Lesions of the respiratory organs of a non-inflammatory nature. Pulmonary edema in dogs and cats

Lung diseases in animals are subdivided depending on the nature of the disease into non-inflammatory and inflammatory diseases. Non-inflammatory include hyperemia and pulmonary edema, emphysema, and inflammatory - pneumonia and gangrene of the lungs.
emphysema can be alveolar and interstitial, and pneumonia, according to Domrachev's classification, are divided into lobar (croupous) and lobular (bronchopneumonia, atelectatic, hypostatic, metastatic).

Hyperemia and pulmonary edema - a disease characterized by overflow of blood vessels and sweating of blood plasma into the alveoli and interalveolar tissue.
The cause of active hyperemia and pulmonary edema is sun and heat stroke, hard work in the hot season, inhalation of irritating gases, and the passive cause is heart failure, chronic intoxication in lung diseases and other diseases.

Bronchopneumonia - an animal disease characterized by the development of an inflammatory process in the bronchi and alveoli and sweating of catarrhal or catarrhal-purulent exudate into the latter. The disease is seasonal, occurring mainly in the late autumn and early spring months. The occurrence of the disease is due to a number of factors. Most often, it occurs due to an unfavorable microclimate: the content of elevated concentrations of ammonia, hydrogen sulfide in the indoor air, strong microbial or dust pollution, the presence of drafts, high humidity, etc. The conditionally pathogenic microflora of the respiratory tract plays an important role in the onset of the disease, which, with a decrease in the body's natural resistance may be the main etiological factor. Vascular disorders in the lungs, allergic factors, suppression of the protective mechanisms of the respiratory system play a significant role in the development of the disease.

Croupous pneumonia (Pneumonia cruposa) - acute fibrinous inflammation, capturing entire lobes of the lung, with severe symptoms of allergy and typical changes in the stages of the fibrinous inflammatory process. The disease is diagnosed mainly in horses, less often in other animal species. Recently, most researchers consider croupous pneumonia as a disease of allergic origin, namely, as hyperergic inflammation in a previously sensitized organism or sensitized lung tissue. Allergens in this case are respiratory tract microorganisms, and irritating gases, hypothermia, injuries, etc. can act as resolving factors. In this case, pneumonia in a sensitized animal develops as a result of exposure to factors of non-antigenic origin (heteroallergy). In addition, microorganisms, both participating in sensitization and not participating in it (paraallergy), can be resolving factors. The development of croupous pneumonia occurs in four stages.

