Respiratory function

An effective respiratory pattern is usually quickly established in nonstressed newborns, as evidenced by vigorous activity, adequate tissue perfusion, and pink or acrocyanotic color. However, infants with a potential for respiratory depression at birth because of asphyxia, maternal analgesia or illness, pulmonary immaturity, or congenital malformations may exhibit cyanosis, gasping or ineffective respirations, decreased tissue perfusion, retractions, nasal flaring, tachypnea, decreased muscle tone, or a combination of these problems.

Numerous problems may affect the respiratory system of preterm infants and may include the following:

In combination, these deficits severely hinder the infant’s respiratory efforts and can produce respiratory distress or respiratory failure. Early signs of respiratory distress include tachypnea, nasal flaring, and expiratory grunting. Depending on the severity of the respiratory distress and the cause, retractions can begin as subcostal, intercostal, or suprasternal. Increasing respiratory effort (e.g., paradoxical breathing patterns, retractions, nasal flaring, expiratory grunting, tachypnea, or apnea) indicates increasing distress. As a result of pulmonary immaturity and residual function, very low-birth-weight (VLBW) and ELBW infants may progress rapidly from respiratory distress to complete respiratory failure. Initially a compromised infant’s color can be cyanotic centrally or pale. Acrocyanosis is a normal finding in the neonate, but central cyanosis indicates poor oxygenation.

Periodic breathing is a respiratory pattern commonly seen in preterm infants. Such infants exhibit 5- to 10-second respiratory pauses followed by 10 to 15 seconds of compensatory rapid respirations. Such periodic breathing should not be confused with apnea, which is a cessation of respirations of 20 seconds or more. The nurse must be prepared to provide supplemental oxygen and artificial ventilation as necessary when the newborn demonstrates an inability to initiate or maintain adequate respiratory function.

Cardiovascular function

Evaluation of heart rate and rhythm, color, blood pressure, perfusion, pulses, oxygen saturation, and acid-base status provides information on cardiovascular status. The nurse must intervene if symptoms of hypovolemia, shock, or both are found. These symptoms include prolonged capillary refill (>3 seconds), pale color, poor muscle tone, lethargy, tachycardia initially then bradycardia, and continued respiratory distress despite the provision of adequate oxygen and ventilation. Hypotension may initially be present or can occur in some infants as a late sign of shock.

Blood pressure (BP) is monitored routinely in the sick neonate by either internal or external means. Direct recording with arterial catheters is often used but carries the risks inherent in any procedure in which a catheter is introduced into an artery. An umbilical venous catheter can also be used to monitor the neonate’s central venous pressure. Oscillometry (Dinamap) is a noninvasive, effective means for detecting alterations in systemic BP (hypotension or hypertension) and for identifying the need to implement appropriate therapy to maintain cardiovascular function.

Body temperature

Preterm infants are susceptible to temperature instability as a result of numerous factors. Factors that place preterm infants at risk for temperature instability include the following:

The goal of thermoregulation is a neutral thermal environment (NTE), which is the environmental temperature at which oxygen consumption and metabolic rate are minimal but adequate to maintain the body temperature (Blackburn, 2007). The NTE range for preterm infants weighing less than 1000 g is very narrow, and the prediction of NTE for each infant is impossible. Extremely immature infants may require environmental temperatures equal to skin and core temperature or possibly higher to achieve thermoneutrality (Blackburn). With knowledge of the four mechanisms of heat transfer (i.e., convection, conduction, radiation, evaporation) the nurse can create an environment for the preterm infant that promotes temperature stability (see Chapter 16). Given that overheating produces an increase in oxygen and calorie consumption, the infant is also jeopardized if he or she becomes hyperthermic (apnea and flushed color may indicate hyperthermia). The preterm infant is not able to sweat and thus dissipate heat.

Central nervous system function

The preterm infant’s central nervous system (CNS) is susceptible to injury as a result of the following problems:

In the preterm neonate, neurologic function is dependent on gestational age, associated illness factors, and predisposing factors such as intrauterine asphyxia, which can cause neurologic damage. Clinical signs of neurologic dysfunction can be subtle, nonspecific, or specific. Five categories of clinical manifestations should be thoroughly evaluated in the preterm infant: seizure activity, hyperirritability, CNS depression, elevated intracranial pressure (ICP), and abnormal movements such as decorticate posturing. Primary and tendon reflexes are generally present in preterm infants by 28 weeks of gestation; evaluation of these reflexes should be part of the neurologic examination. Ongoing assessment and documentation of these neurologic signs are needed both for the purposes of discharge teaching and for making follow-up recommendations.

