Clinical Manifestations

Infants with RDS can develop respiratory distress either acutely or over a period of hours, depending on the acuity of pulmonary immaturity, associated illness factors, and gestational maturity. The observable signs produced by the pulmonary changes usually begin to appear in infants who apparently achieve normal breathing and color soon after birth. In a matter of a few hours, breathing gradually becomes more rapid (>60 breaths/min). Infants may display retractions—suprasternal or substernal, and supracostal, subcostal, or intercostal—which result from a compliant chest wall. Weak chest wall muscles and the highly cartilaginous rib structure produce an abnormally elastic rib cage, resulting in indrawing, or retraction, of the skin between the ribs. During this early period the infant’s color may remain satisfactory, and auscultation reveals air entry. Some of the criteria for evaluating respiratory distress in infants are illustrated in Fig. 10-14.

Within a few hours, respiratory distress becomes more obvious. The respiratory rate continues to increase (to 80 to 120 breaths/min), and breathing becomes more labored. It is significant to note that infants increase the rate rather than the depth of respiration when in distress. Substernal retractions become more pronounced as the diaphragm works hard in an attempt to fill collapsed air sacs. Fine inspiratory crackles can be heard over both lungs, and there is an audible expiratory grunt. This grunting, a useful mechanism observed in the earlier stages of RDS, serves to increase end-expiratory pressure in the lungs, thus maintaining alveolar expansion and allowing gas exchange for an additional brief period. Flaring of the nares is also a sign that accompanies tachypnea, grunting, and retractions in respiratory distress. Central cyanosis (a bluish discoloration of oral mucous membranes and generalized body cyanosis) is a late and serious sign of respiratory distress. Initially supplemental oxygen may eliminate cyanosis. The use of pulse oximetry and arterial blood gas sampling obviates the necessity for dependence on color to determine oxygen requirements.

Severe RDS is often associated with a shocklike state, as manifested by diminished cardiac inflow and low arterial blood pressure. As a result of extreme pulmonary immaturity, decreased glycogen stores, and lack of accessory muscles, the ELBW and VLBW infant may have severe RDS at birth, bypassing the aforementioned steps in the development of RDS.

Infants with RDS who are treated with exogenous surfactant have a good chance for recovery. Complications of RDS include those described as complications of positive pressure ventilation (see p. 353). Associated complications (of prematurity and RDS) include PDA and congestive heart failure, retinopathy of prematurity, IVH, BPD, NEC, and neurologic sequelae.

Diagnostic Evaluation

Laboratory data are nonspecific, and the abnormalities observed are identical to those observed in numerous biochemical abnormalities of the newborn (i.e., the findings of hypoxemia, hypercapnia, and acidosis). Specific tests are used to determine complicating factors, such as blood glucose (to test for hypoglycemia), blood gas measurements for serum pH (to test for acidosis), and Pao₂ (to test for hypoxia). Pulse oximetry is an important component for determining hypoxia. Other special examinations may be used to diagnose or rule out complications.

Radiographic findings characteristic of RDS include (1) a diffuse granular pattern over both lung fields that resembles ground glass and represents alveolar atelectasis and (2) dark streaks, or air bronchograms, within the ground glass areas that represent dilated, air-filled bronchioles. It is important to distinguish between RDS and pneumonia in infants with respiratory distress.

Therapeutic Management

The treatment of RDS includes all the general measures required for any preterm infant, as well as those instituted to correct imbalances. The supportive measures most crucial to a favorable outcome are (1) maintain adequate ventilation and oxygenation with an oxygen hood, continuous positive airway pressure (CPAP), or mechanical ventilation; (2) maintain acid-base balance; (3) maintain a neutral thermal environment; (4) maintain adequate tissue perfusion and oxygenation; (5) prevent hypotension; and (6) maintain adequate hydration and electrolyte status. Nipple and gavage feedings are avoided in any situation that creates a marked increase in respiratory rate because of the greater hazards of aspiration.

Nursing Care Management

Care of infants with RDS involves all the observations and interventions previously described for high-risk infants. In addition, the nurse is concerned with the complex problems related to respiratory therapy and the constant threat of hypoxemia and acidosis that complicates the care of patients in respiratory difficulty.

The respiratory therapist, an important member of the neonatal intensive care team, is often responsible for maintenance and regulation of respiratory equipment. Nevertheless, nurses should understand the equipment and be able to recognize when it is not functioning correctly. The most essential nursing function is to observe and assess the infant’s response to therapy. Continuous monitoring and close observation are mandatory because an infant’s status can change rapidly and because oxygen concentration and ventilation parameters are prescribed according to the infant’s blood gas measurements, tcPo₂, and pulse oximetry readings.