First stage - active hyperemia or tide - characterized by blood damming of the pulmonary capillaries; the epithelium covering the alveoli swells and exfoliates, liquid exudate accumulates in the alveoli with an admixture of leukocytes and a large number of erythrocytes. There is much less air in the affected area than in the healthy one, and by the end of the stage it is completely forced out of the alveoli. The tide stage lasts from several hours to a day.
Second stage - red hepatization - lasts 2-3 days. At this stage, the filling of the alveoli with exudate containing erythrocytes and fibrinogen continues. Then the exudate coagulates, as a result of which the alveoli and bronchioles of the affected area are filled with clotted fibrin with an abundant admixture of erythrocytes, deflated epithelium and a small amount of leukocytes.
At the third stage - stages of gray hepatization - the migration of leukocytes begins. The number of erythrocytes gradually decreases, and the number of leukocytes increases. Under the influence of leukocyte enzymes, fibrin and other components of the exudate are destroyed and take on a gray color. The duration of this stage is 2-3 days.
Fourth stage - resolution stage - characterized by the fact that with an increase in the number of leukocytes, the exudate is split and liquefied and thus acquires the ability to be absorbed. Exudate liquefaction is based on processes occurring under the influence of lipolytic and proteolytic enzymes of leukocytes. Under their influence, fibrin is converted into soluble albumoses and amino acids (leucine, tyrosine, etc.). Liquefied exudate is partially absorbed, partially removed with sputum when coughing. Most of the absorbed exudate is excreted in the urine. Air gradually enters the alveoli released from the exudate, at the same time the regeneration of the alveolar epithelium occurs. The duration of the stage is from 2 to 5 days.
At autopsy of animals that died from bronchopneumonia, inflammatory foci of various sizes are found in the lungs, painted in red-brown, gray-red or gray-white, rising above the surface of the lung. The bronchi contain mucous or mucopurulent exudate. In a chronic course, fibrous fusion of the pulmonary pleura with the costal, and often with the pericardium, is found;
Pathological changes with croupous pneumonia depend on the stage of development of the disease. At the stage of the tide, the lung is plethoric, increased in size. The cut surface is smooth and shiny. At the stage of red hepatization, the affected part of the lung is without air, enlarged, resembles a liver on a cut, sinks in water. The cut surface is red, granular, due to the fact that the alveoli are filled with clotted fibrinous exudate and protrude above the cut surface. At the stage of gray hepatization, the lung initially has a gray tint, and at the resolution stage it acquires a yellowish color. Along with the above staged changes, an increase in bronchial lymph nodes and degeneration of parenchymal organs can be detected. At the resolution stage, the lung resembles the spleen in consistency.
Symptoms in acute alveolar emphysema, they are manifested by severe shortness of breath, horn-shaped expansion of the nostrils during inhalation and protrusion of the anus during exhalation. On auscultation, weakened vesicular breathing is heard, and if the cause of emphysema is bronchitis, wheezing is established. The posterior border of the lungs is pushed back by 1-2 ribs, the percussion sound is boxy.
In chronic alveolar emphysema, expiratory dyspnea is well expressed, exhalation is biphasic. The chest is barrel-shaped. When exhaling, retraction of the intercostal spaces is noted, and an ignition groove is formed along the costal arch. With auscultation, depending on the origin of emphysema, wheezing or weakening of vesicular breathing is established, and with percussion, an increase in the boundaries of the lungs and a boxed percussion sound.
Interstitial emphysema is acute and develops rapidly. It is characterized by rapidly increasing shortness of breath, increased heart rate. On auscultation, weakened vesicular breathing and crepitant rales are heard. When air penetrates under the skin, a crepitus noise is detected.
Hematological examination in horses can detect an increase in the number of red blood cells and hemoglobin.
The first symptoms of bronchopneumonia are characterized by depression of the animal, general weakness, body temperature usually rises by 1-2 ° C, scanty serous-mucous or muco-purulent outflow is observed from the nasal cavities. Shortness of breath is usually mixed. The mucous membranes are cyanotic. Breathing shallow, rapid, tachycardia. During auscultation of the chest, hard vesicular breathing, fine bubbling rales are heard, sometimes bronchial breathing can be heard. Percussion - foci of dullness. Cough at first dry, painful, later becomes wet and less painful.
In a hematological study in patients with bronchopneumonia, neutrophilic leukocytosis is established with a shift of the nucleus to the left to myelocytes, lympho- and eosinophilia, monocytosis, a decrease in acid capacity, blood serum, an acceleration of ESR, a decrease in hemoglobin.
Croupous pneumonia begins suddenly. The onset of the disease is characterized by rapidly appearing oppression of the animal, refusal to feed, increased thirst. With slight movement, shortness of breath and a painful cough appear. The temperature rises to 41-42 ° C and stays at this height for 6-8 days with slight daily fluctuations, i.e. the type of fever is constant. In its clinical manifestation, three stages are distinguished: hyperemia, hepatization and resolution. A typical symptom of croupous pneumonia at the onset of the disease is a discrepancy between an increase in body temperature and an increase in heart rate. If the temperature rises by several degrees, then the pulse during this period is accelerated by 10-15 beats. High temperature usually lasts until the end of the hepatization stage (6-8 days), and then either drops to normal within 12-36 hours (crisis), or reaches normal gradually over 3-6 days (lysis). Visible mucous membranes are icteric, sometimes lemon-yellow. These phenomena are soon joined by symptoms specific to croupous pneumonia, which vary depending on the stage of the disease.
During percussion at the first stage, a tympanic sound is established in the affected lobe, which during the period of hepatization becomes dull and dull. The bluntness can be of different sizes, its borders have a different shape, but the upper border is always arched upwards. At the stage of resolution, the percussion sound acquires a tympanic shade, and as the normal state of the lung tissue is restored, it becomes clear, atympanic.
During auscultation at the stage of hyperemia, increased vesicular breathing is first detected, and by the end of the stage, fine bubbling rales are heard in the inspiratory phase. With the development of the stage of hepatization, wheezing disappears, a gradual disappearance of vesicular and the appearance of bronchial breathing is established, sometimes breath sounds in the lesion are not heard at all. At the resolution stage, rough, moist rales are heard, which become more and more numerous and drown out bronchial breathing. Then the sonority of wheezing gradually decreases, bronchial breathing weakens and turns into normal vesicular noise.
A characteristic symptom of croupous pneumonia is the appearance at the stage of hepatization of a saffron-yellow or rusty-brown discharge from the nose. It is observed before the start of the resolution stage.
Certain changes in croupous pneumonia are noted in the activity of the cardiovascular system. The pulse is quickened from the very beginning of the disease, but this increase is not proportional to the increase in body temperature (the temperature rises by 3-4 ° C, and the pulse quickens by 10-15 beats). This discrepancy is typical for the initial stage of the disease. Heart sounds are usually loud, clear, the 2nd tone is often accentuated. A significant increase in heart rate, its weakness and arrhythmia with a sharp drop in blood pressure indicate developing cardiovascular insufficiency. It should be noted that the degree of cardiac dysfunction is usually directly proportional to the degree of damage to the lung tissue.
Croupous pneumonia is also accompanied by functional disorders in the activity of the urinary and digestive systems. In the blood, neutrophilic leukocytosis, lymphopenia, eosinopenia, and an increase in ESR are detected.
Diagnostics diseases of animals with hyperemia and pulmonary edema are carried out on the basis of anamnesis and clinical manifestations. In differential terms, one should keep in mind heat stroke, poisoning and intoxication.
Diagnosis of emphysema put on the basis of the anamnesis and characteristic clinical symptoms (progressive dyspnea, cyanosis of the mucous membranes, two-phase inspiration, horn-shaped expansion of the nostrils, the presence of an ignition groove, a boxed percussion sound), and with interstitial - a very rapid development of the disease, crepitating wheezing, the presence of subcutaneous emphysema in the neck , chest, back. Emphysema should be differentiated from pneumonia and pleural diseases (pleurisy, hydrothorax and pneumothorax).
When diagnosing bronchopneumonia take into account the data of anamnesis, clinical manifestations, laboratory tests. It is necessary to exclude infectious and parasitic diseases that occur with respiratory syndrome, as well as croupous pneumonia and other lobular pneumonia.
The disease of animals with croupous pneumonia is diagnosed taking into account the analysis of anamnestic data (suddenness of the disease), characteristic clinical signs (permanent fever, saffron-yellow fibrinous outflow from the nasal cavities, staging of the development of the disease, damage to the entire lobe of the lung with an upper arcuate line), laboratory blood tests. In differential diagnosis, infectious diseases such as contagious equine pleuropneumonia, peripneumonia in cattle, swine influenza, etc., should be excluded.
Treatment animals suffering from pulmonary congestion should be urgent. To prevent the development of pulmonary edema, bloodletting is done (0.5-1% of body weight). Intravenous administration of a 10% solution of calcium chloride 100-150 ml or intramuscular injection of calcium gluconate 40-50 ml in a 10% solution is indicated, hypertonic solutions of glucose, sodium chloride can be administered intravenously. At the same time, cardiac preparations are administered to the animal, rubbing of the chest is carried out. Good results are obtained from novocaine blockade of stellate or lower cervical sympathetic nodes.
In the treatment of animals with alveolar emphysema of the lungs, to reduce shortness of breath, it is also recommended to use sedatives, such as chloral hydrate (30.0-40.0 g) with a mucous decoction in the form of small enemas, bromine preparations inside (10.0-30.0 g 3-4 times a day) or intravenously 10% solution, at a dose of 100-150 ml per week for horses. For the same purpose, a 0.1% solution of atropine or a 5% solution of ephedrine is administered subcutaneously daily for 5-7 days (horses 10-15 ml per injection), eufilin 0.1-0.2 g is used orally appointment. Treatment of patients with interstitial emphysema is to provide them with rest, the use of cardiac drugs, antitussive drugs, as well as solutions of atropine or ephedrine.
The highest efficiency in the treatment of animals with bronchopneumonia is obtained with timely initiation of complex therapy for patients with an acute course of the disease. First of all, it is necessary to create optimal conditions for feeding and keeping animals. Of the means of etiotropic therapy, antibiotics are prescribed, taking into account the sensitivity of the microflora of the respiratory tract to them. Antibiotics are preferably used in combination with sulfonamides. The latter are administered orally, and soluble salts of sulfonamides can also be used intravenously. Antibacterial drugs can also be administered in the form of aerosols. For this purpose, antibiotics are used, which are administered on average at 400,000-500,000 U / m3, iodinol - 2 ml / m3, camphor serum according to Kadykov - 15 mg / m1, etc. From the means of pathogenetic therapy, non-specific stimulating drugs are used (gamma- globulins, nonspecific polyglobulins, hydrolysin, hemotherapy), regulating neurotrophic functions (novocaine blockade of the stellate ganglion or splanchnic nerves and sympathetic trunks according to Shakurov), antiallergic and symptomatic agents.
Treatment of animals with lobar pneumonia begins with their isolation. At the first stage of the disease, in order to reduce pulmonary congestion, it is recommended to carry out bloodletting (in horses 2-3 liters), antibiotics and sulfonamides are used from antibacterial agents. Before use, the most active drug is determined by the sensitivity of the microflora of the respiratory tract to it. The most commonly used antibiotics are such drugs as penicillin, streptomycin, tetracycline, oxytetracycline, and of the new ones - cephalosporins, aminoglycosins, hipols. Antibiotics are used 3-4 times a day for 8-10 days, in doses depending on the type of animal and its weight. Of the means of pathogenetic therapy, antiallergic drugs are used (diphenhydramine, sodium thiosulfate, sodium chloride, suprastin, pipolfen, etc.), novocaine blockade of the stellate or lower cervical sympathetic ganglion, rubbing the chest with irritating ointments, cupping, etc. From symptomatic therapy, they use cardiac, expectorant, diuretic.
Warning diseases of animals with hyperemia and pulmonary edema lies in the organization of the correct mode of operation, protection from overheating, inhalation of irritating and poisonous gases. Preventive measures for the occurrence of pulmonary emphysema are also non-specific and are aimed at proper operation and especially the timely and complete treatment of bronchitis.
Prevention diseases of animals with bronchopneumonia should include a complex of economic, zootechnical and veterinary measures. It is necessary to constantly monitor the microclimate of premises for animals, a balanced diet for all major nutrients and vitamins, especially for vitamin A. the principle "everything is empty - everything is busy", etc.). Of the means of pharmacotherapy, drugs are used that increase the natural resistance of the body, including physiotherapy agents (aeroionization, ultraviolet irradiation).

