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

[1], [2], [3], [4], [5], [6], [7],

Hemoptysis and bleeding

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

A ogochnoe bleeding - the outpouring of a significant amount of blood into the bronchial lumen. Liquid, or mixed with sputum, the blood of the patient, as a rule, coughs. The difference between pulmonary hemorrhage and hemoptysis is mainly quantitative. Experts of the European Respiratory Society (ERS) pulmonary hemorrhage is defined as a condition in which the patient loses from 200 to 1000 ml of blood within 24 hours.

In case of pulmonary hemorrhage, the blood is coughed up in significant quantities simultaneously, continuously or intermittently. Depending on the amount of blood extracted in Russia, it is customary to distinguish bleeding small (up to 100 ml), medium (up to 500 ml) and large, or profuse (over 500 ml). It should be borne in mind that patients and their surroundings tend to exaggerate the amount of allocated blood. Patients may not cough up some of the blood from the respiratory tract, but aspirate or swallow. Therefore, a quantitative assessment of blood loss in pulmonary hemorrhage is always approximate.

Profuse pulmonary hemorrhage is a great danger to life and can lead to death. Causes of death are asphyxia or such further complications of bleeding, such as aspiration pneumonia, progression of tuberculosis, and pulmonary heart disease. Mortality in case of profuse bleeding reaches 80%, and at smaller volumes of blood loss - 7-30%.

[8], [9], [10], [11], [12], [13], [14], [15]

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 is more often complicated by infiltrative forms, caseous pneumonia, fibro-cavernous tuberculosis. Sometimes bleeding occurs with cirrhotic tuberculosis or post-tuberculosis pulmonary fibrosis. Profuse pulmonary bleeding can occur in case of aortic aneurysm rupture into the left main bronchus. Other causes of pulmonary hemorrhage are fungal and parasitic lesions of the lungs, and in the first place - aspergilloma in the residual cavity or air cyst. Less commonly, the source of bleeding is associated with bronchial carcinoid, bronchiectasis, broncho-lithitis, a foreign body in the lung tissue or in the bronchi, pulmonary infarction, endometriosis, mitral valve disease with hypertension in the pulmonary circulation, complications after lung operations.

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

[16], [17], [18]

Symptoms of pulmonary hemorrhage

Pulmonary hemorrhage is observed more often in middle-aged and elderly men. It begins with hemoptysis, but may occur suddenly, against the background of a good condition. Provide the possibility and time of bleeding, as a rule, impossible. Scarlet or dark blood is cleared through the mouth in pure form or with sputum. Blood can also be excreted through the nose. Blood is usually frothy and not clotted. It is always important to establish the nature of the underlying pathological process and determine the source of the bleeding. Such diagnosis of pulmonary hemorrhage is often very difficult, even when using modern x-ray and endoscopic methods.

When clarifying the history pay attention to diseases of the lungs, heart, blood. The information obtained from the patient, his relatives or the doctors who watched him may have important diagnostic value. So. With pulmonary bleeding. Unlike bleeding from the esophagus or stomach, blood is always excreted with a cough and is foamy. The scarlet color of blood indicates its intake from the bronchial arteries, and the dark one from the pulmonary artery system. 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 in the sputum secreted by patients with pulmonary hemorrhage, acid-resistant bacteria can be detected, which immediately causes a reasonable suspicion of tuberculosis. Patients themselves rarely feel from which lung or from which area the blood is released. Subjective feelings of the patient are very often not true 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 blood pressure. The underestimation of arterial hypertension can negate all subsequent medical 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 otorhinolaryngologist. Over the area of pulmonary hemorrhage listen wet rales and crepitus. After the usual physical examination, radiography in two projections is necessary in all cases. The most informative CT and bronchial arteriography. 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.

The venous blood test must necessarily include platelet counts. Assessment of hemoglobin content and determination of coagulability indices, Determination of hemoglobin over time is an available indicator of blood loss.

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

Bronchoscopy for pulmonary hemorrhage was considered contraindicated 20-25 years ago. At present, thanks to the improvement of anesthesia and the research technique, bronchoscopy has become the most important method for the diagnosis and treatment of pulmonary hemorrhages. While this is the only way that allows you to inspect the respiratory tract and directly see the source of bleeding or accurately determine the bronchus from which blood is released. For bronchoscopy in patients with pulmonary hemorrhage, both rigid and flexible bronchoscope (fibrobronchoscope) are used. Rigid bronchoscope allows more efficient suction of blood and better ventilation of the lungs, and flexible - to view the smaller bronchi.

