Acute and emergency conditions in tuberculosis: causes, symptoms, diagnosis, treatment. Phthisiology tests "emergency conditions in patients with tuberculosis" test on the topic Emergency care for patients with pulmonary tuberculosis

T. V. Pariyskaya, O. A. Borisova, O. A. Zhiglyavskaya, A. E. Polovinko Emergency conditions in children. Newest

9. Emergency conditions

Emergency conditions Emergency conditions mean various acute diseases, exacerbations of chronic pathologies, injuries, poisoning and other conditions that threaten human life. They require urgent medical attention to alleviate the condition

Chapter 9 Emergency conditions for diseases of the cardiovascular system Collapse Collapse is a condition in which, due to acute vascular insufficiency, a sharp decrease in blood pressure occurs. This leads to a decrease in blood supply to organs, which

Chapter 10 Emergency conditions in neurology Fainting Fainting is a sudden short-term loss of consciousness, in which a sharp decrease in muscle tone occurs, and the activity of the cardiovascular and respiratory systems is weakened. Fainting represents

Chapter 11 Emergency conditions for respiratory diseases A number of life-threatening conditions arise as a result of significant problems with organs related to the respiratory system. A person can live without oxygen for several minutes, and primarily from it

Chapter 12 Emergency conditions for diseases of the digestive system Acute abdomen Acute abdomen is severe pain in the abdomen due to diseases of the internal organs. It is often difficult to immediately identify the source of pain and make an accurate diagnosis, which is why this is used

Chapter 13 Emergency conditions for diseases of the urinary system Renal colic This is an attack of pain that develops when the outflow of urine is disrupted. More common in urolithiasis. Causes: Obstruction to the outflow of urine from the renal pelvis

Chapter 17 Emergency conditions in psychiatry and narcology A feature of conditions requiring emergency care in psychiatry and narcology is that the patient often does not understand the significance of the current situation. He may not be aware of his condition or behavior, not

Chapter 2 Diseases, poisonings, emergencies Allergic dermatitis This is an acute inflammation of the skin that occurs under the influence of external or internal factors - allergens. The disease has a short course, as it disappears after elimination

Emergency conditions In emergency conditions related to insufficiency syndrome (acute vascular insufficiency - fainting, collapse, shock), it is necessary to tone acupressure points; with excess syndrome (severe pain, asthmatic crisis, heat stroke,

Classification of pulmonary hemorrhages

All hemoptysis and pulmonary hemorrhages are divided into:

• true, in which blood is released from the lungs;


• false (pseudohemoptysis), when their source may be the gums, nasal pharynx, esophagus, stomach. False hemoptysis is less often accompanied by a cough; in such cases, blood is released during vomiting, expectorated from the nasal part of the pharynx, and does not contain alveolar cells. As a rule, aspiration pneumonia does not occur after false hemoptysis. In cases of false hemoptysis, clots quickly form, while blood from the lung does not always coagulate.

Etiology and pathogenesis

Bleeding and hemoptysis are complications of pulmonary diseases, which have a depressing effect on the patient’s psyche, often leading to the progression of the disease, and sometimes ending in death. Among lung diseases, tuberculosis is one of the most common causes of hemorrhagic complications, ranging from 32 to 66.3%, followed by diseases such as bronchiectasis, lung abscess, lung cancer, congestive changes in the lungs, and blood diseases. Most of the bleeding of tuberculous etiology is explained by many reasons: the prevalence of tuberculosis of the lungs, the chronic course of this process, periodic exacerbations, the presence of destruction in the lungs with the growth of granulation tissue in their walls, perifocal inflammation and tuberculosis damage to the walls of blood vessels, as well as the nature of chemotherapy. There are a number of factors that contribute to the occurrence of hemoptysis and pulmonary hemorrhage: cold, large fluctuations in atmospheric pressure and air temperature, high positive ionization of air, sudden changes in weather, highlands, overheating of the body, the use of anticoagulants that reduce blood clotting, less often - the action of proteolytic enzymes , catalyzing the cleavage of peptide bonds in proteins and peptides, acute and chronic alcohol poisoning of the human body. Long-term intoxication due to lung disease, massive antibiotic therapy, chemotherapy (usually with sulfonamides), frequent respiratory failure and circulatory disorders affect the functional state of organs and systems. In particular, the functions of the liver and lungs suffer, as a result of which the synthesis and regulation of factors of the blood coagulation system are disrupted.

Clinical picture

Hemoptysis or bleeding of the lungs can be one-time or repeated (recurrent). As a rule, they are associated with vascular arrosion or may be a consequence of diapedesis. In clinical practice, the characteristics of bleeding from the lung are used, based on the amount of blood released: small, in which up to 100 ml of blood is released, medium - up to 500 ml and heavy (profuse) - more than 500 ml of blood. Hemoptysis means more or less blood in the sputum. The presence of mucous sputum mixed with blood suggests that blood is not the main substrate released from the lungs; it is the result of diapedesis of blood cells as one of the manifestations of the inflammatory process or local circulatory disorders with increased permeability of the walls of capillaries and small vessels. When the processes of hemoptysis and pulmonary hemorrhage have just begun, their duration can never be predicted, and there is never any certainty that they will not resume after cessation. Therefore, patients with even mild hemoptysis should be hospitalized, carefully examined and given appropriate treatment. With true hemoptysis and pulmonary hemorrhage, the blood is scarlet, foamy and usually has no tendency to coagulate. At first, there is a feeling of soreness in the throat, sometimes a feeling of pinching and pain behind the sternum, then a cough with bubbling in the throat, and slight suffocation are noted. Patients feel the smell and salty taste of blood. The clinical picture of profuse pulmonary hemorrhage consists of the following symptoms of anemia and collapse: severe pallor, dizziness, rapid pulse, weakness, and decreased blood pressure. Hemoptysis and even short-term pulmonary hemorrhages, as a rule, are not accompanied by anemia and low blood pressure.

The outcome of profuse bleeding can be fatal, the cause of which is asphyxia due to blockage of the airways by blood clots and simultaneously occurring bronchospasm.

Diagnostics pulmonary hemorrhage and hemoptysis comes down mainly to identifying their source. With a unilateral type of disease, the cause is tumors, cavities, cavities of bronchiectasis, abscesses, pneumosclerotic changes, which are determined clinically and radiologically.

