home Auditorium 8 Non-inflammatory lesions of the respiratory system. Lung diseases hyperemia and pulmonary edema - hyperaemia et oedema pulmonum

Non-inflammatory lesions of the respiratory system. Lung diseases hyperemia and pulmonary edema - hyperaemia et oedema pulmonum

Hyperemia and pulmonary edema is a disease characterized by blood overflow of the pulmonary capillaries with subsequent exudation of blood plasma in the lumen of the bronchi, bronchioles and alveolar cavities and infiltration of interlobar effusion connective tissue. There are active and passive hyperemia, active and hypostatic pulmonary edema. Etiology: active hyperemia and active pulmonary edema usually occur during intense and rapid breathing during racing in sports horses, during long hunts in dogs, when animals inhale hot air, exposure to highly irritating gases, and excitement. Catarrhal active hyperemia can develop with pneumothorax and thrombosis pulmonary artery. Passive hyperemia and hypostatic pulmonary edema register for decompensated heart defects, traumatic pericarditis, myocarditis, intoxication, prolonged forced lying alive, etc. Symptoms: active hyperemia and pulmonary edema develops very quickly. Within a few hours, excitement, violence, and fear appear. Breathing becomes rapid and intense, shortness of breath is clearly noticeable; to facilitate breathing, animals stand with their limbs spread wide apart, the nostrils are widened, and during coughing, foam with a reddish tint is released from the nose holes. During auscultation, moist coarse and fine bubble rales and hard vesicular breathing are heard in the trachea, bronchi, and lungs. Treatment: the etiological factors of the disease are eliminated, the animals are transferred to a moderately cool, clean, well-ventilated room. Intravenously administered in small doses hypertensive solutions calcium chloride, glucose. If pulmonary edema develops, moderate bloodletting is recommended (0.5% of body weight once). For passive hyperemia, hypostatic edema and the development of heart failure, cardiac drugs are administered subcutaneously; caffeine, cordiamine, ether. Prevention: aimed at compliance with the regime of operation and training of sports and working animals, protection from overheating, from inhalation of irritating and toxic gases.

Bronchopneumonia (catarrhal pneumonia) is a lobular inflammation of the bronchi and lungs, accompanied by the formation of catarrhal exudate and filling the lumen of the bronchi and alveolar cavities with it. The disease is polyetiological and usually occurs as a result of a combined effect on the or-m unfavorable factors, stress), weakening resistance. This is increased humidity in the air in the room, damp floors and walls, maintenance without bedding on cement or asphalt unheated floors, drafts, excess accumulation ammonia, hydrogen sulfide, etc. into the room. In acute cases, already on the first day, when inflammation passes to the lungs, general weakness and apathy, weakened or loss of appetite, increased body temperature to low-grade or febrile. Depending on the degree of lung damage, decreased appetite, emaciation, stunted growth, decreased productivity and performance, a tendency to constantly lie down, pallor and cyanosis of the mucous membranes, tousled hair or coat are noted. The lungs show strong bronchial and vesicular respiration, wet fine-bubble or dry wheezing in the form of a squeak, whistle. Treatment: sick animals are placed in a separate room or specially equipped pens (stalls). When choosing an antibiotic for treatment, it is necessary to titrate it to determine the sensitivity of the microflora to it. Complex treatment most effectively and economically feasible in initial stage diseases. Animals with chronic diseases, as well as those with confluent progressive purulent-necrotic foci in the lungs, as a rule, are not treated.

Purulent pneumonia - characterized by purulent inflammation of the lungs as a result of drift purulent beginning and other pathological foci of the body. Fundamentally this secondary disease, arose as a complication of septic processes of various origins: purulent inflammation uterus, washes, pharyngitis, ulcers, purulent wounds, abscesses, surgical interventions. Auscultation reveals weakening breath sounds, wheezing, bronchial or amphoric breathing. In the presence of small foci, percussion does not establish deviations from the norm, and in the case of large foci - dullness or nearby tympanic sound, evidence of the development of vicarious emphysema. Symptoms: the most characteristic is shortness of breath, painful cough, refusal to feed. Subsequently, with the development of abscesses in the lungs, the condition of the animals sharply worsens, the temperature increases to 40-41 C, the nature of daily fluctuations in body temperature, and in the majority - sweating. Treatment; sick animals are provided with good maintenance, autohemotherapy is carried out, anti-streptococcal serum is administered, immune drugs. Heat in all its forms is shown on the chest.

