Acute and emergency conditions in tuberculosis: causes, symptoms, diagnosis, treatment

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Hemoptysis and bleeding

Hemoptysis is the presence of streaks of scarlet blood in sputum or saliva, the release of individual spitting of liquid or partially coagulated blood.

Pulmonary hemorrhage is the release of a significant amount of blood into the lumen of the bronchi. The patient usually coughs up liquid blood or blood mixed with sputum. The difference between pulmonary hemorrhage and hemoptysis is mainly quantitative. Experts from the European Respiratory Society (ERS) define pulmonary hemorrhage as a condition in which the patient loses from 200 to 1000 ml of blood within 24 hours.

In pulmonary hemorrhage, blood is coughed up in significant quantities at one time, continuously or intermittently. Depending on the amount of blood released, in Russia it is customary to distinguish between small (up to 100 ml), medium (up to 500 ml) and large, or profuse (over 500 ml) hemorrhages. It should be borne in mind that patients and those around them tend to exaggerate the amount of blood released. Patients may not cough up some of the blood from the respiratory tract, but aspirate or swallow it. Therefore, a quantitative assessment of blood loss in pulmonary hemorrhage is always approximate.

Profuse pulmonary hemorrhage is a major life-threatening event and can lead to death. The causes of death are asphyxia or further complications of bleeding, such as aspiration pneumonia, progression of tuberculosis, pulmonary heart failure. Mortality in profuse bleeding reaches 80%, and in smaller volumes of blood loss - 7-30%.

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Pathogenesis of pulmonary hemorrhage

The causes of pulmonary hemorrhage are very diverse. They depend on the structure of pulmonary diseases and the improvement of their treatment methods. In patients with tuberculosis, pulmonary hemorrhage often complicates infiltrative forms, caseous pneumonia, fibro-cavernous tuberculosis. Sometimes bleeding occurs with cirrhotic tuberculosis or post-tuberculous pneumofibrosis. Profuse pulmonary hemorrhage can occur in the case of a rupture of an aortic aneurysm into the left main bronchus. Other causes of pulmonary hemorrhage are fungal and parasitic lesions of the lungs, and first of all - aspergilloma in a residual cavity or air cyst. Less often, the source of bleeding is associated with bronchial carcinoid, bronchiectasis, broncholithiasis, a foreign body in the lung tissue or in the bronchus, pulmonary infarction, endometriosis, mitral valve defect with hypertension in the pulmonary circulation, complications after lung surgery.

The morphological basis for bleeding in most cases is aneurysmically dilated and thinned bronchial arteries, tortuous and fragile anastomoses between the bronchial and pulmonary arteries at different levels, but mainly at the level of arterioles and capillaries. The vessels form hypervascularization zones with high blood pressure. Erosion or rupture of such fragile vessels in the mucous membrane or in the submucous layer of the bronchus causes hemorrhage into the lung tissue and bronchial tree. Pulmonary hemorrhage of varying severity occurs. Less often, bleeding occurs due to destruction of the vascular wall during a purulent-necrotic process or from granulations in the bronchus or cavern.

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Symptoms of pulmonary hemorrhage

Pulmonary hemorrhage is more often observed in middle-aged and elderly men. It begins with hemoptysis, but can occur suddenly, against the background of a good condition. As a rule, it is impossible to foresee the possibility and time of bleeding. Scarlet or dark blood is coughed up through the mouth in pure form or together with sputum. Blood can also be released through the nose. Usually, the blood is foamy and does not clot. It is always important to establish the nature of the underlying pathological process and determine the source of bleeding. Such diagnostics of pulmonary hemorrhage is often very difficult even with the use of modern X-ray and endoscopic methods.

When taking the anamnesis, attention is paid to diseases of the lungs, heart, and blood. Information received from the patient, his relatives, or the doctors who observed him may be of great diagnostic value. Thus, in case of pulmonary hemorrhage, unlike bleeding from the esophagus or stomach, blood is always released with a cough and is foamy. The scarlet color of the blood indicates that it is coming from the bronchial arteries, and the dark color indicates that it is coming from the pulmonary arteries. Blood from the vessels of the lung has a neutral or alkaline reaction, and blood from the vessels of the digestive tract is usually acidic. Sometimes acid-fast bacteria can be found in the sputum released by a patient with pulmonary hemorrhage, which immediately raises a reasonable suspicion of tuberculosis. Patients themselves rarely feel from which lung or from which area of it the blood is released. The patient's subjective sensations very often do not correspond to reality and should be assessed with caution.