It is more difficult to establish the localization of pulmonary bleeding and hemoptysis in a bilateral pathological process. In this case, patients reflexively reduce the respiratory movements of that half of the chest where the source of bleeding is located. Auscultation reveals crepitus and fine rales in the basal segments of the lungs on the bleeding side; Segmental atelectasis and aspiration pneumonia may develop. In this case, resorption fever first occurs, and after 2-3 days aspiration pneumonia occurs on the bleeding side and, less often, on the opposite side. Aspiration pneumonia tends to regress slowly. Atelectasis appears at the end of the first day or on the second day after bleeding due to obstruction (blockage) of the small bronchi with blood clots. A rare complication of hemoptysis may be secondary anemia.

Differential diagnosis. When bleeding from the tonsils or paranasal sinuses, a mucous or purulent secretion streaked with blood is released. With nosebleeds, the blood is dark in color, flows out profusely on one side, and with severe bleeding it can enter the nasal part of the throat. Bleeding from varicose veins of the esophagus begins suddenly and, as a rule, is profuse in nature. In this case, patients are most often diagnosed with liver cirrhosis. Gastric bleeding is characterized by vomiting dark blood mixed with juice, and sometimes when blood clots in the stomach, the vomit contains dark clots.

Heavy bleeding from a stomach ulcer, especially with achylia (lack of gastric juice secretion), is accompanied by the release of blood with vomit. In all these cases, the blood does not foam; coughing, as a rule, does not precede bleeding and does not accompany this pathogenic process.

Treatment. Hemostatic therapy should be aimed primarily at the main cause and leading pathogenetic link of emerging pulmonary hemorrhages and hemoptysis. Their immediate causes are ruptures in the walls of the blood vessels of the lungs due to hypertension (increased hydrostatic pressure) in the vessels of the pulmonary circulation, disorders of the blood coagulation system, activation of fibrinolysis, and increased permeability of the vascular walls.

If a patient with tuberculosis begins hemoptysis or pulmonary hemorrhage, the following measures must be taken: if blood loss is more than 500-1000 ml (but not at once), when a patient with tuberculosis has a particularly significant increase in plasma fibrinolysis, it is necessary to observe strict bed rest and recommend the position of the patient with an elevated headboard Apply tourniquets to the proximal limbs for 30-40 minutes (the pulse on the radial artery and lower leg should be palpable). It is necessary to administer fibrinolysis inhibitors intravenously: vikasol, fresh frozen plasma, 6% solution of aminocaproic acid (ACA) - 100.0 drops (50-60 drops per minute) or contrical (gordox, ingitril, trasylol) - 10-20 thousand. ATRE in 100 ml of 0.85% sodium chloride solution drop by drop. 1-2 hours after intravenous administration of any fibrinolysis inhibitor, ACC should be prescribed orally 5.0 4-6 times a day (with an interval of 4-6 hours). In total, on the first day you need to take 20.0-30.0 ml of ACC.

To reduce blood pressure in the vessels of the pulmonary circulation, it is advisable to administer ganglion-blocking drugs that disrupt the transmission of nervous excitation at the synapses of the autonomic ganglia, since they are mainly used to treat diseases accompanied by spasms of blood vessels or internal organs: 1.5% ganglerone 1.0 -2.0 ml subcutaneously, 5% pentamin 1.0-2.0 subcutaneously, benzohexonium 0.1 ml orally 3-6 times a day for 2-3 days and a number of other drugs with a similar spectrum of action.

In order to reduce the permeability of the capillary wall and obtain a desensitizing effect, i.e., reduce or disappear the body’s increased sensitivity to repeated administration of a drug, intravenous administration of 10 ml of a 10% solution of calcium chloride, pipolfen or diphenhydramine subcutaneously or orally is recommended, as well as 3 -5 ml of 5% ascorbic acid solution intramuscularly or 0.1 ml orally 3-5 times a day. You can add the drug andraxon 1 ml of 0.025% solution intramuscularly or subcutaneously 1-4 times a day. This is an adrenaline drug, but it does not increase blood pressure and does not affect the activity of the heart. Its main effect is to promote spasm of small blood vessels, so it is used to stop parenchymal and capillary bleeding. It is necessary to pay attention to the fact that it is not recommended to prescribe codeine (an alkaloid contained in opium poppy, used as an analgesic and sedative) and other narcotic substances to the patient, as they help suppress the cough reflex and suppress the respiratory center, which leads to stagnation of blood clots and sputum in the respiratory tract with the development of aspiration pneumonia as a result.

If the above measures are ineffective, it is recommended to apply pneumoperitoneum or artificial pneumothorax, which cause compression of the diseased lung and collapse of the cavity (depending on the form of the process), or, if surgical intervention is possible, it is advisable to transfer the patient to the surgical department. The risk of surgery is reduced by 10-15 times if it is performed during the “cold period,” that is, at least with a temporary stop of bleeding.

In case of hemoptysis, the patient is advised to rest in bed and take ACC 5 g orally 3-4 times a day for 3-5 days (with a 6-8 hour interval between doses). This therapy can be supplemented with 10% calcium chloride, 1 tbsp. l. 3-4 times (after meals), ascorbic acid 0.1 g 3-4 times a day, desensitizing agents. Rational treatment allows 90-95% of newly diagnosed patients to stop bacterial excretion, and in 80-90% to close cavities in the lungs. Modern means of hemostatic therapy are very effective and can achieve cessation of hemoptysis or pulmonary hemorrhage in the vast majority of patients (95-98%).

Hemoptysis and bleeding Hemoptysis is the presence of streaks of scarlet blood in sputum or saliva, the release of separate spits of liquid or partially coagulated blood. Pulmonary hemorrhage is the outpouring 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

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

Pathogenesis of pulmonary hemorrhage The morphological basis for bleeding in most cases is aneurysmally 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 hypervascular zones with high blood pressure. Arrosion or rupture of such fragile vessels in the mucous membrane or submucosal layer of the bronchus causes hemorrhage into the lung tissue and into the bronchial tree. Pulmonary hemorrhage of varying severity occurs. Less commonly, bleeding occurs due to destruction of the vascular wall during a purulent-necrotic process or from granulations in the bronchus or cavity.

