RDS primarily occurs in preterm newborns. In the United States, approximately 24,000 newborns develop RDS each year. The incidence of RDS is inversely related to gestational age: 60% of infants are born at less than 28 weeks, 30% of those are born at 28 to 34 weeks’ gestation, and less than 5% of those born after 34 weeks are affected (Warren & Anderson, 2009). The mortality rate for RDS across all gestational ages is about 10%, attributable to improved prenatal and postnatal management (Dudell & Stoll, 2007; Warren & Anderson, 2009). RDS is caused by insufficient amounts of surfactant or delayed or impaired surfactant synthesis. Surfactant is a mixture of phospholipids and proteins synthesized, packaged, and excreted by alveolar type II cells that lowers surface tension in the alveoli and functions as a stabilizer to prevent atelectasis and alveolar collapse at end expiration (Cole, Nogee, & Hamvas, 2006). Without surfactant, atelectasis (alveolar collapse) occurs, resulting in a series of events that progressively increase disease severity. These events include hypoxemia (decreased concentration of oxygen), hypercapnia (increased concentration of carbon dioxide), mismatch of ventilation with perfusion, acidosis, pulmonary vasoconstriction, alveolar endothelial and epithelial damage, and subsequent protein-rich interstitial and alveolar edema. This cascade of events further decreases surfactant synthesis, storage, and release and leads to pulmonary failure (Dudell & Stoll, 2007; Warren & Anderson, 2009).

Passage of meconium in utero or perinatally is primarily seen in term and postterm infants and those experiencing stress such as growth-restricted infants or those with cord complications compromising uteroplacental circulation (Dudell & Stoll, 2007). Meconium passage occurs as a response to hypoxia, as relaxation of the anal sphincter allows passive escape of meconium into the amniotic fluid. Under normal intrauterine conditions, amniotic fluid does not enter the fetal lung. However, when the fetus experiences hypoxemia, gasping may result in aspiration of meconium-stained amniotic fluid. Of newborns, 8% to 20% are exposed to amniotic fluid stained by meconium; of these, 5% to 10% will go on to develop MAS (American College of Obstetricians and Gynecologists [ACOG], 2006; Dudell & Stoll, 2007; van Lerland & de Beaufort, 2009).

Preventive strategies have been evaluated for cases at risk for MAS, including amnioinfusion and direct tracheal suctioning of the neonate. Although amnioinfusion appears to be a reasonable treatment for repetitive variable decelerations, its sole use as a technique to prevent MAS is not warranted (ACOG, 2006; Xu, Wei, & Fraser, 2008). When aspirated by the fetus before or during birth, meconium can obstruct the airways, leading to severe hypoxia, inflammation, and infection and cause significant respiratory difficulties. Past evidence suggested that intrapartum suctioning before the first breath would decrease the risk of MAS; however, subsequent evidence from a large multicentered randomized trial did not show benefit from routine intrapartum oropharyngeal and nasopharyngeal suctioning (Velaphi & Vidyasagar, 2006; van Lerland & de Beaufort, 2009). Currently, the NRP no longer recommends that all meconiumstained babies routinely receive intrapartum suctioning (AAP & AHA, 2011; Vain, Szyld, Prudent, & Aguilar, 2009).

Pneumonitis is an inflammatory response likely secondary to bile salts present in aspirated meconium. Pneumonitis results in acute lung injury with proteinrich interstitial and alveolar edema. In situations where meconium only partially obstructs the airway, a ball-valve effect results. Air enters the lower airways on inspiration but cannot escape on expiration. This causes overdistension of alveoli, leading to alveolar rupture and pulmonary air leaks. Pneumonitis and airway obstruction result in hypoxemia and acidosis, which cause increased PVR and subsequent PPHN (Steinhom & Farrow, 2007).

Pneumonia is acquired through vertical or horizontal transmission of a pathogenic organism and may present clinically as early-onset sepsis develops in the neonate. Vertical transmission occurs in utero in association with chorioamnionitis, intraamniotic infection, transplacental transmission of organisms, or aspiration of infected amniotic fluid. It may also occur following prolonged rupture of the membranes due to loss of the bacteriostatic protection of amniotic fluid. Horizontal transmission occurs in the nursery as pathogenic organisms spread from hospital personnel, equipment, or families or present as secondary infections as the result of some other primary infection. Pneumonia causes an inflammatory process, disrupting the normal barrier function of the pulmonary endothelium and epithelium, leading to abnormal protein permeability and edema of lung tissue. Hypoxemia and acidosis result, causing increased PVR and potential sequelae such as PPHN (Stoll, 2007a).