Atelectatic pneumonia is an inflammation of the lungs of a lobular nature, resulting from the presence of atelectasis or hypopneumatosis in the lungs. Mostly hypotrophic, weakened and emaciated animals, mainly sheep, become ill. Common reason- V malnutrition pregnant animals. As a result, young animals are born hypotrophic and with increased susceptibility to the disease. Patients experience progressive emaciation, general weakness, movement chest walls when breathing, it is faintly visible, shallow breathing, rapid breathing. Body temperature is often normal, sometimes even lowered. On auscultation of the pulmonary field, breathing is weakened, vesicular, and in areas of pneumonia there are moist rales. Treatment: drug treatment aimed at restoring bronchial patency, suppressing bacterial flora and activation of function, expectorants and absorbents are prescribed: oral ammonium chloride, potassium or sodium iodide, inhalations with menthol, etc. In case of exacerbation and increase in body temperature, a course of treatment with antibiotics or sulfa drugs. For young animals, natural solar or artificial ultraviolet radiation is provided.

Lobar (fibrinous) pneumonia - characterized by acute lobar pneumonia, distributed mainly to entire lobes of the lungs (lobar pneumonia) and a staged course. Horses are more likely to get sick. Usually occurs suddenly and is accompanied by severe chills, significant sharp increase temperature, depressed state of animals, weakness, depression and loss of appetite. The pulse is rapid and tense, breathing is rapid, the skin is dry, hot, the temperature is unevenly distributed. The mucous membranes are hyperemic and icteric. The fever is of a constant type and remains at a high level, usually 41-42 C, regardless of the time of day and other factors. The middle impulse is knocking, the second tone is intensified. Treatment: single or double intravenous administration novarsenol, maximum dose of titrated antibiotics for a long course of therapy (7-10 days), active pathogenetic and symptomatic therapy (gamma globulin, rubbing the skin, irritating ointments on the chest area, novocaine blockade of stellate ganglia)

Mycotic pneumonia - the disease occurs due to damage to the bronchi and alveoli mainly by mold fungi. Molds are almost always present in the respiratory tract, where they enter with inhaled air. Particularly dangerous for animals is prolonged inhalation of a large number of fungal spores, when the animals have already had damage to the respiratory tract, as a result of which immune status in them was reduced, mainly acquired when feeding heavily affected animals, especially dry food, or when using the same bedding. Symptoms: the animal’s general condition worsens, shortness of breath increases, and body condition decreases. Auscultation reveals foci of dullness, and in rare cases acute course usually accompanied by the formation of cavities and the sound of a cracked pot. Patients have a fever. A large number of different fungi are microscopically detected in the nasal discharge. The prognosis is most often unfavorable due to the death of animals or the development of bronchial asthma and emphysema. Treatment; It is recommended to give animals an oral solution of potassium iodide 2.0 g, distilled water - 60 ml (depending on the age of the animals) 2 times a day. Sulfonamide drugs and autohemotherapy are indicated.

Putrefactive pneumonia (pulmonary gangrene) is a purulent-putrefactive melting of lung tissue. It is found mainly in horses, less often in sheep, and isolated cases in other living species. The disease most often arose as a complication of aspiration or metastatic pneumonia. Symptoms: the course of the disease is usually acute, worsening general condition, weakness, loss of appetite, increased shortness of breath, persistent increase in body temperature, fetid putrid smell exhaled air (smell of corpse decomposition), profuse discharge from the nose of a brown-gray, gray-green or chocolate color. The cough is wet, dull, and often painful. Percussion revealed areas of dullness, and in some places the image of caverns was a tympanic sound or the sound of a cracked pot. Auscultation reveals bronchial or amphoric breathing. Treatment; drug therapy directed to suppress purulent-putrefactive microflora in order to localize the process. A course of treatment with novarsenol or antibiotics is carried out by daily intramuscular injections in maximum dosages for 7-10 days. In complex therapeutic measures pathogenetic and symptomatic remedies: bb hydroalcoholic solutions glucose with camphor, hypertonic solutions of calcium chloride, etc.

The disease is also known as fog fever cattle(ABPEE). Essentially, emphysema is acute pneumonia adult animals, which occurs within 4-10 days during the transition from dry pastures or dry food to green pastures rich in lush grass. The pathological condition develops rapidly.