Changes in oxygen concentration are based on these observations. The nurse determines the amount of oxygen administered, expressed as the fraction of inspired air (Fio₂), on an individual basis according to pulse oximetry and/or direct or indirect measurement of arterial oxygen concentration. Capillary samples collected from the heel (see Chapter 27 for procedure) are useful for pH and Paco₂ determinations but not for oxygenation status. Continuous pulse oximetry readings are recorded at least hourly or more often as required. Blood sampling is performed after ventilator changes for the acutely ill infant and thereafter when clinically indicated.

In infants with RDS who are acutely ill or extremely preterm, an umbilical arterial catheter (UAC) may be used to draw arterial blood for monitoring oxygenation. This method, although initially invasive and therefore performed by the practitioner with sterile precautions, allows for blood sampling without repeated peripheral arterial punctures. The catheter is inserted via one of the umbilical arteries to the premeasured desired position (either at the level of the diaphragm, T6-10, or between L3-4) and rests in the descending aorta. Continuous arterial pressure monitoring may be carried out with an “in-line” transducer. Practices vary regarding medication administration via a UAC. The nurse is aware of the potential hazards associated with these catheters (infection, hemorrhage, thrombus formation and subsequent vessel occlusion, arterial vasospasm) and implements monitoring and observation strategies to promptly intervene should complications occur (see Hydration, p. 322). An umbilical venous catheter (UVC) may be used separately or in conjunction with the UAC, depending on the severity of the infant’s illness, the fluid requirements, and preferred medical practice.

Mucus may collect in the respiratory tract as a result of the infant’s pulmonary condition. Secretions interfere with gas flow and may obstruct the passages, including the ET tube. Suctioning should occur only when necessary and should be based on individual infant assessment, which includes auscultation of the chest, evidence of decreased oxygenation, excess moisture in the ET tube, or increased infant irritability. When nasopharyngeal passages, the trachea, or the ET tube is being suctioned, insert the catheter gently but quickly; intermittent suction is applied as the catheter is withdrawn. It is imperative that the catheter obstruct the airway for no more than 5 seconds, since continuous suction removes air from the lungs along with the mucus. It is recommended that, where possible, an in-line suction device be used on infants who are acutely ill and who do not tolerate any procedure without profound decreases in oxygen saturation, blood pressure, and heart rate. The purpose of suctioning an artificial airway is to maintain patency of that airway, not the bronchi. Suction applied beyond the ET tube can cause traumatic lesions of the trachea.

Research indicates that suctioning to a point where the catheter meets resistance and is then withdrawn causes trauma to the tracheobronchial wall. To remove secretions without damage to the tracheobronchial mucosa, the suction catheter is premeasured and inserted to a predetermined depth to avoid extension beyond the ET tube. The practice of suctioning patients on mechanical ventilation has undergone close scrutiny in recent years; further studies are needed to validate this practice and to determine the best methods for maintaining a patent airway without compromising the patient’s well-being.

The most advantageous positions for facilitating an infant’s open airway are with the infant on the side with the head supported in alignment by a small folded blanket or with the infant on the back, positioned to keep the neck slightly extended. With the head in the “sniffing” position, the trachea is opened to its maximum; hyperextension reduces the tracheal diameter in neonates (see Therapeutic Positioning, p. 336). The pulse oximeter is observed before, during, and after suctioning to provide an ongoing assessment of oxygenation status and to prevent hypoxemia.

Inspection of the skin is part of routine infant assessment. Position changes and the use of gel mattresses are helpful in guarding against skin breakdown.

Mouth care is especially important when infants are receiving nothing by mouth, and the problem is often aggravated by the drying effect of oxygen therapy. The nurse can prevent drying and cracking by good oral hygiene using sterile water. Irritation to the nares or mouth that occurs from appliances used to administer oxygen may be reduced by the use of a water-soluble ointment (see Skin Care, p. 329; see Nursing Care Plan).

Nursing care of an infant with RDS is demanding. Pay meticulous attention to subtle changes in the infant’s oxygenation status. The importance of attention to detail cannot be overemphasized, particularly in regard to medication administration.

Pathophysiology

MAS involves the passage of meconium in utero as a result of hypoxic stress. It occurs primarily in full-term and postterm infants but has been reported in infants at less than 37 weeks of gestation. Once the fetus ingests meconium, any gasping activity occurring as a result of intrauterine stress may cause the rather sticky and tenacious substance to become aspirated into the lower airways. The net results are partial airway obstruction, air trapping, hyperinflation distal to the obstruction, and atelectasis caused by surfactant deactivation. A “ball-valve” situation exists wherein gas flows into the lungs on inspiration but is trapped there on exhalation as a result of the small airway diameter. As the infant struggles to take in more air (air hunger), even more meconium may be aspirated. Hyperinflation, hypoxemia, and acidemia result in increased PVR.