TTNB occurs in approximately 0.3% to 0.5% of newborns, although the exact incidence is unknown
(Yurdakok, 2010). Generally, TTNB is a mild, selflimiting disorder of term and near-term infants (NTIs), lasting from 12 to greater than 72 hours. Fetal lungs are fluid filled during gestation, although production of lung fluid decreases at birth with the onset of breathing and secondary to other influences of labor. Fluid is then absorbed from the air spaces through blood vessels, lymphatics, and the upper airways (Yurdakok, 2010). In certain infants, however, the residual fluid in the alveoli persists, alters oxygen exchange, and increases work of breathing. Several pathophysiologic mechanisms have been suggested for TTNB. Historically, this condition was thought to be related to delayed reabsorption of lung fluid by the pulmonary lymphatic system. Retained fluid causes bronchiolar collapse with air trapping or hyperinflation of the alveoli. Hypoxia results when poorly ventilated alveoli are perfused, and hypercarbia results from mechanical interference with alveolar ventilation by fluid. Decreased lung compliance results in tachypnea and increased energy needed to do the work of breathing. It is known that stimuli during labor and at the time of birth cause active transport of chloride from plasma into the fetal lung fluid to cease. As the concentration of chloride becomes higher in the plasma, fetal lung fluid begins to be reabsorbed. Two thirds of the fetal lung fluid is absorbed before birth. Newborns without the benefit of labor and those born prematurely do not have the same amount of time to reabsorb lung fluid as those born after a normal course of labor. Infants delivered by elective cesarean section also have a higher incidence of TTNB (Jain & Eaton, 2006). Some also suggest that TTNB may result from mild immaturity of the surfactant system, which may explain cases of TTNB in late preterm infants (Yurdakok, 2010).

PPHN is defined as a failure of the pulmonary vasculature to relax at birth, resulting in delivery of unoxygenated blood to the systemic circulation. In fetal circulation, pulmonary blood vessels are constricted, causing most blood flow to bypass the lungs. This is appropriate for the fetus because the placenta rather than the fetal lung acts as the organ of gas exchange. PPHN is the result of a sustained elevation of the PVR after birth, preventing transition to the normal pattern of circulation. When the PVR remains elevated, blood bypasses the lungs by flowing through the foramen ovale or ductus arteriosus. This pattern of circulation is referred to as right-to-left shunting because blood is diverted from the venous circulation on the right side of the heart to the arterial circulation on the left side of the heart without going through the pulmonary vascular system. In approximately 1/500 to 1/1,500 live births, severe, prolonged hypoxemia (decreased oxygen in the blood) progresses to hypoxia (decreased oxygen in the tissues) and results in metabolic acidosis and worsening pulmonary vasoconstriction. A vicious cycle ensues. PPHN may be idiopathic, caused by abnormal development of pulmonary vessels, or may result from pathopysiologic events such as asphyxia, MAS, pneumonia, and RDS (Dudell & Stoll, 2007; Lapointe & Barrington, 2011; Stayer & Liu, 2010; Steinhom & Farrow, 2007). Infants with PPHN are typically labile and often require sedation to control competing respiratory effort, vasodilators to overcome pulmonary vasoconstriction, and vasopressors to support systemic blood pressure. A small percentage with refractory hypoxemia may require extracorporeal membrane oxygenation (ECMO) for survival (Dudell & Stoll, 2007).

Clinical signs of respiratory distress may be present at birth or occur at any time in the early neonatal period. These signs include tachypnea, grunting, retractions, nasal flaring, and cyanosis. Tachypnea is defined as a sustained respiratory rate greater than 60 to 70 breaths per minute (Gardner, Enzman-Hines, & Dickey, 2011). Tachypnea develops when the newborn attempts to improve ventilation. Because of the very compliant chest wall, especially in the preterm newborn, it is more energy efficient for the newborn to increase the respiratory rate rather than the depth of respirations. However, persistent tachypnea results in muscular fatigue and, over time, further compromises pulmonary status.

On exhalation, a grunting sound is sometimes heard in newborns with respiratory distress. Grunting is the result of forceful closure of the glottis in an attempt to increase intrapulmonary pressure, keep alveoli open, and create residual lung gas volume (functional residual capacity). Keeping alveoli open during exhalation is a compensatory response to decreased partial pressure of oxygen (PO2) and allows more time for gas exchange to occur (Gardner et al., 2011).