Diagnosis of pulmonary hemorrhage

The most important moment in the initial examination of a patient with hemoptysis and pulmonary hemorrhage is the measurement of arterial pressure. Underestimation of arterial hypertension can negate all subsequent treatment procedures.

To exclude bleeding from the upper respiratory tract, it is necessary to examine the nasopharynx, in a difficult situation with the help of an otolaryngologist. Moist rales and crepitations are heard over the area of pulmonary bleeding. After a routine physical examination, radiography in two projections is necessary in all cases. CT and bronchial arteriography are the most informative. Further diagnostic tactics are individual. It depends on the patient's condition, the nature of the underlying disease, the continuation or cessation of bleeding and should be closely related to treatment.

Analysis of venous blood must necessarily include a platelet count, an assessment of hemoglobin content and determination of coagulation parameters, Determination of hemoglobin in dynamics is an accessible indicator of blood loss.

In modern conditions, digital radiography provides rapid visualization of the lungs, specifies the localization of the process. However, according to ERS experts, in 20-46% it does not allow determining the localization of bleeding, since either it does not reveal pathology, or the changes are bilateral. High-resolution CT allows visualization of bronchiectasis. The use of contrast helps in identifying vascular integrity disorders, aneurysms and arteriovenous malformations.

Bronchoscopy for pulmonary hemorrhage was considered contraindicated 20-25 years ago. Currently, thanks to the improvement of anesthetic support and examination techniques, bronchoscopy has become the most important method for diagnosing and treating pulmonary hemorrhages. So far, this is the only method that allows you to examine the respiratory tract and directly see the source of bleeding or accurately determine the bronchus from which the blood is released. For bronchoscopy in patients with pulmonary hemorrhage, both a rigid and flexible bronchoscope (fibrobronchoscope) are used. A rigid bronchoscope allows for more effective blood suction and better ventilation of the lungs, and a flexible one allows for examining smaller bronchi.

In patients with pulmonary hemorrhage, the etiology of which seems unclear, bronchoscopy and especially bronchial arteriography often allow to identify the source of bleeding. To perform bronchial arteriography, it is necessary to puncture the femoral artery under local anesthesia and, using the Seldinger method, insert a special catheter into the aorta and then into the mouth of the bronchial artery. After the introduction of a radiopaque solution, direct or indirect signs of pulmonary hemorrhage are detected on the images. A direct sign is the release of the contrast agent beyond the vascular wall, and if the bleeding has stopped, its occlusion. Indirect signs of pulmonary hemorrhage are the expansion of the bronchial artery network (hypervascularization) in certain areas of the lung, aneurysmal vascular dilations, thrombosis of the peripheral branches of the bronchial arteries, the appearance of a network of anastomoses between the bronchial and pulmonary arteries.

Treatment of pulmonary hemorrhage

There are three main steps in the management of patients with profuse pulmonary hemorrhage:

• resuscitation and respiratory protection;
• determining the location of bleeding and its cause;
• stopping bleeding and preventing its recurrence.

The possibilities of effective first aid for pulmonary hemorrhage, unlike all external hemorrhages, are very limited. Outside a medical institution, the correct behavior of medical workers is important for a patient with pulmonary hemorrhage, from whom the patient and his environment require quick and effective actions. These actions should consist of emergency hospitalization of the patient. At the same time, they try to convince the patient not to be afraid of blood loss and not to instinctively hold back a cough. On the contrary, it is important to cough up all the blood from the respiratory tract. In order to better conditions for coughing up blood, the patient's position during transportation should be sitting or semi-sitting. It is necessary to hospitalize a patient with pulmonary hemorrhage in a specialized hospital with conditions for bronchoscopy, contrast X-ray examination of blood vessels and surgical treatment of lung diseases.

Treatment algorithm for patients with pulmonary hemorrhage:

• lay the patient on the side where the source of bleeding in the lung is located;
• prescribe oxygen inhalations, etamsylate (to reduce the permeability of the vascular wall), tranquilizers, antitussives;
• reduce blood pressure and pressure in the pulmonary circulation (ganglion blockers: azamethonium bromide, trimethophan camsylate; clonidine);
• perform a bronchoscopy;
• determine the optimal scope of surgical intervention (lung resection, pneumonectomy, etc.);
• perform the operation under general anesthesia with intubation using a two-channel tube or blockade of the affected lung by inserting an endobronchial single-channel tube;
• perform a sanitizing bronchoscopy at the end of the operation.

Methods for stopping pulmonary hemorrhage can be pharmacological, endoscopic, X-ray-endovascular and surgical.