Theme Target

To study the pathomorphology of lung atelectasis, pulmonary emphysema, edema and pneumonia, pleura and their differential diagnosis.

The focus is on the following issues:

Definition of the concepts of atelectasis, emphysema, edema, pneumonia, pleurisy. Etiology.
Types of lung atelectasis and morphological characteristics.
Types of emphysema, macro - micro pictures.
Pulmonary edema. Morphological characteristics of edema.
Types of pneumonia. Brief morphological characteristics of serous, catarrhal, fibrinous, purulent and other pneumonias.
Morphological characteristics of pleurisy.

Respiratory diseases occur under the influence of various biological pathogens (viruses, bacteria, mycoplasmas, helminths, etc.), physical and chemical elements entering the respiratory tract and lungs from the external environment or with lymph and blood. The predisposing role is played by hereditary, age and acquired features of the body. Of the protective barriers of the respiratory system, one should take into account the state of aerodynamic filtration (mucocellular transport system), humoral and cellular factors of general and local protection. With all the variety of clinical and morphological manifestations of respiratory diseases, they all have a non-inflammatory (atelectasis, emphysema, tumors), inflammatory (rhinitis, bronchitis, tracheitis, bronchiolitis, pneumonia) or allergic nature. The pathology of the respiratory organs includes narrowing - stenosis of the nasal passages, inflammation of the nasal mucosa - rhinitis of various etiologies, stenosis or expansion, inflammation of the larynx - laryngitis, inflammation of the trachea - tracheitis and bronchial tubes - bronchitis. Most often in animals, the lungs are affected. The pathology of a non-infectious nature includes atelectasis - collapse, emphysema - expansion, collapse or airless state of the lungs.

Lung atelectasis

Lung atelectasis refers to the collapse of the lungs, their airless state.

It can be congenital or acquired, general and local.

congenital atelectasis observed in stillborns or in animals in the first days after birth, when air does not enter individual lobules, and the alveoli remain unexpanded, collapsed. As a rule, congenital atelectasis is observed in underdeveloped newborn animals, more often in pigs.

Acquired atelectasis occurs in the lungs, which were previously in a normal state.

Compression atelectasis- collapse of the pulmonary alveoli as a result of their compression during the accumulation of exudate, edematous fluid, air in the pleural cavity, or during the formation of tumors. Air does not normally enter the compressed areas of the lung.

In neonatal atelectasis and obstructive lesions, the areas are sharply delineated, as they correspond exactly to the anatomical boundaries of the pulmonary lobules served by the occluded bronchi. With compression atelectasis, the collapse covers large areas, and sometimes the entire right or left lung. Areas of atelectasis are reduced in volume (collapsed), sometimes significantly sunk relative to the total surface of the lung. They are dense, dark red in color, the cut surface is dry, a piece of the lung sinks in water, the pleura is wrinkled. By these signs, atelectasis differs from bronchopneumonia, in which the affected areas of the lung are also dense, reddened, usually protruding above the general surface of the lung, and wet on the cut, columns of catarrhal exudate stand out from the bronchi. When the causes of the disease are eliminated, the lung function is restored, but in the case of chronic pelvic ateliers, the alveoli of the connective tissue may become overgrown. This condition is called pneumofibrosis.

Emphysema

Emphysema is an overflow of the lungs with air. The reason for the development of emphysema may be a heavy load with a fast ride in horses, in hunting dogs; with microbronchitis, asphyxia, weakening of cardiac activity, pneumonia, etc.

Distinguish between alveolar and institial emphysema. With the first, air accumulates in the alveoli, with the second, it is in the interstitial tissue and under the pleura.

Alveolar emphysema can be acute and chronic, cover the entire lung or its individual parts (lobular form).

The lung in acute alveolar emphysema is enlarged, pale colored, fluffy, makes a crunchy sound (crepites) when touched, a piece of the lung easily floats in water like foam, the cut surface is bloodless. Under the microscope, the alveoli are stretched, the walls are thinned (pressure atrophy), the capillaries are narrowed, and contain few red blood cells. The essence of the process of excessive stretching of the lungs in emphysema is that when the body's need for oxygen increases, inhalation has more power, more volume of inhaled air than during exhalation. Therefore, in the etiology of emphysema, especially acute, a large role belongs to hard work with stress in horses, long-term rapid transportation of cattle to a meat processing plant, hounds during the hunting season, deer during the rut, etc.

Acute lobar emphysema occurs most often as a compensatory process in the lungs adjacent to areas of pneumonia. With long-acting causes, emphysema becomes chronic. Chronic alveolar emphysema is characterized by atrophy of the alveolar septa due to their prolonged stretching, followed by rupture and fusion of individual alveoli into large air cavities. The lungs are strongly swollen and enlarged, pale, fluffy. Enlarged air streaks are visible even to the unarmed Lung, sometimes giving the lungs a spongy appearance on cut (bubbly emphysema). Accompanied by chronic alveolar emphysema, as a rule, hypertrophy of the right ventricle of the heart - a compensatory phenomenon with difficulty in blood circulation through the compressed capillaries of the lung. With decompensation, the right ventricle of the heart expands.

Interstitial emphysema occurs when ruptures of the lung tissue (for example, with a penetrating injury to the lung). Air from the alveoli passes into the interstitial tissue of the lung, spreads through the tissue cracks along the interlobular tissue, under the pleura whole air cords are formed, penetrating the lobes of the lung in the form of a grid. Interstitial emphysema is observed as an agonal condition when cutting the trachea in meat processing plants during the slaughter of animals.

Pulmonary edema

Pulmonary edema refers to the accumulation of edematous fluid in the interstitial tissue and the lumen of the lung alveoli. The causes of edema are mainly venous congestion, cardiac weakness, toxic substances entering the lungs, and an agonal state.

It may have a mechanism of venous congestion with a weakening of cardiac activity or be atonal in nature. May occur as a result of poisoning with toxic poisonous gases.

Morphological changes in pulmonary edema are of the same type, regardless of the cause that caused it. Lungs with edema not sleeping, the pleura is smooth. On palpation, a fossa remains, the consistency is test-like.

The cut surface is smooth, juicy, light red or dark red. With congestive edema, the lungs have a bluish tint. From the surface of the incision, a foamy light or bloody, or cloudy-pink liquid flows or is squeezed out. With serous-inflammatory edema, gelatinous strands of interstitial connective tissue are clearly visible. Pieces of the lung, lowered into the water, float heavily, most of them are immersed in water.