Retractions are depressions observed between the ribs, above the sternum, or below the xiphoid process during inhalation. Retractions are the result of a very compliant chest wall and noncompliant lung. Compliance refers to the stiffness or distensibility of the chest wall and lung parenchyma. As the amount of negative intrathoracic pressure increases on inspiration, the rib cage expands until the soft tissue of the thorax and weak intercostal muscles are pulled inward toward the spine. The result is worsening atelectasis with marked oxygenation and ventilation abnormalities (Cifuentes, Segars, & Carlo, 2003; Gardner et al., 2011).

Nasal flaring occurs with respiratory distress as the newborn attempts to decrease airway resistance and increase the inflow of air through dilation of the alae nasi (Gardner et al., 2011).

Cyanosis results from inadequate oxygenation caused by atelectasis, poor lung compliance, and right-to-left shunting. Although the newborn’s color may be an indicator of oxygenation, variables such as skin temperature and perfusion affect the accuracy of this finding. Precise measurement of oxygen and acid-base status may be necessary for the management of respiratory distress using tools such as pulse oximetry and blood gases (Gardner et al., 2011; Rohan & Golembek, 2009).

Care for newborns with respiratory distress focuses on oxygenation and ventilation as well as controlling factors that increase oxygen demands such as hypothermia or stress. Adequate oxygenation and ventilation requires supportive mechanisms ranging from supplemental oxygen only to application of assisted ventilation with techniques such as continuous positive airway pressure (CPAP) or mechanical ventilation. Pulse oximetry and direct arterial blood gas monitoring are methods used to ensure adequate gas exchange. In a preterm newborn, delivery of oxygen should be sufficient to maintain arterial oxygen tension at 50 to 70 mm Hg, corresponding to a pulse oximetry reading of approximately 85% to 95% (Dudell & Stoll, 2007). Because oxygen may be toxic to some tissue, care should be taken to avoid excessive tissue oxygenation, which might have toxic effects such as chronic lung disease or retinopathy of prematurity. In a term newborn at risk for PPHN, oxygen delivery should be sufficient to maintain normoxemia yet avoid hypoxia, which is a potent stimulus for vasoconstriction (Lapointe & Barrington, 2011). Infants with suspected PPHN will need to be transferred to a tertiary care center for further evaluation and management, including potential use of high-frequency ventilation (HFOV), inhaled nitric oxide (i-NO), or ECMO for severe hypoxemia (Stayer & Liu, 2010).

Select pharmacologic agents may be used in the prevention or management of neonatal respiratory distress. Prenatally, at-risk mothers may receive antenatal steroids to stimulate surfactant synthesis in an effort to prevent RDS. Postnatally, commonly used preparations include airway-instilled surfactant (for RDS prophylaxis or treatment), antibiotics (for pneumonia prophylaxis or treatment), and inhaled or vascularly delivered pulmonary vasodilators (for PPHN treatment) (Konduri & Kim, 2009; Warren & Anderson, 2009).

A neutral thermal environment (NTE) is crucial in the care of a newborn with respiratory distress. Hypothermia or hyperthermia both increase metabolic demands, leading to decreased oxygenation, metabolic acidosis, and worsening respiratory distress (Cifuentes et al., 2003). Newborns with respiratory distress are cared for under a radiant warmer or in an incubator.

Adequate nutrition frequently requires the administration of intravenous (IV) fluids during the early neonatal period. Care is taken to prevent hypoglycemia that may occur from respiratory distress and increased metabolic demands (Rohan & Golembek, 2009).

The cardiovascular system begins to develop in the third week of gestation and is fully developed by the end of the eighth week. It is the first major organ system to develop in the embryo. In the United States, an estimated 32,000 infants are expected to be affected with CHD annually. Of these, an approximate 25% require invasive treatment in the first year of life (AHA, 2012). Heart defects are among the most common birth defects and are the leading cause of birth defect-related deaths. However, the overall mortality has significantly declined over the past few decades (AHA, 2012). The cause of CHD cannot be ascribed to any single factor. Most cases are multifactorial, involving genetic predisposition, familial recurrence, and environmental factors. A family history of CHD is significant; if the mother has a history of a child with CHD, her risk of recurrence increases by threefold (Kenney, Hoover, Williams, & Iskersky, 2011). CHD can also be associated with chromosomal abnormalities (i.e., trisomies 21, 18, 13; chromosome deletion syndromes; DiGeorge deletion 22q; Turner syndrome; and Cornelia de Lange) and maternal-environmental factors, such as drugs (i.e., thalidomide, anticonvulsants, lithium, retinoic acid) and alcohol exposure, or diseases (e.g., insulin-dependent diabetes, maternal lupus erythematosus) and infections (e.g., rubella, Coxsackie B, and enteroviruses) (Kenney et al., 2011).

