Neonatal Pneumothorax

　　1. Etiology

　　A few cases are spontaneous pneumothorax, without a clear cause; the vast majority of air leaks have underlying pulmonary diseases, such as meconium aspiration, hyaline membrane disease, bullous lung disease, localized emphysema, pneumonia, congenital pulmonary malformation, congenital pulmonary cysts, and others, often due to rupture of overinflated alveoli leading to air leaks. Excessive positive pressure during artificial ventilation is also a common cause.

　　2. Pathogenesis

　　The lungs are airless in the fetal stage due to the high surface tension of pulmonary fluid and the immaturity of the lung elastic tissue, so in order to expand the neonatal lungs and maintain normal functional residual capacity, the initial 1-2 breaths have a pulmonary alveolar pressure of 3.9 kPa (40 cmH2O), which can transiently reach 9.8 kPa (100 cmH2O). The pulmonary alveolar pressure is generally not more than 2.9 kPa (30 cmH2O). Excessive pressure can lead to alveolar rupture, causing gas to enter the pulmonary interstitium and become interstitial emphysema. Gas is usually located near lymphatic vessels and blood vessels, with diffuse pulmonary intralobular and pleural type, and sometimes the emphysema expands into a cystic form known as a pseudopulmonary cyst. Interstitial emphysema can directly break into the pleura and become a pneumothorax. The gas from the emphysema can reach the mediastinum along blood vessels, lymphatic vessels, or bronchi, forming mediastinal emphysema. In neonates, due to the larger thymus and smaller mediastinum, the gas entering the mediastinum mainly accumulates in the area where the pulmonary vessels and the heart are connected. If the gas enters the subcutaneous tissue along large blood vessels, it becomes subcutaneous emphysema. If it enters the pericardium, it becomes pericardial effusion. If it passes through the diaphragm along the esophagus and vascular intervals into the abdominal cavity, it becomes an abdominal empyema. Then, it enters the scrotum to become a scrotal emphysema. The gas in interstitial emphysema and mediastinal emphysema occasionally can enter the pulmonary veins and lymphatic vessels to form systemic intravascular air embolism. Due to compressed lung tissue, shortness of breath, decreased blood volume, abnormal ventilation and perfusion leading to intrapulmonary shunting, increased hypoxia, reduced lung compliance, secondary ventilation dysfunction, compression of the heart, reduced cardiac output, increased pulmonary vascular resistance, and central venous pressure, bradycardia and hypotension can occur and shock can occur.

　　Interstitial emphysema shows pulmonary enlargement on pathological examination, appearing pale, with the pleura surface being tense and concave upon palpation. Free gas is seen in the mediastinum, pericardium, thoracic and abdominal cavities. Microscopic examination of the lung tissue shows alveolar expansion, with some alveoli破裂, and there is a large amount of air around the blood vessels and bronchi and in the connective tissue of the lung acini.

　　Pulmonary distress and shock can occur concurrently, as can persistent pulmonary hypertension, intracranial hemorrhage, hypercapnia, bronchopulmonary dysplasia, pericardial tamponade, air embolism, and others. In severe cases, it can compress small airways and reduce lung compliance, leading to difficulty breathing, wheezing, hypoxia, and CO2 retention. When the inferior vena cava is compressed, it can cause peripheral venous dilation, liver enlargement, reduced cardiac output, decreased pulse pressure, weakened pulse, and decreased blood pressure.

　　1.Pneumothorax

　　Mild cases may have no clinical symptoms, and signs are often not obvious. They are often discovered during X-ray examination. In severe cases, the child may only show rapid breathing; in severe cases, the child may be irritable, have difficulty breathing, cyanosis, and the typical sign is that the chest on the affected side is more bulging than the healthy side, the intercostal spaces are full, percussion sounds are hyperresonant, and respiratory sounds are absent or reduced. When the intrathoracic pressure is higher than atmospheric pressure, it is called high-pressure pneumothorax, which can cause the mediastinum to shift towards the healthy side, the diaphragm to descend, and when the caval vein is compressed, it can cause peripheral venous dilation, liver enlargement, reduced cardiac output, decreased pulse pressure, weakened pulse, and decreased blood pressure.

　　2.Mediastinal emphysema

　　Less common than pneumothorax, usually asymptomatic. When there is a lot of mediastinal gas, it can also cause respiratory distress and symptoms of pericardial tamponade, especially when combined with pericardial effusion, subcutaneous emphysema can occur in the neck or upper chest, with a local 'snow pressing' sensation, indicating the presence of mediastinal emphysema.

　　3.Pneumoperitoneum

　　Gases can enter the abdominal cavity from the mediastinum, causing pneumoperitoneum, manifested as abdominal distension, tympany on percussion, which needs to be differentiated from gastrointestinal perforation. However, the latter often has edema of the abdominal wall, indentation marks, and peritoneal irritation signs, which can be distinguished from this disease.