Under the microscope, hyperemia of blood vessels is visible. With serous inflammatory edema, hyperemia is expressed in the respiratory capillaries. With congestive edema, the capillaries of the interalveolar septa and veins of the interlobular connective tissue are dilated and crowded. Especially small veins. In the alveoli - air and transudate, in the bronchi - liquid with air bubbles. There are few cellular elements in the transudate. With serous-inflammatory edema, serous exudate accumulates in the alveoli. Perivascular, peribronchial connective tissue is swollen, collagen fibers are thickened.

Dropsy of the chest cavity

Dropsy of the chest cavity - hydrothorax. The reason is congestion in the vessels due to compression by tumors or inflammation of the lungs.

Pleurisy

Inflammation of the pleura as a result of hypothermia, trauma to the chest wall, infection, the transition of inflammation from the lungs - pleuropneumonia.

Primary develop when the chest cavity is damaged, with bacteremia. More often there are secondary pleurisy in pneumonia, pericarditis, when the inflammatory process passes to the pleura.

Pleuropneumonia is therefore observed in such serious diseases as epidemic pneumonia in cattle, contagious pleuropneumonia of horses, and also in pulmonary tuberculosis (cattle pearl oyster). Pleurisy is most often found in cattle and pigs due to the looser specific structure of the pleura and the abundance of lymphatic vessels in it. They usually proceed according to the type of exudative inflammation and can be divided into serous, serous-fibrinous, purulent and hemorrhagic. In all cases, the pleura swells, grows dull, hyperemic, and banded hemorrhages appear on it. The lungs are compressed, breathing becomes difficult, it becomes, coughing increases, cardiac activity is difficult. There is intoxication of the body, dystrophy in parenchymal organs, temperature appears. In the acute course of pleurisy, the exudate can resolve and the pleura is restored. With a protracted course of pleurisy, adhesions (synechia) form between the pulmonary and costal pleura, and sometimes the pleural strip is overgrown in significant areas or completely (adhesive pleurisy). Specific productive pleurisy is characterized by the formation of specific tuberculous, actinomycosis granulomas on the pleura. They can also be with glanders, aspergillosis and coligranulomatosis.

Pleurisy is also divided by origin, course, type of exudate. In acute pleurisy, the exudative process predominates, and in chronic pleurisy, the proliferation of connective tissue and the development of adhesions. More often there are pleurisy of the exudative type.

With serous pleurisy, a cloudy liquid with fibrin flakes is determined in the pleural cavity. The pleura is dull, hyperemic, with hemorrhages, swollen. Such changes can be either diffuse or focal.

With fibrinous pleurisy, fibrin is visible in the form of grayish-white films on the pleura. In fresh cases, the films are easily separated; in chronic cases, fibrinoid overlays grow into connective tissue. The surface of the overlays is rough, after their removal, a dull, hyperemic pleura is visible, with hemorrhages.

Rice. 189. Fibrinous pleurisy in a sheep.

With purulent pleurisy, pus is found in the cavity and on the surface of the pleura. The pleura is dull, swollen, hyperemic. Visible hemorrhage, erosion. Chronic pleurisy is characterized by the formation of adhesions (senechia). Productive pleurisy develops in infectious diseases (tuberculosis, glanders, actinomycosis, etc.). In this case, typical changes are formed on the pleura with signs characteristic of these diseases.

Rice. 190. Ulcers in the lungs of a ram.

Exudative pneumonia is serous, catarrhal, fibrinous, purulent, hemorrhagic, ichorous and mixed.

At serous pneumonia the lung is compacted, red in color, the pleura is smooth, edematous, vitreous, a large amount of slightly cloudy liquid flows from the cut surface of the damaged area

Catarrhal bronchopneumonia. According to the size of the affected areas, catarrhal pneumonia can be lobular and lobar. At first, only individual lobules are affected, but as the process develops, the inflammation becomes lobar.

In acute catarrhal bronchopneumonia, the affected area of the lung is red in color, compacted (testy) in consistency, resembling the spleen (splenization). Muddy liquid is squeezed out from the incision surface, and viscous mucus is squeezed out of the bronchi.

In chronic catarrhal bronchopneumonia, the lung is dense, fleshy, similar to the pancreas, often bumpy on the surface and granular on the cut. On a red background, serous foci and veins of various shapes are visible, in the middle of them a lumen of the bronchus is noticeable. In pigs, the lung is often white, dense, similar to fat (sebaceous pneumonia). A purulent mucous mass is squeezed out from the surface of the incision from the bronchi.

Fibrinous (croupous) pneumonia- severe inflammation of the lungs in farm animals.

With her, the lobarity of the lung lesion from the very beginning. Marbling of the drawings of the affected areas both from the surface and in the section. Some lobules are red, others are gray, and others are yellowish (this color gives the organ a marbling pattern). The strands of interlobular connective tissue are sharply dilated. Lymphatic vessels gape. Thrombosis and embolism are seen. Fibrin plugs can be removed from the bronchi and alveoli. Often the process passes to the pleura and fibrinous pleurisy is noted.

Rice. 191. Inflammation of the right lung of the lamb: catarrhal - anterior and middle lobes;
Fibrinous-necrotic - posterior lobe.

Fibrinous, croupous pneumonia is characterized by:

The formation of fibrinous exudate and dryness of the incision surface;

Lobar lesion;

The spread of the process along the lymphatic pathways of the lungs, i.e. along the interstitial connective tissue, where the lymphatic vessels are located:

The staging of the development of pneumonia;

In a number of diseases, the slow development of inflammation and the non-simultaneous involvement of individual lobules, therefore, a motley (marble) pattern of the lung is characteristic.

First stage- hyperemia, rush of blood. Expressed vascular reaction, inflammatory hyperemia. All vessels are sharply dilated and filled with blood. The capillaries of the lung septa are tortuous, kidney-shaped protrude into the cavities of the alveoli. The affected areas are dark red, soft consistency. There is no exudate in the alveoli yet.

Second stage red hepatization (hepatization). Hyperemia is pronounced, alveoli and small bronchi are filled with exudate. It contains fibrinogen, which turns into fibrin in the alveoli, as well as a lot of red blood cells, an admixture of neutrophils and desquamated cells of the epithelium of the alveoli and bronchi (alteration component). Alternative processes are also manifested by a change in collagen bundles in the stroma of the lungs, their expansion and defibration. Vessel thrombosis and the development of necrosis as a result of this are pronounced.

Rice. 192. Fibrinous-necrotic pneumonia in a sheep.

Proliferative processes are detected in the form of infiltration with fibrinous-cellular exudate of the stroma of the lung. The lung takes on the consistency of the liver (hepatization), thickens. The color of the affected areas is red.

Third stage gray hepatization or gray hepatization. Vessels squeezed by alveoli filled with exudate collapse. Hyperemia subsides. In the exudate, the number of leukocytes increases, the enzymes of which contribute to the dissolution of fibrin. The affected areas remain dense, but acquire a grayish, gray-yellowish color.

Fourth stage permissions. It comes in three forms:

Yellow hepatization, when, under the influence of leukocyte enzymes, fibrin is absorbed, the alveoli are released from exudate. Lung areas are yellowish in color.
carnification. At the same time, fibrin is resorbed and the alveoli are overgrown with connective tissue. Lung areas take on the appearance of meat.
Sequestration. In this case, the areas of pneumonia are necrotic and encapsulated.

