Pulmonary hemorrhage

Diffuse alveolar hemorrhage syndrome is persistent or recurrent pulmonary hemorrhage.

Over the past decades, about a hundred different nosological forms complicated by pulmonary hemorrhage (PH) have been described. However, such hemorrhages are most often diagnosed with pulmonary tuberculosis (40-66%), suppurative lung diseases (30-33%), and lung cancer (10-15%). Sometimes other, rarer systemic diseases are accompanied by the development of pulmonary hemorrhage. Before the advent of antibacterial drugs, the mortality rate due to pulmonary hemorrhage was 2%, and currently it is 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), death of patients occurs in 70% of cases.

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

What causes pulmonary hemorrhage?

Isolated immune pulmonary capillaritis is a microvascular vasculitis limited to the pulmonary vessels; its only manifestation is alveolar pulmonary hemorrhage, occurring in people aged 18-35 years.

Idiopathic pulmonary hemosiderosis is a syndrome of diffuse alveolar hemorrhage in which no underlying disease can be identified. Pulmonary hemorrhage occurs primarily in children under 10 years of age and is thought to result from a defect in the alveolar capillary endothelium, possibly due to autoimmune injury.

Some of these diseases can also cause glomerulonephritis, in which case the patient is said to have pulmonary-renal syndrome.

Main sources of pulmonary hemorrhage

• Rasmussen's aneurysm (aneurysm of the pulmonary artery passing through a tuberculous cavity).
• Varicose veins passing 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 plexuses (like hemangiomas) that form in areas of chronic inflammation and pneumosclerosis.
• Inflamed or calcified bronchopulmonary lymph nodes, their presence causes the formation of vascular wall necrosis.
• Diapedetic pulmonary hemorrhages that develop due to impaired capillary permeability as a result of inflammation of the vascular wall or exposure to toxins.

At present, it is impossible to clearly identify the source of pulmonary hemorrhage. The main source of such bleeding is the bronchial arteries, which are part of the systemic circulation (according to various publications). According to some experts, most often pulmonary hemorrhages arise from the pulmonary artery system (small circulation). There is also a compromise point of view: the main source of pulmonary hemorrhage in acute processes is the pulmonary artery, and in chronic ones - the bronchial artery. The basis of disagreement is considered to be data on the frequent occurrence of pulmonary hemorrhage from anastomoses between the bronchial and pulmonary vessels.

As studies have shown, 90% of fatal pulmonary hemorrhage cases are associated with pulmonary hypertension. Against the background of hypertension, rupture of sclerotic and aneurysmally altered vessels occurs, leading in some cases to profuse bleeding and subsequent death. Back in 1939 in the USA, Auerbach, who studied Rasmussen's aneurysm, proved that the formation of a thrombus in the area of the vessel defect and the subsequent cessation of bleeding occur if the thrombus is able to withstand the pressure of blood pressure.

Most specialists associate the problem of pulmonary hemorrhage with the coagulopathic factor. However, as studies conducted during the 20th century (starting from the 1920s) have shown, hypocoagulation, hypercoagulation and normocoagulation can be detected in patients with pulmonary tuberculosis with LC. Similar data were obtained in the study of suppurative lung diseases. Anti-tuberculosis chemotherapy often affects the coagulation system. Thus, long-term use of phthivazid causes hypocoagulation, and streptomycin - hypercoagulation. Intercoagulation leads to increased fibrinolytic activity, decreased activity of the fibrin-stabilizing factor and rapid dissolution of fibrin clots. Many authors consider this fact to be the main cause of pulmonary hemorrhage.

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

Symptoms of pulmonary hemorrhage

Symptoms and signs of mild diffuse alveolar pulmonary hemorrhage syndrome include dyspnea, cough, and fever; however, many patients develop acute respiratory failure. Hemoptysis is common but may be absent in up to one-third of patients. Children with idiopathic pulmonary hemosiderosis may have severe developmental delays. Physical examination does not reveal specific symptoms.

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

Complications

Asphyxia is the most dangerous complication of pulmonary hemorrhage. Sometimes atelectasis is detected. As a result of pulmonary hemorrhage, the underlying process progresses, this is observed both in tuberculosis and in purulent lung diseases.