Pharmacological methods include controlled arterial hypotension, which is very effective in bleeding from the vessels of the systemic circulation - bronchial arteries. Reducing systolic blood pressure to 85-90 mm Hg creates favorable conditions for thrombosis and stopping bleeding. For this purpose, one of the following drugs is used.

• Trimethophane camsylate - 0.05-0.1% solution in 5% glucose solution or 0.9% sodium chloride solution intravenously by drip (30-50 drops per minute and then more).
• Sodium nitroprusside - 0.25-10 mcg/kg per minute, intravenously.
• Azamethonium bromide - 0.5-1 ml of 5% solution, intramuscularly - action in 5-15 minutes.
• Isosorbide dinitrate - 0.01 g (2 tablets under the tongue), can be used in combination with angiotensin-converting enzyme inhibitors.

In cases of bleeding from the pulmonary artery, the pressure in it is reduced by intravenous administration of aminophylline (5-10 ml of a 2.4% aminophylline solution is diluted in 10-20 ml of a 40% glucose solution and administered intravenously over 4-6 minutes). For all pulmonary hemorrhages, to slightly increase blood clotting, a fibrinolysis inhibitor can be administered intravenously by drip - 5% aminocaproic acid in 0.9% sodium chloride solution - up to 100 ml. Intravenous administration of calcium chloride. The use of etamsylate, menadione sodium bisulfide, aminocaproic acid, aprotinin are not significant for stopping pulmonary hemorrhage and therefore cannot be recommended for this purpose. In cases of minor and moderate pulmonary hemorrhage, as well as in cases where it is impossible to quickly hospitalize the patient in a specialized hospital, pharmacological methods can stop pulmonary hemorrhage in 80-90% of patients.

An endoscopic method for stopping pulmonary hemorrhage is bronchoscopy with direct action on the source of bleeding (diathermocoagulation, laser photocoagulation) or occlusion of the bronchus into which the blood flows. Direct action is especially effective in case of bleeding from a bronchial tumor. Bronchial occlusion can be used in case of massive pulmonary hemorrhages. A silicone balloon catheter, foam sponge, and gauze tamponade are used for occlusion. The duration of such occlusion may vary, but usually 2-3 days are enough. Bronchial occlusion prevents blood aspiration into other parts of the bronchial system and sometimes finally stops the bleeding. If subsequent surgery is necessary, bronchial occlusion makes it possible to increase the time for preparation for surgery and improve the conditions for its implementation.

In patients with stopped bleeding, bronchoscopy should be performed as soon as possible, preferably in the first 2-3 days. In this case, it is often possible to determine the source of bleeding. Usually, it is a segmental bronchus with remnants of clotted blood. Bronchoscopy, as a rule, does not provoke resumption of bleeding.

An effective method for stopping pulmonary hemorrhage is X-ray endovascular occlusion of the bleeding vessel. The success of bronchial artery embolization depends on the skills of the physician. It should be performed by an experienced radiologist skilled in angiography. Arteriography is first performed to determine the site of bleeding from the bronchial artery. For this, such signs as vessel size, degree of hypervascularization, and signs of vascular shunting are used. Various materials are used for embolization, but primarily polyvinyl alcohol (PVA) in the form of small particles suspended in a radiopaque medium. They are not resorbable and thus prevent recanalization. Another agent is a gelatin sponge, which, unfortunately, leads to recanalization and is therefore used only as an addition to PVA. Isobutyl-2-cyanoacrylate, as well as ethanol, is not recommended due to the high risk of tissue necrosis. The immediate response of bronchial artery embolization success is noted in 73-98% of cases. Quite a few complications have been described, the most common of which is chest pain. Most likely, it is of ischemic origin and usually passes. The most dangerous complication is spinal cord ischemia, which occurs in 1% of cases. The probability of this complication can be reduced by using a coaxial microcatheter system for so-called supraselective embolization.

Surgical treatment is considered as a treatment option for patients with an established source of massive bleeding and when conservative measures are ineffective or conditions that directly threaten the patient's life. The most compelling indication for surgical intervention in pulmonary hemorrhage is the presence of aspergilloma.

Operations for pulmonary hemorrhages can be emergency, urgent, delayed and planned. Emergency operations are performed during bleeding. Urgent operations are performed after the bleeding has stopped, and delayed or planned operations are performed after the bleeding has stopped, a special examination and full preoperative preparation. Expectant tactics often lead to repeated bleeding, aspiration pneumonia, and disease progression.

