Bronchopulmonary dysplasia, symptoms and treatment
PathogenesisI will give the main factors contributing to the development of bronchopulmonary dysplasia:
- hyaline-membrane disease;
- oxygen therapy;
- periodic auxiliary ventilation with positive pressure;
- interstitial emphysema;
- uncontrolled arterial duct;
- difficulty diuresis;
- excessive fluid administration;
- pulmonary infections;
- familial bronchial asthma;
- deficiency of vitamins A or E.
Bronchopulmonary dysplasia may occur as a result of lung damage in a premature infants with hyaline-membrane disease. The increased permeability of the pulmonary epithelium, characteristic of this disease, persists with its transition to dysplasia. Known bronchopulmonary dysplasia after mechanical ventilation of the lungs, carried out for other pulmonary disorders. It has been experimentally proved that oxygen therapy can become an important toxic factor. In newborns who received oxygen without forced ventilation, chronic changes in the small airways developed, but the disease was not observed in any case. It has been established that free oxygen radicals, such as peroxide anions, are responsible for the destruction of lung tissue in newborns, and peroxide dismutase neutralizes peroxide anions and thereby reduces the severity of the disease with hyaline-membrane disease. According to Reynolds, artificial ventilation with low respiratory rate and low maximum inspiratory pressure reduces the likelihood of bronchopulmonary dysplasia. The role of barotrauma in pathogenesis is confirmed by the fact that mechanical ventilation without the use of oxygen also causes a prolonged increase in the resistance of the respiratory tract."Oxygen plus pressure plus time," as Philip states, is the cause of the damage to the immature lung. The development of bronchopulmonary dysplasia is also associated with interstitial emphysema of the lung and uninfected arterial duct. However, it remains unclear what determines the severity of the pathological process in the lungs. It is believed that there is a relationship between the delay of diuresis, the excessive introduction of fluid into the body, enhancing chronic edema of the lung tissue, and the severity of bronchopulmonary dysplasia. Intubation of the trachea, in which the secret accumulates and a secondary infection develops, aggravates the process of tissue damage. In a family history of some newborns with bronchopulmonary dysplasia, there are indications of bronchial asthma from relatives. From this it can be concluded that the genetically determined reactivity of the respiratory tract increases the risk of developing the disease. Many premature babies are deficient in vitamin A and vitamin E at birth, and if it is not possible to cope with hypovitaminosis, bronchopulmonary dysplasia may develop.
PathophysiologyThe essence of pathological changes in bronchopulmonary dysplasia is a violation of tissue growth in combination with the development of scar tissue and the regeneration process. Histological signs of the disease are often found in newborns who died before the clinical signs of this condition appeared. When dysplasia is resolved, the exudate can be absorbed by the walls of the alveoli, which leads to interstitial fibrosis. In other cases, exudate is organized in situ, obliterating the alveolar space. During the first week, the cells of the alveolar epithelium and the endothelium of the capillaries are destroyed, and the edema of the interstitial and perivascular space develops. There are necrosis of bronchioles, squamous metaplasia, smooth muscle hypertrophy, disappearance of cells of ciliated epithelium. On the 2-3rd week, the number of macrophages, plasma cells and fibroblasts increases. Damage to bronchioles of different orders, which in severe cases leads to obliterating bronchiolitis. In the following weeks, atelectasis zones with interstitial and peribronchial fibrosis are combined with foci of compensatory or destructive emphysema. Lymphatic vessels are convoluted, in the walls of the alveoli the number of reticular, collagen and elastic fibers is increased. You can find signs of active regeneration of the epithelium, but the process of multiplying the alveoli is disturbed, at least in some areas.
Significant narrowing of small and medium arteries due to thickening of the intima significantly complicates the pulmonary blood flow. With pulmonary hypertension, accompanying dysplasia, the reactivity of the vascular bed is preserved and vasoconstriction is reversible under the effect of oxygen therapy.
The resistance of lung tissue is increased at the 1st week of life in newborns, in whom bronchopulmonary dysplasia subsequently develops. Respiratory disorders observed during the first year of life include relative hypoxia, carbon dioxide retention, increased respiratory rate, decreased respiratory volume, increased minute ventilation, low dynamic extensibility, impaired general ventilation. Factors that determine the weakness of the respiratory muscles include increased oxygen consumption and increased work of breathing. Emphysema and atelectasis of the lobe of the lung with bronchopulmonary dysplasia can be explained by the difficulty of outflow of air from the lungs. Severe obstructive airway disease is sometimes associated with hyperreactivity of the bronchi.
Symptoms ofBronchopulmonary dysplasia develops, as a rule, in prematurity requiring mechanical ventilation of the lungs, but after initial initial improvement, persistent respiratory failure occurs. In light cases, one can observe only the impossibility of reducing the oxygen concentration and softening the parameters of mechanical ventilation for 1-2 weeks. Severe forms of bronchopulmonary dysplasia last for months and lead either to the death of the patient from increasing respiratory failure, or to a late onset recovery. The chronic process is characterized by prolonged respiratory distress, periodic apnea and bradycardia, the impossibility of abandoning mechanical ventilation. Anteroposterior size of thorax is enlarged. Retraction of ribs, tachypnea;can be observed stridor. Frequent complications include relapsing pneumonia, atelectasis and aspiration of food masses. Due to pulmonary hypertension, a pulmonary heart can develop.
