Pulmonary hemorrhage

Syndrome of diffuse alveolar bleeding is a persistent or recurring pulmonary hemorrhage.

Over the past decades, about a hundred different nosological forms, complicated by pulmonary hemorrhage (LC), have been described. However, more often such bleeding is diagnosed in pulmonary tuberculosis (40-66%), suppurative lung diseases (30-33%), and lung cancer (10-15%). Sometimes other, more rare systemic diseases are accompanied by the development of pulmonary hemorrhage. Prior to receiving antibacterial drugs, mortality due to pulmonary hemorrhage was 2%, currently 10-15%. It is believed that with the loss of more than 600 ml of blood in a short period of time (less than four hours), the death of patients occurs in 70% of cases.

[1], [2], [3], [4]

What causes pulmonary bleeding?

Isolated immune pulmonary capillary disease - microvascular vasculitis, limited to vascular lesions of the lungs; its only manifestation is alveolar pulmonary hemorrhage that occurs in people aged 18–35 years.

Idiopathic pulmonary hemosiderosis is a syndrome of diffuse alveolar bleeding, in which it is impossible to identify the underlying disease. Pulmonary hemorrhage occurs mainly in children under 10 years of age and is thought to be due to a defect in the alveolar capillary endothelium, possibly due to autoimmune damage.

Some of these diseases can also cause glomerulonephritis, in which case it is said that the patient has pulmonary and renal syndrome.

Major sources of pulmonary hemorrhage

• Rasmussen's aneurysm (pulmonary artery aneurysm passing through the tubercular cavity).
• Varicose veins that pass through fibrous, peribronchial, and intraalveolar cirrhotic tissue.
• Branches of the pulmonary artery.
• Bronchial arteries.
• Anastomoses between the pulmonary artery and bronchial arteries.
• Thin-walled vascular plexus (such as hemangiomas) that form in areas of chronic inflammation and pneumosclerosis.
• Inflamed or petrified bronchopulmonary lymph nodes, their presence causes the formation of vascular wall necrosis.
• Diapedesic pulmonary hemorrhage, developed due to a violation of capillary permeability as a result of inflammation of the vascular wall or exposure to toxins.

Currently, it is impossible to clearly identify the source of pulmonary hemorrhage. The main source of such bleeding is the bronchial arteries that are part of the systemic circulation (based on various publications). According to some experts, most often pulmonary hemorrhages arise from the pulmonary artery system (the small circulation). There is a compromise point of view; the main source of pulmonary hemorrhage in acute processes is the pulmonary artery, and in chronic processes it is the bronchial artery. The basis of controversy is the data on the frequent occurrence of LC from the anastomoses between the bronchial and pulmonary vessels.

Studies have shown that 90% of deaths of pulmonary hemorrhage are associated with pulmonary hypertension. Against the background of hypertension, the sclerotic and aneurysmatically altered vessels rupture, leading in some cases to profuse bleeding and subsequent death. Back in 1939, in the USA, Auerbach, who investigated Rasmussen's aneurysm, proved that the formation of a blood clot in the area of a vessel defect and the subsequent arrest of bleeding occur if a blood clot is able to withstand the pressure of blood pressure.

Most specialists associate the problem of pulmonary hemorrhage with the coagulopathic factor. However, as shown by studies conducted during the 20th century (since the 1920s), hypocoagulation, hypercoagulation, and normal coagulation can be detected in patients with pulmonary tuberculosis with LC. Similar data were obtained in the study of suppurative diseases of the lungs. Often, anti-tuberculosis chemotherapy also has an effect on the coagulation system. So, long-term use of ftivazid causes hypocoagulation, and streptomycin - hypercoagulation. The intracoagulation leads to an increase in fibrinolytic activity, a decrease in the activity of a fibrin-stabilizing factor and the rapid dissolution of fibrin clots. Many authors consider this fact the main cause of the development of pulmonary hemorrhage.

