, there may be no radiographic changes.

"Honeycomb lung" on an x-ray

Changes on radiographs in allergic alveolitis are the same and vary from normal (in acute and subacute forms) to severe fibrosis and “ cellular lung". It is also possible that there are no changes on the radiograph even with fibrous changes in the biopsy material and hypoxemia in the patient. In acute and subacute forms, changes of the type “ frosted glass" Changes in X-ray of the lungs in acute alveolitis resolve within 4-6 weeks, if repeated contact with the allergen is excluded. The situation is much more complicated in the chronic form, which reaches the “ cellular lung».

CT scan

Helps to reliably make a diagnosis and judge the degree of activity. Diagnostic accuracy reaches 90%. Signs " cellular lung"are found in 70% of cases, compared to 15-20% with radiography. The changes are localized mainly in the basal parts of the lungs.

Phenomenon " frosted glass" manifests itself with slight thickening of the walls of the alveoli and interstitium and a slight filling of the alveoli with fluid or cells. CT picture " frosted glass"is a more favorable prognostic sign. Such patients respond well to treatment steroids , and the improvement in their condition is reflected by an improvement in the CT scan. An inflammatory reaction (namely alveolitis) is an indication for corticosteroid therapy, from which an effect can be expected. This examination assesses the extent of the lesion when compared with a biopsy sample taken from a single area.

In the presence of emphysema, a CT examination allows one to assess its severity and distinguish it from cystic changes that reflect the final stage of the disease. Computed tomography performed over time gives an idea of changes in hemodynamics in the lungs and pulmonary hypertension . Thus, this examination is comparable in importance to a biopsy, which is considered the “gold standard” for diagnosing this disease. The use of CT is important to monitor the effectiveness of treatment. In the case of the allergic nature of the disease, the changes have much in common. Once contact with the agent disappears, changes may diminish and even disappear.

Respiratory function test

The total capacity of the lungs decreases, bronchial patency is significantly reduced, and the ability to straighten the lung tissue is lost. A valuable indicator in this study is the diffusion capacity of the lungs. It is closely related to the symptom dyspnea , and its pronounced decrease indicates the development pulmonary hypertension . Functional changes in EAA are nonspecific and completely coincide with the indicators in ELISA.

Bronchoalveolar lavage

This is a method of obtaining washouts from bronchioles and alveoli for subsequent various types research. It is important that in this study material is obtained from the lower parts of the pulmonary tree. When compared with, in this examination the material is obtained from a larger number of alveoli. The method is non-invasive (sampling is carried out through bronchoscope ), it can be repeated many times, and it has diagnostic significance, since the course and prognosis of fibrosing alveolitis is assessed.

Eosinophilia is often associated with a poor prognosis and such patients have an insufficient response to steroid therapy, and treatment and in combination gives a good result. The number of neutrophils and eosinophils correlates with activity. Sometimes revealed lymphocytosis (increased content of lymphocytes), which indicates severe alveolar inflammation and in the absence of “honeycomb lung”, steroid therapy gives a good result.

Diagnostic value and other components

For example, circulating immune complexes, which are significantly elevated in this disease. Some studies have shown that when their levels are high, steroid therapy is effective. Immunoglobulin G is also increased. The lipid composition reflects the state of the surfactant, which changes significantly (the amount of phospholipids decreases and the ratio of fractions changes). The more phospholipids in the wash, the more favorable the prognosis. Another surfactant component (surfactant protein A) is a marker of activity, but its content in ELISA is significantly reduced.

Blood gas study

In the early stages, the blood gas analysis at rest remains almost unchanged, but when physical activity noted desaturation (decreased blood oxygen saturation). As it progresses hypoxemia (decrease in oxygen content) is recorded at rest and, in addition, is accompanied hypocapnia (excess CO 2 content) in the terminal stages.

impossibility of establishing a diagnosis;
absence " cellular lung»;
choice of treatment method.

This method is necessary to reliably establish a diagnosis and prescribe the correct treatment, which has serious side effects, therefore it is unacceptable to subject a patient to an unspecified diagnosis. A biopsy can identify the specific factor causing fibrosis (eg, asbestosis ), and also allows you to confirm other diagnoses (, alveolar carcinoma , lymphoma , eosinophilic pneumonia ).

The diagnostic yield of this method is more than 94%, and the number of complications ranges from 6–19%.

There are several biopsy methods:

open biopsy;
transbronchial;
video thoracoscopic;
percutaneous puncture.

Open biopsy performed if it is impossible to perform a less traumatic biopsy. It is performed under through incisions of the chest wall from the areas with the greatest changes, which are determined on radiography (CT), and from the area where the parenchyma is still preserved. 2–4 samples are taken from the lower and upper lobes. The material is used for morphological, bacteriological studies, as well as other studies (immunofluorescent, immunohistochemical). For patients who have severe functional impairment of the lungs, surgery is a difficult intervention and is contraindicated.

Transbronchial performed during bronchoscopy by collecting tissue through a puncture of the bronchus. The disadvantage of this type of biopsy is the small sample size and less information content. With ELISA it is not of great importance and information content, but with EAA it is used. The advantage is safety compared to the previous option.

Video thoracoscopic is gaining great popularity due to the least traumatization (two small punctures are made), but it allows samples to be taken in the same quantity as with open method. Research and collection are carried out under visual control thoracoscope , which is administered through punctures. This examination reduces complications and the length of the patient's stay in the hospital.

Percutaneous biopsy . It is performed under general anesthesia with a cutting needle, the device of which allows you to cut out a piece of parenchyma or aspirate the material. The entry site is selected under CT guidance. Information content is 70%.

The listed procedures are more often performed by younger patients and those with mild functional impairments.