The main operation for pulmonary hemorrhage is lung resection with removal of the affected part and the source of bleeding. Much less frequently, mainly in cases of bleeding in patients with pulmonary tuberculosis, collapse surgical interventions (thoracoplasty, extrapleural filling), as well as surgical bronchial occlusion, ligation of the bronchial arteries can be used.

Mortality with surgical intervention varies from 1 to 50%. If there are contraindications to surgery (eg, respiratory failure), other options are used. Attempts have been made to introduce sodium or potassium iodide into the cavity, instillation of amphotericin B with or without N-acetylcysteine through a transbronchial or percutaneous catheter. Systemic antifungal therapy for aspergilloma leading to bleeding has so far been disappointing.

After profuse bleeding, it may sometimes be necessary to partially replace the lost blood. For this purpose, red blood cell mass and fresh frozen plasma are used. During and after surgery for pulmonary hemorrhage, bronchoscopy is necessary to sanitize the bronchi, since the remaining liquid and coagulated blood in them contributes to the development of aspiration pneumonia. After stopping pulmonary hemorrhage, broad-spectrum antibiotics and anti-tuberculosis drugs must be prescribed to prevent aspiration pneumonia and exacerbation of tuberculosis.

The basis for preventing pulmonary hemorrhages is timely and effective treatment of lung diseases. In cases where surgical treatment of lung diseases is necessary with a history of bleeding, surgical intervention should be performed in a timely and planned manner.

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Spontaneous pneumothorax

Spontaneous pneumothorax is the entry of air into the pleural cavity, which occurs spontaneously, as if by itself, without damage to the chest wall or lung. However, in most cases of spontaneous pneumothorax, both a certain form of lung pathology and factors that contributed to its occurrence can be established.

It is difficult to estimate the frequency of spontaneous pneumothorax, since it often occurs and is eliminated without an established diagnosis. Men make up 70-90% of patients with spontaneous pneumothorax, mainly between the ages of 20 and 40. Pneumothorax is observed on the right somewhat more often than on the left.

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What causes spontaneous pneumothorax?

Currently, spontaneous pneumothorax is most often observed not in pulmonary tuberculosis, but in widespread or local bullous emphysema as a result of the rupture of air bubbles - bullae.

Generalized bullous emphysema is often a genetically determined disease, which is based on the deficiency of the inhibitor of elastase α ₁ -antitrypsin. Smoking and inhalation of polluted air are important in the etiology of generalized emphysema. Localized bullous emphysema, usually in the area of the apex of the lungs, can develop as a result of tuberculosis, and sometimes a nonspecific inflammatory process.

In the formation of bullae in local emphysema, the damage of small bronchi and bronchioles with the formation of a valve obstructive mechanism is important, which causes increased intra-alveolar pressure in the subpleural parts of the lung and ruptures of overstretched interalveolar septa. Bullae can be subpleural and barely bulge above the surface of the lung or represent bubbles connected to the lung by a wide base or a narrow stalk. They can be single or multiple, sometimes in the form of bunches of grapes. The diameter of the bullae is from a pinhead to 10-15 cm. The wall of the bullae is usually very thin, transparent. Histologically, it consists of a scant amount of elastic fibers covered from the inside by a layer of mesothelium. In the mechanism of spontaneous pneumothorax in bullous emphysema, the leading place belongs to an increase in intrapulmonary pressure in the area of thin-walled bullae. Among the causes of increased pressure, the most important are the patient's physical exertion, lifting weights, pushing, and coughing. At the same time, the valve mechanism at its narrow base and wall ischemia can contribute to the increase in pressure in the bulla and the rupture of its wall.

In addition to bullous widespread or local emphysema, the following factors may be important in the etiology of spontaneous pneumothorax:

• perforation of the tuberculous cavity into the pleural cavity;
• rupture of the cavity at the base of the pleural cord when applying artificial pneumothorax;
• damage to lung tissue during transthoracic diagnostic and therapeutic puncture:
• abscess rupture or gangrene of the lung;
• destructive pneumonia;
• pulmonary infarction, rarely - lung cyst; cancer. metastases of malignant tumors, sarcoidosis, berylliosis, histiocytosis X, fungal lung lesions and even bronchial asthma.

A special type of spontaneous pneumothorax is associated with the menstrual cycle. The cause of such pneumothorax is the rupture of localized emphysematous bullae, which are formed by intrapulmonary or subpleural implantation of endometrial cells.

