Lung atelectasis: disc-shaped, right, left, upper, lower, middle lobe

In clinical pulmonology, the complex of symptoms accompanying the compaction of areas of the lung parenchyma and the absence of air in their gas exchange zone (alveoli and alveolar ducts) is called pulmonary atelectasis, that is, incomplete expansion of its individual lobes or segments with loss of alveolar function.

Atelectasis leads to a significant reduction in respiratory volume and ventilation of the lungs, and in the case of total damage to the air-bearing tissue of the lungs, to respiratory failure with a fatal outcome.

According to ICD-10, this pathological condition has the code J98.1.

[ 1 ], [ 2 ]

Epidemiology

According to the American Journal of Respiratory and Critical Care Medicine, pulmonary atelectasis after inhalation anesthesia occurs in 87% of American surgical patients, and in 54-67% of Canadian patients. The incidence of this pulmonary complication after open cardiac surgery in developed countries currently stands at 15% with a patient mortality rate of 18.5%, which is 2.79% of the total mortality from complications of surgical interventions.

Over the past 20 years, the number of premature babies has been steadily increasing worldwide, according to WHO. Premature births (occurring before the 37th week of gestation) account for 9.6% of 12.6 million births per year. However, this figure varies across regions, with the highest proportion of premature births in Africa (11.8%) and the lowest in Europe (6.3%).

In the United States, neonatal respiratory distress syndrome is one of the top five causes of infant death, accounting for 5.6% of deaths.

And congenital atelectasis is the cause of 3.4% of newborn deaths.

Atelectasis is also common in young children because their airways are narrower and many structures are still forming.

[ 3 ], [ 4 ], [ 5 ], [ 6 ], [ 7 ], [ 8 ]

Causes atelectasis of the lung

There is no single cause of pulmonary atelectasis for all varieties of this pathology. Thus, the types that differ in the size of the affected area - partial atelectasis (focal, isolated or segmental atelectasis) and total atelectasis or collapse of the lung - may have different etiologies.

Explaining the pathogenesis of pulmonary atelectasis, it should be recalled that the bronchopulmonary alveoli look like bubbles separated by connective tissue partitions, penetrated by a network of capillaries in which arterial blood undergoes oxygenation (i.e. absorbs inhaled oxygen), and venous blood gives off carbon dioxide. With atelectasis, ventilation of part of the lungs is disrupted, the partial pressure of oxygen in the air filling the alveoli drops, which leads to disruption of gas exchange in the pulmonary circulation.

Pulmonologists determine the types of atelectasis either depending on the features of its localization in the air-bearing structures - atelectasis of the right lung, atelectasis of the left lung, atelectasis of the lobe of the lung (lower, middle or upper), or taking into account its pathogenesis. Thus, primary atelectasis, also known as congenital atelectasis, occurs in newborns with abnormalities in lung opening (especially in cases of prematurity); more about it will be discussed below - in the section Atelectasis in newborns.

All other cases are considered secondary or acquired conditions, among which are obstructive or obstructive atelectasis and non-obstructive (including compression and distension atelectasis).

Since the right middle lobe of the lung is the narrowest and surrounded by a large volume of lymphoid tissue, atelectasis of the middle lobe of the lung is considered the most common.

Obstructive atelectasis (in most cases partial) is diagnosed when the collapse of the lung occurs due to aspiration of the respiratory tract by a foreign body (blocking the passage of air) or masses entering during gastroesophageal reflux disease; blockage of the bronchi by mucous exudate during obstructive bronchitis, severe tracheobronchitis, emphysema, bronchiectasis, acute and chronic eosinophilic and interstitial pneumonia, asthma, etc.

For example, atelectasis in tuberculosis (usually segmental) most often develops when the bronchi are obstructed by blood clots or caseous masses from caverns; also, in tuberculosis, overgrown granulomatous tissues can press on the bronchiole tissue.

The stages of total obstructive atelectasis, regardless of location, progress from one to another with a rapid deterioration in the patient’s condition – as oxygen, carbon dioxide and nitrogen are absorbed in the “blocked” alveoli and the overall composition of blood gases changes.