Nutrition status

The initial goal of neonatal nutrition in the preterm infant is to prevent catabolism and excess fluid loss. Once the infant’s respiratory and cardiac functions are stabilized, the goal of nutrition is to promote optimal growth and development. The preterm infant’s metabolic functions are compromised by a limited store of nutrients, a decreased ability to digest proteins and absorb nutrients, and immature enzyme systems.

The nurse must continuously assess the infant’s nutritional status. Preterm infants often require gavage or intravenous (IV) feedings instead of oral feedings, depending on the gestational age, birth weight, and existing illness factors such as respiratory distress.

Renal function

The preterm infant’s immature renal system is unable to (1) excrete metabolites and drugs adequately, (2) concentrate urine, or (3) maintain acid-base, fluid, or electrolyte balance. Therefore intake and output, as well as specific gravity, are assessed. Laboratory tests are performed to assess acid-base and electrolyte balance. Medication levels are monitored in preterm infants because metabolism via renal and hepatic routes is often hindered. Because of the great variability in drug metabolism, serum levels are obtained to ensure an adequate therapeutic range for treatment and to prevent toxicity.

Hematologic status

The preterm infant is predisposed to hematologic problems because of the following conditions:

Infants are assessed for any evidence of bleeding from puncture sites, the GI tract, and pulmonary system. They are also examined for signs of anemia (e.g., decreased hemoglobin and hematocrit levels, pale skin, increased apnea, lethargy, tachycardia, poor weight gain). In high risk infants the amount of blood withdrawn for laboratory testing is monitored.

Infection prevention

Even though protection from infection is an integral part of all newborn care, preterm and sick infants are particularly susceptible to infectious organisms. As with all aspects of care, strict handwashing is the single most important measure to prevent nosocomial infections. Personnel with known infectious disorders are barred from the unit until they are no longer infectious. Standard Precautions are instituted in all nursery areas as a method of infection control to protect infants and staff.

Neonates are highly susceptible to infection as a result of diminished nonspecific (inflammatory) and specific (humoral) immunity, such as impaired phagocytosis, delayed chemotactic response, minimal or absent immunoglobulin A (IGA) and immunoglobulin M (IgM), and decreased complement levels. Because of the infant’s poor response to pathogenic agents, in most instances, no local inflammatory reaction is seen at the portal of entry to signal an infection, and the resulting symptoms tend to be vague and nonspecific. Consequently, diagnosis and treatment may be delayed. Preterm and term infants exhibit various nonspecific signs and symptoms of infection (Box 24-2). Early identification and treatment of sepsis is essential.

Physical care

The preterm infant’s environmental support typically consists of the following equipment and procedures:

Various metabolic support measures that may be instituted consist of the following:

Maintain body temperature

The preterm infant is susceptible to heat loss and its complications (see Fig. 16-2 on p. 444). In addition, low-birth-weight (LBW) infants may be unable to increase their metabolic rate because of impaired gas exchange, caloric intake restrictions in relation to high expenditure, or poor thermoregulation. Transepidermal water loss is greater than in the term infant because of skin immaturity in ELBW and VLBW infants (i.e., those weighing less than 1000 g and 1500 g, respectively) and can contribute to temperature instability. The preterm infant should be transferred from the birth room in a prewarmed incubator; ELBW infants may be placed in a polyethylene bag to decrease heat and water loss (Fig. 24-1). Skin-to-skin contact (kangaroo care) between the stable preterm infant and parent is a viable option for interaction because of the maintenance of appropriate body temperature by the infant (see p. 767 for further discussion of kangaroo care).

Preterm and other high risk infants are cared for in the NTE created by use of an external heat source. A probe applied to the infant is attached to an external heat source supplied by a radiant warmer or a servo-controlled incubator. Optimal thermoneutrality cannot be predicted for every preterm infant’s needs. The American Academy of Pediatrics and the American Heart Association Neonatal Resuscitation Program recommends that the first axillary temperature not be below 36.5° C (Kattwinkel, 2006). Standard guidelines for maintaining NTE in the LBW infant are published (Blake & Murray, 2006). Further research is needed to define an NTE for the ELBW infant.