In some patients, spontaneous pneumothorax develops sequentially on both sides, but there are known cases of simultaneous bilateral pneumothorax. Complications of pneumothorax include the formation of exudate in the pleural cavity, usually serous, sometimes serous-hemorrhagic or fibrinous. In patients with active tuberculosis, cancer, mycosis, with an abscess or gangrene of the lung, the exudate is often infected with non-specific microflora and purulent pleurisy (pyopneumothorax) joins the pneumothorax. Rarely, with pneumothorax, air penetration into the subcutaneous tissue, into the mediastinal tissue ( pneumomediastinum ) and air embolism are observed. A combination of spontaneous pneumothorax and intrapleural bleeding (hemopneumothorax) is possible. The source of bleeding is either the site of perforation of the lung or the edge of the rupture of the pleural adhesion. Intrapleural bleeding can be significant and cause symptoms of hypovolemia and anemia

Symptoms of spontaneous pneumothorax

Clinical symptoms of spontaneous pneumothorax are caused by air entering the pleural cavity and the occurrence of lung collapse. Sometimes spontaneous pneumothorax is diagnosed only by X-ray examination. However, more often the clinical symptoms are quite pronounced. The disease usually occurs suddenly, and patients can accurately indicate the time of its onset. The main complaints are chest pain, dry cough, shortness of breath, palpitations. The pain can be localized in the upper abdomen, and sometimes concentrated in the heart area, radiating to the left arm and shoulder blade, to the hypochondrium. In some cases, the picture may be similar to acute coronary circulatory failure, myocardial infarction, pleurisy, perforated ulcer of the stomach or duodenum, cholecystitis, pancreatitis. The pain may gradually subside. The origin of the pain is not entirely clear, since it appears even in the absence of pleural adhesions. At the same time, when artificial pneumothorax is imposed, there is usually no significant pain.

In severe cases of spontaneous pneumothorax, pale skin, cyanosis, cold sweat, tachycardia with increased blood pressure are characteristic. Symptoms of shock may be expressed. Much depends on the speed of development of pneumothorax, the degree of lung collapse, displacement of mediastinal organs, age and functional state of the patient.

A small spontaneous pneumothorax is not always diagnosed using physical methods. With a significant amount of air in the pleural cavity on the side of the pneumothorax, a box percussion sound is detected, respiratory sounds are sharply weakened or absent. Air penetration into the mediastinum sometimes causes mediastinal emphysema, which is clinically manifested by a hoarse voice.

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Diagnosis of spontaneous pneumothorax

The most informative method for diagnosing all types of spontaneous pneumothorax is X-ray examination. Images are taken during inhalation and exhalation. In the latter case, the edge of the collapsed lung is better revealed. The degree of lung collapse, localization of pleural adhesions, position of the mediastinum, presence or absence of fluid in the pleural cavity are established. It is always important to identify the pulmonary pathology that caused spontaneous pneumothorax. Unfortunately, conventional X-ray examination, even after air aspiration, is often ineffective. CT is necessary to recognize local and widespread bullous emphysema. It is also often indispensable for distinguishing spontaneous pneumothorax from a lung cyst or a large, inflated, thin-walled bulla.

The air pressure in the pleural cavity and the nature of the opening in the lung can be assessed using manometry, for which a puncture of the pleural cavity is performed and the needle is connected to the water manometer of the pneumothorax apparatus. Usually the pressure is negative, i.e. lower than atmospheric, or approaches zero. The changes in pressure during the process of air suction can be used to judge the anatomical features of the pulmonary-pleural communication. The clinical course of pneumothorax largely depends on its features.

When a small bulla is perforated, only a one-time flow of air into the pleural cavity is often observed. After the lung collapses, the small hole in such cases closes on its own, the air is absorbed, and the pneumothorax is eliminated within a few days without any treatment. However, with continued, even a very small flow of air, pneumothorax can exist for many months and years. Such pneumothorax, in the absence of a tendency for the collapsed lung to straighten out and in conditions of late or ineffective treatment, gradually becomes chronic ("pneumothorax disease" in the old terminology). The lung is covered with fibrin and connective tissue, which form a more or less thick fibrous shell. Later, connective tissue from the visceral pleura grows into the rigid lung and grossly disrupts its normal elasticity. Pleurogenic cirrhosis of the lung develops, in which it loses the ability to straighten out and restore normal function even after surgical removal of the shell from its surface; patients often experience progressive respiratory failure, and hypertension develops in the pulmonary circulation. Long-term pneumothorax can lead to pleural empyema.

