Meconium aspiration pneumonia is characterized bytachypnea, hypoxia, hypercapnia, and small airway obstruction causing a ball-valve effect, leading to air trapping, over-distention, and extra-alveolar air leaks. Complete small airway obstruction produces atelectasis. Within 24 to 48 hours, a chemical pneumonitis develops in addition to the mechanical effects of airway obstruction. Abnormal pulmonary function may be caused by the meconium, in part, through inactivation of surfactant. Primary pulmonary hypertension of the newborn (PPHN) frequently accompanies meconium aspiration, with right-to-left shunting caused by increased pulmonary vascular resistance. The chest radiograph reveals patchy infiltrates, overdistention, flattening of the diaphragm, increased anteroposterior diameter, and a high incidence of pneumomediastinum and pneumothoraces. Comorbid diseases include those associated with in utero asphyxia that initiated the passage of meconium.
Treatment of meconium aspiration includes general supportive care and assisted ventilation. Infants with a PPHN-like presentation should be treated for PPHN. If severe hypoxia does not subside with conventional or high-frequency ventilation, surfactant therapy, and inhaled nitric oxide, extracorporeal membrane oxygenation (ECMO) may be beneficial.
Prevention of meconium aspiration syndrome involvescareful in utero monitoring to prevent asphyxia. When meconium-stained fluid is observed, the obstetrician should suction the infant’s oropharynx before delivering the rest ofthe infant’s body. If the infant is depressed with poor tone,minimal respiratory effort, and cyanosis, the infant’s oropharynx should be suctioned, the vocal cords visualized,and the area below the vocal cords suctioned to remove anymeconium from the trachea. Saline intrauterine amnioinfusion during labor may reduce the incidence of aspiration andpneumonia.
PPHN occurs in post-term, term, or near-term infants. PPHN is characterized by severe hypoxemia, without evidence of parenchymal lung or structural heart disease. PPHN is often seen with asphyxia or meconium-stained fluid. The chest radiograph usually reveals normal lung fields rather than the expected infiltrates and hyperinflation that may accompany meconium aspiration. Additional problems that may lead to PPHN are congenital pneumonia, hyperviscosity-polycythemia, congenital diaphragmatic hernia, pulmonary hypoplasia, congenital cyanotic heart disease, hypoglycemia, and hypothermia. Total anomalous venous return associated with obstruction of blood flow may produce a clinical picture that involves severe hypoxia and that is initially indistinguishable from PPHN; however, a chest radiograph reveals severe pulmonary venous engorgement and a small heart. Echocardiography or cardiac catheterization confirms the diagnosis.
Significant right-to-left shunting through a patent foramen ovale, through a PDA, and through intrapulmonary channels is characteristic of PPHN. The pulmonary vasculature often shows hypertrophied arterial wall smooth muscle, suggesting that the process of or predisposition to PPHN began in utero as a result of previous periods of fetal hypoxia. After birth, hypoxia, hypercapnia, and acidosis exacerbate pulmonary artery vasoconstriction, leading to further hypoxia and acidosis. Some infants with PPHN have extrapulmonary manifestations as a result of asphyxia. Myocardial injuries include heart failure, transient mitral insufficiency, and papillary muscle or myocardial infarction. Thrombocytopenia, right atrial thrombi, and pulmonary embolism also may be noted.