With fibrinous pneumonia, pieces of the lung, lowered into the water, sink (sink) to the bottom.

The non-simultaneity of the development of stages in different lobules of the lung gives the inflamed areas a marble pattern specific to this type of inflammation. The resemblance to a marble pattern is increased by a strong swelling of the interlobular septa, which are especially pronounced in the form of grayish gelatinous stripes in the lungs of cattle and pigs.

The outcome of lobar pneumonia depends on the degree of filling of the alveoli and the associated circulatory disorders. Yellow hepatization can occur with the cleansing of the alveoli from fibrin and the restoration of their function, or carnification, characterized by the germination of fibrin by connective tissue and blood vessels, as a result of which the pneumonic areas resemble meat in color and consistency. This is observed with a delay in the resorption of fibrin, when the affected areas of the lungs, overgrown with connective tissue, can no longer return to normal. The outcome in the form of sequestration is associated with the necrosis of the inflamed areas, their separation from the surrounding tissue. This occurs in severe croupous pneumonia, when fibrin accumulates in the alveoli in such an amount that the blood circulation in them stops, the lymphatic vessels often undergo thrombosis. Melting of the dead area of the lung occurs at its border with living tissue, and a connective tissue capsule often develops here. At autopsy, the sequester can be completely removed and the anatomical structures of the lung can be distinguished in it. The outcome in sequestration is sometimes observed in cattle with epidemic pneumonia.

Purulent inflammation it is expressed by the formation of abscesses of various sizes in the lungs (abscessing pneumonia) or catarrhal-purulent diffuse inflammation. Abscesses in the lungs can form on their own or as a complication of a particular inflammation. They are of different sizes, consist of accumulations of purulent bodies, colonies of pyogenic microorganisms and neutrophilic leukocytes in varying degrees of degeneration. Often, abscesses are also enclosed in a capsule, which consists of an inner (pyogenic) and outer (fibrous connective tissue) layers.

The lung is not collapsed, sharply hyperemic, with multiple hemorrhages; purulent-softened areas of various sizes of gray-yellow and yellow color clearly appear on the surface of the cut. A thick mucopurulent mass is squeezed out of the bronchi.

Hemorrhagic pneumonia characterized by the predominance of a large number of red blood cells in the exudate. It is observed in a number of infectious diseases (anthrax, swine fever), which occur with a violation of the integrity of the walls of blood vessels and the death of red blood cells. The interstitial connective tissue is saturated with erythrocytes, becomes dark red. Histologically, a mass of erythrocytes is observed in the alveoli.

The affected area is light dark red in color, flabby in consistency, dark red liquid is squeezed out from the cut surface. Interlobular tissue is also dark red, edematous.

The outcome of such pneumonia is usually fatal, and in the best cases, small necrotic areas are encapsulated.

Differential Diagnosis

For pleurisy, the distinguishing feature is the state of the pleura: it is dull, swollen, hyperemic, on its surface there may be threads or fibrin deposits, hemorrhages.

Differentiate pleurisy from post-mortem accumulation of cadaveric transudate, hypostasis, dropsy of the chest cavity. Cadaveric transudate is a clear, watery, reddish or dark red liquid. There is more of it in the half on which the corpse lay. With hypostases of the pleura, hyperemia of the vessels is expressed on the side of the lying corpse, and on the opposite side the pleura is pale. In slaughtered animals, the pleura is anemic on both sides. With dropsy, the liquid is colorless or slightly colored. The pleura is smooth, pale, shiny.

Serous pneumonia is differentiated from pulmonary edema. Edema is characterized by diffuse damage to the lung, when entire lobes or the entire lung are covered. Hyperemia is weakly expressed, in the trachea and bronchi - foamy liquid. The stroma of the organ is not edematous. With serous pneumonia, a cloudy exudate is released from the cut surface, the stroma is thickened, gelatinous.

Catarrhal bronchopneumonia is differentiated from atelectasis. With atelectasis, the cut surface of the lung is dry, there is no discharge from the bronchi. In case of catarrhal bronchopneumonia, a bloody fluid flows from the incision surface, plugs of the mucosal turbid mass are released from the bronchi. With fibrinous pneumonia - fibrin plugs.

test questions

Lung atelectasis, types, causes, morphological features.
Pulmonary edema, its symptoms.
Emphysema, types. Morphological features.
Pneumonia and bronchopneumonia. What is the difference? Kinds.
Morphological characteristics of catarrhal bronchopneumonia and fibinous pneumonia.
Differential diagnosis of respiratory diseases.

Museum preparations

Wet preparations:
pneumonia N 190, 187, 170, 37, 12, 10, 11;

emphysema N171.
Histopreparations:
serous pneumonia N 56;

catarrhal bronchopneumonia N 57c;

fibrinous pneumonia N 66a, 666;

purulent pneumonia N 70a;

emphysema N 10.84;

edema and congestive hyperemia of the lungs N 446/50.

Literature

Pain K.G., Pain B.K. Fundamentals of pathological anatomy of page - x. animals. - M.: Selkhozizdat, 1954.
Kokurichev P.I. Atlas of pathological anatomy of page - x. animals. - M.: Kolos, 1973. S. 16-20, 32-63, 42, 77-79.
pathological anatomy of animals page - x. animals / Ed. Shishkova V.P. -M.: Kolos, 1980.
Pichugin L.M., Akulov A.V. Workshop on pathological anatomy of page - x. animals. -M.: Kolos, 1980. S. 100-102, 105, 110-112, 126, 198.
Shishkov V.P., Zharkov A.V., Naletov N.A. Autopsy and pathoanatomical diagnosis of diseases of page - x. animals. - M.: Kolos, 1982.
Smerdova M.D. Workshop on pathological anatomy of page - x. animals. - Krasnoyarsk: KrasGAU, 1994. S. 88-90, 92-93, 98-99, 101, 108, 115, 123, 120-130.
Zharov A.V. pathological anatomy of animal animals. – M.: 1995.

Pulmonary edema is a pathological condition in which there is an accumulation of fluid and electrolytes in the interstitial space (interstitium) of the lungs and / or in the pulmonary alveoli. Depending on the cause that caused respiratory failure, cardiogenic and non-cardiogenic pulmonary edema in animals is distinguished.

Cardiogenic pulmonary edema develops with left-sided heart failure (most often mitral valve insufficiency). Due to valvular insufficiency, the ejected blood backs up into the heart (regurgitation). Increased pressure in the left side of the heart leads to congestion of venous blood in the lungs and increased fluid extravasation into the interstitium and alveoli.

Non-cardiogenic pulmonary edema- swelling caused by any other reasons. This type of respiratory failure is caused by an increase in the permeability of the pulmonary vessels (with cardiogenic edema, the hydrostatic pressure in the vessels increases, and not their permeability).

Causes of non-cardiogenic pulmonary edema in cats and dogs:

1) Neurogenic edema - electrical trauma, craniocerebral trauma, convulsions.

2) Inflammatory edema - infectious and non-infectious diseases.

3) Reduced levels of albumin in the blood, leading to a decrease in plasma oncotic pressure - gastrointestinal disorders, liver disease, glomerulopathy, overhydration, starvation.