Treatment of alveolitis

How to treat fibrosing alveolitis? For 30 years, treatment approaches have remained unchanged and are based on anti-inflammatory therapy. For this purpose, basic drugs are used - glucocorticosteroids And cytostatics , Sometimes immunosuppressants .

How effective are these drugs? In most patients, they do not have a significant effect on their life expectancy. However, in 40% of patients, treatment with corticosteroids leads to improvement, and combined treatment with cytostatics significantly increases the effectiveness and allows reducing drug doses. There are no universal treatment regimens and an individual approach is required in each case.

The doctors

Medicines

Corticosteroids

Corticosteroids used . The mechanism of the anti-inflammatory action of the drug is multifaceted. It suppresses the release of inflammatory mediators and reduces vascular permeability. In addition, it reduces the sensitivity of receptors to inflammatory mediators. Its immunosuppressive effect is also important - it reduces the production of antibodies, prevents the migration of lymphocytes and blocks the synthesis of interferons. The clinical effect is manifested by a decrease in inflammation and swelling of tissues, suppression of the development of connective tissue.

The drug is prescribed at 1.0-1.5 mg per kg of body weight per day (or its equivalent in an equivalent dose) for the first 4 weeks. If improvement is noted, then over the next 3 months the dose is reduced to 0.5 mg and gradually reduced to 0.25 mg per kg of weight over 6 months - this is the minimum period of treatment. Most often, the entire dose is prescribed in the morning after breakfast. Treatment with GCS is effective in only 15–20% of patients. The main mechanisms of action of corticosteroids are: suppression of migration of neutrophils and monocytes into the lung tissue, suppression of the release of cytokines and suppression of the immune response.

Cytostatics

If, despite treatment with sufficiently high doses of corticosteroids, a deterioration in clinical and functional parameters occurs, the issue of prescribing cytostatics - second-line drugs - is decided.

From this group they are most often used . The main mechanism of its action is blockade of DNA synthesis, suppression of the number of lymphocytes (T- and B-lymphocytes, the proliferation of which is one of the components of the immune response) and antibody synthesis. It is prescribed at a dose of 2-3 mg per kg of weight (maximum daily dose 150-200 mg). Treatment begins with 25 mg, increasing by 25 mg every two weeks to the maximum dose.

From the group of cytostatics can be prescribed . Its effect is expressed in a decrease in the number of lymphocytes. The drug suppresses the proliferation of predominantly B-lymphocytes, which are involved in the immune response. Prescribe 2 mg per kg of weight (the maximum dose is also 150 mg per day). The prescription regimen is the same as the previous drug: from the minimum dose to the maximum.

With rapid progression, intravenous courses are effective 250 mg (pulse therapy) every 6 hours or administration cyclophosphamide 2 mg/day for 3–4 days in a row.

, compared to the latter drug, has less immunosuppressive effect, but has a stronger anti-inflammatory effect. The effectiveness of treatment with cytostatics is assessed after 3 months.

Immunosuppressants

Treatment with cytostatics requires mandatory monitoring of blood leukocytes and platelets. If their level decreases, treatment is either suspended or the dose is reduced by 50%. The degree of recovery of leukocytes and platelets is monitored weekly. If their quantity is not restored, cytostatics are canceled until the blood composition normalizes.

In addition to the negative effect on the blood, has a pronounced hepatotoxic effect. Therefore, patients are determined monthly transaminases . If their level exceeds the norm by 3 times, treatment is suspended or the dose of the drug is reduced. Upon admission Cyclophosphamide Hemorrhagic cystitis may develop, so patients are advised to drink plenty of fluids and check their urine test twice a month. During the entire treatment period, in addition to monitoring clinical and biochemical blood tests, the patient is subjected to spirometry once a month.

Treatment of exogenous allergic alveolitis

The principles of treating EAA of any form are the same, but the main point is elimination of the allergen. If contact is maintained, there is a risk of developing an irreversible chronic disease. This is why early diagnosis is important so that progression can be prevented.

The use of systemic corticosteroids remains the only treatment method. In acute cases, a dose of prednisolone of 0.5 mg per 1 kg of weight is sufficient, which is recommended for 3-4 weeks. According to the treatment regimen, for subacute and chronic allergic alveolitis, the dose increased to 1 mg per kg of weight and prescribed for up to 2 months. Then gradually reduce to 5-10 mg per day. The drug is discontinued when improvement is achieved, as well as if there is no effect. The possibilities of inhaled use of corticosteroids have not been sufficiently studied.

If there is no effect, it is prescribed D-penicillamine And Colchicine . Successful treatment results have been obtained in animal models Cyclosporine .

Consequences and complications

At the stage of development of emphysematous bullae, a complication is pneumothorax when swollen pulmonary acini spontaneously burst. Pneumothorax can recur several times and be complicated by infection, which requires mandatory hospitalization.

As the disease progresses, respiratory failure increases, cor pulmonale develops, and this condition becomes more complicated pulmonary edema . These serious complications and are the cause of death of patients.

Forecast

Early detection of the disease and the prescription of glucocorticoids and cytostatic agents increases the effectiveness of treatment and improves the prognosis. Therefore, an important task is early diagnosis, which is possible with working together therapist, pulmonologist and radiologist. However, the survival rate of patients from the moment of diagnosis is 3-4 years. According to one study, 50% of patients die within 5 years. The prognosis is more favorable in women, young patients and with a short duration of the disease (less than one year).

Allergic and toxic alveolitis have a more favorable course, which, when the provoking factor (occupational, household or environmental) is eliminated in the early stages, can regress. With adequate and timely treatment, long-term remission is achieved and the disease does not progress.

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