BPD, or bronchopulmonary dysplasia, is a chronic disease that develops in premature infants due to performing artificial lung ventilation. As a result, the child experiences injury to the underdeveloped bronchi and lungs with high-concentration oxygen, which is manifested by persistent obstructive disorders.
The question arises: Why cannot a premature baby breathe independently and must be connected to an artificial lung-ventilating machine (ALVM)?
Own opinion: the act of breathing is unconditional and begins with the movement of the muscle called the diaphragm, which creates vacuum in the lungs, and air enters there under pressure as into the pump. The amount of incoming air depends on whether the intercostal muscles can stretch completely or not.
In mature infants, the intercostal muscles stretch completely, the alveoli in the lungs are completely filled with air and accumulate no mucus.
In premature infants, the intercostal muscles cannot completely stretch, therefore part of the alveoli is not filled with air. The alveoli do not conglutinate owing to surfactant, the substance in the lungs, which does not allow them to conglutinate when exhaling.
To be certain of this, I looked through an electron microscope at a cut of the intercostal muscle of a premature infant, who died of pulmonary muscle swelling arising from bronchopulmonary dysplasia or BPD.
The electron microscope shows muscle swelling in the intercostal muscle.
Explanation of the above photo:
Red color marks the muscle fibers, which are at a distance from each other. Normally, the muscle fibers are parallel and pressed together.
Yellow color in the photo marks a muscle swelling pressing on the muscle fibers and disorganizing them.
This muscle swelling pushes cell nuclei (dark points) from the center to the periphery and hampers the work of mitochondria generating energy for muscle stretching.
To avoid the child’s death from suffocation, he/she is connected to the artificial lung ventilation unit.
Drug-free treatment of bronchopulmonary dysplasia in infants
You can ask a quite impartial question: "Why do I succeed in releasing a premature baby from bronchopulmonary dysplasia?" I am a myologist and I approach treatment of BPD from the point of view of a specialist in muscles. When the child after my emendic procedures gets rid of rattles, bronchitis, and begins to recover, then the correctness of my explanations becomes clear.
Look at how the muscle swelling in the intercostal muscles decreases in children with bronchopulmonary dysplasia during the emendic procedure:
The first photo shows a very severe muscle swelling: the child cannot breathe independently and is connected to the artificial lung-ventilating machine (ALVM).
The second photo shows a reduced muscle swelling as a result of my work. In this condition, the intercostal muscles can stretch longer. Alveoli completely fill with air, obstructive bronchitis no longer occurs. The child has no apnea observed.
This is a result of treating a newborn child with bronchopulmonary dysplasia by emendic procedure.
In the third photo, the muscle swelling of intercostal muscles has further decreased. Emendic procedures continue. The child's rattles stopped, his breathing became clear and even.
Causes of intercostal muscle swelling
In this part of the paper, I will tell about the causes of muscle swelling occurrence in intercostal muscles in premature infants from the point of view of 21st-century knowledge.
Professor Kiyotoshi Sekiguchi, Osaka University, Japan:
A primitive (up to 9 weeks of embryo development) lymphatic system ceases to grow and does not branch because endothelial and mesenchyme cells do not produce structural protein polydom.
Muscle cells grow, and lymphatic vessels do not grow.
Lymph takes metabolism products away from cells and removes them from the child's organism. But since the lymph vessels become smaller relative to the muscle fibers, not all waste is excreted by lymph. So swelling in the intercostal muscle fibers begins.
The immature lungs of premature infants have a deficit of surfactant - a natural surface-active substance that prevents the alveoli from conglutinating during exhalation and is necessary for the removal of mucus by the ciliated epithelium. The surfactant begins to be synthesized on 20-24 weeks of gestation, the required level of surfactant is reached by 35-36 weeks.
Neurologists note that BPD, i.e. bronchopulmonary dysplasia, has iatrogenia.
Artificial ventilation of lungs, especially in severe conditions, leads to barotrauma of bronchial and pulmonary tissues, at that toxic effect of high concentrations of oxygen in inhaled gaseous mixture also leads to epithelial damage, the development of pulmonary muscle swelling and its impregnation with protein. As a result, both factors lead to a decrease in the alveolar extensibility.
Own opinion: in the premature infant, on one side, intercostal muscles are not stretched, and, on another side, a large concentration of oxygen “burns” the mucous membrane inside the alveoli. As soon as it is ceased to give oxygen to the infant, an infection develops in oxygen-damaged places of alveoli.
Conclusions on the results of pathoanatomical studies of pulmonary tissue and alveoli in the premature infants deceased from pneumonia, which developed after the removal of the infant from breathing oxygen, made it possible to establish the stages of BPD development.
There are 4 stages in developing the diagnosis of bronchopulmonary dysplasia:
Stage 1 BPD (day 1-3 of life of the newborn) – severe alveolar muscle swelling with hyaline membranes, atelectasis and endothelial necrosis of bronchioles.
Stage 2 BPD (day 4-10 of life of the infant) – atelectasis becomes more widespread, alternates with areas of emphysema. Necrotic masses fill the airways.
Stage 3 BPD (day 11-30 of life) – widespread metaplasia and hyperplasia of the epithelium in bronchi and bronchioles, areas of emphysema, fibrosis and muscle swelling with thinning of the alveolar basal membranes.
Stage 4 BPD in premature infants (the second month of life) – massive pulmonary fibrosis with destruction of alveoli and airway walls.
During Stage 4, hypertrophy of the muscular bronchioles layer and a decrease in the number of pulmonary arterioles with hypertrophy of the muscular layer of arterioles and venules are especially pronounced.
Neonatologists treat premature infants diagnosed with bronchopulmonary dysplasia symptomatically: they continue oxygen therapy.
Own opinion: neonatologists “burn” alveolar mucosa more intensively. They use bronchodilators, diuretics, glucocorticosteroids, antioxidants and antibiotics.
In acute period at a severe BPD, when there is a concern about life, the prescribed medication is justified. After eliminating the inflammatory process, the prescription of drugs will not solve the problem of muscle swelling of the intercostal muscles.
The only way to eliminate muscle swelling from the intercostal muscles is emendic procedures.
Consequences and complications in bronchopulmonary dysplasia
The predominant number of infants, who have survived BPD in their early life, suffer from impaired respiratory function at an older age, when they reach adolescence. Manifestations of breathing disorders are the following symptoms:
Impaired bronchial patency;
decreased diffusing lung capacity;
All this results in the following diseases:
Recurrent bronchoobstructive syndrome (RBOS);
acute bronchiolitis, especially that associated with respiratory syncytial viral infection;
chronic respiratory failure;
syndrome of chronic microaspiration;
Combinations of bronchopulmonary dysplasia with croup syndrome, congenital lung malformations, transformation into chronic bronchiolitis with obliteration (BOS), bronchial asthma, relapsing obstructive bronchitis (ROB) are described.