Symptoms of pulmonary hemorrhage 1. 2. 3. Pulmonary hemorrhage is observed more often in middle-aged and elderly men. It begins with hemoptysis, but can occur suddenly, against the background of good health. with pulmonary hemorrhage. Unlike bleeding from the esophagus or stomach, the blood is always coughed up and is foamy. Sometimes acid-fast bacteria can be found in the sputum secreted by patients with pulmonary hemorrhage, which immediately raises a reasonable suspicion of tuberculosis.

Treatment of pulmonary hemorrhage, resuscitation and airway protection; determining the location of bleeding and its cause; stopping bleeding and preventing its recurrence. It is important to cough up all blood from the respiratory tract. For 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 facilities for bronchoscopy, contrast X-ray examination of blood vessels and surgical treatment of lung diseases.

Methods for stopping pulmonary hemorrhage can be pharmacological, endoscopic, x-ray endovascular and surgical. Pharmacological methods include controlled arterial hypotension, which is very effective for bleeding from the vessels of the systemic circulation of the bronchial arteries. Decrease in systolic blood pressure to 85 -90 mm Hg. creates favorable conditions for thrombosis and stopping bleeding. For this purpose, use one of the following medications. Trimethophan camsilate - 0.05 -0.1% solution in 5% glucose solution or 0.9% sodium chloride solution intravenously (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, intramuscular action after 5-15 minutes. Isosorbide dinitrate - 0.01 g (2 tablets under the tongue), can be combined with angiotensin-converting enzyme inhibitors.

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

An effective method for stopping pulmonary hemorrhage is X-ray endovascular occlusion of a bleeding vessel. 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 able to dissolve and thus prevent recanalization. Another agent is gelatin sponge, which unfortunately leads to recanalization and is therefore used only as an adjunct to PVA.

The surgical method is considered as a treatment option for patients with an identified source of massive bleeding and in cases of ineffectiveness of conservative measures or conditions that directly threaten the patient’s life.

Spontaneous pneumothorax is the entry of air into the pleural cavity, which occurs spontaneously, as if spontaneously, without damage to the chest wall or lung.

in the etiology of spontaneous pneumothorax the following factors may be important: perforation into the pleural cavity of the tuberculous cavity; rupture of the cavity at the base of the pleural cord when applying an artificial pneumothorax; damage to lung tissue during transthoracic diagnostic and therapeutic puncture: breakthrough of an abscess or gangrene of the lung; destructive pneumonia; pulmonary infarction, rarely - pulmonary cyst; cancer. metastases of malignant tumors, sarcoidosis, histiocytosis X, fungal infections of the lungs and even bronchial asthma.

Symptoms of spontaneous pneumothorax 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, and to the hypochondrium. In severe cases of spontaneous pneumothorax, pale skin, cyanosis, and cold sweat are characteristic. tachycardia with increased blood pressure.

Diagnosis of spontaneous pneumothorax The most informative method for diagnosing all variants of spontaneous pneumothorax is x-ray examination. Pictures are taken during inhalation and exhalation. In the latter case, the edge of the collapsed lung is better identified. Determine the degree of lung collapse, localization of pleural adhesions, position of the mediastinum, presence or absence of fluid in the pleural cavity

A particularly severe and life-threatening form of spontaneous pneumothorax is tension, valve, valve or progressive pneumothorax. It occurs in cases of formation of valvular pulmonary pleural communication at the site of perforation of the visceral pleura. During inhalation, air enters through the perforation into the pleural cavity, and during exhalation, the closing valve prevents it from leaving the pleural cavity. As a result, with each breath, the amount of air in the pleural cavity increases, and intrapleural pressure increases.

In patients with tension pneumothorax, severe shortness of breath, cyanosis appear, the timbre of the voice changes, and patients feel the fear of death. Usually a forced sitting position and restlessness and agitation of the patient are noted. Accessory muscles are involved in breathing. The chest wall on the side of the pneumothorax lags behind during breathing, the intercostal spaces smooth out or bulge. Subcutaneous emphysema may be detected. Acute respiratory failure with severe hemodynamic disorders that develops during tension pneumothorax can quickly lead to the death of the patient in the absence of therapeutic measures.

Treatment of spontaneous pneumothorax must be carried out in a hospital. If there is a thin layer of air between the lung and the chest wall, no special treatment is often required. In cases of a larger amount of air, puncture of the pleural cavity is necessary with suction, if possible, of all the air. In case of tension pneumothorax, the patient needs emergency assistance - 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 trocars into the pleural cavity. This technique allows you to reduce intrapleural pressure and eliminate the immediate threat to the patient’s life. For bilateral spontaneous pneumothorax, aspiration drainage of both pleural cavities is indicated.

Pulmonary embolism is a life-threatening condition in which the circulation of a significant part of the lungs can be impaired.

Symptoms of pulmonary embolism Clinical symptoms of thromboembolism are nonspecific, patients complain of shortness of breath, cough, fear, rapid breathing, tachycardia. During auscultation, an increase in the second tone above the pulmonary artery and signs of bronchospasm (dry wheezing) are heard. In case of infarction-pneumonia and limited thromboembolism in the pulmonary artery system, clinical symptoms such as chest pain and hemoptysis are characteristic.

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 typical with the sudden development of massive thromboembolism. X-rays reveal a decrease in lung volume and sometimes pleural effusion, the appearance of local zones of reduced blood supply and dilatation of the hilar arteries proximal to the thrombosed area. Auxiliary methods for diagnosing pulmonary embolism (echocardiography, ventilation-perfusion scintigraphy, angiopulmonography) in severe condition of patients with tuberculosis and suddenly developed thromboembolism are practically unavailable.

Treatment of pulmonary embolism immediately after clarification of the diagnosis requires intravenous administration of 10 thousand units of sodium heparin, subsequently the drug should be administered every hour at 11.5 thousand units until an increase of 1.5-2 times compared to the initial aPTT value. you can start with an infusion of sodium heparin at a dose of 80 units/kg per hour, then you should 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 oral anticoagulants of indirect action (warfarin, ethyl biscoumacetate) until the prothrombin time increases by 1.5 times; oxygen therapy 3 -5 l/min; when a diagnosis of massive pulmonary embolism is made 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 units/kg for 10 minutes, then 4000 units/kg intravenously for 12-24 hours, or streptokinase intravenously at a dose of 250 thousand units for 30 minutes, then 100 units /hour for 12 -72 hours; when determining the exact location of the embolus or when anticoagulant or thrombolytic therapy is ineffective, embolectomy is indicated.