The reason for the development of edema in the lungs in cows

Affected animals fed dry feed for a long period of time have special rumen fermentation adapted to this situation. With changes in diet, protein concentration changes dramatically. The culprit of enphysema is one of the amino acids contained in plant protein.

Tryptophan (an amino acid) contained in the feed is instantly converted by bacteria in the rumen into a substance called 3-methylindole (3-MI). The finished 3-MI is absorbed through the rumen wall and distributed throughout the body. 3-MI is toxic to the essential cells that line the inside of the lungs. Thus, high levels 3-MI passing from the scar to the lungs destroys lung tissue.

Symptoms of emphysema

The following signs are observed in animals:

labored breathing;
cough;
foam at the mouth;
anxiety state (separation from the group);
death of the animal.

Treatment of acute pulmonary edema

There is no specific treatment for fog fever. Some mild attacks may go away on their own. The most seriously affected cattle do not respond to any treatment and die within a day or two. Removing cows from pasture often does not help, and some scientists believe that moving sick animals may make the condition worse.

Prevention

Limiting grazing time during the first 10 days when moving to a new pasture will reduce the risk of developing pulmonary edema. It is advisable to limit grazing to 2 hours a day.

It is also believed that feeding monensin or chlortetracycline for the first 10 days may help control the situation.

Pulmonary edema- This pathological condition, in which the liquid portion of the blood sweats out and accumulates in the intercellular space (interstitium) of the lungs or pulmonary alveoli.

Lungs– main organ respiratory system, this is where gas exchange occurs. The right and left lungs are formed by bronchi, bronchioles, alveolar ducts and alveoli surrounded by connective tissue. Direct gas exchange in the lungs occurs in the acini. It is the functional unit of the lung, represented by bronchioles, alveolar ducts and alveoli. Alveoli are vesicles through which capillaries carrying blood pass. Inner surface The alveoli are lined with specific epithelial cells - respiratory epithelium. Its cells are closely adjacent to the cells blood vessels , making it possible to enrich the blood with oxygen.

What could be the reasons and what is happening?

Pulmonary edema can develop due to 3 main mechanisms:

- Increased hydrostatic pressure in the vessels of the pulmonary circulation (when, with an acute increase in pressure in the capillary, its permeability is disrupted and the liquid part of the blood enters the interstitial tissue of the lung). This occurs with various heart defects, cardiomyopathy, endocarditis and other heart diseases, as well as with volume and rapid intravenous infusions.

- Decrease in blood oncotic pressure(in this case there is a difference between the oncotic pressure of the blood and the oncotic pressure intercellular fluid, and in order to equalize this difference, fluid from the vessel exits into the extracellular space - the interstitium). This mechanism develops with hypoproteinemia.

- Increased permeability of capillary-alveolar membranes(as a result of any damage, the protein structure of the capillary-alveolar membranes is disrupted with the release of fluid into the interstitial space). This process is observed in pneumonia, various intoxications, and disseminated intravascular coagulation syndrome.

Development of pulmonary edema can also contribute renal failure , snake bite, heatstroke, electrical injury, traumatic brain injury.

Thus, taking into account the mechanism by which pathology develops, we distinguish cardiogenic, non-cardiogenic And mixed pulmonary edema.

Cardiogenic(so-called cordial) pulmonary edema develops due to an increase in hydrostatic pressure in the pulmonary circulation system, leading to the occurrence of acute left ventricular failure. In this case, any reason leading to an increase in pressure in the pulmonary artery is important. Rapidly increasing hydrostatic pressure in the pulmonary circulation leads to pathological effusion of fluid into the lung tissue, and then into the alveoli. Most often, cardiogenic pulmonary edema develops against the background arterial hypertension, cardiosclerosis, various heart defects.

Non-cardiogenic pulmonary edema is an accumulation of fluid in the interstitial lung tissue and alveoli, not related to heart disease. It arises rather due to increasing capillary permeability, and not as a result of increased hydrostatic pressure, in contrast to cardiogenic pulmonary edema. Occurs mainly in dogs, less common in cats. The most common reasons include upper airway obstruction (laryngeal paralysis, foreign bodies , abscesses), traumatic brain injury, smoke poisoning, sepsis, anaphylactic shock in cats.

What are the clinical signs with pulmonary edema?