4) Toxic edema - various ways of penetration of toxic substances into the body, for example, inhalation of carbon monoxide, snake bite, poisoning, uremia, etc.

5) Allergic reactions, anaphylaxis.

6) Sepsis.

7) Neoplasms - obstruction of the lymphatic vessels.

Development mechanism

The general mechanism by which pulmonary edema develops in dogs and cats is a violation of the water exchange between the vessels of the lungs and the lung tissue due to the reasons described above, as a result of which fluid enters the interstitium and alveoli. Increased fluid content in the lung markedly reduces its elasticity and reduces volume. In the alveoli, the presence of fluid leads to the thinning of the surfactant (a substance that prevents the collapse of the lung), the collapse of the lung alveoli and the displacement of air. All this interferes with normal gas exchange in the lungs.

Symptoms

The main symptoms of pulmonary edema in dogs and cats include restlessness, shortness of breath, rapid breathing, cyanosis (cyanosis) of the mucous membranes, abdominal breathing with an open mouth. At the beginning, the animals take a forced posture, stand with their limbs wide apart. Then, as the pathology worsens, they take a lateral recumbent position. In some cases, expectoration of liquid contents is observed. In severe cases, wheezing can be heard.

Diagnostics

The diagnosis of pulmonary edema in cats and dogs is made on the basis of auscultation (listening) of the chest, as well as an x-ray of the chest cavity. Auscultation can reveal moist rales in the lungs. With cardiogenic pulmonary edema, heart murmurs and rhythm disturbances (eg, gallop rhythm) may be heard. An X-ray image is usually performed in two projections, frontal and lateral. The picture shows a darkening of the pulmonary field, stagnation is traced in large vessels, and small ones are poorly contrasted. In the case of cardiogenic edema, an increase in the cardiac shadow is often observed. With left-sided heart failure, you can see an increase in the left half of the heart. Alveolar edema is characterized by strong compaction of the lung at the base of the heart. If the animal is in critical condition, it is first stabilized and then x-rayed.

Therapeutic measures

If pulmonary edema is suspected, the treatment of dogs and cats is carried out immediately and consists in prompt resuscitation. An animal that can breathe on its own is given oxygen therapy. In the absence of productive respiratory movements, tracheal intubation is performed, followed by aspiration of the contents from the tube and artificial ventilation of the lungs. As a rule, diuretics and corticosteroids are used intravenously. The rest of the treatment depends on the pathology that caused the pulmonary edema. The electrolyte composition of the blood is also monitored by means of a gas analyzer.

If you find any breathing problems in your pet, contact the clinic immediately. Such conditions, as a rule, are urgent, and if medical assistance is not provided in time, the animal may die.

Veterinary center "DobroVet"

Bronchopneumonia of calves is a disease that is common and leads to large economic losses in farms. There are other diseases caused by hypothermia in calves, the most common of which is bronchitis. With untimely and incorrect treatment, the calf develops a deep dysfunction of the respiratory organs, which causes intoxication of the body. Irreversible processes occur in the bronchopulmonary organs. The protective functions in the body are reduced, which increases the activity of microbes that develop intoxication and disrupt the functioning of all body systems, cardiovascular and digestive functions are affected, and a cough appears.

Bronchopneumonia in calves develops from hypothermia

Thanks to timely diagnostic measures, prevention and treatment of this disease, it is possible to successfully solve the problem of preserving and successfully breeding cattle, increasing meat and dairy production. Scientists are developing effective ways to deal with this pathology. But even history and conducted scientific research do not answer questions on the etiology, pathogenesis, treatment and prevention of the disease, what needs to be done, and why actions do not always lead to successful treatment. This is most true for calves with catarrhal bronchopneumonia.

Even an adult and strong cow can be susceptible to this disease, which is common in all regions of Russia, and is the second in a row - the first place is occupied by diseases that occur in the gastrointestinal tract. After the animal recovers from bronchopneumonia, it weakly gains average daily weight, productive and breeding parameters noticeably worsen.

Causes of the disease

Diseases of the respiratory organs in calves appear as a result of:

decrease in protective properties and poor adaptability of young animals,
occurrence of stress
being in conditions of great closeness,
nutrition with food with insufficient amounts of vitamins,
the presence of hypovitaminosis,
finding young individuals in unventilated areas.

Walking in the fresh air and good nutrition is an excellent prevention of bronchopneumonia

Diseases that affect the respiratory organs of calves develop rapidly. Inflammatory processes begin from the bronchi due to the fluid accumulated in the alveoli. At the beginning of the disease, exudate collects in the lungs, which has serous contents, causing coughing. Then the pathology affects the bronchi of the young animal, and bronchopneumonia begins in the calf.

The following causes cause bronchopneumonia in calves

Weak work of the respiratory organs due to a long stay in a small room.
Exposure to cold and damp, causing colds.
Overheat. Underdeveloped calves that are under the sun for a long time lose their normal thermoregulation. This is accompanied by increased body temperature and an increase in respiratory rate, increased heart rate.
The presence of calves in rooms containing a high concentration of ammonia or hydrogen sulfide in the air, which occurs when the ventilation system is not working properly and the sewer system is faulty.
Hypovitaminosis A, D.
Prolonged diseases of the gastrointestinal tract.
Unfavorable microflora in the air and the body, containing streptococci, staphylococci, pneumococci, diplococci - harmful and dangerous microorganisms.

Prolonged exposure to the scorching sun can lead to impaired thermoregulation of the body.

How the disease affects the body of the calf

A favorable soil is created that disrupts the functions of the respiratory and circulatory organs. The pulmonary system begins to work poorly, a large amount of dust, ammonia and water vapor enters the lungs, causing diseases of the respiratory apparatus. History cites many cases where prevention saves the lives of young animals.

The adverse effect that the calf's nervous system experiences disrupts the functioning of nerve cells, reduces the protective functions of the young animal's body, the concentration of lysozyme and histamine decreases, and the globulin fraction of proteins increases.

These factors cause blood to stagnate in the lungs, their mucous membranes swell, leukocytes become less active and the movement of mucus accumulated in the bronchi slows down, a strong cough appears.

The animal begins to suffer from shortness of breath, it begins to get nervous, the activity of the cardiovascular system begins, the tone in the blood vessels decreases and blood pressure decreases. The occurrence of stagnant processes leads to the occurrence of dystrophy, affecting the heart muscle, changing the functioning of the liver. The content of chlorides in the blood decreases, and hydrochloric acid is observed in the stomach, which exceeds the norm. The kidneys lose their ability to filter, releasing too much protein into the urine.

Shortness of breath and nervous behavior are the first symptoms of bronchopneumonia in calves

Preventive measures in the event of an epidemic

The reasons for the occurrence of diseases can be different. For mating, it is necessary to choose the right pairs, it is desirable that the cow and bull are strong and healthy, otherwise offspring with a weak and susceptible to disease organism, which has unusual anatomical features, may be born:

Short trachea.
Narrowed bronchial tree.
Not elastic fabrics.
Increased content of blood vessels.

When the functions of the internal organs are disturbed, the calf is subject to the rapid development of pathology: streptococci, pneumococci, staphylococci and Escherichia coli, viruses, various fungi, which become the most active, begin to multiply rapidly in the microflora. With an increased concentration of microbes and toxins, necrotic inflammation begins in the mucous membranes, causing coughing.