Acute lung injury syndrome (ALI) and adult acute respiratory distress syndrome (ARDS) are pulmonary edema of non-cardiogenic etiology with severe respiratory failure and severe hypoxia, resistant to oxygen therapy. The reason for the development of nostrils 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.

Symptoms of acute lung injury syndrome Clinical manifestations of acute lung injury syndrome do not appear immediately, as with cardiogenic shock, but gradually: increasing shortness of breath, cyanosis, wheezing in the lungs (“wet lung”). X-ray reveals bilateral pulmonary infiltration against the background of a previously unchanged pulmonary pattern.

Diagnosis of acute lung injury syndrome Radiologically, with acute lung injury syndrome, a reticulated pulmonary pattern, blurred shadows of blood vessels, especially in the lower sections, and an increase in the vascular pattern in the root of the lung (“blizzard”, “butterfly”, “wings of the angel of death”) are noted. Changes in the gas composition of the blood: arterial hypoxemia with the subsequent 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 in these patients. The differences between POPL and ARDS are mainly in the quantitative manifestation of the severity of lung damage and in changes in the oxygenation index. With nostril, the oxygenation index may be below 300, and with ARDS even below 200 (the norm is 360 -400 or more).

Treatment of acute lung injury syndrome: continuous controlled oxygen therapy; antibacterial therapy taking into account the sensitivity of the microflora; glucocorticoids (prednisolone, methylprednisolone, hydrocortisone); non-steroidal 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); analgesics (morphine, trimeperidine, lornoxicam); antioxidants; cardiac glycosides (strophanthin-K, lily of the valley glycoside, etc.) in the absence of contraindications; Ventilation with positive end-expiratory pressure if necessary.

A. G. Khomenko

Drug-induced anaphylactic shock is usually caused by antibiotics, most often penicillin, bicillin and streptomycin, but can also be caused by chemotherapy drugs and other drugs, mainly when administered parenterally.

The typical clinical picture of anaphylactic shock includes the following main signs: arterial hypotension, impaired consciousness up to its loss, respiratory failure, convulsive syndrome and cutaneous autonomic-vascular reactions. Clinical manifestations develop acutely during or shortly after administration of the drug: severe weakness, a feeling of a rush of blood to the head, tingling and itching of the skin, pain in the heart, difficulty breathing with wheezing and foam at the mouth, loss of consciousness, convulsions, frequent threadlike pulse, sharp decrease in blood pressure.

According to A. S. Lopatin, in addition to such typical symptoms, anaphylactic shock can be characterized mainly by symptoms of impaired cardiovascular activity: pain in the heart, weak or absent pulse, a significant decrease in blood pressure, heart rhythm disturbances (hemodynamic variant), it is also possible asphyxial, cerebral and abdominal variants.

With the asphyxial variant, swelling of the larynx develops, leading to a narrowing or complete closure of its lumen, and bronchospasm, which causes acute respiratory failure. The cerebral variant is characterized by symptoms of psychomotor agitation, convulsions, and loss of consciousness. The abdominal variant is characterized by the appearance of an “acute abdomen” syndrome with severe pain, tension in the abdominal muscles, and signs of irritation of the peritoneum.

Medical care for anaphylactic shock should be provided immediately: it is necessary to stop the administration of the drug that caused the shock, put the patient on his back, lower and throw back his head, turn it to the side, push the lower jaw to prevent the tongue from retracting, raise the legs, clear the upper respiratory tract. In case of respiratory arrest - artificial respiration (mouth to mouth), in case of cardiac arrest - external cardiac massage. It is necessary to inject adrenaline intramuscularly (1 ml of 0.1% solution); if blood pressure remains low, then epinephrine or norepinephrine should be administered intravenously, as well as prednisolone.

Based on the clinical manifestations, you should also administer 2-4 ml of a 2.5% solution of pipolfen or a 2% solution of suprastin, or 5 ml of a 1% solution of diphenhydramine. Cordiamine, caffeine are also administered, and for bronchospasm - aminophylline intravenously (1-2 ml of a 24% solution or 20 ml of a 2.4% solution). The order of administration of the above medications is not so important; the main thing is to immediately provide emergency care to the patient using the available means.

Due to the severity of this complication, before starting chemotherapy, it is necessary to ask the patient about how he tolerates various medications, whether he has had allergic symptoms such as hay fever, food allergies, or a disease manifested by allergic runny nose, swelling, etc. For patients who have previously had drug allergic shock, antibiotics or other drugs that caused this serious complication should not be prescribed.

Pulmonary hemorrhage and hemoptysis- very severe complications of many pulmonary diseases: tuberculosis, bronchiectasis, lung cancer, pneumonia, bronchitis, etc. Severe pulmonary bleeding occurs when the integrity of the vascular wall is damaged, which is destroyed when it is involved in the necrosis zone; The cause of bleeding can also be rupture of varicose veins and arterial aneurysms in the bronchiectasis of the bronchial system.

Hemoptysis can occur in the absence of ruptures of the vascular wall due to increased permeability. The clinical manifestations of hemoptysis are quite striking; when coughing, sputum streaked with blood is released or a clot of sputum is completely stained with blood, the blood is bright red and foamy. Even more striking symptoms of pulmonary hemorrhage are observed in cases where liquid blood is released when coughing, the amount of which varies within a very wide range - from 30-50 to 200-400 ml or more.

When the airways are blocked by blood, instant death from asphyxia can occur, so when the first signs of pulmonary hemorrhage appear, measures must be taken to prevent it. For this purpose, it is necessary to suck out all the contents of the bronchi that can be removed through the endotracheal tube using a vacuum pump. Then the patient needs to be calmed down and placed in a semi-sitting position.

To eliminate hemoptysis or minor pulmonary hemorrhage, hemostatic agents are used: aminocaproic acid 2 g 3-4 times a day, ascorbic acid 0.1 g 3-5 times a day, calcium gluconate 10 ml of a 10% solution intravenously. In case of large blood loss - up to 400 ml - a blood or red blood cell transfusion is recommended. 10 ml of a 2.4% aminophylline solution is administered intravenously, and pyrylene 0.01 g or benzohexonium 0.1-0.2 g 2 times a day are also prescribed (I. S. Pilipchuk).