Cardiac lesions are classified as cyanotic, acyanotic, or according to the hemodynamic characteristics related to pulmonary blood flow. Five of the most commonly occurring cardiac lesions presenting in the early neonatal period include ventricular septal defect (VSD), tetralogy of Fallot (TOF), PDA, atrial septal defect (ASD), and d (dextro)-transposition of the great arteries (d-TGA).

The assessment to exclude CHD includes the following:

The newborn with CHD or persistence of a fetal shunt may present shortly after birth or within the first weeks of life with cyanosis or symptoms of congestive heart failure (CHF). The newborn becomes cyanotic when gas exchange is impaired by pulmonary edema, blood flow to the lungs is restricted as a result of a structural abnormality, or blood flow is shunted away from the lungs. In the newborn with CHD, central cyanosis (bluish discoloration of the skin, nail beds, and mucous membranes) is one of the most common presenting signs and is generally not visible until there is 4 to 5 g/dL of deoxygenated hemoglobin in the arterial system (Mahle et al., 2009). Both the severity of hypoxemia and the hemoglobin concentration determine the degree of cyanosis (Kenney et al., 2011). It is important to differentiate central cyanosis from acrocyanosis (cyanosis of the extremities is commonly seen in newborns because of reduced blood flow through the small capillaries), which is considered a normal finding (Lott, 2007; Kenney et al., 2011).

When the heart is unable to meet the metabolic demands of the tissues, CHF ensues. Unlike infants with CHD, infants with CHF typically present with significant respiratory distress. Common clinical signs associated with CHF (Kenney et al., 2011; Lott, 2007):

A murmur, if present, varies in quality and intensity, depending on the particular cardiac lesion present. If a VSD or ASD is present, allowing mixing of oxygenated and unoxygenated blood, only mild cyanosis occurs. If there is no intracardiac shunt, severe cyanosis is observed. With the exception of cyanosis, the physical examination is often otherwise unremarkable. In the newborn with a large VSD or ASD, signs of CHF develop over time as the PVR falls and the pulmonary blood flow increases. In newborns without an intracardiac shunt, severe hypoxemia and metabolic acidosis develop, followed by a rapid demise if emergency measures are not instituted.

Routine newborn screening for critical congenital heart disease (CCHD) using pulse oximetry is recommended to prevent mortality and morbidity (Secretary’s Advisory Committee on Heritable Disorders in Newborns and Children, 2011). Hypoplastic left heart syndrome, pulmonary atresia (with intact septum), transposition of the great arteries, truncus arteriosus, tricuspid atresia, tetralogy of Fallot, and total anomalous pulmonary venous return are among the seven CCHDs that are primary targets for the routine screening in the well infant and intermediate nurseries (Mahle et al., 2009; Kemper et al., 2012).

Newborns with known or suspected CHD usually require transfer to a tertiary center for treatment and follow-up. The complete diagnostic workup and subsequent repairs or palliative surgery are performed in centers with pediatric cardiac capabilities. Before transport, close observation and supportive care and treatment are warranted. Nursing care for newborns with known or suspected CHD includes the following:

Metabolic acidosis is treated with sodium bicarbonate, pulmonary edema with respiratory distress is treated with diuretics, and shock is treated with vasopressors and calcium gluconate. A lesion such as d-TGA without an intracardiac shunt is treated with prostaglandin E1 to maintain patency of the ductus arteriosus until surgical correction takes place (Kenney et al., 2011).

During fetal life, insulin is secreted by the fetal pancreas in response to glucose that readily crosses the placenta. At birth, the newborn’s blood glucose level is approximately 70% to 80% that of the mother. After removal of placental circulation, the newborn must maintain glucose homeostasis. This requires initiation of various metabolic processes, including gluconeogenesis (e.g., forming glucose from noncarbohydrate sources such as protein and fat) and glycogenolysis (e.g., conversion of glycogen stores to glucose), as well as an intact regulatory mechanism and an adequate supply of substrate (Kayiran & Gurakan, 2010; Sperling & Menon, 2004). While this is effective for the well or term infant, the sick or preterm infant is constrained in effectively mobilizing or utilizing fuel sources.

Hypoglycemia can occur at variable times in neonatal life, depending on its cause. Hypoglycemia during the first few hours of life can be a transient result of developmental immaturity or perinatal stress and may occur in preterm or small-for-gestational-age (SGA) infants. Beyond the first few hours of life, hypoglycemia is more common due to hyperinsulinemia, as with the infant of a diabetic mother. Persistent hypoglycemia, a rare event, may represent inborn metabolic errors of metabolism or endocrine disorders (Sperling & Menon, 2004).

