I. Overview Bronchopulmonary dysplasia was first named by Northway et al. in 1961. The etiology of this disease is now thought to be related to prematurity, positive pressure ventilation, high concentration of oxygen administration, and pulmonary infection. Diagnosis is based on the use of mechanical ventilation for one week after birth, the subsequent need for oxygen to maintain Pa02 > 6.67 kPa (50 mmHg) for more than 28 d, and the presence of persistent dense shadows on chest radiographs with irregular translucent areas. The incidence of this disease is high in very low birth weight infants, but the reports vary greatly, and many foreign hospitals report an incidence ranging from 10% to 80% in very low birth weight infants under 1500g. The high concentration of oxygen in the lung forms a large number of oxygen-based oxygen radicals oxidizing unsaturated lipids on the surface of cell membranes, interfering with intracellular enzyme metabolism and thus destroying cell structure and function, and the antioxidant enzyme system for scavenging oxygen radicals in the lungs of preterm infants is insufficient, so the high concentration of oxygen is more damaging to the lungs of preterm infants. 2.Pneumatic pressure injury High peak pressure of pressurized breathing, excessive inspiratory time, and high average airway pressure make the lung over-expanded, damage the alveolar structure, inhibit the synthesis of alveolar surface active substances to reduce, the transfer is impaired, so that the alveolar surface tension is increased to form alveolar emphysema and pulmonary atelectasis. 3, premature birth Premature birth is prone to RDS often requires high concentrations of oxygen and mechanical ventilation, and the ventilation pressure is high. At the same time, it is easy to occur arteriovenous catheter failure resulting in pulmonary edema, followed by the legacy of bronchial wall thickening, alveolar interstitial fibroplasia. 4, excessive fluid load Vitamin A, vitamin E deficiency, intravenous drip fat milk, intrauterine infections and Ureaplasma urealyticum infections can contribute to the occurrence of bronchopulmonary dysplasia. Bacterial secondary infection can aggravate lung damage. Impaired lung function due to the above causes causes hypoxemia, carbon dioxide retention, increased respiratory rate, decreased lung compliance, increased resistance, decreased tidal volume, and increased functional residual air volume. Emphysema, pulmonary atelectasis, small airway obstruction, and airway hyperresponsiveness increase respiration, increase oxygen consumption, and respiratory muscle fatigue. Clinical manifestations Commonly seen in premature infants with RDS and severe pneumonia with mechanical ventilation and beyond. Oxygen supply is still required to maintain normal oxygen saturation. Mild cases often require oxygen or mechanical ventilation for several weeks. In severe cases, death may occur after several months of progressive respiratory failure, or recovery may be gradual and may extend over months to years. Survivors often have pulmonary dysfunction. During tracheopulmonary dysplasia and recovery, recurrent pneumonia, pulmonary atelectasis, bronchospasm causing croup, gastroesophageal reflux, aspiration pneumonia, apnea, hypertension, and growth disorders may occur. The lung X-ray changes in different periods may show reduced lung field translucency, granular lung field shadow and bronchial inflation shadow, round transparent area in lung field and striated pulmonary atelectasis. V. Treatment 1. Bronchopulmonary dysplasia is dependent on oxygen and ventilator therapy. At this time, it is necessary to avoid oxygen and air pressure damage to the lung, but also to maintain the blood Pa02 at 6.2-9.33kPa (50-70mmHg) and PaC02 at 5.3-6.7kPa (40-50mmHg). Therefore, ventilator-assisted breathing mostly uses intermittent command mode (IMV) to facilitate the child’s spontaneous breathing, with end-breath pressure of 0.12-0.39 kPa (2-4 cmHzO) and controlled peak inspiratory pressure. When the number of ventilations drops to 4-6 times per minute and the peak pressure drops below 20cmHzO, continuous positive pressure (CPAP) can be used intermittently, with CPAP pressure at 2-4cmH2O and normal blood gas analysis can be maintained, that is, the ventilator can be gradually withdrawn and other means of oxygen supply can be used, and then oxygen supply can be gradually stopped. 2.Water and heat supply Since pulmonary edema is a change of bronchopulmonary dysplasia, the fluid should be appropriately restricted and can be reduced appropriately according to the physiological needs of preterm infants at daytime age, and the serum electrolytes should be monitored and appropriately supplemented to maintain them at normal levels. On the basis of ensuring water-electrolyte balance, appropriate use of diuretics can help improve pulmonary compliance, resistance, minute ventilation, alveolar ventilation, reduce the need for oxygen and shorten the time of ventilator application, often using tachypnea 1mg/kg each time, 2 times/d. In bronchopulmonary dysplasia, growth and development are backward and energy consumption increases, so adequate calories should be provided, generally at 627.6kj/(kg.d ) [150call (kg.d)] is appropriate, and calorie supplementation is best by oral feeding or tube feeding, and if fasting or oral feeding is difficult, part of the nutrition can be supplemented intravenously or intravenous high nutrition. 3, bronchodilators (1) due to bronchospasm pulmonary resistance increases, can use theophylline to reduce airway resistance, the dose is 2mg/kg, every 12h intravenous drip. (2) When theophylline is not effective, the following bronchodilators can be used for nebulized inhalation. ①Ethylisoprenaline: 1% 0.25ml nebulized inhalation for 5min. ②Isoprenaline: 0.1% 5ml nebulized inhalation for 5min. ③Oxynaline: 0.3% solution 2ml nebulized inhalation for 5min. ④Salbutamol sulfate: 0.02mglkg dissolved in 1.5ml saline, nebulized for 5~lOmin. ⑤Isoproterenol: 2.5rug/kg dissolved in 1.5ml saline. kg dissolved in 1.5ml saline, nebulize for 10-15min. 6) Atropine: 0.08mg/kg dissolved in 2ml saline, nebulize for 10-15min. 4) Dexamethasone Dexamethasone can increase the synthesis of alveolar surface active substances, stabilize lysosomes and cell membranes, increase β-adrenergic nerve activity, relax bronchospasm, reduce inflammatory response and lung and bronchial Increase the level of serum vitamin A. Decreases lung compliance and resistance, which helps to reduce the need for oxygen and mechanical ventilation. To shorten the duration of oxygenation and mechanical ventilation, dexamethasone 0.3-0.5mg/(kg.d) is usually administered intravenously in 2 doses for 3 d. It has also been reported that 0.6mg/(kg.d)-week is used. The use of dexamethasone should be aware of the following side effects, such as hypertension, stress ulcers, spread of infection, increased proteolysis resulting in growth retardation. 5. Alveolar surface active substance can improve lung compliance and supplement its insufficient synthesis after lung injury. The dosage is 150mg/kg, 1 time every 6 heart hours, 3 times in a row. 6, intravenous gammaglobulin 400mg/(kg.d) intravenous, for 3-5d. Prevention 1, prenatal application of corticosteroids can reduce its occurrence, corticosteroids and thyrotropin-releasing hormone can promote fetal lung maturation, prevention effect is better. 2, early postnatal use of dexamethasone for severe RDS can reduce lung injury. 3.Alveolar surface active substance replacement therapy can reduce the occurrence of this disease. 4, early use of nasal CPAP and higher inhalation gas temperature (above 36.5 ℃) to facilitate wetting can reduce the occurrence of this disease and reduce the duration of mechanical ventilation. 5, high frequency ventilation can reduce the occurrence of this disease. 6, the early role of vitamin A, indomethacin off PDA, treatment of the original disease, the control of infection are conducive to reducing the occurrence of this disease.