If the bleeding does not stop, then pneumoperitoneum can be applied for hemostatic purposes. Some patients with fibrocavernous tuberculosis undergo surgical intervention for urgent and life-saving reasons. Bronchoscopy may be performed to identify the source of bleeding.

In the initial forms of tuberculosis, with the help of hemostatic agents, as a rule, it is possible to stop pulmonary hemorrhage and, especially, hemoptysis. However, it should be borne in mind that spilled blood that enters the respiratory tract can cause aspiration pneumonia, therefore, if body temperature rises, leukocytosis develops, or persistent wheezing appears, an x-ray examination must be performed.

If pneumonia is detected, it is necessary to treat with antibiotics (penicillin, lincomycin, gentamicin, etc.). It should be added that in patients with tuberculosis, nonspecific aspiration pneumonia can develop into a progressive tuberculosis process, accompanied by the formation of cavities. Such patients also require anti-tuberculosis chemotherapy.

Spontaneous (spontaneous) pneumothorax characterized by the development of lung collapse. The severity of collapse can vary: from total compression of the lung due to the penetration of a large amount of air into the pleural cavity, accompanied by an increase in positive pressure, to partial collapse and the formation of a relatively small gas bubble.

The causes of spontaneous pneumothorax are different: rupture of the parietal, subpleural, tuberculous cavity into the pleural cavity or rupture of the bulla. Spontaneous pneumothorax can form during bronchological examination and pleural puncture (puncture pneumothorax).

Depending on the cause of spontaneous pneumothorax, two groups of patients should be distinguished: patients with tuberculosis and patients with spontaneous pneumothorax of non-tuberculous etiology. The first group is characterized by the fact that soon after the occurrence of spontaneous pneumothorax due to a breakthrough into the pleural cavity of the tuberculous cavity, patients develop pneumopleuritis and empyema. The clinical picture of spontaneous pneumothorax is varied. It can develop gradually without pronounced clinical manifestations, and only with increasing lung collapse does shortness of breath occur.

Possible rapid development of lung collapse with pronounced clinical manifestations: severe pain in the corresponding half of the chest and shortness of breath, cyanosis and tachycardia are noted. The further course of the disease depends on the mechanisms of communication of the pleural cavity with atmospheric air through the system of draining bronchi.

There are open spontaneous pneumothorax, in which constant communication with atmospheric air is maintained; valvular (the most severe), when, due to the action of the “valve mechanism” in the pleural cavity, the amount of air increases, positive pressure increases, and the mediastinal organs shift to the opposite side; closed, in which after air penetrates the pleural cavity, communication between it and atmospheric air stops.

Diagnosis of spontaneous pneumothorax is not difficult; in addition to clinical symptoms of respiratory failure, patients have a tympanic sound during percussion, weakened breathing over the corresponding half of the chest. The presence of a gas bubble and lung collapse is confirmed by x-ray examination.

Treatment of spontaneous pneumothorax consists of providing emergency care for severe respiratory failure in the event of lung collapse: cordiamine, sulfocamphocaine, oxygen inhalation. It is necessary to put the patient to bed, since physical stress is contraindicated. Often this is enough and the collapsed lung gradually straightens out. Some patients require pleural puncture and air aspiration if high positive pressure is created in the pleural cavity.

Sometimes such aspirations need to be repeated or an underwater drain can be installed. Patients with open or valve pneumothorax, if there is no effect from conservative treatment, need to undergo surgery (V. A. Ravich-Shcherbo, V. S. Savelyev and Ch. D. Konstantinovn).

Acute respiratory failure develops in patients in case of insufficient oxygen supply to the body and carbon dioxide retention in it. At the same time, P02 decreases to 55 mm Hg. Art., and PaCO2 is 50 mm Hg. Art. and higher. The causes of acute respiratory failure are varied; it can occur in many diseases.

In patients with tuberculosis, acute respiratory failure can develop during and after surgical interventions, when complications occur such as spontaneous pneumothorax, rapidly formed atelectasis, rapid accumulation of fluid in the pleural cavity, anaphylactic shock, asphyxia caused by pulmonary hemorrhage, disseminated intravascular coagulation syndrome, as well as with decompensation of the pulmonary heart.

The clinical picture is characterized by a variety of symptoms: shortness of breath, tachycardia, arrhythmia, decreased blood pressure, cyanosis. In such cases, it is necessary to conduct an urgent study of the blood gas composition to reliably establish the presence of acute respiratory failure. In this regard, first of all, emergency treatment measures are carried out, of which the main one is long-term (10-12 hours, and sometimes continuously for 1 day) use of oxygen, which is supplied to the patient using nasal catheters or a mask. Long-term use of oxygen has a positive effect in the hypoxemic form of acute respiratory failure.

Often, additional methods are used to reduce the level of carbon dioxide in the blood, in particular positive end-expiratory pressure, and if there is no effect, extracorporeal membrane oxygenation and carbon dioxide elimination. When apnea occurs, intubation or artificial ventilation of the lungs is performed through a tracheostomy using breathing apparatus of various systems. With a slight excursion of the diaphragm, it can be electrically stimulated. Patients who experience acute respiratory failure must be urgently hospitalized in intensive care units (wards) or intensive care units. In addition to these measures, drug therapy is carried out according to indications.

Pulmonary edema- pathological accumulation in non-vascular fluid in lung tissue. A complication develops in cases where the amount of fluid filtered through the arterial sections of the capillaries of the lung exceeds the amount that can be resorbed through the venous sections of the capillaries and transported by the lymphatic vessels (R. R. Albert).

The most common cause of pulmonary edema is circulatory disorders of the left ventricular type, which can occur as a consequence of chronic diseases and acute conditions. In patients with tuberculosis, pulmonary edema develops due to decompensation of the cor pulmonale with circulatory disorders of the left ventricular type. Pulmonary edema occurs when tuberculosis is complicated by renal amyloidosis and the development of uremia, as well as when various chemicals (chemical toxic substances, gasoline vapors) are inhaled in high concentrations with sufficiently long exposure.

The clinical picture is characterized by pronounced shortness of breath, taking on the character of “cardiac asthma”, bubbling breathing, a large number of moist rales in the lungs, which are heard mainly in the lower sections. Emergency care involves the use of diuretics (Lasix, furosemide, etc.); intravenous infusions of aminophylline, 10 ml of a 2.4% solution, as well as cardiac medications (strophanthin, korglykon, etc.) are used to relieve the pulmonary circulation.