Dysfunction of the lung tissue caused by compression atelectasis is the result of its extrathoracic or intrathoracic compression by hypertrophied lymph nodes, enlarged fibrous neoplasms, large tumors, pleural effusion, etc., which leads to collapse of the alveoli. Specialists quite often observe atelectasis in lung cancer, thymomas or lymphomas localized in the mediastinum, bronchoalveolar carcinoma, etc.

In case of total damage of the lung parenchyma, total atelectasis and lung collapse can be diagnosed. When, due to chest trauma, its tightness is broken with air entering the pleural cavity, tension pneumothorax develops with atelectasis (but atelectasis is not a synonym for pneumothorax).

The so-called discoid or lamellar atelectasis is a compression atelectasis, and it got its name from the image of the shadow on the X-ray image - in the form of elongated transverse stripes.

Distension atelectasis or functional (most often segmental and subsegmental, localized in the lower lobes) is etiologically associated with the suppression of the activity of neurons of the respiratory center of the medulla oblongata (in injuries and tumors of the brain, with general inhalation anesthesia, administered through a mask or an endotracheal tube); with a decrease in the functions of the diaphragm in bedridden patients; with an increase in pressure in the abdominal cavity due to dropsy and increased gas formation in the intestine. In the first case, there are iatrogenic causes of atelectasis: with endotracheal anesthesia, the pressure and absorption of gases in the lung tissues change, causing collapse of the alveoli. As surgeons note, atelectasis is a common complication of various abdominal surgeries.

Some sources distinguish contractile atelectasis (constricting), which is caused by a decrease in the size of the alveoli and an increase in surface tension during bronchial spasms, injuries, surgical interventions, etc.

Atelectasis can be a symptom of a number of interstitial lung diseases that damage the tissues surrounding the alveoli: exogenous allergic alveolitis (allergic pneumonitis or pneumoconiosis), pulmonary sarcoidosis, obliterating bronchiolitis (cryptogenic pneumonia), desquamative interstitial pneumonia, pulmonary Langerhans histiocytosis, idiopathic pulmonary fibrosis, etc.

[ 9 ], [ 10 ], [ 11 ], [ 12 ], [ 13 ]

Risk factors

Risk factors for atelectasis include:

• age under three or over 60 years;
• prolonged bed rest;
• impaired swallowing function, especially in the elderly;
• lung diseases (see above);
• rib fractures;
• premature pregnancy;
• abdominal surgeries under general anesthesia;
• respiratory muscle weakness due to muscular dystrophy, spinal cord injury, or other neurogenic condition;
• chest deformities;
• the use of drugs whose side effects extend to the respiratory system (in particular, sleeping pills and sedatives);
• obesity (excess body weight);
• smoking.

[ 14 ], [ 15 ], [ 16 ], [ 17 ]

Symptoms atelectasis of the lung

The first signs of incomplete lung function are shortness of breath and decreased expansion of the chest wall when inhaling.

If the pathological process has affected a small area of the lungs, the symptoms of pulmonary atelectasis are minimal and are limited to a feeling of lack of air and weakness. When the lesion is significant, the person turns pale; his nose, ears and fingertips become bluish (cyanosis); stabbing pains appear on the affected side (not often). Fever and increased heart rate (tachycardia) may be observed when atelectasis is accompanied by an infection.

In addition, the symptoms of atelectasis include: irregular, rapid, shallow breathing; a drop in blood pressure; cold feet and hands; a decrease in temperature; cough (without sputum).

If atelectasis develops against the background of bronchitis or bronchopneumonia, and the lesion is extensive, a sudden exacerbation of all symptoms is observed, and breathing becomes rapid, shallow and arrhythmic, often with wheezing.

Symptoms of atelectasis in newborns are manifested by wheezing, moaning exhalation, irregular breathing with apnea, flaring of the nostrils, cyanosis of the face and all skin, retraction of the skin in the spaces between the ribs - when inhaling (from the side of atelectasis development). Also noted are increased pulse rate, decreased body temperature, muscle rigidity, convulsions.