Pneumonia, traditionally called hemoaspiration pneumonia, is a typical and frequently occurring complication of pulmonary hemorrhage. ICD-10 contains two different concepts: pneumonia (an infectious lung disease) and pneumonitis (a condition caused by hemoaspiration). Hemaspiration pneumonia is understood to mean pneumonitis that occurs as a result of blood aspiration, complicated by the addition of infectious flora. Clinically and radiologically, such pneumonia is determined on the 2nd-5th day after hemoaspiration. Localization of the lesion on the side of the bleeding source and below it (Sternberg's sign, 1914) is radiologically determined as broncholobular or with the presence of small broncholobular foci. Statistical literature data on the prevalence of hemoaspiration pneumonia are extremely contradictory. According to the data of the City Clinical Hospital No. 7 of Moscow, the disease is registered in 9% of patients with confirmed hemoaspiration. In the intensive care unit, where patients with moderate and 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 conditions are clearly distinguished: hemoptysis (streaks or admixture of blood in sputum) and pulmonary hemorrhage. About 20 classifications of pulmonary hemorrhage have been published recently. According to V. I. Struchkov's classification, there are three degrees of blood loss. With grade I blood loss, the patient loses less than 300 ml per day, with grade II - up to 700 ml, with grade III - more than 700 ml. Yu. V. Rzhavskov's classification takes into account blood loss that occurs within an hour. With grade I blood loss, the amount of leaked blood does not exceed 20 ml, with grade II - up to 50 ml, with grade III - up to 200 ml or more. The simplest and most common classification includes minor (blood loss - up to 100 ml), moderate (blood loss - up to 500 ml) and large or profuse (blood loss - 500 ml or more) pulmonary hemorrhages. In English-language literature, you can find the concept of massive pulmonary hemorrhage. Massive is defined as the leakage of 600 ml or more of blood within 24 hours.

The main drawback (or rather flaw) of all classifications based on external blood secretion is considered to be the lack of consideration of the volume of blood remaining in the lower parts of the lungs and the volume of blood entering the contralateral lung.

Gastrointestinal bleeding is a condition that often masks pulmonary hemorrhage. Sometimes, blood is swallowed rather than coughed up. LC is not detected during life in approximately 19% of patients, and the presence of blood in the gastrointestinal tract is recorded in 74% of patients. Nosebleeds are often mistaken for pulmonary hemorrhage, especially when blood is coughed up, rather than flowing out. In isolated cases, pulmonary hemorrhage is mistakenly diagnosed as AS, for example, with a suppressed cough reflex and blood flowing into 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 hemorrhages, often mistaken for pulmonary hemorrhage.

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

Diagnosis of pulmonary hemorrhage

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

The diagnosis is often suggested by the finding of widespread bilateral alveolar infiltrates on chest radiography. Urinalysis is indicated to exclude glomerulonephritis and pulmonary-renal syndrome. Other studies include blood count and platelet count, coagulation studies, and serologic tests ( antinuclear antibodies, anti-double-stranded DNA antibodies, anti-glomerular basement membrane antibodies [anti-CBM antibodies], antineutrophil cytoplasmic antibodies [ANCA], antiphospholipid antibodies) to identify underlying disease; ANCA titers may be elevated in some cases of isolated immune pulmonary capillaritis. 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 evidence of microvascular vasculitis (pulmonary capillaritis) or other diseases.

Other studies depend on the clinical situation. Pulmonary function tests may be performed to document pulmonary function; increased diffusing capacity for carbon monoxide due to increased uptake by intraalveolar hemoglobin is associated with pulmonary hemorrhage. Echocardiography may be indicated to exclude mitral stenosis. Bronchoalveolar lavage usually yields fluid that remains hemorrhagic even after several successive lavages. Lung biopsy is often necessary if the underlying cause remains unclear.

Diffuse alveolar hemorrhage syndrome is an independent diagnostic syndrome, since it requires differential diagnosis and a certain sequence of studies and treatment. Pulmonary hemorrhage should be differentiated from such conditions as: autoimmune diseases, including systemic vasculitis and Goodpasture's syndrome; antiphospholipid syndrome; pulmonary infections; exposure to toxic substances; drug reactions; bone marrow and other organ transplantation; heart defects, such as mitral stenosis; coagulation disorders caused by diseases or anticoagulant drugs; isolated immune pulmonary capillaritis and idiopathic pulmonary hemosiderosis.

[ 27 ], [ 28 ]

Treatment of pulmonary hemorrhage

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

In addition to drug (conservative) therapy, there are semi-radical (bronchological and endovascular) and surgical methods of treating pulmonary hemorrhages. It should be noted that during operations at the moment of maximum bleeding intensity, patients often die, and various hemoaspiration complications arise. Such data have been 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 probability of developing hemoaspiration complications often exceeds 50%. According to some data, postoperative aspiration pneumonia develops in 4% of patients after delayed operations, and in 42% of patients after emergency surgical interventions.