　　4.Interstitial lung emphysema

　　Gases can spread along the loose interstitium around the bronchi and blood vessels to the hilum of the lung. In severe cases, it can compress the small airways and reduce lung compliance, leading to difficulty breathing, wheezing, hypoxia, and CO2 retention.

　　1. Attention should be paid to avoiding premature birth and post-term birth.

　　2. Preventing intrauterine and peripartum asphyxia.

　　3. The吸入物of the respiratory tract after birth, such as meconium, should be promptly removed.

　　4. During mechanical ventilation, close monitoring is required, and peak inspiratory pressure should not be too high. For suspected cases, dynamic changes should be observed, and timely treatment should be provided.

　　5. The use of muscle relaxants (Pancuronium) and pulmonary surfactant can reduce the occurrence of air leaks.

　　1. X-ray examination

　　Diagnosis mainly relies on X-ray examination. In the case of pneumothorax, the outer margin of the chest where air is accumulated can be seen to be overly translucent, without lung markings, forming a clear edge with the compressed lung on the inside. In the case of high-pressure pneumothorax, the mediastinum can be seen to shift towards the healthy side, with the diaphragm on the same side being flat. In the case of mediastinal emphysema, there can be a gas shadow with high transparency around the heart margin, located between the heart margin and the sternum. The thymus can be elevated by the superior mediastinal gas, and the frontal film can show a sail-like shadow. When there is pericardial effusion, the heart shadow contracts, and the pericardial cavity can be seen to contain air, with the outer edge showing the shadow of the pericardial wall. In the case of pneumoperitoneum, there can be air accumulation below the diaphragm, which needs to be differentiated from gastrointestinal perforation.Interstitial pulmonary emphysema can be seen as a narrow strip of light transmission from the hilum along the trachea and blood vessels.

　　2. Transillumination method

　　Critically ill children cannot be moved, and cold light transillumination can be used to determine the location of air leaks, facilitating puncture and decompression.

　　3. Ultrasound examination

　　Ultrasound examination can assist in diagnosing atypical mediastinal emphysema and can be used to differentiate between pleural effusion and mediastinal emphysema.

　　4. Endoscopic examination

　　Endoscopic examination can assist in diagnosis and treatment of cervical mediastinal emphysema.

　　Attention should be paid to avoid premature birth and post-term delivery, and prevent intrauterine and perinatal asphyxia. The respiratory tract inhaled after birth, such as meconium, should be aspirated in time. Close monitoring should be conducted during mechanical ventilation, and the peak inspiratory pressure should not be too high. Dynamic changes in suspected cases should be observed and treated in a timely manner. The use of sedatives and/or pulmonary surfactant can reduce the occurrence of pneumatocele.

　　I. Treatment

　　1. Keep quiet and closely observe

　　For patients with clinical symptoms or mild symptoms, close observation is required, and the child should be kept quiet to prevent the air leak from worsening due to crying and fussing. If the pulmonary air leak does not continue, most free gas can be absorbed spontaneously. Abdominal air usually absorbs spontaneously, and it is advisable to feed in small amounts multiple times to prevent gastric distension from affecting ventilation.

　　2. Oxygen inhalation

　　Oxygen inhalation should be administered when there is difficulty breathing, and the absorption of free gas in the pleural cavity can be accelerated by inhaling pure oxygen, but there is a risk of oxygen toxicity.

　　3. Decompression and exhaust

　　For severe cases with a large amount of air accumulation and respiratory and circulatory failure, immediate decompression and exhaust measures should be taken, such as chest puncture or insertion of a catheter for decompression and exhaust on the second intercostal space on the anterior chest of the affected side in severe high-pressure pneumothorax; closed drainage surgery can also be performed if time permits. For mediastinal emphysema and pericardial air, excessive gas can be drained separately by puncturing behind the sternum and pericardial puncture using a syringe. For severe interstitial emphysema, selective bronchial intubation is often effective.

　　4. Treatment of the primary disease

　　In addition, targeted treatment should be carried out for the primary lung disease. In cases of mechanical ventilation, the positive pressure should be reduced, the exhalation time extended, and the symptoms can usually be improved.

　　5. Conservative treatment

　　Applicable to pulmonary air leaks with a small amount of gas, without persistent air leaks, and without obvious clinical symptoms and signs. The child is placed in an incubator or under the infrared therapy table, kept quiet, and prevented from crying and fussing. Oxygen is administered, heart rate and respiration are monitored closely, blood pressure is measured or a transcutaneous oxygen saturation monitor (tcPO2 or SO2) is used for continuous monitoring, and X-ray imaging is followed up if necessary.

　　II. Prognosis

　　The mortality rate is related to the timeliness of diagnosis and treatment, the severity of lung lesions, and the severity of complications. The mortality rate of this disease is high.