Northway and co-authors described four consecutive stages of radiographic changes in bronchopulmonary dysplasia. The first stage is indistinguishable from the hemolytic disease of the newborn, the second is a pulmonary pleura, as in the non-spreading of the ductus arteriosus. On the 2-3th week after the birth, multiple cysts of different sizes appear, which is characteristic of the third "bubbly" stage. The fourth stage is characterized by cardiomegaly, increased transparency of the lung tissue, especially in the lower lobes, and lace-like seals that extend to the periphery of the pulmonary fields. Recent evidence suggests that the radiographic signs of bronchopulmonary dysplasia are not as specific as previously thought, and the sequence of development of the process through the stages is not constant. Often lung damage is more homogeneous, with multiple distinct lace-like dense foci going to the periphery.
Because bronchopulmonary dysplasia is a continuous process, Bancolari and co-authors proposed the following criteria for establishing an accurate clinical diagnosis:
1) at the first week of life, for at least 3 days, a mechanical ventilation of the lungs with positive pressure is performed;
2) chronic respiratory distress, characterized by tachypnea, chest retraction and respiratory noise, lasts no less than 28 days;
3) to maintain RaO2 above 50 mm Hg. Art. Oxygen therapy is applied for 28 days;
4) during X-ray examination dense foci alternate with areas of increased transparency.
Intermittent forced ventilation is performed with such parameters to maintain RACO2 within the range of 50-55 mm Hg. Art. To stabilize the volume of the lungs, the end-expiratory pressure should be 2-4 cm of water.
The transition from intermittent forced ventilation to independent breathing is a slow process that lasts for severe bronchopulmonary dysplasia for many months. Since an important component of this condition is pulmonary edema, measures aimed at early closure of the arterial duct, namely the restriction of the injected fluid to 150 ml /( kg-day), the administration of furosemide and aldactone at a dose of 1-1.5 mg / kg of each drugtwice a day. Kao and co-authors showed that furosemide reduces airway resistance and improves the dynamic extensibility of lung tissue in bronchopulmonary dysplasia. Similarly, theophylline acts, improving lung function and shortening the period of transition to spontaneous breathing. Significantly reduce the frequency of breathing, peak inspiratory pressure, oxygen concentration in the inspired air and alveolar-arterial oxygen gradient was achieved with dexamethasone.
To ensure normal growth of the child, adequate nutrition is needed. Hematocrit should be maintained at a level above 40% in order to increase the oxygen capacity of the blood. At present, there is no evidence that vitamin E affects the frequency or severity of bronchopulmonary dysplasia. Energetic measures require pulmonary infections;Physiotherapy and other methods that stimulate the development of the child should be in the arsenal of the doctor.
After discontinuation of intubation, oxygen can be fed through the nasal catheter if a gas mixture containing less than 30% oxygen is required. Inhaling a low-density gas mixture, for example, helium-oxygen, significantly reduces lung resistance and reduces the energy costs of breathing in bronchopulmonary dysplasia. Consequently, such a mixture is shown with weakness of the respiratory musculature, it saves the energy necessary for the growth and recovery of the child. The time spent in the hospital can be significantly reduced if a system of managing the patient at home, including oxygen therapy, is introduced.
ForecastThe turning point in the patient's condition occurs usually in the middle of the period of mechanical ventilation. This improves PaCO2, breathing is cut, pauses in forced ventilation are well tolerated, body weight is increasing. Long-term hospitalization with bronchopulmonary dysplasia is significantly associated with psychosocial and economic factors. In hospitals, most deaths in the post-neonatal period among newborns with a very low body weight are those who developed bronchopulmonary dysplasia. For clinical evaluation of the disease, repeated echocardiography is advisable. In cases that subsequently led to death, hypertrophy of the left ventricle was noted, and the ratio between the period preceding the expulsion and the phase of blood ejection for the right ventricle exceeded 0.3, indicating a great resistance in the pulmonary vessels.
Mortality in the first year of life was within 23-36%.The rate of sudden death among children with bronchopulmonary dysplasia is 7 times greater than in children with the same birth weight, but without this disease. Persistent tachypnea, periodic stridor, repeated pneumonia occur much more frequently in the first year of life than in the second year. Such conditions require hospitalization. With age, respiratory rates normalize, but bronchial hyperreactivity persists on average to 8 years of age. It is possible that it is the cause of episodic attacks of suffocation, requiring inhalation of bronchodilators. In the first year of life, transient systemic hypertension is also possible, which is well controlled by hypotensive drugs. The growth and development of the child is closely related to the severity and duration of the breathing disorder, as well as to other pathological conditions in the perinatal period. The growth retardation was noted in 1/3, and other deviations from the norm - in 25-40% of the survivors.
Women's magazine www. BlackPantera.com: Victor Yu