In patients with pulmonary hemorrhage, the etiology of which is unclear, bronchoscopy and especially bronchial arteriography often reveal the source of the bleeding. To conduct bronchial arteriography, it is necessary to puncture the femoral artery under local anesthesia and, using the Seldinger method, conduct a special catheter into the aorta and further to the mouth of the bronchial artery. After the introduction of the radiopaque solution in the pictures reveal direct or indirect signs of pulmonary hemorrhage. A direct symptom is the emergence of a contrast substance beyond the limits of the vascular wall, and in case of stopped bleeding, its occlusion. Indirect signs of pulmonary hemorrhage are the expansion of the network of bronchial arteries (hypervascularization) in certain areas of the lung, aneurysmal vascular dilatation, thrombosis of the peripheral branches of bronchial arteries, the appearance of an anastomotic network 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 protection of the respiratory tract;
• determination of the bleeding site and its causes;
• stop bleeding and prevent its recurrence.

The possibilities of effective first aid for pulmonary hemorrhage, in contrast to all external bleeding, are very limited. Outside of a medical institution, in a patient with pulmonary hemorrhage, it is important that the correct behavior of health workers, from which the patient and his environment require quick and effective action. These actions should consist in emergency hospitalization of the patient. In parallel, they try to convince the patient not to be afraid of blood loss and not instinctively restrain a cough. On the contrary - it is important to cough up all the blood from the respiratory tract. For the purpose of better conditions for coughing up blood, the position of the patient during transportation should be sedentary or semi-sitting. It is necessary to hospitalize a patient with pulmonary hemorrhage in a specialized hospital with the presence of conditions for bronchoscopy, contrast x-ray of the vascular and surgical treatment of lung diseases.

Algorithm for the treatment of patients with pulmonary hemorrhage:

• place the patient on the side where the source of bleeding in the lung is located;
• assign oxygen inhalation, etamzilat (to reduce the permeability of the vascular wall), tranquilizers, antitussives;
• reduce blood pressure and pressure in the pulmonary circulation (ganglioblockers: azametonium bromide, trimethophan camsilate; clonidine);
• perform bronchoscopy;
• determine the optimal volume of surgical intervention (resection of the lung, pneumonectomy, etc.);
• perform the operation under anesthesia with the intubation of a two-channel tube or blockade of the affected lung by the introduction of an endobronchial single-channel tube;
• carry out 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 large circulation, the bronchial arteries. Decrease in systolic blood pressure to 85-90 mm Hg creates favorable conditions for thrombosis and stop bleeding. For this purpose, use one of the following drugs.

• Trimethophan camsilate - 0.05-0.1% solution in 5% glucose solution or in 0.9% sodium chloride solution intravenously (30-50 drops per minute and then more).
• Sodium nitroprusside - 0.25-10 µg / kg per minute, intravenously.
• Azametonium bromide - 0.5-1 ml of 5% solution, intramuscularly - action after 5-15 minutes.
• Isosorbide dinitrate - 0.01 g (2 tablets under the tongue), can be combined 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 2.4% solution of aminophylline is diluted in 10-20 ml of 40% glucose solution and injected into a vein within 4-6 minutes). For all pulmonary hemorrhages, for some increase in blood coagulability, an inhibitor of fibrinolysis — 5% solution of aminocaproic acid in 0.9% sodium chloride solution — up to 100 ml can be administered intravenously. Intravenous administration of calcium chloride. The use of etamzilat, menadione sodium bisulfide, aminocaproic acid, aprotinin is not essential for stopping pulmonary hemorrhage and therefore cannot be recommended for this purpose. In case of small and medium pulmonary hemorrhages, as well as in cases where it is impossible to quickly hospitalize a patient in a specialized hospital, pharmacological methods allow stopping pulmonary hemorrhage in 80-90% of patients.