Oxygen therapy

The goals of oxygen therapy are to provide adequate oxygen to the tissues, prevent lactic acid accumulation resulting from hypoxia, and at the same time avoid the potentially negative effects of hyperoxia and free radicals. Numerous methods have been devised to improve oxygenation (Fig. 24-2). All of these methods require that the gas be warmed and humidified before entering the respiratory tract. If the infant does not require mechanical ventilation, oxygen can be supplied by plastic hood placed over the infant’s head, by nasal cannula, or by nasal continuous positive airway pressure (CPAP) to supply variable concentrations of humidified oxygen. Because oxygen therapy is not without inherent hazards, each infant must be closely monitored to prevent hyperoxemia and hypoxemia.

Mechanical ventilation (respiratory support providing predetermined amount of oxygen through endotracheal tube) must be implemented if other methods of therapy cannot correct abnormalities in oxygenation. Ventilator settings are determined by the infant’s particular needs. The ventilator is set to provide a predetermined amount of oxygen to the infant during spontaneous respirations and to provide mechanical ventilation in the absence of spontaneous respirations. Newer technologies in ventilation allow oxygen to be delivered at lower pressures and in assist modes, thereby preventing the overriding of the infant’s spontaneous breathing and providing distending pressures within a physiologic range, decreasing barotrauma and associated complications such as pneumothorax and pulmonary interstitial emphysema.

Neonatal resuscitation

In 2010 the American Heart Association published neonatal resuscitation guidelines (Kattwinkel, Perlman, Aziz, et al., 2010). A rapid assessment of infants can identify those who do not require resuscitation: those born at term gestation, with no evidence of meconium or infection in the amniotic fluid, those who are breathing or crying, and those with good muscle tone. If any of these characteristics is absent, the infant should receive the following actions in sequence: (1) initial steps in stabilization: provide warmth by placing the baby under a radiant warmer, position the head in a position to open the airway, clear the airway with a bulb syringe or suction catheter, dry the baby, stimulate breathing, and reposition the baby; (2) ventilation; (3) chest compressions; and (4) administration of epinephrine or volume expansion or both. The decision to move from one category of action to the next is based on the assessment of respirations, heart rate, and color. Rapid decision making is imperative; 30 seconds are allotted for each step. The condition of the infant is reevaluated and the decision made whether to progress to the next step (Fig. 24-3).

Resuscitation of asphyxiated newborns with 21% oxygen rather than 100% oxygen shows promise. Proponents for room air resuscitation suggest that fewer complications are associated with oxidative stress and hyperoxemia when room air is administered. The 2010 American Heart Association resuscitation standards for neonatal resuscitation stress that resuscitation may begin with no supplemental oxygen (i.e., 21% or room air) but that if the infant’s condition does not improve within 90 seconds, supplemental oxygen should be available for use. The stated goal is to minimize oxygen free radicals by preventing hyperoxia using supplemental oxygen at levels less than 100% (Kattwinkel, et al., 2010). A review of several studies indicates that neonatal mortality is reduced by 30% to 40% when room air instead of 100% oxygen is used for neonatal resuscitation (Saugstad, 2007). Fluctuations in oxygen saturation are also deemed harmful. Experts recommend that oxygen saturations for ELBW infants be maintained between 85% and 93% but definitely not exceeding 95% (Saugstad). Rates of retinopathy of prematurity and bronchopulmonary dysplasia are reduced in infants whose arterial oxygen saturation (SaO₂) is kept between 93% and 95%.

Surfactant replacement therapy

Surfactant is a surface-active phospholipid secreted by the alveolar epithelium. Acting much the same as a detergent, this substance reduces the surface tension of fluids that line the alveoli and respiratory passages, resulting in uniform expansion and maintenance of lung expansion at low intraalveolar pressure. Without surfactant, infants are unable to keep their lungs inflated and therefore exert a great deal of effort to reexpand the alveoli with each breath. With increasing exhaustion, infants are able to open fewer and fewer alveoli. This inability to maintain lung expansion produces widespread atelectasis.