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

Pulmonary hemorrhage is the outpouring 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.

With pulmonary hemorrhage, blood is coughed up in a significant amount at once, 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 bleeding (over 500 ml). 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 rather aspirate or swallow it. Therefore, the quantitative assessment of blood loss during pulmonary hemorrhage is always approximate.

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

Pathogenesis of pulmonary hemorrhage

The morphological basis for bleeding in most cases is aneurysmally 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 hypervascular zones with high blood pressure. Arrosion or rupture of such fragile vessels in the mucous membrane or submucosal layer of the bronchus causes hemorrhage into the lung tissue and into the bronchial tree. Pulmonary hemorrhage of varying severity occurs. Less commonly, bleeding occurs due to destruction of the vascular wall during a purulent-necrotic process or from granulations in the bronchus or cavity.

Symptoms of pulmonary hemorrhage

Pulmonary hemorrhage is observed more often in middle-aged and elderly men. It begins with hemoptysis, but can occur suddenly, against the background of good health. As a rule, it is impossible to predict the possibility and time of bleeding. Scarlet or dark blood is coughed out through the mouth in pure form or along with sputum. Blood may 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 diagnosis of pulmonary hemorrhage is often very difficult even when using modern radiological and endoscopic methods.

When clarifying the medical history, attention is paid to diseases of the lungs, heart, and blood. Information received from the patient, his relatives or the doctors who observed him can have important diagnostic value. So. with pulmonary hemorrhage. Unlike bleeding from the esophagus or stomach, the blood is always coughed up and is foamy. The scarlet color of the blood indicates that it comes from the bronchial arteries, and the dark color indicates that it comes 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 acid-fast bacteria can be found in the sputum secreted by patients with pulmonary hemorrhage, which immediately raises a reasonable suspicion of tuberculosis. Patients themselves rarely feel from which lung or from which area of ​​it 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 point in the initial examination of a patient with hemoptysis and pulmonary hemorrhage is measuring blood 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 crepitus are heard above the area of ​​pulmonary hemorrhage. After a routine physical examination, radiography in two projections is necessary in all cases. The most informative are 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.

A venous blood test must include a platelet count. assessment of hemoglobin content and determination of coagulation parameters. Determination of hemoglobin in dynamics is an available indicator of blood loss.

In modern conditions, digital radiography provides quick visualization of the lungs and clarifies the localization of the process. However, according to ERS experts, in 20-46% it does not allow to determine the localization of bleeding, since it either does not reveal pathology, or the changes are bilateral. High-resolution CT allows visualization of bronchiectasis. The use of contrast aids in the identification of vascular disruption, aneurysms, and arteriovenous malformations.

Bronchoscopy for pulmonary hemorrhage was considered contraindicated 20-25 years ago. Currently, thanks to the improvement of anesthesia and research techniques, bronchoscopy has become the most important method for diagnosing and treating pulmonary hemorrhages. So far, this is the only way that allows you to examine 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 bronchoscopes (fiber bronchoscopes) are used. A rigid bronchoscope allows you to suction blood more efficiently and better ventilate the lungs, while a flexible one allows you to examine smaller bronchi.

In patients with pulmonary hemorrhage, the etiology of which is unclear, bronchoscopy and especially bronchial arteriography can often identify 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, insert a special catheter into the aorta and then into the mouth of the bronchial artery. After the administration 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 when the bleeding has stopped, its occlusion. Indirect signs of pulmonary hemorrhage are expansion of the network of bronchial arteries (hypervascularization) in certain areas of the lung, aneurysmal dilation of blood vessels, thrombosis of the peripheral branches of the bronchial arteries, and 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 airway protection;
• determining the location of bleeding and its cause;
• stopping bleeding and preventing its recurrence.

The possibilities for effective first aid for pulmonary hemorrhage, unlike all external bleeding, are very limited. Outside a medical institution, in a patient with pulmonary hemorrhage, the correct behavior of medical workers is important, 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 instinctively not to hold back his cough. On the contrary, it is important to cough up all the blood from the respiratory tract. For 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 facilities for bronchoscopy, contrast X-ray examination of blood vessels and surgical treatment of lung diseases.

Treatment algorithm for patients with pulmonary hemorrhage:

• place 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 camsilate; clonidine);
• perform bronchoscopy;
• determine the optimal volume of surgical intervention (pulmonary resection, pneumonectomy, etc.);
• perform the operation under anesthesia with intubation with a two-channel tube or blockade of the affected lung by introducing 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 for bleeding from the vessels of the systemic circulation - the bronchial arteries. Decrease in systolic blood pressure to 85-90 mm Hg. creates favorable conditions for thrombosis and stopping bleeding. For this purpose, use one of the following medications.

• Trimethophan camsilate - 0.05-0.1% solution in 5% glucose solution or 0.9% sodium chloride solution intravenously (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, intramuscular - action in 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 a 2.4% aminophylline solution is diluted in 10-20 ml of a 40% glucose solution and injected into a vein over 4-6 minutes). For all pulmonary hemorrhages, to slightly enhance blood clotting, a fibrinolysis inhibitor can be injected intravenously - a 5% solution of aminocaproic acid in a 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 essential for stopping pulmonary hemorrhage and therefore cannot be recommended for this purpose. For small and medium-sized pulmonary hemorrhages, 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 impact on the source of bleeding (diathermocoagulation, laser photocoagulation) or occlusion of the bronchus into which the blood flows. Direct exposure is especially effective for bleeding from a bronchial tumor. Bronchial occlusion can be used for massive pulmonary hemorrhages. For occlusion, a silicone balloon catheter, a foam sponge, and a gauze tamponade are used. The duration of such occlusion may vary, but usually 2-3 days are sufficient. Bronchial occlusion prevents aspiration of blood into other parts of the bronchial system and sometimes completely stops bleeding. If a subsequent operation 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 early as possible, preferably in the first 2-3 days. In this case, the source of bleeding can often be determined. Usually this is a segmental bronchus with remnants of coagulated blood. Bronchoscopy, as a rule, does not provoke resumption of bleeding.