An endoscopic method for stopping pulmonary hemorrhage is bronchoscopy with a direct effect on the source of bleeding (diathermocoagulation, laser photocoagulation) or occlusion of the bronchus into which blood flows. Direct exposure is particularly effective when bleeding from a bronchial tumor. Occlusion of the bronchus can be used for massive pulmonary hemorrhages. For occlusion using a silicone balloon catheter, foam sponge, gauze tamponade. The duration of such an occlusion may vary, but usually 2-3 days are sufficient. Occlusion of the bronchus prevents the aspiration of blood to other parts of the bronchial system and sometimes stops the bleeding completely. If necessary, the subsequent operation of the occlusion of the bronchus makes it possible to increase the time to prepare for surgery and to improve the conditions for its implementation.

In patients with stopped bleeding, bronchoscopy should be performed as early as possible, preferably in the first 2-3 days. It is often possible to determine the source of bleeding. This is usually the segmental bronchus with remnants of clotted blood. Resumption of bleeding bronchoscopy, as a rule, does not provoke.

An effective method for stopping pulmonary hemorrhage is x-ray enovascular occlusion of a bleeding vessel. The success of embolization of the bronchial arteries depends on the skills of the doctor. It should be performed by an experienced radiologist who owns angiography. First, arteriography is performed to determine the site of bleeding from the bronchial artery. To do this, use signs such as the size of the vessels, the degree of hypervascularization, as well as signs of vascular bypass surgery. Various materials are used for embolization, but first of all polyvinyl alcohol (PVA) in the form of small particles suspended in X-ray contrast medium. They are not able to dissolve and thus prevent recanalization. Another agent is a gelatin sponge, which, unfortunately, leads to recanalization and therefore is used only as a supplement to PVA. Isobutyl-2-cyanoacrylate, as well as ethanol, is not recommended, due to the high risk of developing tissue necrosis. Immediate response to the success of bronchial artery embolization was noted in 73-98% of cases. At the same time, quite a lot of complications have been described, among which the most frequent is chest pain. Most likely, it has an ischemic nature and usually goes away. The most dangerous complication is spinal cord ischemia, which occurs in 1% of cases. The likelihood of this complication can be reduced by using a coaxial microcatheter system for conducting so-called supraselective embolization.

The surgical method is considered as a treatment option for patients with an established source of massive bleeding and with the ineffectiveness of conservative measures or conditions that directly threaten the patient’s life. The most weighty indications for surgery for pulmonary hemorrhage is the presence of aspergilloma.

Operations for pulmonary hemorrhage can be emergency, urgent, delayed and planned. Emergency surgery is performed during bleeding. Urgent - after stopping bleeding, and delayed or planned - after stopping bleeding, 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 resection of the lung with the removal of its affected part and 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 occlusion of the bronchus, ligation of bronchial arteries can be used.

Mortality in surgical intervention varies from 1 to 50%. If there are contraindications to surgery (for example, respiratory failure), other options are used. Attempts were 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 of asperigilloma, leading to bleeding, while disappointing.

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

The basis for the prevention of pulmonary hemorrhage is the timely and effective treatment of pulmonary diseases. In cases of the need for surgical treatment of pulmonary diseases with bleeding in history, surgical intervention should be carried out in a timely manner and in a planned manner.

[19], [20]

Spontaneous pneumothorax

Spontaneous pneumothorax - the flow of air into the pleural cavity, which occurs spontaneously, as if spontaneously, without damaging the chest wall or lung. However, in most cases with spontaneous pneumothorax, both a definite form of lung disease and factors that contributed to its occurrence may well be established.

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

[21], [22], [23]

What causes spontaneous pneumothorax?

Nowadays, most often spontaneous pneumothorax is observed not with pulmonary tuberculosis, but with widespread or local bullous emphysema as a result of the bursting of air bubbles - bull.

Common bullous emphysema is often a genetically determined disease, which is based on the insufficiency of the α ₁ antitrypsin elastase inhibitor. In the etiology of common emphysema, smoking, inhalation of polluted air are important. Localized bullous emphysema, usually in the apex of the lungs, may develop as a result of a previous tuberculosis. And sometimes non-specific inflammatory process.