Early feeding will contribute to stabilization of newborn blood sugar. Breastfed term infants have lower blood glucose levels but higher concentrations of ketone bodies than formula-fed infants (Hawdon, Ward Platt, & Aynsley-Green, 1992). Utilization of this alternate fuel source may allow them to tolerate lower serum glucose levels without sequelae (Committee on Fetus and Newborn & Adamkin, 2011; Cornblath et al., 2000).

Identification of those infants at risk for developing hypoglycemia facilitates planning and implementation of appropriate nursing care. This process begins with a review of maternal prenatal and intrapartum history for risk factors associated with neonatal hypoglycemia and a careful physical examination. Symptoms of hypoglycemia are nonspecific and not easily differentiated from many other common neonatal conditions (Display 21-1).

Universal blood glucose screening before clinical signs develop is not currently recommended by the AAP (Committee on Fetus and Newborn & Adamkin, 2011). Selective screening of at-risk newborns is more appropriate and does not appear to decrease quality of care or result in adverse outcomes.

Newborns at risk should be screened within 30 to 60 minutes after birth. Use of proper screening techniques is one of the most important nursing functions. Point-of-care testing (POCT), performed using a bedside glucose oxidase stick method, will provide an expedient estimation of glucose values. Although glucose oxidase sticks are widely used, accuracy of the results from these screening tests depends on the hematocrit, blood source, and operator’s skill. They have been shown to have considerable variance from actual blood glucose levels, which may be due to the source of blood used for testing. Venous blood samples have glucose levels that are approximately 10% less than capillary or arterial specimens (Deshpande & Ward Platt, 2005). Other factors limiting accuracy are improper storage, outdated shelf life of test strips, or contamination with isopropyl alcohol, which falsely elevates the glucose result. It is also important to remember that these POCT use whole blood, which will affect the ability to accurately detect glucose at extremes of hematocrit. The timing of glucose measurements may also result in inaccurate values, as failure to run the test promptly after sampling may result in red blood cell (RBC) oxidation of glucose and produce falsely low values. Blood samples should be transported on ice and analyzed quickly.

Newborns with asymptomatic hypoglycemia should be fed immediately and then retested. Invasive interventions on the basis of low values detected by screening are not warranted as long as infants are assessed and are found to be without clinical findings attributable to hypoglycemia. A low glucose in the asymptomatic newborn may initially be managed by offering breastfeeding or providing expressed breast milk or formula. The infant should be reassessed within 2 to 4 hours and, if the glucose remains low for a second measurement, should be fed again or have IV therapy started (Cornblath et al., 2000).

Newborns with symptomatic hypoglycemia, particularly those with neurologic signs and low POCT bedside blood glucose, should be treated immediately with an IV infusion of glucose, and a blood sample should be drawn and sent to the laboratory for glucose evaluation. Infusion rates should be similar to that expected with endogenous hepatic glucose production (approximately 5 mg/kg/min depending on maturity and weight for gestation—equivalent to 10% dextrose at approximately 70 to 80 mL/kg/day or 3 mL/kg/hr and titrated based on response) (Williams, 2005). Gradual increases in glucose infusion rate should not exceed 2 mg/kg/min each hour. Newborns who are unable to nipple feed and those whose blood glucose levels do not respond to oral feedings or have very low glucose levels (e.g., < 20 mg/dL) should receive a 200 mg/kg (2 mL/kg) bolus of 10% dextrose in water intravenously over 1 minute, followed by a continuous infusion at the rates given previously until the blood glucose is stabilized (Cornblath et al., 2000; Rozance & Hay, 2010). Correction of hypoglycemia should result in resolution of the symptoms. IV administration is tapered off slowly, and the blood glucose level is monitored frequently, every 1 to 2 hours initially, and then intermittently before feedings until stable (Williams, 2005).

Newborns who experience persistent hypoglycemia may require an increased concentration of glucose, such as 12.5%, 15%, or 20%; dextrose solutions with concentrations greater than 12.5% require placement of a central line because of the risk of tissue extravasation. Other treatments for persistent or refractory hypoglycemia include glucagon, which promotes glycogenolysis and requires adequate stores, and corticosteroids, which induce gluconeogenic enzyme activity (Jain et al., 2010).

Hypoglycemia severe enough to warrant IV therapy, or which persists or recurs, requires further investigation to rule out underlying pathology, particularly infection or metabolic and endocrine disease (Deshpande & Ward Platt, 2005). The focus of nursing care is to prevent hypoglycemia when possible. Newborns should be fed within the first 2 hours of life. Care is taken to avoid cold stress and to recognize signs of respiratory distress and sepsis, which can increase the newborn’s risk for developing hypoglycemia.