Respiratory disorders are the most frequent cause of admission to the special care nursery both in term and preterm infants. Pediatricians and primary care providers may encounter newborn infants with respiratory distress in their office, emergency room, delivery room, or during physical assessment in the newborn nursery. The authors have proposed a practical approach to diagnose and manage such infants with suggestions for consulting a neonatologist at a regional center. Their objective is that practicing pediatricians should be able to assess and stabilize such infants, and transfer to or consult a neonatologist, cardiologist, or pulmonologist after reading this article.
Key points
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Respiratory disorders are the most frequent cause of admission to the special care nursery both in term and preterm infants.
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In critically ill infants or when the diagnosis in unclear, a neonatologist, cardiologist, pulmonologist, or ear, nose, and throat (ENT) surgeon must be promptly consulted.
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The need for referral to a tertiary perinatal-neonatal center for fetal intervention or early neonatal intervention, such as congenital diaphragmatic hernia, other congenital malformations, or delivery of very low-birth-weight (BW) infants is of paramount importance.
Respiratory disorders are the most frequent cause of admission to the special care nursery both in term and preterm infants. Pediatricians and primary care providers may encounter newborn infants with respiratory distress in their office, emergency room, delivery room, or during physical assessment in the newborn nursery. Often these infants may be in distress because of the failure of transition from fetal to extrauterine environment due to retained lung fluid commonly seen in neonates born by cesarean delivery, being immature with relative surfactant deficiency, or having meconium aspiration syndrome (MAS). In some instances, the cause of respiratory distress may pose a diagnostic challenge, especially in differentiating from cardiac diseases. Significant advances have been made in fetal diagnosis, pathophysiology, and early management of these diseases. Therefore, referral to a tertiary perinatal-neonatal center for fetal intervention or early neonatal intervention for congenital diaphragmatic hernia, other congenital malformations, or delivery of a very low-BW infant is of paramount importance.
In this article, the authors have proposed a practical approach to diagnose and manage such infants with suggestions for consulting a neonatologist at a regional center ( Box 1 ). For an in-depth review, the reader is encouraged to preview a text on the subject. The authors’ objective is that practicing pediatricians should be able to asses and stabilize a newborn infant with respiratory distress, and transfer to or consult a neonatologist, cardiologist, or pulmonologist after reading this article.
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Inability to stabilize or ventilate infant, or requiring vasopressors
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Suspect cardiac disease
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Meconium aspiration with and without pulmonary hypertension
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Sepsis with pneumonia
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Pulmonary hemorrhage
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Pneumothorax or pneumomediastinum
Physiologic changes at birth
Before birth, the lung is fluid filled, receiving less than 10% to 15% of the total cardiac output, and fetal oxygenation occurs by the placenta. The transition from intrauterine to extrauterine life requires establishment of effective pulmonary gas exchange. This complex process entails rapid removal of fetal lung fluid controlled by ion transport across the airway and pulmonary epithelium with varying roles of catecholamines, glucocorticosteroids, and oxygen-regulating sodium uptake in alveolar fluid clearance. During fetal life, the high pulmonary vascular resistance directs most of the blood from the right side of the heart through the ductus arteriosus into the aorta. At birth, clamping the umbilical vessels removes the low-resistance placental circuit with increase in systemic blood pressure and relaxation of the pulmonary vasculature. Adequate expansion of the lungs and increase in Pa o 2 values results in an 8- to 10-fold increase in pulmonary blood flow and constriction of the ductus arteriosus. The cardiopulmonary transition takes approximately 6 hours, resulting in rise in Pa o 2 values and decrease in P co 2 values as the intrapulmonary shunt decreases, and the functional residual capacity (FRC) after crying establishes adequate lung volume. Initially the respiratory pattern may be irregular but soon becomes rhythmic modulated by chemoreceptors and stretch receptors, with rates of 40 to 60 breaths per minute. Respiratory distress is common in preterm infants because of poor respiratory drive, weak muscles, compliant chest wall, and surfactant deficiency.