In the formation of bulls with local emphysema, the defeat of the small bronchi and bronchioles is important, with the formation of a valve obstructive mechanism, which causes increased intraalveolar pressure in the subpleural regions of the lung and ruptures of the over-stretched interalveolar septa. Bullae can be subpleural and barely protrude above the surface of the lung or be bubbles associated with a light broad base or narrow stem. They are single and multiple, sometimes in the form of bunches of grapes. The diameter of a bull from a pinhead is up to 10-15 cm. The wall of a bull is usually very thin and transparent. Histologically, it consists of a meager amount of elastic fibers, covered from the inside with a layer of mesothelium. In the mechanism of the occurrence of spontaneous pneumothorax in bullous emphysema, the leading role belongs to the increase in intrapulmonary pressure in the zone of thin-walled bulla. Among the reasons for the increase in pressure are the main importance of physical stress of the patient, lifting of gravity, push, cough. At the same time, pressure increase in the bulla and rupture of its wall can be promoted by the valve mechanism at its narrow base and wall ischemia.

In addition to the common bullous or localized emphysema, the etiology of spontaneous pneumothorax may be of the following factors:

• perforation into the pleural cavity of the tubercular cavity;
• rupture of the cavern at the base of the pleural cord during the imposition of artificial pneumothorax;
• lung tissue damage during transthoracic diagnostic and therapeutic puncture:
• breakthrough abscess or gangrene of the lung;
• destructive pneumonia;
• pulmonary infarction, rarely - lung cyst; crayfish. Metastases of malignant tumors, sarcoidosis, berylliosis, histiocytosis X, pulmonary fungal and even asthma.

A special type of spontaneous pneumothorax is associated with the menstrual cycle. The cause of this pneumothorax becomes a rupture of localized emphysematous bull, which are formed during intrapulmonary or subpleural implantation of endometrial cells.

In some patients, spontaneous pneumothorax consistently develops on both sides, but there are cases of simultaneous bilateral pneumothorax. The complications of pneumothorax include the formation of fluid in the pleural cavity, usually serous, sometimes serous hemorrhagic or fibrinous. In patients with active tuberculosis, cancer, mycosis, with abscess or gangrene of the lung, the exudate is often infected with nonspecific microflora and purulent pleurisy (pyopneumothorax) joins pneumothorax. With pneumothorax, air infiltration into the subcutaneous tissue, mediastinal tissue ( pneumomediastinum ) and air embolism are rarely observed. Possible combination of spontaneous pneumothorax with intrapleural bleeding (hemopneumothorax). The source of bleeding is either a place of perforation of the lung, or the edge of the rupture of pleural adhesions. Intrapleural bleeding can be significant and cause symptoms of hypovolemia and anemia.

Symptoms of spontaneous pneumothorax

Clinical symptoms of spontaneous pneumothorax are caused by the flow of air into the pleural cavity and the appearance of a collapse of the lung. Sometimes spontaneous pneumothorax is diagnosed only on x-ray examination. However, most often the clinical symptoms are quite pronounced. The disease is usually. Occurs suddenly, and patients can accurately indicate the time of its beginning. The main complaints are chest pain, dry cough, shortness of breath, palpitations. Pain can be localized in the upper abdomen, and sometimes concentrated in the heart, radiating to the left arm and scapula, in the hypochondrium. In some cases, the picture may be similar to acute insufficiency of the coronary circulation, myocardial infarction, pleurisy, perforated gastric or duodenal ulcer, cholecystitis, pancreatitis. Gradually, the pain may subside. The origin of the pain is not entirely clear, as it appears in the absence of pleural adhesions. At the same time, with the imposition of an artificial pneumothorax, there is usually no significant pain.

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

Small spontaneous pneumothorax with the help of physical methods are not always diagnosed. With a significant amount of air in the pleural cavity on the side of pneumothorax, a boxed percussion sound is determined, the respiratory sounds are sharply attenuated or absent. Air infiltration into the mediastinum sometimes causes mediastinal emphysema, which is clinically manifested in a hoarse voice.

[24],

Diagnosis of spontaneous pneumothorax

The most informative method for diagnosing all variants of spontaneous pneumothorax is x-ray examination. Pictures are made on the inhale and exhale. In the latter case, the edge of the collapsed lung is better detected. Establish the degree of collapse of the lung, the localization of pleural adhesions, the position of the mediastinum, the presence or absence of fluid in the pleural cavity. It is always important to identify pulmonary pathology, which was the cause of spontaneous pneumothorax. Unfortunately, a routine X-ray examination, even after aspiration of air, is often ineffective. CT is necessary for recognition of local and widespread bullous emphysema. It is often indispensable for distinguishing spontaneous pneumothorax from a lung cyst or a large, swollen, thin-walled bulla.