[5], [6], [7], [8]

Symptoms of pulmonary hemorrhage

Symptoms and manifestations of moderate diffuse alveolar pulmonary hemorrhage syndrome - shortness of breath, cough and fever; however, many patients develop acute respiratory failure. Hemoptysis is common, but a third of patients may be absent. Children with idiopathic pulmonary hemosiderosis may have a pronounced lag in development. Physical examination does not detect specific symptoms.

[9], [10], [11], [12]

Complications

Asphyxia is the most dangerous complication of pulmonary hemorrhage. Sometimes atelectasis is found. As a result of pulmonary hemorrhage, the main process progresses; this is noted in tuberculosis and purulent lung diseases.

Pneumonia, traditionally called hemoaspiration, is a typical and frequently occurring complication of pulmonary hemorrhage, ICD-10, contains two different concepts of pneumonia (an infection of the lungs of an infectious nature) and pneumonitis (a condition caused by hemoaspiration). Hemoaspiration pneumonia is understood to mean pneumonitis resulting from blood aspiration, complicated by the addition of infectious flora. Clinically and radiologically, such pneumonia is determined on days 2-5 after hemoaspiration. Localization of the lesion on the side of the source of the bleeding and below it (Sternberg's sign, 1914) is radiologically determined as broncholobular or with small broncholobular foci. Statistical literature data on the prevalence of hemoaspiration pneumonia are extremely controversial. According to TKB No. 7 of Moscow, the disease is recorded in 9% of patients with confirmed hemoaspiration. In the intensive care unit, where patients with moderate to large (profuse) bleeding are treated, this form of pneumonia is diagnosed in 44.9% of cases, and in 23% of cases the pathological process is characterized by bilateral localization.

[13], [14], [15], [16], [17], [18], [19], [20]

Classification

According to ICD-10, two states of hemoptysis (streaks or blood in sputum) and pulmonary hemorrhages are clearly distinguished. Recently published about 20 classifications of pulmonary hemorrhage. According to the classification of V. I. Struchkov there are three degrees of blood loss. With I degree of blood loss, the patient loses less than 300 ml per day, with II degree - up to 700 ml, with III degree - more than 700 ml. The classification of Yu. V. Rzhavskova takes into account blood loss that occurs within an hour. With the first degree of blood loss, the amount of leaked blood does not exceed 20 ml, with the second - up to 50 ml, with the third - up to 200 ml or more. The simplest and most common classification includes small (blood loss - up to 100 ml), medium (blood loss - up to 500 ml) and large or profuse (blood loss - 500 ml or more) pulmonary hemorrhage. In the English literature can be found the concept of massive pulmonary hemorrhage. Massive is called the expiration of 600 ml or more of blood during the day.

The main disadvantage (or more precisely the defect) of all classifications based on external blood excretion is considered to be the lack of accounting for the volume of blood remaining in the lower parts of the lungs and the volume of blood trapped in the contralateral lung.

Gastrointestinal bleeding is a condition that often masks pulmonary hemorrhage. Sometimes it is not coughing up blood, and its swallowing of LC during life is not detected in approximately 19% of patients, and the presence of blood in the gastrointestinal tract is recorded in 74% of patients. Often, nosebleeds are taken for pulmonary hemorrhage, especially when coughing up blood, rather than bleeding it out. In isolated cases, pulmonary hemorrhage is mistakenly diagnosed as an AS, for example, with a suppressed cough reflex and blood flowing to the lower parts of the lungs. The presence of a tumor of the root of the tongue and larynx also leads to the development of bleeding, often taken for pulmonary hemorrhage.

[21], [22], [23], [24], [25], [26]

Diagnosis of pulmonary hemorrhage

In the diagnosis of pulmonary hemorrhage, radiography and CT are of great importance. However, the most informative diagnostic method is considered bronchoscopy, which allows to determine not only the side of bleeding, but also to find its source.

