Respiratory distress syndrome in newborns

Respiratory distress syndrome of the newborn is caused by a deficiency of surfactant in the lungs of infants born at less than 37 weeks' gestation. The risk increases with the degree of prematurity. Symptoms of respiratory distress syndrome include wheezing, use of accessory muscles of breathing, and nasal flaring, beginning shortly after birth. Diagnosis is clinical; risk can be assessed prenatally with lung maturity tests. Treatment includes surfactant therapy and supportive care.

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What causes neonatal respiratory distress syndrome?

Surfactant is a mixture of phospholipids and lipoproteins secreted by type II pneumocytes; it reduces the surface tension of the water film that lines the inside of the alveoli, thus reducing the tendency of the alveoli to collapse and the work required to fill them.

With surfactant deficiency, diffuse atelectasis develops in the lungs, which provokes the development of inflammation and pulmonary edema. Since the blood passing through the areas of the lung with atelectasis is not oxygenated (forming a right-left intrapulmonary shunt), the child develops hypoxemia. The elasticity of the lungs decreases, so the work spent on breathing increases. In severe cases, weakness of the diaphragm and intercostal muscles, accumulation of CO2 and respiratory acidosis develop.

Surfactant is not produced in adequate quantities until relatively late in pregnancy; therefore, the risk of respiratory distress syndrome (RDS) increases with the degree of prematurity. Other risk factors include multiple gestations and maternal diabetes mellitus. Risk is reduced by small fetal size, preeclampsia or eclampsia, maternal hypertension, late rupture of membranes, and maternal glucocorticoid use. Rare causes include congenital surfactant defects caused by mutations in the surfactant protein genes (SVG and SVG) and ATP-binding cassette transporter A3. Boys and whites are at greater risk.

Symptoms of Respiratory Distress Syndrome

Clinical symptoms of respiratory distress syndrome include rapid, wheezing, and dyspneic breathing beginning immediately after birth or within a few hours of delivery, with retraction of the pliable areas of the chest and flaring of the alae nasi. As atelectasis and respiratory failure progress, the symptoms become more severe, with cyanosis, lethargy, irregular breathing, and apnea.

Babies with a birth weight of less than 1000 g may have lungs so rigid that they are unable to initiate and/or maintain breathing in the delivery room.

Complications of respiratory distress syndrome include intraventricular hemorrhage, periventricular white matter injury, tension pneumothorax, bronchopulmonary dysplasia, sepsis, and neonatal death. Intracranial complications include hypoxemia, hypercapnia, hypotension, blood pressure fluctuations, and low cerebral perfusion.

Diagnosis of respiratory distress syndrome

Diagnosis is based on clinical presentation, including identification of risk factors; arterial blood gases showing hypoxemia and hypercapnia; and chest radiography. Chest radiography shows diffuse atelectasis, classically described as a ground-glass appearance with prominent air bronchograms; the radiographic appearance is closely related to severity.

Differential diagnosis includes group B streptococcal pneumonia and sepsis, transient tachypnea of the newborn, persistent pulmonary hypertension, aspiration, pulmonary edema, and congenital cardiopulmonary anomalies. Patients typically require cultures of blood, CSF, and possibly tracheal aspirate. The diagnosis of group B streptococcal pneumonia is extremely difficult to establish clinically; therefore, antibiotic therapy is usually initiated pending culture results.

The risk of developing respiratory distress syndrome can be assessed prenatally using lung maturity tests that measure surfactant obtained by amniocentesis or taken vaginally (if the membranes have already ruptured). These tests help determine the optimal time for delivery. They are indicated for selected deliveries before 39 weeks if fetal heart sounds, human chorionic gonadotropin levels, and ultrasound cannot confirm gestational age, and for all deliveries between 34 and 36 weeks. The risk of developing respiratory distress syndrome is lower if the lecithin/sphingomyelin ratio is greater than 2, phosphatidyl inositol is present, the foam stability index is 47, and/or the surfactant/albumin ratio (measured by fluorescence polarization) is greater than 55 mg/g.

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Treatment of respiratory distress syndrome

Respiratory distress syndrome has a favorable prognosis with treatment; mortality is less than 10%. With adequate respiratory support, surfactant production begins over time, and respiratory distress syndrome resolves within 4-5 days, but severe hypoxemia can lead to multiple organ failure and death.

Specific treatment consists of intratracheal surfactant administration; tracheal intubation is necessary, which may also be necessary to achieve adequate ventilation and oxygenation. Less premature infants (>1 kg) and infants with lower oxygen supplementation requirements (fraction of O [H ] in the inspired mixture less than 40-50%) may only require 02 support.

Surfactant therapy speeds recovery and reduces the risk of pneumothorax, interstitial emphysema, intraventricular hemorrhage, bronchopulmonary dysplasia, and in-hospital mortality in the neonatal period and at 1 year. However, infants who received surfactant for respiratory distress syndrome are at higher risk of developing apnea of prematurity. Surfactant replacement options include beractant (bovine lung fat extract supplemented with proteins B and C, colfosceryl palmitate, palmitic acid, and tripalmitin) 100 mg/kg q 6 h as needed for up to 4 doses; poractant alfa (modified minced pig lung extract containing phospholipids, neutral lipids, fatty acids, and proteins B and C) 200 mg/kg, then up to 2 doses of 100 mg/kg as needed after 12 hours; calfactant (calf lung extract containing phospholipids, neutral lipids, fatty acids, and proteins B and C) 105 mg/kg after 12 hours up to 3 doses as needed. Lung compliance may improve rapidly after surfactant administration; peak inspiratory pressure may need to be reduced rapidly to reduce the risk of pulmonary air-leak syndrome. Other ventilator parameters (FiO2 rate) may also need to be reduced.

How to prevent respiratory distress syndrome?

If delivery is expected to occur at 24-34 weeks' gestation, giving the mother 2 doses of betamethasone 12 mg 24 hours apart or 4 doses of dexamethasone 6 mg intravenously or intramuscularly 12 hours apart at least 48 hours before delivery stimulates the formation of surfactant in the fetus and reduces the incidence of respiratory distress syndrome or its severity.