The amount of air pressure in the pleural cavity and the nature of the hole in the lung can be assessed using manometry, for which a puncture of the pleural cavity is made and the needle is connected to the water pressure gauge of the pneumothorax apparatus. Usually the pressure is negative, i.e. Below atmospheric, or approaching zero. According to the pressure changes in the process of air suction, one can judge about the anatomical features of the pulmonary pleural message. The clinical course of pneumothorax largely depends on its features.

During perforation of a small bulla, only one-stage admission of air into the pleural cavity is often observed. After the lung collapses, the small opening 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 last for months and years. Such a pneumothorax, in the absence of a tendency to the collapse of a collapsed lung and in conditions of late or ineffective treatment, gradually becomes chronic (“pneumothorax disease” according to the old terminology). The lung is covered with fibrin and connective tissue, which form a more or less thick fibrous shell. Later, the connective tissue on the part of the visceral pleura grows into a rigid lung and roughly violates its normal elasticity. A pleurogenic cirrhosis of the lung develops, in which it loses its ability to smooth out and restore normal function even after surgical removal of the shell from its surface, patients often have respiratory failure, develop hypertension in the pulmonary circulation. Long-existing pneumothorax can lead to pleural empyema.

A particularly severe and life-threatening form of spontaneous pneumothorax is a stressful, valve, valve or progressive pneumothorax. It occurs in cases of formation of valvular pulmonary-pleural communication in the place of perforation of the visceral pleura. During inhalation, air enters through the perforation hole into the pleural cavity, and during exhalation, the closing valve prevents it from escaping from the pleural cavity. As a result, with each breath, the amount of air in the pleural cavity increases, the intrapleural pressure increases. The lung on the side of the pneumothorax is completely collapsed. There is a shift of the mediastinum organs in the opposite direction with a decrease in the volume of the second lung. Displace, bend and squeeze the main veins, decreases blood flow to the heart. Falls down and becomes a flat dome of the diaphragm. Gaps between adhesions of the parietal and visceral pleura with the formation of hemopneumothorax easily occur.

In patients with intense pneumothorax, severe dyspnea and cyanosis appear, the tone of voice changes, patients feel the fear of death. Usually note a forced sitting position and anxiety, excitement of the patient. Auxiliary muscles are involved in breathing. The chest wall on the side of the pneumothorax lags behind when breathing, the intercostal spaces smooth or emit. Sometimes the supraclavicular fossa protrudes. On palpation, the displacement of the apical impulse of the heart is set in the direction opposite to the pneumothorax, the voice tremor on the side of the pneumothorax is absent. Subcutaneous emphysema may be detected. With percussion, high tympanitis and displacement of the mediastinum organs are noted, with auscultation - the absence of respiratory noise on the side of the pneumothorax. Occasionally, body temperature rises. X-ray examination confirms and clarifies the clinical data. Acute respiratory failure with severe hemodynamic disturbances in the absence of therapeutic measures that develops with intense pneumothorax can quickly lead to the death of the patient.

[25], [26]

Treatment of spontaneous pneumothorax

Treatment of spontaneous pneumothorax should be carried out in a hospital. With a thin layer of air between the lung and chest wall, no special treatment is often required. In cases of a larger amount of air, a puncture of the pleural cavity is necessary with suction, if possible, of the entire air. Puncture is performed under local anesthesia in the midclavicular line in the second intercostal space. If it is not possible to remove all the air and it continues to flow into the needle “without end”, a silicone catheter must be inserted into the pleural cavity for continuous aspiration of air. In hemopneumothorax, a second catheter is inserted along the mid-axillary line in the sixth intercostal space. Constant aspiration with a vacuum of 10-30 cm of water. Art. In most cases, leads to the cessation of air flow from the pleural cavity. If at the same time, according to the X-ray examination data, the lung was straightened, aspiration was continued for another 2-3 days. And then the catheter is removed. However, sometimes the flow of air through the catheter lasts 4-5 days. In such a situation, they often use the introduction of bicarbonate or tetracycline solutions into the pleural cavity of the sodium, as well as the spraying of pure talcum powder, which cause the development of pleural adhesions. An attempt may be made to seal the lung by electrocoagulation or biological glue through a thoracoscope introduced into the pleural cavity. However, more often with prolonged air flow, surgical treatment is resorted to by means of a mini-invasive video-assisted thoracoscopic or open surgery.