Soon, the scattered areas affected by the disease begin to merge and form large foci of inflammation that thicken the tissues of the lungs. The calf begins to cough and snort, breathe rapidly, because ventilation in the lungs is disrupted, and the remaining healthy areas of the lung have to function doubly.

The blood vessels of the animal become less elastic, the heart muscle suffers from congestion, an increase in intoxication adversely affects the performance of the kidneys, the central nervous system fails, the processes of thermoregulation of the calf are disturbed, which is accompanied by fever.

Bronchopneumonia in a calf leads to the rapid development of pathologies of internal organs

Symptoms of bronchopneumonia

The development of catarrhal bronchopneumonia can occur in various forms of severity:

in acute form.
In substandard form.
in a chronic form.

Characteristics of the acute form of the disease

The acute form of the disease lasts from 5 to 10 days. During this period, the calf becomes lethargic, his appetite decreases, and a slight malaise is noticeable. The animal does not breathe through the nose, but through an open mouth. Hyperemia appears on the mucous membranes of the nose and eyes. The serous exudate that collects in the nose becomes purulent.

The calf begins to cough at first sharply and dryly, then the cough becomes frequent, weak and wet.

The animal's health is rapidly deteriorating, it breathes hard, wet rales are heard, muffled heart tones, a blood test shows an increase in leukocytes. By the third day, a sick calf has a sharp increase in body temperature up to 42 C. There is a deterioration in the general condition, the appearance of hypodynamia, rapid and difficult breathing.

With bronchopneumonia, an increase in the concentration of leukocytes in the blood of a calf is observed.

The acute course of bronchopneumonia changes the mucous membranes of most animals - they become noticeably pale. The upper airways swell, and the bronchi and bronchioles contain a large amount of exudate. Enlarged bronchial lymph nodes

Characteristics of the subacute form of the disease

The main symptoms of the subacute form of the disease are a decrease in appetite and a decrease in fatness within a month, malnutrition develops. This phase is accompanied by an evening increase in body temperature by 1–2°C, the calf breathes with shortness of breath, accompanied by a wet cough. If there is an exacerbation of the disease, the condition may worsen: shortness of breath increases, hypoxia develops, digestion fails, diarrhea appears. The animal becomes exhausted, a large amount of purulent mucus appears in the bronchi. The bronchi themselves are edematous, hyperemic, hemorrhage is possible. The pleura contains a lot of fluid, the liver is enlarged

Characteristics of the chronic form

A calf with a chronic form of bronchopneumonia lags far behind a healthy calf in growth and becomes hypotrophic. He does not stop coughing, serous fluid flows from the nose, the mucous membranes become cyanotic, the body temperature rises slightly, when listening in the lungs, dry wheezing is heard. There is a constant change in appetite.

A healthy calf has pink mucous membranes and a good weight.

Diagnosis of the disease

Why is it necessary to do diagnostics? When diagnosing a disease, the conditions in which young animals are kept, their behavior indoors and outdoors, and the state of the entire livestock economy are taken into account. To determine the correct diagnosis, the following indicators are used:

General condition of the calf.
Clinical manifestations.
Blood test scores.
Laboratory data.

X-ray examinations show local obscurations in the lungs of varying degrees. Conducting bronchopulmonary and biochemical analyzes allows you to find out about the presence and degree of the inflammatory process for the appointment of effective treatment. Differential diagnosis allows to recognize the rapid spread of the disease and determine the pathogen. With streptococcal infection, the articular bones of the calf are affected.

X-ray light makes it possible to accurately diagnose bronchopneumonia

Getting rid of the disease

The conditions of stay of calves affect the effectiveness and time of treatment of bronchopneumonia. A sick calf should not be kept together with healthy ones, and treatment is prescribed by a veterinarian, who takes into account the form and stage of the disease, before prescribing the intake or injection of drugs in the form of antibiotics, macrolide and sulfanilamide solutions and procedures. The timeliness and dosages of the drugs used determine how long and successfully the treatment of the disease is.

Despite the rapid development of the disease and the difficulties arising from this, if the treatment is timely and correct, and the course of the disease is favorable, its foci are quickly eliminated, recovery occurs relatively quickly - no more than a week and a half.

If the process went unfavorably, purulent and necrotic changes may occur, leading to the formation of pleurisy, pericarditis, and secondary immune deficiency.

It is not always effective to treat calves with bronchopneumonia using known drugs. This delays the healing process, and the acute course of the disease passes into other stages. The functions that protect the body are impaired, immunity is reduced. It is difficult to cure the disease if it has become protracted or chronic. Etiotropic therapy is to ensure a sufficient concentration of certain drugs in the foci of inflammation.

A sick calf should be separated from the herd

During the acute and subacute phases of the disease, calves are treated with antimicrobial agents that quickly penetrate the histohematogenous barriers. Prolonged treatment processes cause edema, cell infiltration with vascular sclerosis appears, as well as squeezing of capillaries near inflammatory foci in the body of sick calves. This makes it difficult for drugs to enter the body.

Therefore, the appointment of antimicrobial drugs should be made in a timely manner. The use of immunostimulating drugs is effective.

Prevention of bronchopneumonia

Diseases are better to prevent than to cure - everyone knows about this. Preventive measures are carried out in a complex that includes:

Correct content.
Proper feeding of calves and cows.

How to keep calves

Calves must be kept in premises where zoohygienic standards are observed. Valid values:

relative humidity not exceeding 70%.
The air temperature difference should fluctuate within 5°C.
concentrations of ammonia vapors and hydrogen sulfide - not higher than 5 mg / m.

Calves need to be walked more often; during the summer heat, pastures should be equipped with special awnings from the sun. In the premises for calves, it is necessary to follow all the rules of the sanitary regime, keep them clean, use disinfectant solutions for cleaning - this prevention should be carried out regularly.

The calf should regularly walk outside

It is recommended to vaccinate newborn calves, use aerosols, use individual and herbal medicine: add medicinal plants to milk that can increase the body's resistance and improve the functioning of the immune system.

Preventive measures to be taken by a veterinarian

Create better living conditions and proper feeding for the pregnant cow and newborn calf.
Provide the necessary microclimate in the room.
Feed calves granulated grass meal.
Feed calves steamed concentrated feed.
Periodically massage the chest of the calves.
Create a sanitary regime with systematic maintenance of cleanliness in the premises in which the calves are kept.
Perform ongoing disinfection and refurbishment of the premises.
May-August transfer calves to summer buildings with shady canopies and flooring.
Use drugs that increase resistance - supplements containing a sufficient amount of vitamins with minerals.
To raise calves, observing the necessary conditions for their maintenance and adaptation, to prevent the development of dyspepsia and other diseases.
To equip livestock farms with healthy calves.
Timely identify and treat diseased calves, and subject the rest to preventive treatment.

For the prevention of bronchopneumonia, good care should be provided to both the calf and the cow.

How to feed calves

To strengthen young organisms, it is necessary to introduce vitamin supplements with minerals in sufficient quantities into the food of animals. Do not overfeed calves with coarse, dry and concentrated types of feed.