Pulmonary edema in animals is critical condition , requiring emergency care and accompanied by the following symptoms: dyspnea, rapid breathing, restless behavior, cyanosis (cyanosis) mucous membranes oral cavity , copious discharge frothy pink sputum , which can be mistaken for vomit or saliva, tachycardia, breathing with open mouth in cats. Symptoms may appear suddenly depending on the cause of the swelling and lead to severe respiratory failure posing a threat to the life of the animal.

How is pulmonary edema diagnosed in cats and dogs?

Diagnosis is based on clinical signs, auscultation(auditions) lungs, X-ray data. On auscultation, diffuse moist rales. At laboratory research blood is sometimes noted leukocytosis, hyperazotemia, increased activity of liver enzymes. An echocardiographic examination can exclude cardiac pathologies leading to pulmonary edema.

The gold standard for diagnosing pulmonary edema is X-ray of the chest cavity in two mutually perpendicular projections. On x-ray identify decrease transparency lung tissue, expansion and " blur» roots of the lungs. These changes can be either diffuse and affect all lobes of the lungs, or focal, which is less common.

Pulmonary edema is differentiated from other pathologies accompanied by shortness of breath: tracheal collapse, laryngeal paralysis, upper respiratory tract obstruction, neoplasms, thromboembolism in cats.

How to treat pulmonary edema in cats and dogs?

Treatment includes limitation physical activity animal, minimizing stress, oxygen therapy(oxygen inhalation), drug support. It is necessary to prescribe diuretic drugs ( furosemide, mannitol), glucocorticoids ( dexamethasone, prednisolone), in some cases it is advisable to use sedatives (acepromazine). The use of vasodilators is also indicated ( nitroglycerine), bronchodilators ( aminophylline). For non-cardiogenic pulmonary edema, treatment of the underlying disease is carried out, in particular treatment of hypoproteinemia. These measures are aimed at relieving respiratory failure, correcting the increasing oxygen starvation, prevention of shock.

Intensive therapy for pulmonary edema should be carried out until the animal’s condition is completely stabilized. Most often, such patients requires inpatient observation for continuous monitoring, the possibility of additional examinations and resuscitation measures in case of deterioration.

Recovery and prognosis depend on the underlying cause of pulmonary edema. On average, recovery occurs most often within 24-72 hours and then does not require special therapy. IN severe cases the so-called respiratory distress syndrome which leads to the death of the animal.

Timely request for help for animals with symptoms of dyspnea and immediate assistance to such patients necessary to prevent complications and improve prognosis in the treatment of this condition.

Pulmonary edema is observed with both active and passive hyperemia. Consequently, its origin will be based on the same reasons as for pulmonary hyperemia. Additional reasons are weakening of the left ventricle, which contributes to the development of congestion in the lungs, and porosity of the pulmonary vessels, caused by certain types of intoxication or prolonged congestion. Therefore, pulmonary edema can only occur when external or internal reasons created the combination necessary for its origin, i.e., hyperemia of the lungs, weakness of the left ventricle with stagnation of blood in the lungs and vascular porosity. This happens with pneumonia, poisoning, severe intoxication, inhalation of poisonous gases, prolonged weakness of the left ventricle with congestion in the lungs, with bicuspid valve defects and some infectious diseases(anthrax, malignant edema, etc.).

Pathogenesis. The pathological significance of pulmonary hyperemia is that overcrowded capillaries reduce the lumen of the alveoli and small bronchi. With congestive hyperemia, the flow of blood also decreases. With pulmonary edema, the exudation of edematous fluid is accompanied by the release of sebum into the alveoli and bronchioles, which leads to congestion of the lungs and very severe breathing problems.

Symptoms External signs hyperemia and pulmonary edema are similar and consist of rapidly progressing shortness of breath and attacks of suffocation. At first, the breathing is accelerated and tense, but clean; later wheezing appears. Animals during attacks of suffocation express fear and anxiety. The mucous membranes are cyanotic.

Vesicular breathing with pulmonary hyperemia is slightly weakened or harsh, and with edema it is also weakened and in some places is not audible at all. In addition, with pulmonary edema there is always abundant diffuse, often moist, fine-bubbling and crepitating rales caused by serous fluid, penetrated the alveoli and then into the bronchi. Moving it to the top Airways causes a short, muffled cough and is accompanied by the appearance of a yellowish or, less commonly, reddish, finely foamy bilateral nasal discharge. Such leakages do not occur during hyperemia.