In case of intense pneumothorax, the patient needs emergency help - 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 inserting 1-2 thick needles or trocar into the pleural cavity. This technique allows you to reduce intrapleural pressure and eliminate the immediate threat to the life of the patient. With bilateral spontaneous pneumothorax, aspiration drainage of both pleural cavities is indicated. Treatment of patients with intense and bilateral spontaneous pneumothorax is desirable to be carried out in intensive care units, intensive care units or specialized pulmonary surgical units.

In 10-15% of patients, spontaneous pneumothorax after treatment with punctures and drainage recurs, if the reasons for its occurrence and the free pleural cavity remain. For relapses, it is advisable to make a video-assisted thoracoscopy and determine the subsequent treatment tactics depending on the pattern revealed.

Pulmonary embolism

Pulmonary thromboembolism is a life-threatening condition in which the blood circulation of a significant part of the lungs may be impaired.

[27], [28], [29]

Causes of pulmonary embolism

Pulmonary embolism can occur in patients with widespread fibro-cavernous pulmonary tuberculosis or tuberculous empyema, in elderly patients and in patients with chronic pulmonary heart disease, often after extensive surgical interventions.

Blood clots from the deep veins of the lower extremities and pelvic veins with the blood flow into the right atrium, then into the right ventricle, where they are fragmented. From the right ventricle blood clots fall into 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 total vascular resistance in the lungs. There is an overload of the right ventricle, a fall in cardiac output and the development of acute cardiovascular insufficiency.

Symptoms of pulmonary embolism

Clinical symptoms of thromboembolism are not specific, patients complain of shortness of breath, cough, fear, shortness of breath, tachycardia. When auscultation listen to the strengthening of the second tone of the pulmonary artery, signs of bronchospasm (dry wheezing). With myocardial pneumonia and limited thromboembolism in the pulmonary artery system, clinical symptoms such as chest pain and hemoptysis are characteristic. Patients noted pain along the deep veins of the extremities and edema of the leg.

[30], [31]

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. X-ray examination reveals a decrease in lung volume and sometimes pleural effusion, the appearance of local areas of reduced blood filling and expansion of the root arteries proximal to the thrombated area. Auxiliary methods for the diagnosis of pulmonary embolism (echocardiography, ventilation-perfusion scintigraphy, angiopulmonography) in severe condition of patients with tuberculosis and suddenly developed thromboembolism are practically inaccessible.

Treatment of pulmonary embolism

• immediately after the diagnosis is clarified, 10 thousand U of sodium heparin should be injected intravenously, then the drug should be administered every hour by 1-1.5 thousand. You can start with the infusion of sodium heparin at a dose of 80 U / kg per hour, then you should continue the subcutaneous administration of sodium heparin by 3-5 thousand. Units under the control of indicators of coagulation;
• at the same time or after 2-3 days, it is advisable to administer orally indirect anticoagulants (warfarin, ethyl biscumacetate) until the prothrombin time is 1.5 times longer;
• oxygen therapy 3-5 l / min;
• when a diagnosis of massive pulmonary thromboembolism is established and thrombolytic therapy is prescribed, anticoagulant therapy should be canceled as excessive;
• with massive thromboembolism, it is recommended to use urokinase intravenously at a dose of 4000 U / kg for 10 minutes, then for 12-24 hours intravenously at 4000 U / kg, or streptokinase for intravenous doses of 250 thousand U for 30 minutes, then 100 U / h for 12-72 h;
• when determining the exact localization of the embolus or with the ineffectiveness of anticoagulant or thrombolytic therapy, embolectomy is indicated.

Acute lung injury syndrome

Acute lung injury syndrome (SOPL) and adult acute respiratory distress syndrome (ARDSV) - pulmonary edema of non-cardiogenic etiology with severe respiratory failure and severe oxygen-resistant hypoxia. The reason for the development of NEDS and ARDSV is damage to the pulmonary capillaries and alveolar endothelium due to inflammation and an increase in the permeability of the pulmonary vessels with the development of interstitial pulmonary edema, arteriovenous shunting, disseminated intravascular coagulation and microthrombogenesis. Interstitial pulmonary edema results in damage to the surfactant and decreases the elasticity of the lung tissue.