[ 18 ], [ 19 ]

Atelectasis in newborns

Atelectasis in newborns or primary atelectasis is the main cause of the so-called respiratory distress syndrome of the newborn (ICD-10 code – P28.0-P28.1).

Congenital atelectasis occurs due to airway obstruction by amniotic fluid or meconium aspiration, which lead to increased pressure in the lungs and pleural cavity and damage to the alveolar epithelium. This pathology can also be a consequence of intrauterine underdevelopment of lung and bronchial tissues (Wilson-Mikiti syndrome), bronchopulmonary dysplasia (in children born at a gestational age of less than 32 weeks), congenital alveolar or alveolar-capillary dysplasia, intrauterine pneumonia, and congenital disorder of surfactant secretion.

The latter factor is of particular importance in the pathogenesis of congenital atelectasis. Normally, the alveolar walls do not stick together due to the surfactant produced by special cells of the alveolar basement membrane (type II alveolocytes) – a protein-phospholipid substance with surface-active properties (the ability to reduce surface tension), which covers the alveolar walls from the inside.

Synthesis of surfactant in the fetal lungs begins after the 20th week of embryonic development, and the surfactant system of the child's lungs is ready to expand at birth only after the 35th week. So any delays or abnormalities in fetal development and intrauterine oxygen starvation can cause a surfactant deficiency. In addition, a connection has been found between this disorder and mutations in the genes of surfactant proteins SP-A, SP-B and SP-C.

According to clinical observations, with a deficiency of endogenous surfactant, dysontogenetic disseminated atelectases develop with edema of the lung parenchyma, excessive stretching of the lymph vessel walls, increased capillary permeability and blood stagnation. Their natural result is acute hypoxia and respiratory failure.

In addition, atelectasis in premature infants, in cases of placental abruption, perinatal asphyxia, diabetes mellitus in pregnant women, and surgical delivery may be a symptom of the presence of coagulated fibers of the fibrillar protein hyaline on the walls of the alveoli (hyaline membrane syndrome, pulmonary hyalinosis, endoalveolar hyalinosis of the newborn, or respiratory distress syndrome type 1). In full-term infants and young children, atelectasis may be provoked by such a genetically determined disease as cystic fibrosis.

[ 20 ], [ 21 ], [ 22 ]

Complications and consequences

The main consequences and complications of atelectasis:

• hypoxemia (a decrease in the level of oxygen in the blood due to impaired respiratory mechanics and a reduction in pulmonary gas exchange);
• decreased blood pH (respiratory acidosis);
• increased load on the respiratory muscles;
• pneumonia from atelectasis (with the development of an infectious inflammatory process in the atelectatic part of the lung);
• pathological changes in the lungs (overstretching of intact lobes, pneumosclerosis, bronchiectasis, cicatricial degeneration of part of the lung parenchyma, retention cysts in the bronchial zone, etc.);
• asphyxia and respiratory failure;
• narrowing of the lumen of the arterial and venous vessels of the lungs.

[ 23 ], [ 24 ]

Diagnostics atelectasis of the lung

To diagnose atelectasis, the doctor records all complaints and symptoms and conducts a physical examination of the patient with auscultation of his lungs with a stethoscope.

To identify the cause, blood tests are required - general, biochemical, blood pH and gas composition, fibrinogen, antibodies (including to Mycobacterium tuberculosis), rheumatoid factor, etc.

Instrumental diagnostics consists of spirometry (determining lung volume) and pulse oximetry (determining the level of blood oxygen saturation).

The main diagnostic method for this pathology is a chest X-ray in proximal-distal and lateral projections. An X-ray for atelectasis allows one to examine the condition of the thoracic organs and see a shadow in the area of atelectasis. The image clearly shows the trachea, heart, and the root of the lung itself that have deviated to the side, as well as changes in the intercostal distances and the shape of the diaphragm vault.

High-resolution CT can detect pulmonary atelectasis: to visualize and clarify fine details of interstitial lung diseases. High-resolution CT images can help confirm a diagnosis of, for example, idiopathic pulmonary fibrosis and avoid the need for a lung biopsy.