The diagnosis is often suggested when common bilateral alveolar infiltrates are detected during chest X-ray. Analysis Urinalysis is prescribed to exclude glomerulonephritis and pulmonary renal syndrome. Other studies include the determination of blood formula and content platelets, coagulation studies and serologic tests ( antinuclear antibodies, antibodies to double-stranded DNA, antibodies to glomerular basement membrane [anti-CBM antibodies], antineutrophil cytoplasmic antibodies [ANCA], antibodies to phospholipids) for the detection of the underlying disease; ANCA titers may be elevated in some cases of an isolated immune pulmonary capillary. The diagnosis of idiopathic pulmonary hemosiderosis includes the presence of iron deficiency anemia and hemosiderin-saturated macrophages in bronchoalveolar lavage or lung biopsy in the absence of signs of microvascular vasculitis (pulmonary capillaritis) or other diseases.

Other studies depend on the clinical situation. Pulmonary function tests can be performed to document lung function; An increase in the ability to diffuse carbon monoxide due to its increased absorption by intraalveolar hemoglobin is combined with pulmonary hemorrhage. Echocardiography may be indicated to exclude mitral stenosis. In case of bronchoalveolar lavage, a liquid is usually obtained, which remains hemorrhagic even after successive production of several wash waters. Lung biopsy is often a necessary study if the underlying cause is unclear.

Syndrome of diffuse alveolar bleeding is an independent diagnostic syndrome, because it requires a differential diagnosis and a specific sequence of research and treatment. Pulmonary hemorrhage should be differentiated by the following conditions: autoimmune diseases, including systemic vasculitis and Goodpasture's syndrome; antiphospholipid syndrome; pulmonary infections; exposure to toxic substances; drug reactions; transplantation of bone marrow and other organs; heart defects, such as mitral stenosis; coagulation disorders caused by diseases or anticoagulant drugs; isolated immune pulmonary capillary and idiopathic pulmonary hemosiderosis.

[27], [28]

Treatment of pulmonary hemorrhage

Pulmonary hemorrhage should be treated if the cause is eliminated. Glucocorticoids and possibly cyclophosphamide are used in the treatment of vasculitis, connective tissue diseases and Goodpasture syndrome. Glucocorticoids are also used in the treatment of idiopathic pulmonary hemosiderosis; in resistant cases, immunosuppressants are added.

In addition to medical (conservative) therapy, there are semi-radical (bronchological and endovascular) and surgical methods for the treatment of pulmonary hemorrhage. It should be noted that during operations at the time of maximum intensity of bleeding, patients often die, and there are various hemoaspirated complications. Such data were obtained in almost all countries of the world. Mortality mainly depends on the intensity of pulmonary hemorrhage and is 20% in France and 15-80% in Russia. The likelihood of hemoaspiration complications often exceeds 50%. According to some data, postoperative aspiration pneumonia develops with delayed operations in 4% of patients, with emergency surgical interventions in 42% of patients.

In the treatment of pulmonary hemorrhage must take into account some of the fundamental points. Pulmonary hemorrhage, as a rule, develops over a long time (from several hours to days). Hemorrhagic shock when LC is diagnosed rarely. Bleeding either stops or patients die from asphyxiation. It is not recommended to conduct emergency massive ITT, often contributing to the enhancement or recurrence of pulmonary hemorrhage.

Most experts believe that the use of hemostatics is the main method of pharmacotherapy. Moreover, these drugs are used, without taking into account the mechanism of their action, the state of the coagulation system and the pathogenesis of bleeding. Currently prescribed calcium, vikasol, ascorbic acid and ascorutin, which do not have a serious hemostatic effect in pulmonary hemorrhage. Moreover, cases of increased bleeding when using calcium chloride due to its effect on hemodynamics are described. Usually prescribed etamzilat, which increases the amount of mucopolysaccharides of high molecular weight in the capillary walls, correcting plasma factors, the level of fibrinolysis and fibrinase activity, which increases the intensity of platelet function.

In standard hemostatic therapy include inhibitors of proteolysis and fibrinolysis (aminocaproic acid, pride, contrycal and some others), contributing to the formation of a dense fibrin clot. It can be argued that the use of hemostatics as the main method of pharmacotherapy has a beneficial effect mainly in diapedemic bleeding. When the destruction of the vascular wall inhibitors of proteolysis and fibrinolysis are considered only as ancillary drugs. The basis for stopping pulmonary hemorrhage is considered to be the pharmacological effect of drugs on the pressure in the bleeding vessels. Its reduction leads to the fixation of a blood clot in the area of the defect.