Surfactant can be administered as an adjunct to oxygen and ventilation therapy (see Medication Guide: Surfactant Replacement). Generally, infants born before 32 weeks of gestation do not have adequate amounts of pulmonary surfactant to survive extrauterine life. In many centers the use of prophylactic surfactant is reserved for infants younger than 29 weeks who will likely have respiratory distress syndrome (RDS) (see Table 24-2) (Hagedorn, Gardner, Dickey, & Abman, 2006). The American Academy of Pediatrics (AAP) Committee on Fetus and Newborn (Engle & AAP Committee on Fetus and Newborn, 2008) recommends the use of surfactant in infants with RDS as soon as possible after birth, especially ELBW infants and those not exposed to maternal antenatal steroids. The administration of antenatal steroids to the mother and surfactant replacement has decreased the incidence of RDS and concomitant morbidities.

Additional therapies

Inhaled nitric oxide (INO), extracorporeal membrane oxygenation (ECMO), and liquid ventilation are additional therapies used in the treatment of respiratory distress and respiratory failure in neonates. INO is used in term and late preterm infants with conditions such as persistent pulmonary hypertension, meconium aspiration syndrome, pneumonia, sepsis, and congenital diaphragmatic hernia to decrease or reverse pulmonary hypertension, pulmonary vasoconstriction, acidosis, and hypoxemia. Nitric oxide is a colorless, highly diffusible gas that can be administered through the ventilator circuit blended with oxygen. INO therapy may be used in conjunction with surfactant replacement therapy, high-frequency ventilation, or ECMO.

ECMO may be used in the management of term infants with acute severe respiratory failure for the same conditions as those mentioned for INO. This therapy involves a modified heart-lung machine, although in ECMO the heart is not stopped, and blood does not entirely bypass the lungs. Blood is shunted from a catheter in the right atrium or right internal jugular vein by gravity to a servo-regulated roller pump, pumped through a membrane lung where it is oxygenated, through a small heat exchanger where it is warmed, and then returned to the systemic circulation via a major artery such as the carotid artery to the aortic arch. ECMO provides oxygen to the circulation, allowing the lungs to “rest,” and decreases pulmonary hypertension and hypoxemia in such conditions as persistent pulmonary hypertension of the newborn, congenital diaphragmatic hernia, sepsis, meconium aspiration, and severe pneumonia. ECMO is not used in preterm infants younger than 34 weeks of gestation because of the anticoagulant therapy required in the pump and circuits, which can increase the potential for intraventricular hemorrhage in such infants. In some centers the success of high-frequency ventilation and INO has greatly decreased the demand for and use of ECMO.

Weaning from respiratory assistance

The infant is ready to be weaned from respiratory assistance when the ABG and SaO₂ levels are maintained within normal limits and the infant is able to establish spontaneous ventilation sufficient to maintain acid-base balance. A spontaneous, adequate respiratory effort must be present and the infant must show improved muscle tone during increased activity. Weaning is accomplished in a stepwise and gradual manner, which may consist of the infant being extubated, placed on nasal CPAP, and then weaned to oxygen by means of a hood or nasal cannula. Throughout the weaning process the infant’s oxygen levels are monitored by pulse oximetry, transcutaneous partial pressure of oxygen (tcPO₂) monitoring, and by assessing blood gas levels.

Frequent skin assessments are essential when the infant is receiving supplemental oxygen with any of the methods described herein but particularly in infants with poor perfusion and in those requiring equipment that comes in continuous contact with the infant’s skin (e.g., nasal CPAP, nasal cannula, pulse oximetry probes). A greater-than-normal incidence of skin breakdown is noted in infants and children who require the use of medical devices (e.g., nasal prongs, pulse oximetry probes) (Noonan, Quigley, & Curley, 2006).

Some infants are not able to be weaned from all oxygen support by the time of discharge from the hospital and may require home oxygen therapy for several months. Bronchopulmonary dysplasia or congenital anomalies such as repaired congenital diaphragmatic hernia or tracheal defect or a neurologic insult with resultant dysfunction may preclude weaning.

The parents need to be given consistent information and be reassured about the infant’s respiratory progress. Decisions regarding the nature of continued interventions should be included in a multidisciplinary plan of care, and the therapy should be explained frequently to the family.