Bronchoscopy for atelectasis (inserting a flexible bronchoscope into the lungs through the mouth or nose) is performed to examine the bronchi and obtain a small tissue sample. Bronchoscopy is also used for treatment purposes (see below). However, if more lung tissue from a specific area identified by X-ray or CT is needed for histological examination, surgical endoscopic biopsy is used.

[ 25 ], [ 26 ]

Differential diagnosis

The differential diagnostics carried out during X-ray examination of patients is intended to distinguish this pathology from pneumonia, chronic inflammatory process in the bronchi, bronchostenosis due to tuberculosis infection, pulmonary sequestration, cystic and tumor formations, etc.

Treatment atelectasis of the lung

Treatment for atelectasis varies depending on the etiology, duration, and severity of the disease in which it develops.

Atelectasis in newborns is treated with tracheotomy to open the airway, respiratory support (positive pressure breathing), and oxygen administration. However, high concentrations of oxygen used for long periods of time worsen lung tissue damage and can lead to the development of retrolental fibroplasia in premature infants. In most cases, artificial ventilation is required to ensure oxygenation of the blood in the arteries.

Medicines for atelectasis in newborns - surfactant substitutes Infasurf, Survanta, Sukrim, Surfaxim - are administered into the child's trachea at equal intervals, and the dose is calculated depending on body weight.

If atelectasis is caused by airway obstruction, the causes of the blockage are eliminated first. This may involve removing clots with an electric suction device or by bronchoscopy (followed by rinsing the bronchi with antiseptic solutions). Sometimes postural drainage with coughing is sufficient: the patient coughs while lying on his side, with his head lower than his chest, and everything that is blocking the airways comes out with the cough.

Antibiotics are prescribed to combat the infection that almost always accompanies secondary obstructive atelectasis – see Antibiotics for pneumonia

In the case of development of distension atelectasis with hypoxia in bedridden patients, physiotherapeutic treatment is carried out using constant pressure during inhalation of a mixture of oxygen with carbon dioxide; UHF sessions, electrophoresis with drugs. A positive effect is provided by respiratory gymnastics for atelectasis (increasing the depth of breathing and its rhythm) and therapeutic massage for pulmonary atelectasis, which allows for accelerated evacuation of exudate.

If the cause of atelectasis is a tumor, chemotherapy, radiation, and surgery may be necessary. Surgery is also used in cases where the affected area of the lung must be removed due to necrosis.

According to doctors, emergency care for atelectasis can only be provided with urgent hospitalization. In a medical facility, patients are given injections of strophanthin, camphor, and corticosteroids. To stimulate breathing, drugs from the respiratory analeptic group can be used, for example, Nicotinic acid diethylamide (Nicetamide) - parenterally 1-2 ml up to three times a day; drops are taken orally (20-30 drops two or three times a day); Ethimizole (in the form of tablets - 50-100 mg three times a day; in the form of a 1.5% solution - subcutaneously or intramuscularly). Side effects of both drugs include dizziness, nausea, increased anxiety, and sleep disturbances.

Prevention

First of all, atelectasis prevention concerns patients who are scheduled for surgery under inhalation anesthesia or who have already had surgery. To prevent lung damage, you should quit smoking at least one and a half to two months before the planned surgical treatment and increase your water intake. And for patients who have had surgery, breathing exercises and sufficient humidity in the rooms are necessary. In addition, doctors do not recommend "lying around" in bed and moving whenever possible (at the same time, this is a good way to prevent postoperative adhesions).

Doctors also strongly recommend treating respiratory diseases correctly (especially in children) and not allowing them to become chronic.

[ 27 ], [ 28 ]

Forecast

Doctors give a favorable prognosis for the outcome of this pathological condition of the lungs in compression and distension atelectasis. And the outcome of obstructive atelectasis depends on many factors: its cause, the patient's condition, the quality and timeliness of medical care.

As for atelectasis in newborns, today the mortality rate of infants with primary atelectasis and respiratory distress syndrome of the newborn is 15-16 out of every hundred cases.

[ 29 ], [ 30 ], [ 31 ]