Starting from the 60s of the 20th century, ganglioblockers (mainly pentamine and benzohexonium) were introduced into the practice of pharmacological arrest of pulmonary hemorrhages, which, causing systemic hypotension in the small and large circulation, help stop pulmonary hemorrhage. The method of using ganglioblokatorov is quite simple, it can be demonstrated on the example of pentamine. The drug is administered subcutaneously or intravenously in a dose of 0.5-1.0 ml 2-3 times a day until systolic blood pressure is reduced (to 80-90 mm Hg). Then use ganglioblockers, taken orally (3-6 times a day). The effectiveness of the method is 66-88%. Contraindications to the use of ganglioblokatori consider initially low blood pressure, severe renal and hepatic failure, thrombophlebitis, CNS damage. Currently, this group of drugs has not lost its value, but they are more often used to stop bleeding, and not for a course of treatment.

A powerful effect on hemodynamics have nitrates. Studies have shown that taking high pharmacopoeial doses of nitrates leads to a decrease in pulmonary hypertension. These drugs are administered intravenously (injectable form preparations) or are taken sublingually. However, the use of a standard dose (10 mg) of isosorbide dinitrate sublingually does not produce a tangible effect. Bleeding is recorded only in 23% of patients. With the appointment of maximum single doses (20 mg 4-6 times a day) of isosorbide dinitrate, pulmonary hemorrhage stops in 88% of patients. Often, nitrates are used in combination with ganglioblokatorami.

If it is impossible to achieve stable drug hypotension with monotherapy with nitro drugs, they are combined with rhythm-slowing calcium antagonists (verapamil, diltiazem) used in therapeutic doses. Calcium antagonists and nitrates are referred to peripheral vasodilators. In the most severe cases, ACE inhibitors are prescribed in addition to nitrates and calcium antagonists.

The combined use of two or three groups of drugs can stop the bleeding in 94% of patients. At the same time maintaining systolic blood pressure at 80-90 mm. Hg Art. For several days does not lead to serious complications. Adequate daily diuresis and no change in creatinine and urea levels are noted. Impact on hemodynamics in pulmonary hemorrhage leads to the deposition of blood in the abdominal cavity and increased gastrointestinal bleeding, therefore, in the treatment of bleeding from the gastrointestinal tract, other procedures are performed. Non-drug treatment.

Such methods of treatment of pulmonary hemorrhage, such as bleeding, the imposition of harnesses on the limbs, the introduction of atropine for the deposit of blood in the abdominal cavity today, mainly have historical significance.

Tracheal intubation for pulmonary hemorrhage

There is a common opinion, described in serious guidelines, but not confirmed by statistical data that with massive bleeding, treatment should begin with tracheal intubation, and then consistently insert the endotracheal tube into the right and left bronchus to localize the side of the bleeding and perform a separate intubation with a double lumen tube. The author considers this technique incorrect and even vicious. In addition, documented cases of patient rescue using separate intubation could not be found. This approach cannot be recommended, it should be considered solely as a method of "despair".

In developed countries, embolization of the bronchial arteries is considered one of the main methods of treating massive pulmonary hemorrhage. If embolization cannot be performed or its effect is insufficient, emergency surgical intervention is carried out, despite the high mortality and high risk of complications. In some situations, the embolization of the bronchial arteries is not performed due to the low expected efficiency. As shown by one of the French studies, 38 of 45 patients died from Rasmussen's aneurysm rupture. There are two cases of successful application of transcatheter occlusion of the branches of the pulmonary artery. In our country, these methods due to insufficient technical equipment of medical institutions are not available to the vast majority of patients with pulmonary tuberculosis and pulmonary hemorrhage.

What is the prognosis for pulmonary hemorrhage?

Recurrent diffuse alveolar pulmonary hemorrhage syndrome leads to the development of pulmonary hemosiderosis and fibrosis, which develop when ferritin accumulates in the alveoli and has toxic effects. COPD occurs in some patients with recurrent alveolar hemorrhage syndromes due to microscopic polyarteritis.

[29], [30]