Bronchitis in calves

Bronchitis in calves is a common disease caused by the presence of any inflammatory process affecting the mucous membranes and submucosal layers of the bronchi. A young and strong cow is not susceptible to this type of disease that affects a young, old or weakened body. Bronchial diseases are massively spread among young individuals on special farms where they fatten and breed cows with non-compliance with zoohygienic conditions. Prevention helps to avoid the disease that causes severe coughing. History knows many cases of complete recovery of diseased animals.

Disease classification

The disease is classified according to:

The course (acute or chronic).
Origin (primary or secondary).
Characteristics of inflammation (catarrhal, purulent, hemorrhagic or fibrinous).

There are the following types of bronchitis:

Macro-bronchitis, which affects the large bronchi.
Micro-bronchitis affecting the small bronchi.
Bronchiolitis, in which the bronchioles are affected.

Treatment of bronchitis should be comprehensive: in addition to medicines, it is necessary to give calves fees and infusions of medicinal herbs, which contain a sufficient amount of vitamins. as well as effective inhalation using aerosols with antimicrobial properties. The versatile influence of medicinal plants on pathogenesis is known, they provide pronounced symptomatic effects and a certain etiotropic effect, alleviate the course of the disease, reduce its duration, improve the outcome, and save money spent on drugs.

With a lethal outcome in the acute period (on the 1st-2nd day), pallor with a gray-earthy tinge of the skin and mucous membranes is noted. A slightly frothy fluid is released from the mouth and nose (sometimes only with pressure on the chest).

The lungs are sharply enlarged in volume. Their mass is also increased and reaches 2-2.5 kg instead of 500-600 g in the norm.

The surface of the lungs has a characteristic mottled (marble) appearance due to the alternation of pale pink protruding areas of emphysema, dark red depressed areas of atelectasis and bluish areas of edema (Fig. 27).

Rice. 27. Pulmonary edema. Foamy "marble" appearance of the surface of the lungs.

Rice. 28. Diphosgene pulmonary edema in a rat (microphoto, small

increase). The lung alveoli are filled with edematous fluid.

On incision, a copious amount of serous foamy fluid is released from the lungs, especially when pressed.

The trachea and bronchi are filled with edematous fluid, but their mucosa is smooth and shiny, slightly hyperemic. Microscopic examination in the alveoli reveals an accumulation of edematous fluid, which is stained pink with azure-eosin (Fig. 28).

The heart is moderately dilated, with dark blood clots in its cavities. Parenchymal organs are congestively plethoric. The meninges and brain substance are plethoric, in some places there are pinpoint hemorrhages, sometimes vascular thrombosis and softening foci.

In the case of later death (3-10 days), the lungs take on a picture of confluent bronchopneumonia, in the pleural cavities there is a small amount of serous-fibrinous fluid. The heart muscle is flabby, Other organs are congestively full-blooded.

6.5. Treatment of toxic pulmonary edema

Due to the absence of specific antidotes, pathogenetic and symptomatic therapy is used, which is aimed at reducing pulmonary edema, combating hypoxia and stopping other symptoms, as well as combating complications.

The provision of maximum rest and warming of the affected person is an absolutely essential requirement for treatment, without which all other therapeutic measures may be ineffective. In the stage of edema, even slight muscle efforts can dramatically worsen the patient's condition. Absolute rest, warm wrapping, heating pads reduce the body's need for oxygen and facilitate the transfer of oxygen starvation. Not only should patients not be allowed to get up and walk, but they should not be disturbed at all, shifted, it is better to give them a semi-sitting position. In order to stop neuropsychic excitation, they give phenazepam or seduxen in tablets.

In the pathogenetic and symptomatic therapy of toxic pulmonary edema, primarily agents that reduce the permeability of the pulmonary capillaries (EA Luzhnikov, 1979), dehydration and cardiovascular agents, and oxygen therapy are used. In order to reduce vascular permeability, as well as reduce hyperergic inflammatory processes in the lungs, it is recommended to widely use_glucocorticoids: intravenous prednisone at a dose of 30-60 mg or drip at a dose of up to 150-200 mg. It also shows the introduction of antihistamines (pipolphen, diphenhydramine), ascorbic acid (5% solution of 3-5 ml), chloride or calcium gluconate 10 ml of a 10% solution intravenously in the first hours, during the period of increasing edema.

Importance is attached to dehydration therapy, which reduces edema and promotes reabsorption of edematous fluid. A 30% solution of urea is injected intravenously at the rate of 1 g of the substance per 1 kg of the patient's weight (60 ml of solution). The dehydration effect is also observed with the introduction of furosemide (Lasix) and glucose (10 ml of a 40% solution).

Oxygen starvation is the most important symptom of pulmonary edema, a pathogenetic factor in metabolic and cardiovascular disorders, so oxygen therapy is important. It begins at the first symptoms of oxygen deficiency and continues for a long time, until pulmonary respiration improves. Sufficiently effective inhalation of an oxygen-air mixture with a content of 30-40% oxygen for 15-30 minutes with interruptions of 10-15 minutes, depending on the patient's condition. Foaming of edematous fluid in the bronchi, which prevents the passage of air into the lungs, has a very unfavorable effect. Therefore, antifoaming surfactants should be used. The oxygen-air mixture is passed through a Bobrov vessel, into which 72-96% alcohol or a 10% alcohol solution of antifomsilane is poured (in the field, gauze moistened with alcohol can be put into the inhaler mask). Cardiovascular agents according to indications (with the appearance of tachycardia, hypotension): cordiamine, sulfocamphocaine, corglicon or strophanthin, eufillin to reduce stagnation in the pulmonary circulation, with a decrease in blood pressure - 1 ml of 1% mezaton solution. In cases of blood clotting, in order to prevent thromboembolic complications, it is recommended to administer heparin (5000 IU), trental can be used.

In order to reduce stagnation in the pulmonary circulation, bloodletting of 300-400 ml is recommended (in the initial stages of edema without signs of hypotension) or bloodless bloodletting by applying venous tourniquets to the limbs. Currently, these procedures are treated very carefully, they can only be carried out at the advanced stages of evacuation (MPB, MPP) in the initial stages of edema without pronounced cardiac disorders.

With pulmonary edema, sedatives are indicated (phenazepam, seduxen, elenium). The introduction of adrenaline, which can increase edema, morphine, which depresses the respiratory center, is contraindicated. It may be advisable to introduce an inhibitor of proteolytic enzymes, in particular kininogenases, which reduce the release of bradykinin - trasylol (kontrykal) 100,000-250,000 IU in isotonic glucose solution. In severe pulmonary edema, antibiotics are prescribed to prevent secondary infectious pneumonia, especially with an increase in body temperature.

In the gray form of hypoxia, therapeutic measures are aimed at removing the collaptoid state, excitation of the respiratory center and ensuring airway patency. The introduction of corglicon (strophanthin), mezaton, lobelin or cytiton, inhalation of carbogen (a mixture of oxygen and 5-7% carbon dioxide) is shown. To thin the blood, an isotonic 5% glucose solution is administered with the addition of mezaton and vitamin C 300-500 ml intravenously. If necessary, intubation should be done, fluid should be sucked out of the trachea and bronchi, and the patient should be transferred to controlled breathing.