A particularly severe and life-threatening form of spontaneous pneumothorax is tension, valve, valvular or progressive pneumothorax. It occurs when a valvular pulmonary-pleural communication forms at the site of perforation of the visceral pleura. During inhalation, air enters the pleural cavity through the perforation, and during exhalation, the closing valve prevents it from exiting the pleural cavity. As a result, with each inhalation, the amount of air in the pleural cavity increases, and intrapleural pressure increases. The lung on the side of the pneumothorax completely collapses. There is a shift in the mediastinal organs to the opposite side, with a decrease in the volume of the second lung. The main veins shift, bend and become compressed, and blood flow to the heart decreases. The dome of the diaphragm descends and becomes flat. Ruptures of adhesions between the parietal and visceral pleura easily occur, forming hemopneumothorax.

Patients with tension pneumothorax experience severe dyspnea, cyanosis, a change in the timbre of the voice, and fear of death. Usually, a forced sitting position and anxiety and agitation of the patient are noted. Accessory muscles participate in breathing. The chest wall on the side of the pneumothorax lags behind during breathing, the intercostal spaces are smoothed out or bulge. Sometimes the supraclavicular fossa also bulges. Palpation reveals a shift in the apical impulse of the heart to the side opposite to the pneumothorax, and there is no vocal fremitus on the side of the pneumothorax. Subcutaneous emphysema may be determined. Percussion reveals high tympanitis and displacement of the mediastinal organs, and auscultation reveals the absence of respiratory sounds on the side of the pneumothorax. Body temperature occasionally rises. X-ray examination confirms and clarifies the clinical data. Acute respiratory failure with severe hemodynamic disorders developing with tension pneumothorax in the absence of treatment measures can quickly lead to the death of the patient.

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Treatment of spontaneous pneumothorax

Spontaneous pneumothorax should be treated in a hospital. With a thin layer of air between the lung and the chest wall, no special treatment is often required. In cases of a more significant amount of air, a puncture of the pleural cavity is necessary with suction, if possible, of all the air. The puncture is performed under local anesthesia along the midclavicular line in the second intercostal space. If all the air cannot be removed and it continues to flow into the needle "endlessly", a silicone catheter must be inserted into the pleural cavity for continuous aspiration of air. In hemopneumothorax, a second catheter is inserted along the midaxillary line in the sixth intercostal space. Continuous aspiration with a vacuum of 10-30 cm H2O in most cases leads to the cessation of air flow from the pleural cavity. If the lung has straightened according to X-ray examination data, aspiration is continued for another 2-3 days. and then the catheter is removed. However, sometimes the air supply through the catheter continues for 4-5 days. In such a situation, sodium bicarbonate or tetracycline solutions are often introduced into the pleural cavity, as well as spraying pure talc powder, which causes the development of pleural adhesions. An attempt can be made to seal the lung using electrocoagulation or biological glue through a thoracoscope inserted into the pleural cavity. However, with prolonged air supply, surgical treatment is more often resorted to by means of minimally invasive video-assisted thoracoscopic or open surgery.

In case of tension pneumothorax, the patient needs emergency care - drainage of the pleural cavity with constant aspiration of air. Temporary relief of the patient's condition can be achieved in a simpler way - by introducing 1-2 thick needles or a trocar into the pleural cavity. This technique allows to reduce intrapleural pressure and eliminate the immediate threat to the patient's life. In case of bilateral spontaneous pneumothorax, aspiration drainage of both pleural cavities is indicated. Treatment of patients with tension and bilateral spontaneous pneumothorax is preferably carried out in intensive care units, resuscitation units or specialized pulmonary surgical units.

In 10-15% of patients, spontaneous pneumothorax recurs after treatment with punctures and drainage if the causes for its occurrence and a free pleural cavity remain. In case of relapses, it is advisable to perform videothoracoscopy and determine subsequent treatment tactics depending on the identified picture.

Pulmonary embolism

Pulmonary embolism is a life-threatening condition that can disrupt blood flow to a significant portion of the lungs.

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Causes of pulmonary embolism

Pulmonary embolism may occur in patients with widespread fibrocavernous pulmonary tuberculosis or tuberculous empyema, in elderly patients and in patients suffering from chronic pulmonary heart failure, often after extensive surgical interventions.

Thrombi from the deep veins of the lower extremities and pelvic veins enter the right atrium with the blood flow, then into the right ventricle, where they fragment. From the right ventricle, thrombi enter the pulmonary circulation.

The development of massive pulmonary embolism is accompanied by an increase in pressure in the pulmonary artery, which leads to an increase in the total vascular resistance in the lungs. Overload of the right ventricle, a drop in cardiac output and the development of acute cardiovascular failure occur.