Percussion of the lungs during hyperemia usually produces a normal sound. Only with hypostases in lower parts lungs it is slightly dull. In severe cases of edema in parts of the lung where the alveoli are filled with hydrocele, percussion reveals a dull and sometimes tympanic percussion sound.

The activity of the heart during active hyperemia of the lungs is accelerated and intensified. Accordingly, the heartbeat and sounds are increased. With congestive hyperemia and edema, the activity of the heart weakens from the very beginning or subsequently, resulting in overflow of the jugular veins, a weakening of the cardiac impulse and a weak small pulse.

Diagnosis. Both hyperemia and pulmonary edema can be diagnosed based on the above symptoms. In a differential relationship, it is necessary to keep in mind thermal overheating and sunstroke. With them, in contrast to pulmonary hyperemia, in addition to shortness of breath, dullness of consciousness, weakness and elevated temperature are observed.

LUNG DISEASES HYPEREMIA AND PULMONARY EDEMA - HYPERAEMIA ET OEDEMA PULMONUM

The disease is characterized by overflow of the capillaries of the lungs with blood, accompanied by infiltration of interlobular connective tissue and exudation of serous fluid into the cavity of the alveoli. Hyperemia can be active and passive (stagnant), and edema can be hypostatic (stagnant). Horses and pigs get sick more often, sheep, dogs and animals of other species are less common.

Etiology. The main causes of the disease are as follows. Increased blood flow to the lungs as a result of increased breathing, especially in hot, dry weather, sunny and heatstroke, stagnation of blood in the lungs due to heart failure, intoxication and prolonged lying of animals in one position. The disease can also occur during poisoning with certain poisons of plant, animal and mineral origin, as well as during autointoxication. Pulmonary edema may accompany infectious diseases, pasteurellosis, malignant edema, anthrax, contagious pleuropneumonia, canine plague, etc. Factors predisposing to the disease are prolonged overload at work, training, and stress.

Material damage consists of a decrease in productivity, the performance of animals, the cost of treating patients or their possible death.

Pathogenesis. The pathogenetic significance of the disease processes under consideration is very significant. Blood-filled pulmonary capillaries increase in volume, reduce the lumen of the alveoli and bronchi, which causes a decrease in the mobility of the lungs, their ability to expand and, thus, difficulty breathing and the occurrence of shortness of breath. Due to the filling of the alveoli with edematous fluid, favorable conditions for the vital activity and reproduction of opportunistic microflora, the formation and accumulation of its toxins in the lungs. As a result, the functioning of almost all systems in the animal body is disrupted, especially

cardiovascular.

Symptoms More often, the disease is acute and is accompanied by increased breathing, shortness of breath, dilation of the nostrils and the discharge of reddish foam from the nasal openings. Animals usually stand with their forelimbs spread to the sides. Auscultation of the trachea and lungs reveals wheezing. In severe cases, animals may show signs of agitation, fear, and suffocation (asphyxia). The mucous membranes become bluish, the pulse is weak. The percussion sound of the lungs during hyperemia and the onset of pulmonary edema is tympanic, and subsequently dull.

With passive hyperemia and hypostatic pulmonary edema Clinical signs grow slowly, over several days, and are less pronounced.

For all forms of the disease, if the animals are not provided medical assistance, they may die as a result of asphyxia.

Pathomorphological changes. Active hyperemia is accompanied by an increase in lung volume. They look swollen, denser, dark red in color. Pulmonary capillaries overflowing with blood protrude into the lumen of the alveoli. When a lung is cut, blood comes out more than is normal.

With passive hyperemia, the lungs are slightly increased in volume, compacted, and speckled with numerous hemorrhages, which usually occurs with prolonged venous stagnation and is accompanied by further education age spots. As a result, the lungs become brown.

With a long-term course of this form of hyperemia, the alveoli are filled with the exuding liquid part of the blood, which is accompanied by atelectasis of certain areas of the lungs. In this case, in their density and heaviness, as well as in the cut surface, they become similar to the spleen.

With edema, the lungs are increased in volume, swollen, doughy consistency, dark red in color, covered with a thin layer of light liquid. In some places they have hemorrhages. Foamy fluid, often mixed with blood, is found in the bronchi and trachea. When the lung is incised, it is released a large number of foamy, bloody fluid. These pathological changes confirm the presence of pulmonary edema.