Clinical presentation involves tachypnea (rate>60 breaths per minute), cyanosis, expiratory grunting with chest retractions, and nasal flaring. The underlying disease may be due to pulmonary, cardiac, infectious, metabolic, or other systemic disorders. Peripheral cyanosis or acrocyanosis is often observed in normal newborn infants or in ill infants with poor cardiac output. Central cyanosis is assessed by examining the oral mucosa and suggests inadequate gas exchange signifying more than 3 to 5 g/dL of desaturated hemoglobin. Clinical determination of central cyanosis may be unreliable (ie, not observed) in severely anemic patients despite low Pa o 2 values; in contrast, polycythemic infants may appear cyanotic despite normal values of Pa o 2 . Hence, oxygen saturation measured by pulse oximetry (arterial oxygen saturation [Sao 2 ]) is recommended by the American Academy of Pediatrics to screen infants for hypoxemia, and Sao 2 values less than 90% after 15 minutes of age are considered abnormal. Decrease in O 2 saturation, apnea, or both may be present in infants with respiratory distress. Irregular (seesaw) or slow respiratory rates of less than 30 breaths per minute if associated with gasping may be an ominous sign.
Chest retractions occur because the neonatal chest wall is compliant making it susceptible to alterations in lung function resulting in substernal, subcostal, or intercostal retractions. The retractions result from negative intrapleural pressure generated by the contraction of diaphragm and accessory chest wall muscles along with impaired mechanical properties of the lungs and chest wall. Retractions are observed in lung parenchymal diseases such as respiratory distress syndrome (RDS), pneumonia, airway disorders, pneumothorax, atelectasis, or bronchopulmonary dysplasia (BPD).
Nasal flaring is caused by contraction of alae nasi muscles decreasing the resistance in the nares with resultant reduced work of breathing. Neonates primarily breathe through the nose, hence nasal resistance contributes significantly to total lung resistance, which occurs in choanal atresia or obstruction due to secretions. During resuscitation, suction of mouth is followed by suctioning the nose to prevent aspiration of secretions, blood, or meconium. Occasionally, nasal flaring is observed during feeding or active sleep in normal infants.
Grunting is a compensatory effort made during expiration by closure of the glottis, increasing the airway pressure and lung volume with resultant increased ventilation perfusion (V/Q) ratio. Unlike normal breathing, wherein the vocal cords abduct to enhance inspiratory flow, expiration through partially closed vocal cords in some respiratory disorders produces a grunting sound. Depending on the severity of lung disease, grunting may be either intermittent or continuous. Grunting can maintain FRC and values of Pa o 2 equivalent to those during the application of 2 or 3 cm H 2 O of continuous distending pressure.
Accessory respiratory muscles also assist in optimizing upper airway functions. The genioglossus muscle protrudes the tongue and maintains pharyngeal patency, whereas the laryngeal muscles move the vocal cords regulating airflow during expiration.
Assessing a Neonate with Respiratory Distress
It is not surprising that incomplete cardiopulmonary transition results in respiratory distress with approximately 10% of neonates requiring respiratory support immediately after delivery and up to 1% requiring intensive resuscitation. Therefore, the American Heart Association and the American Academy of Pediatrics recommend that the personnel attending to the newborn in the delivery room should be Neonatal Resuscitation Program (NRP) certified. The cause of respiratory distress can be either pulmonary or nonpulmonary in origin.
The initial approach in assessing an infant with respiratory distress involves physical examination and rapid assessment to identify any life-threatening conditions such as tension pneumothorax, chylothorax, congenital diaphragmatic hernia, or upper airway anomalies. Infants with significant respiratory distress and hypoxia should be initially stabilized. When attending a high-risk delivery, antenatal history of oligohydramnios suggests hypoplastic lungs, whereas polyhydramnios may be present in infants with tracheoesophageal fistula (TEF). Infants of diabetic mothers are at risk for RDS, transient tachypnea of newborn (TTN), or cardiac anomalies causing respiratory distress; fetus in distress with meconium-stained amniotic fluid are at risk for developing meconium aspiration pneumonia, pneumothorax, and persistent pulmonary hypertension ( Box 2 ). History of chorioamnionitis may give a clue to the infant developing pneumonia or sepsis. Repeating physical examinations after initial stabilization for temperature instability with worsening clinical status suggests infection; tachycardia may indicate sepsis or hypovolemia. Stridor is often associated with upper airway obstruction. A scaphoid abdomen with bowel sounds auscultated in the left side of chest indicates congenital diaphragmatic hernia. Asymmetric breath sounds suggest tension pneumothorax or inadvertent placement of endotracheal tube in the main stem bronchus.
