Pediatric bronchopulmonary dysplasia

　　I. Etiology

　　The etiology is not completely clear at present, and possible causes of BPD may include:

　　1. High concentration of oxygen.

　　2. Damage from mechanical positive pressure ventilation.

　　3. Chronic inflammation.

　　4. Excessive water and salt intake, i.e., excessive fluid infusion.

　　5, patent ductus arteriosus with heart failure

　　6, poor lung maturity

　　7, asphyxia during childbirth. The disease can also be seen in full-term newborns with meconium aspiration, persistent pulmonary hypertension, congenital heart and lung diseases, intracranial hemorrhage, or sepsis shock after treatment with mechanical ventilation. Some scholars have reported that inhaling high concentrations of oxygen in newborn lambs can cause similar BPD changes regardless of whether mechanical ventilation is used. Some believe that any cause of chronic pulmonary edema can hinder the postnatal lung development of immature lungs. Recent reports have shown that gastroesophageal reflux can prolong the course of bronchopulmonary dysplasia.

　　Second, pathogenesis

　　1, high concentration of oxygen inhalation

　　It has been reported that after inhaling high concentrations of oxygen, intermediate metabolic products of oxygen in the body such as peroxides, free radicals, hydroxyl ions, hydrogen peroxide, and singlet oxygen are highly active free radicals that can oxidize unsaturated lipids in cell membranes and sulfhydryl enzymes, glutathione peroxidase, coenzyme A, and other enzymes within cells, interfere with cell metabolism, and further damage their structure. At the same time, after inhaling high concentrations of oxygen, the cilia activity of epithelial cells disappears, mucus accumulates in the lungs, and the epithelial cells undergo metaplasia, function degeneration, leading to chronic lung lesions.

　　2, barotrauma

　　Positive pressure breathing with excessive peak inspiratory pressure and prolonged inspiratory time can lead to bronchopulmonary dysplasia.

　　3, preterm birth

　　Premature infants have insufficient antioxidant enzyme systems and are sensitive to oxygen; premature infants are prone to pulmonary hyaline membrane disease and require mechanical ventilation. Due to high airway resistance and reduced lung compliance, artificial ventilation is prone to cause alveolar and small bronchial injury; premature infants are prone to patent ductus arteriosus, leading to pulmonary edema; premature infants are deficient in vitamin A and vitamin E.

　　4, other factors

　　Chronic pulmonary inflammation, asphyxia at birth, excessive intake of water and salt, chronic pulmonary edema caused by congenital heart disease and heart failure, impairs postnatal lung development and promotes the occurrence of BPD.

　　Asthma, pulmonary heart disease, poor pulmonary function, pulmonary infection, respiratory failure, etc., survivors often have growth and development delays, leaving chronic asthma, pulmonary fibrosis, poor pulmonary function, pulmonary heart disease, and neurological complications such as intellectual disability and cerebral palsy. Short courses may die within a few weeks, while prolonged courses may last for several months to years. Although there is a possibility of gradual recovery, most die from secondary pulmonary infection, heart failure, pulmonary hypertension, and pulmonary heart disease.

　　For premature infants with hyaline membrane disease after birth or recurrence of respiratory distress and hypoxia, pale complexion, sweating, drowsiness, vomiting, dry cough, shortness of breath, cyanosis, difficulty breathing, mild costal space indentation, pulmonary wet rales and wheezing sounds, with episodes of apnea, requiring oxygen and assisted ventilation, the course of the disease may last for several weeks to several months, leading to progressive respiratory failure and heart failure. There are often symptoms of right heart failure, such as enlarged liver, peripheral edema, and distended jugular veins. Arterial blood gas analysis may reveal hypoxemia and/or hypercapnia. Clinically, children may show growth retardation or stagnation, and recovered children often have recurrent lower respiratory tract infections within 1 to 2 years, surviving on oxygen and ventilators.

　　In addition to measures to prevent preterm birth and hyaline membrane disease, attention should be paid to not exceeding the oxygen concentration during the rescue of neonatal respiratory failure, and not exceeding the pressure during mechanical ventilation to avoid lung injury. Avoid excessive water and sodium, promptly correct patent ductus arteriosus, and appropriately use antibiotics to prevent infection. Some reports show that vitamin E can reduce the occurrence of BPD, but there is no definitive conclusion. In addition, malnutrition, protein, vitamin, and trace element deficiencies can all increase the oxygen toxicity of the lungs, which should be noted.

　　1. X-ray examination

　　Difficult to distinguish from RDS, it can be divided into 4 stages: Stage Ⅰ: Commonly seen increased density shadows in both lungs, with widespread granular shadows and bronchial aeration signs; Stage Ⅱ: almost no transmissibility in both lungs, heart enlargement, indistinct shadow; Stage Ⅲ: pulmonary fields show diffuse small honeycomb-like translucent areas, irregular density, resembling plum blossoms; Stage Ⅳ: Onset for about 1 month, dense streak-like changes in both lungs, and irregularly translucent areas.

　　2. Pulmonary function test

　　Pulmonary function is the most sensitive indicator, with increased airway resistance and decreased lung compliance.

　　Patients with pediatric bronchopulmonary dysplasia should have a light and nutritious diet, such as congee, lotus root powder, egg flower soup, vegetable soup, noodles, etc., and avoid indigestible and irritating foods..

　　1. Treatment

　　Including attention to nutrition and care, moderate oxygen supply and symptomatic treatment, using digoxin and moderate diuretics to control heart failure. Supplying 2-3g/kg of protein and 110kcal/kg of calories each day to ensure growth and development. Limiting the daily sodium intake to 1-2mmol/kg (1-2mEq/kg) to control pulmonary edema, maintain acid-base balance, use bronchodilators, and apply mechanical ventilation when necessary, but the pressure should not be too high.

　　2. Prognosis

　　Poor prognosis, mortality can reach 30% to 40%, more than in infancy die from pulmonary infection and cardiorespiratory failure. Some reports show that about 29% of severe cases have mild sequelae such as growth and development delay, changes in lung X-rays, and abnormal cardiorespiratory function. 34% have moderate or severe sequelae, manifested as intellectual disability, cerebral palsy, deaf-mutism, etc.