Clinical examination data do not always distinguish cardiogenic pulmonary edema (COL) from ARDSV. However, there are some differences in the early stages of development.

Cardiogenic pulmonary edema occurs as a result of an increase in pressure in the pulmonary capillaries against the background of the normal permeability of the pulmonary vessels.

[32], [33], [34],

Symptoms of acute lung injury syndrome

The severity of clinical manifestations of QOLs is rapidly increasing. Patients are agitated, they note a feeling of fear, asphyxiation, pain in the heart area, wheezing, participation in the breathing of the intercostal muscles, auscultative signs of lung congestion, hypoxia with acrocyanosis, coughing up of pink frothy sputum. Radiographic changes occur somewhat later: a decrease in the transparency of the pulmonary fields, expansion of the roots of the lungs, an increase in heart volume and pleural effusion.

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

Diagnosis of acute lung injury syndrome

Radiographically, in the syndrome of acute lung injury, recurrence of the lung pattern, blurred vascular shadows, especially in the lower sections, and increased vascular pattern in the lung root area (“snowstorm”, “butterfly”, “wings of the angel of death”) are noted.

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

The differences between SPL and ARDSV are mainly in the quantitative manifestation of the severity of lung lesions and in the change in the oxygenation index. With SOPL, the oxygenation index may be lower than 300. And with ARDSV even lower than 200 (the norm is 360–400 or more).

[35], [36]

Treatment of acute lung injury syndrome

• constant controlled oxygen therapy;
• antibacterial therapy taking into account the sensitivity of microflora;
• glucocorticoids (prednisone, methylprednisolone, hydrocortisone);
• nonsteroidal anti-inflammatory drugs - NSAIDs (diclofenac);
• direct acting 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);
• antihistamine drugs (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 pressure at the end of expiration if necessary.

Oxygen therapy should be started immediately after the onset of signs of acute respiratory failure. The oxygen supply is carried out through a nasotracheal catheter or mask under the control of pulse oximetry and blood gas composition. The oxygen concentration in the inhaled mixture can be increased from 50 to 90% at the height of ARDSV development for a short period of time to increase the pO ₂ in arterial blood above 60 mm Hg.

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

Anticoagulants are used to prevent the progression of intravascular coagulation and thrombosis.

With the development of ARDSV, in order to reduce the severity or relieve pulmonary edema, intravenous and oral diuretics are prescribed. Preference should be given to furosemide (it has a vasodilating effect on the veins and reduces congestion in the lungs).

Nitrates and peripheral vasodilators promote unloading of the small circle of blood circulation. Nitroglycerin and sodium nitroprusside with ARDSV are used in the form of infusions, the drugs act on the pulmonary vessels, reduce peripheral resistance, increase cardiac output and increase the effect of diuretics.

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

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

Interstitial and alveolar edema of the lungs inevitably leads to damage to the lung surfactant. This is accompanied by an increase in surface tension and the sweating of fluid in the alveoli, therefore, when ARDSV, it is necessary to prescribe inhalations as soon as possible with 3% surfactant-BL emulsion in the form of instillations and with the help of mechanical inhalers. The use of an ultrasonic inhaler is unacceptable, since the surfactant is destroyed when the emulsion is processed by ultrasound.

Progression of ARDSV with severe respiratory failure - an indication for transferring patients to artificial ventilation of the lungs in the mode of creating a positive pressure at the end of expiration (PDKV). The regimen is recommended for maintaining a pO ₂ > 60 mm Hg. With FiO2 ≤0.6.

The use of PEEP during mechanical ventilation allows achieving ventilation of collapsed alveoli, increasing the functional residual capacity and stretchability of the lungs, reducing shunting and improving blood oxygenation. The use of peep with low pressure (less than 12 cm water column) allows you to prevent the destruction of surfactant and damage to the lung tissue from local oxygen exposure. PDKV, exceeding the value of pulmonary resistance, helps to block blood flow and reduce cardiac output, can worsen the oxygenation of tissues and increase the severity of pulmonary edema.

In order to reduce the likelihood of iatrogenic damage to the lungs during mechanical ventilation, the use of pressure-controlled servo fans can be recommended. This prevents the risk of over-stretching of the lungs, providing small tidal volumes and an inverted inspiratory to expiratory ratio during mechanical ventilation in patients with ARDSV.