An effective method for stopping pulmonary hemorrhage is X-ray endovascular occlusion of a bleeding vessel. The success of bronchial artery embolization depends on the skill of the physician. It should be performed by an experienced radiologist skilled in angiography. First, arteriography is performed to determine the site of bleeding from the bronchial artery. For this purpose, such signs as the size of the vessels, the degree of hypervascularization, as well as 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 able to dissolve and thus prevent recanalization. Another agent is gelatin sponge, which unfortunately leads to recanalization and is therefore used only as an adjunct to PVA. Isobutyl-2-cyanoacrylate, like ethanol, is not recommended due to the high risk of tissue necrosis. Immediate response success of bronchial artery embolization was noted in 73-98% of cases. In this case, quite a lot of complications have been described, among which the most common is chest pain. Most likely, it is ischemic in nature and usually resolves. 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 to perform so-called supraselective embolization.

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

Surgeries for pulmonary hemorrhage can be emergency, urgent, delayed or planned. Emergency operations are performed during bleeding. urgent - after stopping the bleeding, and delayed or planned - after stopping the bleeding, special examination and full preoperative preparation. Watchful waiting often leads to repeated bleeding, aspiration pneumonia, and progression of the disease.

The main operation for pulmonary hemorrhage is resection of the lung with removal of its 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 and ligation of the bronchial arteries, can be used.

Mortality during surgical intervention varies from 1 to 50%. If there are contraindications to surgery (for example, 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 asperigilloma leading to bleeding has so far been disappointing.

After profuse bleeding, it may sometimes be necessary to partially replace lost blood. For this purpose, red blood cells 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, 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 timely and effective treatment of lung diseases. In cases where surgical treatment of lung diseases is necessary with a history of bleeding, it is advisable to perform surgical intervention in a timely manner and as planned.

Spontaneous pneumothorax

Spontaneous pneumothorax is the entry of air into the pleural cavity, which occurs spontaneously, as if spontaneously, without damage to the chest wall or lung. However, in most cases with spontaneous pneumothorax, both a certain form of lung pathology and the 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. Among patients with spontaneous pneumothorax, men account for 70-90%. mainly between the ages of 20 and 40. Pneumothorax is observed on the right somewhat more often than on the left.

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 rupture of air bubbles - bullae.

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

In the formation of bullae in local emphysema, damage to small bronchi and bronchioles is important with the formation of a valve obstructive mechanism, which causes increased intraalveolar pressure in the subpleural parts of the lung and ruptures of overstretched interalveolar septa. The bullae may be subpleural and hardly bulge above the surface of the lung, or they may be blisters associated with the lung, 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 the head of a pin to 10-15 cm. The wall of the bullae 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 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 main importance is the patient’s physical stress, lifting heavy objects, jolting, and coughing. In this case, an increase in pressure in the bulla and rupture of its wall can be facilitated by the valve mechanism at its narrow base and ischemia of the wall.

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

• perforation into the pleural cavity of the tuberculous cavity;
• rupture of the cavity at the base of the pleural cord when applying an artificial pneumothorax;
• damage to lung tissue during transthoracic diagnostic and therapeutic puncture:
• breakthrough of an abscess or gangrene of the lung;
• destructive pneumonia;
• pulmonary infarction, rarely - pulmonary cyst; cancer. metastases of malignant tumors, sarcoidosis, berylliosis, histiocytosis X, fungal infections of the lungs 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 during intrapulmonary or subpleural implantation of endometrial cells.

In some patients, spontaneous pneumothorax develops sequentially on both sides, but cases of simultaneous bilateral pneumothorax are known. 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 nonspecific microflora and purulent pleurisy (pyopneumothorax) is added to pneumothorax. Rarely, with pneumothorax, penetration of air into the subcutaneous tissue, into the mediastinal tissue (pneumomediastinum) and air embolism are observed. A combination of spontaneous pneumothorax with intrapleural bleeding (hemopneumothorax) is possible. The source of bleeding is either the site of lung perforation or the edge of the rupture of the pleural commissure. Intrapleural bleeding may be significant and cause symptoms of hypovolemia and anemia

Symptoms of spontaneous pneumothorax

Diagnosis of spontaneous pneumothorax

The most informative method for diagnosing all types of spontaneous pneumothorax is x-ray examination. Pictures are taken during inhalation and exhalation. In the latter case, the edge of the collapsed lung is better identified. The degree of lung collapse, the localization of pleural adhesions, the position of the mediastinum, the presence or absence of fluid in the pleural cavity are determined. It is always important to identify the pulmonary pathology that was the cause of spontaneous pneumothorax. Unfortunately, conventional X-ray examination, even after air aspiration, is often ineffective. CT is required to recognize local and widespread bullous emphysema. It often turns out to be 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 performed 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. By changes in pressure during air suction, one can judge the anatomical features of the pulmonary-pleural communication. The clinical course of pneumothorax largely depends on its characteristics.

When a small bulla is perforated, only a momentary entry 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 very small air intake, pneumothorax can exist for many months and years. Such pneumothorax, in the absence of a tendency to expand the collapsed lung and in conditions of delayed 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, the 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 expand and restore normal function even after surgical removal of the shell from its surface; patients often progress to respiratory failure and develop hypertension 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, valve or progressive pneumothorax. It occurs in cases of formation of valvular pulmonary-pleural communication at the site of perforation of the visceral pleura. During inhalation, air enters through the perforation into the pleural cavity, and during exhalation, the closing valve prevents it from leaving the pleural cavity. As a result, with each breath, 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 displacement of the mediastinal organs in the opposite direction with a decrease in the volume of the second lung. The main veins are displaced, bent and compressed, and blood flow to the heart decreases. The diaphragm dome lowers and becomes flat. Ruptures of the adhesions between the parietal and visceral layers of the pleura easily occur with the formation of hemopneumothorax.

In patients with tension pneumothorax, severe shortness of breath, cyanosis appear, the timbre of the voice changes, and patients feel the fear of death. Usually a forced sitting position and restlessness and agitation of the patient are noted. Accessory muscles are involved in breathing. The chest wall on the side of the pneumothorax lags behind during breathing, the intercostal spaces smooth out or bulge. Sometimes the supraclavicular fossa also bulges. Upon palpation, a displacement of the apex beat of the heart is determined in the direction opposite to the pneumothorax; there is no vocal tremor on the side of the pneumothorax. Subcutaneous emphysema may be detected. On percussion, high tympanitis and displacement of the mediastinal organs are noted; on auscultation, there is an absence of breath sounds on the side of the pneumothorax. Occasionally the body temperature rises. X-ray examination confirms and clarifies clinical data. Acute respiratory failure with severe hemodynamic disorders that develops during tension pneumothorax can quickly lead to the death of the patient in the absence of therapeutic measures.