Diagnosis and differential diagnosis. The diagnosis is made based on medical history, clinical symptoms And special methods research. Radiologically, large areas of shading are identified, mainly in lower parts pulmonary field.

When differentiating the disease, solar and thermal shock should be taken into account; diffuse bronchitis and bleeding from the lungs. In these cases, for thermal and sunstroke The specific etiological factors that cause them are characteristic. Diffuse bronchitis characterized by increased general body temperature, cough, nasal discharge and snoring, as well as negative results percussion. Bleeding from the lungs is excluded by the presence of characteristic increasing anemia of the mucous membranes.

Forecast. Be careful, especially with passive (congestive) hyperemia and pulmonary edema, due to the fact that in these cases the death of animals from asphyxia often occurs.

Treatment. They start by placing the animals in cool room, release up to 0.5% of the animal’s weight at one time and administer intravenously a 10% solution of calcium chloride, calcium gluconate, 0.9% sodium chloride solution, 5% isotonic glucose solution in doses depending on type and age of the animal. For passive hyperemia, hypostatic edema and the development of heart failure, cardiac medications are prescribed. caffeine, cordiamine, corazol, etc. Indicated subcutaneous injections oxygen, blockade of the stellate ganglion with a 0.25% or 0.5% solution of novocaine at the rate of 1 and 0.5 ml per 1 kg of animal weight, respectively, small doses of bronchiolytic drugs (atropine, ephedrine, aminophylline, etc. ), rubbing chest irritating ointments, turpentine, jars and mustard plasters. With the development of hypostatic pneumonia, accompanied by increased general temperature body, undergo a course of treatment with antibiotics, sulfonamide drugs, etc.

Prevention. Avoid overloading and overheating of animals, eliminate cardiovascular diseases.

Hyperemia and pulmonary edema

The diseases are characterized by blood overflow of the pulmonary capillaries with subsequent leakage of plasma into the cavity of the alveoli and infiltration of interlobular connective tissue.

The cause of active hyperemia and pulmonary edema is intense hard work, prolonged fast running, keeping animals in stuffy, poorly ventilated rooms during the hot season, transporting animals in stuffy, crowded carriages, inhaling hot air, poisonous and irritating gases. Passive hyperemia and pulmonary edema occur as a consequence of blood stagnation in the pulmonary circulation in heart failure caused by myocarditis, myocardosis, pericarditis, heart defects, etc.

Pulmonary edema is often a consequence of general overheating of the body (hyperthermia, heat stroke) or hyperinsolation (sunstroke).

The disease develops quickly and is accompanied by increasing shortness of breath mixed type, tachycardia and asthma attacks. The mucous membranes are cyanotic, foam with a reddish tint is released from the nasal openings. During auscultation in the trachea, bronchi and lungs, moist fine bubbling and crepitating rales are heard, caused by serous fluid that has penetrated into the alveoli and bronchi. A muffled cough is possible. In severe cases, animals exhibit agitation, fear, and signs of asphyxia. Often the cause is heart pathologies, myocardial dystrophy, pericarditis, atrioventricular orifice stenosis, bicuspid valve insufficiency, etc.

The diagnosis is made on the basis of anamnesis and characteristic clinical symptoms (progressive shortness of breath, wheezing in the lungs, watery discharge from the nose). Lobar pneumonia and acute infections are excluded.

Animals are provided with a cool, well-ventilated room. If the cause of hyperemia and pulmonary edema is overheating, then the animals are doused cool water. Bloodletting is done immediately (0.5% of blood from the animal’s weight per bloodletting). Large animals usually produce 2-3 liters of blood. After bloodletting, a 10% calcium chloride solution (100-200 ml for large animals) and a 40% glucose solution in appropriate doses are administered intravenously. Timely bloodletting facilitates the work of the heart, reduces blood pressure in the lungs, as a result of which capillary overflow decreases and pulmonary ventilation improves. Cardiac medications are used ( camphor oil, caffeine, cordiamine), diuretics and laxatives. It is advisable to administer 50-100 ml of a 1% solution of novocaine intravenously (to a cow). When hyperemia and pulmonary edema are complicated by hypostatic pneumonia, antibiotics and sulfonamides are prescribed.

Do not allow animals to overheat or keep them in stuffy rooms.