Symptoms of pulmonary embolism

Clinical symptoms of thromboembolism are non-specific, patients complain of shortness of breath, cough, fear, rapid breathing, tachycardia. Auscultation reveals an increase in the second tone over the pulmonary artery, signs of bronchospasm (dry wheezing). Infarction-pneumonia and limited thromboembolism in the pulmonary artery system are characterized by clinical symptoms such as chest pain and hemoptysis. Patients note pain along the deep veins of the extremities and swelling of the lower leg.

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Diagnosis of pulmonary embolism

Changes in gas composition: a decrease in the partial pressure of oxygen in arterial blood (due to blood shunting) and carbon dioxide (a consequence of hyperventilation), which is especially characteristic of the sudden development of massive thromboembolism. Radiologically, a decrease in lung volume and sometimes pleural effusion, the appearance of local zones of reduced blood filling and dilation of the hilar arteries proximal to the thrombosed area are detected. Auxiliary methods for diagnosing pulmonary embolism (echocardiography, ventilation-perfusion scintigraphy, angiopulmonography) are practically unavailable in severe conditions of patients with tuberculosis and suddenly developed thromboembolism.

Treatment of pulmonary embolism

• immediately after diagnosis, it is necessary to administer 10 thousand units of sodium heparin intravenously, subsequently the drug should be administered every hour at 1-1.5 thousand units until it increases by 1.5-2 times compared to the initial value of APTT. It is possible to start with an infusion of sodium heparin at a dose of 80 units/kg per hour, then continue subcutaneous administration of sodium heparin at 3-5 thousand units under the control of coagulogram parameters;
• simultaneously or after 2-3 days, it is advisable to prescribe indirect anticoagulants orally (warfarin, ethyl biscoumacetate) until prothrombin time increases by 1.5 times;
• oxygen therapy 3-5 l/min;
• when a diagnosis of massive pulmonary embolism is established and thrombolytic therapy is prescribed, anticoagulant therapy should be discontinued as unnecessary;
• In case of massive thromboembolism, it is recommended to use urokinase intravenously at a dose of 4000 U/kg for 10 minutes, then intravenously by drip at 4000 U/kg for 12-24 hours, or streptokinase intravenously at 250 thousand U for 30 minutes, then 100 U/hour for 12-72 hours;
• When the exact location of the embolus is determined or when anticoagulant or thrombolytic therapy is ineffective, embolectomy is indicated.

Acute lung injury syndrome

Acute lung injury syndrome (ALIS) and adult acute respiratory distress syndrome (ARDS) are non-cardiogenic pulmonary edema with severe respiratory failure and pronounced hypoxia resistant to oxygen therapy. The cause of ALI and ARDS is damage to the pulmonary capillaries and alveolar endothelium due to inflammation and increased permeability of the pulmonary vessels with the development of interstitial pulmonary edema, arteriovenous shunting, disseminated intravascular coagulation and microthrombosis in the lungs. As a result of interstitial pulmonary edema, surfactant is damaged and the elasticity of the lung tissue decreases.

Clinical examination data do not always allow us to differentiate cardiogenic pulmonary edema (CPE) from ARDS. However, in the early stages of development, there are certain differences.

Cardiogenic pulmonary edema occurs due to increased pressure in the pulmonary capillaries against the background of normal permeability of the pulmonary vessels.

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Symptoms of Acute Lung Injury Syndrome

The severity of clinical manifestations of COL increases rapidly. Patients are agitated, note a feeling of fear, suffocation, pain in the heart area, wheezing, participation of intercostal muscles in respiration, auscultatory signs of pulmonary congestion, hypoxia with acrocyanosis, coughing up pink foamy sputum are characteristic. X-ray changes occur somewhat later: decreased transparency of the lung fields, expansion of the roots of the lungs, increased heart volume and pleural effusion.

Clinical manifestations of acute lung injury syndrome do not appear immediately, as with cardiogenic shock, but gradually: increasing dyspnea, cyanosis, wheezing in the lungs ("wet lung"). Radiologically, bilateral pulmonary infiltration is detected against the background of previously unchanged pulmonary pattern.

Diagnosis of acute lung injury syndrome

Radiologically, in acute lung injury syndrome, a mesh-like pattern of the lungs, blurred shadows of the vessels, especially in the lower sections, and an increase in the vascular pattern in the area of the root of the lung (“snow storm”, “butterfly”, “wings of the angel of death”) are noted.

Changes in blood gas composition: arterial hypoxemia with subsequent addition of hypercapnia and development of metabolic acidosis, while arterial hypoxemia is not eliminated even by high concentrations of oxygen in the inhaled mixture. Development or progression of pneumonia with severe respiratory failure is often the cause of death in these patients.