When treating pulmonary hemorrhage, it is necessary to take into account some fundamental points. Pulmonary hemorrhage, as a rule, develops over a long period of time (from several hours to a day). Hemorrhagic shock in pulmonary hemorrhage is rarely diagnosed. Bleeding either stops, or patients die from asphyxia. It is not recommended to perform emergency massive ITT, which often contributes to the intensification or relapse 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, calcium preparations, vikasol, ascorbic acid and askorutin are prescribed, which do not have a serious hemostatic effect in pulmonary hemorrhage. Moreover, cases of increased bleeding with the use of calcium chloride due to its effect on hemodynamics have been described. Etamsylate is usually prescribed, which increases the amount of high molecular weight mucopolysaccharides in the capillary walls, corrects plasma factors, the level of fibrinolysis and fibrinase activity, increasing the intensity of the platelet apparatus.

Standard hemostatic therapy includes inhibitors of proteolysis and fibrinolysis (aminocaproic acid, gordox, contrical and some others), which promote 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 diapedetic bleeding. In the case of vascular wall destruction, inhibitors of proteolysis and fibrinolysis are considered only as auxiliary drugs. The basis for stopping pulmonary hemorrhages is considered to be the pharmacological effect of drugs on the pressure in the bleeding vessels. Its reduction leads to fixation of the thrombus in the defect area.

Since the 1960s, ganglionic blockers (mainly pentamine and benzohexonium) have been introduced into the practice of pharmacological stopping of pulmonary hemorrhage. They cause systemic hypotension in the pulmonary and systemic circulation, helping to stop pulmonary hemorrhage. The method of using ganglionic blockers is quite simple, it can be demonstrated using pentamine as an example. The drug is administered subcutaneously or intravenously at 0.5-1.0 ml 2-3 times a day until systolic blood pressure decreases (to 80-90 mm Hg). Then ganglionic blockers are used, taken orally (3-6 times a day). The effectiveness of the method is 66-88%. Contraindications to the use of ganglionic blockers include initially low blood pressure, severe renal and hepatic insufficiency, thrombophlebitis, and CNS damage. Currently, this group of drugs has not lost its importance, but they are more often used to stop bleeding rather than for a course of treatment.

Nitrates have a powerful effect on hemodynamics. As studies have shown, taking high pharmacopoeial doses of nitrates leads to a decrease in pulmonary hypertension. These drugs are administered intravenously (injectable forms of drugs) or taken sublingually. However, using a standard dose (10 mg) of isosorbide dinitrate sublingually does not produce a noticeable effect. Bleeding is stopped in only 23% of patients. When prescribing maximum single doses (20 mg 4-6 times a day) of isosorbide dinitrate, pulmonary bleeding is stopped in 88% of patients. Nitrates are often used in combination with ganglionic blockers.

If stable drug-induced hypotension cannot be achieved with monotherapy with nitro drugs, they are combined with rhythm-slowing calcium antagonists (verapamil, diltiazem), used in therapeutic doses. Calcium antagonists and nitrates are classified as 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 allows stopping bleeding in 94% of patients. At the same time, maintaining systolic blood pressure at 80-90 mm Hg for several days does not lead to serious complications. Adequate daily diuresis and no change in creatinine and urea levels are noted. The effect on hemodynamics in pulmonary hemorrhage leads to blood deposition in the abdominal cavity and increased gastrointestinal bleeding, therefore, other procedures are performed in the treatment of gastrointestinal bleeding. Non-drug treatment.

Such methods of treating pulmonary hemorrhage as bloodletting, application of tourniquets to the extremities, and the introduction of atropine to deposit blood in the abdominal cavity today are mainly of historical significance.

Tracheal intubation for pulmonary hemorrhage

There is a widespread opinion, described in serious manuals, but not supported by statistical data, that in case of massive bleeding, treatment should begin with tracheal intubation, and then sequentially insert an endotracheal tube into the right and left bronchi to localize the bleeding side and perform separate intubation with a double-lumen tube. The author considers this method to be incorrect and even vicious. In addition, it was not possible to find documented cases of saving a patient with the help of separate intubation. Such an approach cannot be recommended; it should be considered exclusively as a method of "desperation".

In developed countries, bronchial artery embolization is considered one of the main methods of treating massive pulmonary hemorrhages. If embolization is impossible or its effect is insufficient, emergency surgery is performed, despite the high mortality rate and high risk of complications. In some situations, bronchial artery embolization is not performed due to low expected effectiveness. As one French study showed, 38 out of 45 patients died from a ruptured Rasmussen aneurysm. There are two cases of successful use of transcatheter occlusion of pulmonary artery branches. In our country, these methods are inaccessible to the vast majority of patients with pulmonary tuberculosis and pulmonary hemorrhage due to insufficient technical equipment of medical institutions.

What is the prognosis for pulmonary hemorrhage?

Recurrent diffuse alveolar pulmonary hemorrhage syndrome results in 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 ]