Treatment of spontaneous pneumothorax

Treatment of spontaneous pneumothorax must be carried out in a hospital. If there is a thin layer of air between the lung and the chest wall, no special treatment is often required. In cases of a larger amount of air, 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 constant aspiration of air. For hemopneumothorax, a second catheter is inserted along the midaxillary line in the sixth intercostal space. Constant aspiration with a vacuum of 10-30 cm of water. Art. in most cases it leads to the cessation of air flow from the pleural cavity. If the lung has expanded according to X-ray examination, aspiration is continued for another 2-3 days. and then the catheter is removed. However, sometimes the flow of air through the catheter continues for 4-5 days. In such a situation, they often use the injection of sodium bicarbonate or tetracycline solutions into the pleural cavity, as well as spraying pure talc powder, which causes the development of pleural adhesions. An attempt may be made to seal the lung using electrocoagulation or biological glue through a thoracoscope inserted into the pleural cavity. However, more often, with prolonged air intake, surgical treatment is resorted to through minimally invasive video thoracoscopic or open surgery.

In case of tension pneumothorax, the patient needs emergency assistance - 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 trocars into the pleural cavity. This technique allows you to reduce intrapleural pressure and eliminate the immediate threat to the patient’s life. For 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, intensive care units or specialized pulmonary surgical departments.

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. 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 in which the circulation of a significant part of the lungs can be impaired.

Causes of pulmonary embolism

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

Blood clots from the deep veins of the lower extremities and pelvic veins enter the right atrium, then the right ventricle, where they fragment. From the right ventricle, blood clots 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 overall vascular resistance in the lungs. Overload of the right ventricle occurs, a drop in cardiac output and the development of acute cardiovascular failure.

Symptoms of pulmonary embolism

Clinical symptoms of thromboembolism are nonspecific; patients complain of shortness of breath, cough, fear, rapid breathing, and tachycardia. During auscultation, an increase in the second tone above the pulmonary artery and signs of bronchospasm (dry wheezing) are heard. In case of infarction-pneumonia and limited thromboembolism in the pulmonary artery system, clinical symptoms such as chest pain and hemoptysis are characteristic. Patients note pain along the deep veins of the extremities and swelling of the lower leg.

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 typical with the sudden development of massive thromboembolism. X-rays reveal a decrease in lung volume and sometimes pleural effusion, the appearance of local zones of reduced blood supply and dilatation of the hilar arteries proximal to the thrombosed area. Auxiliary methods for diagnosing pulmonary embolism (echocardiography, ventilation-perfusion scintigraphy, angiopulmonography) in severe condition of patients with tuberculosis and suddenly developed thromboembolism are practically unavailable.

Treatment of pulmonary embolism

• immediately after clarifying the 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 an increase of 1.5-2 times compared to the initial aPTT value. you can start with an infusion of sodium heparin at a dose of 80 units/kg per hour, then you should 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 orally indirect anticoagulants (warfarin, ethyl biscoumacetate) until the prothrombin time increases by 1.5 times;
• oxygen therapy 3-5 l/min;
• when a diagnosis of massive pulmonary embolism is made 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 units/kg for 10 minutes, then 4000 units/kg intravenously for 12-24 hours, or streptokinase intravenously at a dose of 250 thousand units for 30 minutes, then 100 units /hour for 12-72 hours;
• when determining the exact location of the embolus or when anticoagulant or thrombolytic therapy is ineffective, embolectomy is indicated.

Acute lung injury syndrome

Acute lung injury syndrome (ALI) and adult acute respiratory distress syndrome (ARDS) are pulmonary edema of non-cardiogenic etiology with severe respiratory failure and severe hypoxia, resistant to oxygen therapy. The reason for the development of nostrils 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.

Symptoms of acute lung injury syndrome

The severity of clinical manifestations of COL is rapidly increasing. Patients are excited, note a feeling of fear, suffocation, pain in the heart area, wheezing, participation of intercostal muscles in breathing, auscultatory signs of congestion in the lungs, hypoxia with acrocyanosis, coughing up pink foamy sputum. X-ray changes appear somewhat later: decreased transparency of the pulmonary 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 shortness of breath, cyanosis, wheezing in the lungs (“wet lung”). X-ray reveals bilateral pulmonary infiltration against the background of a previously unchanged pulmonary pattern.

Diagnosis of acute lung injury syndrome

Radiographically, in acute lung injury syndrome, a reticulated pulmonary pattern, blurred shadows of blood vessels, especially in the lower sections, and an increase in the vascular pattern in the root of the lung (“blizzard”, “butterfly”, “wings of the angel of death”) are noted.

Changes in the gas composition of the blood: arterial hypoxemia with the subsequent 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 in these patients.

Oxygen therapy should be started immediately after signs of acute respiratory failure appear. Oxygen is supplied 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 the development of ARDS for a short period of time to increase 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 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 capacitive 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.

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

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

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

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

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

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, therefore, in ARDS, inhalation of 3% surfactant-BL emulsion in the form of instillations and using mechanical inhalers should be prescribed as early as possible. The use of an ultrasonic inhaler is unacceptable, since the surfactant is destroyed when the emulsion is treated with ultrasound.

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

The use of PEEP during mechanical ventilation makes it possible to achieve ventilation of collapsed alveoli, increase the functional residual capacity and compliance of the lungs, reduce shunting and improve blood oxygenation. The use of PEEP with low pressure (less than 12 cm of water column) helps prevent the destruction of surfactant and damage to lung tissue from local exposure to oxygen. PEEP that exceeds pulmonary resistance helps to block blood flow and reduce cardiac output, can impair tissue oxygenation and increase the severity of pulmonary edema.

In order to reduce the likelihood of iatrogenic lung injury during mechanical ventilation, the use of pressure-controlled servo ventilators can be recommended. This prevents the risk of lung overdistension by ensuring small tidal volumes and an inverted inspiratory to expiratory ratio during mechanical ventilation in patients with ARDS.