The differences between ALI and ARDS are mainly in the quantitative manifestation of the degree of lung damage and in the change in the oxygenation index. With ALI, the oxygenation index can be below 300, and with ARDS even below 200 (the norm is 360-400 and more).

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Treatment of acute lung injury syndrome

• continuous controlled oxygen therapy;
• antibacterial therapy taking into account the sensitivity of microflora;
• glucocorticoids (prednisolone, methylprednisolone, hydrocortisone);
• nonsteroidal anti-inflammatory drugs - NSAIDs (diclofenac);
• direct anticoagulants (sodium heparin and its analogues);
• nitrates (nitroglycerin) and peripheral vasodilators (sodium nitroprusside);
• cardiotonics (dopamine, dobutamine);
• diuretics (furosemide, ethacrynic acid, spironolactone);
• surfactant emulsion for inhalation (surfactant-BL and surfactant-HL);
• antihistamines (chloropyramine, promethazine);
• analgesic drugs (morphine, trimeperidine, lornoxicam);
• antioxidants;
• cardiac glycosides (strophanthin-K, lily of the valley glycoside, etc.) in the absence of contraindications;
• Artificial ventilation with positive end-expiratory pressure if necessary.

Oxygen therapy should be started immediately after the onset of signs of acute respiratory failure. Oxygen is supplied through a nasotracheal catheter or mask under the control of pulse oximetry and blood gas composition. The concentration of oxygen in the inhaled mixture can be increased from 50 to 90% at the height of ARDS development for a short period of time to increase pO2 _in arterial blood above 60 mm Hg.

Antibacterial therapy with broad-spectrum drugs is often prescribed empirically, without waiting for the results of bacterial testing. In the treatment of ARDS, glucocorticoids are widely used, which reduce edema associated with lung damage, have an anti-shock effect, reduce the tone of resistance vessels and increase the tone of capacitance vessels, and reduce histamine production. It is also advisable to use NSAIDs and antihistamines, which block the accumulation of fibrinogen breakdown products and reduce vascular permeability.

To prevent the progression of intravascular coagulation and thrombus formation, anticoagulants are used.

In the development of ARDS, intravenous and oral diuretics are prescribed to reduce the severity or stop pulmonary edema. Preference should be given to furosemide (it has a vasodilatory effect on veins and reduces congestion in the lungs).

Nitrates and peripheral vasodilators help relieve the pulmonary circulation. Nitroglycerin and sodium nitroprusside are used in ARDS as infusions; the drugs affect the pulmonary vessels, reduce peripheral resistance, increase cardiac output, and enhance the effect of diuretics.

Adrenomimetics with pronounced cardiotonic and inotropic effects (dopamine, dobutamine) are used in complex infusion intensive therapy for low cardiac output and arterial hypotension. Phosphocreatine is used to improve myocardial metabolism and microcirculation, especially in patients with ischemic heart disease.

Morphine not only provides an analgesic and sedative effect, but also reduces venous tone and redistributes blood flow, improving blood supply to peripheral areas.

Interstitial and alveolar pulmonary edema inevitably leads to damage to the pulmonary surfactant. This is accompanied by an increase in surface tension and fluid leakage into the alveoli, so in ARDS, it is necessary to prescribe inhalations of 3% surfactant-BL emulsion as early as possible in the form of instillations and using mechanical inhalers. The use of an ultrasonic inhaler is unacceptable, since the surfactant is destroyed when the emulsion is treated with ultrasound.

Progression of ARDS with severe respiratory failure is an indication for transferring patients to artificial ventilation in the mode of creating positive pressure at the end of expiration (PEEP). The mode is recommended to maintain pO ₂ >60 mm Hg with FiO2 ≤0.6.

The use of PEEP during mechanical ventilation allows for ventilation of collapsed alveoli, an increase in functional residual capacity and lung compliance, a reduction in shunting, and improved blood oxygenation. The use of PEEP with low pressure (less than 12 cm H2O) helps prevent surfactant destruction and lung tissue damage from local exposure to oxygen. PEEP that exceeds the pulmonary resistance contributes to blood flow blockage and a decrease in cardiac output, may worsen tissue oxygenation, and increase the severity of pulmonary edema.

To reduce the risk of iatrogenic lung injury during mechanical ventilation, the use of pressure-controlled servo-ventilators can be recommended. This prevents the risk of lung overinflation by providing small tidal volumes and an inverted inspiratory/expiratory ratio during mechanical ventilation in patients with ARDS.