In turn, shunting of blood through the ductus arteriosus (right to left) occurs because of increased resistance to blood flow through the pulmonary arteries (and to the lungs), leading to further hypoxemia and acidosis. Ductal shunting increases with hypoxia; some blood may enter the left atrium (LA) from the right atrium (RA) via the foramen ovale because there is a net decrease in blood returning to the LA via the pulmonary venous system, thus preventing closure of the foramen ovale. This pathologic process is essentially persistence of the fetal circulation, or PPHN, which is discussed later in this chapter. The air trapping of MAS causes overdistention of the alveoli and often air leaks. There is evidence that meconium contributes to the destruction of surfactant, thus increasing surface tension and further predisposing the alveoli to decreased functional capacity.

Clinical Manifestations

Infants who have released meconium in utero for some time before birth are stained from green meconium stools (those with more recent meconium passage may not be stained), tachypneic, hypoxic, and often depressed at birth. They develop expiratory grunting, nasal flaring, and retractions similar to those experienced by infants with RDS. They may initially be cyanotic or pale as well as tachypneic, and they may demonstrate the classic barrel chest from hyperinflation. The infants are often stressed, hypothermic, hypoglycemic, and hypocalcemic. Severe meconium aspiration progresses rapidly to respiratory failure. These infants exhibit profound respiratory distress with gasping, ineffective ventilations; marked cyanosis and pallor; and hypotonia.

Diagnostic Evaluation

At birth, meconium can often be visualized via laryngoscopy in the respiratory passages and vocal cords. Chest radiographs show uneven distribution of patchy infiltrates, air trapping, hyperexpansion, and atelectasis. Air leaks may be seen as the illness progresses. Oxygenation will be poor, as evidenced by pulse oximetry and arterial blood gases. These infants may quickly develop metabolic and respiratory acidosis. Echocardiography assists in the diagnosis of right-to-left shunting of blood away from the pulmonary system.

Therapeutic Management

Prevention of meconium aspiration begins with suctioning the mouth, nose, and posterior pharynx just after the head is delivered while the chest is still compressed in the birth canal. After delivery, the need for tracheal suctioning is based on infant assessment. Infants who are vigorous with strong, stable respiratory effort, good muscle tone, and heart rate greater than 100 beats/min should not undergo tracheal suctioning but should be closely monitored (Kattwinkel, 2006). On the other hand, infants who demonstrate poor respiratory effort, low heart rate, and poor tone should be rapidly intubated, suctioned appropriately, and resuscitated according to clinical status after suctioning. These management protocols have been supported by ongoing research (Kabbur, Herson, Zaremba, et al, 2005).

Infants with respiratory distress are admitted to the NICU. Management of MAS consists of ventilatory support, exogenous surfactant administration, IV fluids, systemic antibiotics, and in some cases inotropes. Because these infants are prone to development of persistent pulmonary hypertension, they should be supported to maintain normal pH, carbon dioxide, and oxygen levels; they may be candidates for ECMO therapy, HFV, or NO (see Nitric Oxide, p. 354, and Persistent Pulmonary Hypertension of the Newborn, p. 359). Complications are managed symptomatically or as described under the specific disorder.

Nursing Care Management

Nursing care management is the same as for any high-risk neonate (see nursing care in sections on oxygen therapy, persistent pulmonary hypertension, and other complications).

Clinical Manifestations

Spontaneous pneumothorax usually occurs during the first few breaths after birth, primarily in full-term or postterm infants, and is evident by the gradual onset of symptoms of respiratory distress after arrival in the nursery. Use of positive pressure ventilation in resuscitation may cause air leaks. Mechanical positive pressure ventilation may contribute to an increase in the incidence of air leaks; however, in some cases, such as in extreme prematurity and meconium aspiration, air leaks may not be altogether preventable. The nurse suspects an air leak on the basis of respiratory manifestations and a shift in location of maximum intensity of heart sounds and absent or diminished breath sounds (although breath sounds may not be altered because of the small diameter of the chest and auscultation of referred breath sounds).

A tension pneumothorax occurs more frequently in infants requiring ventilatory assistance. In preterm infants being mechanically ventilated, an air leak may be demonstrated by hypotension, bradycardia, decreased or absent breath sounds unilaterally, decreased oxygenation (by pulse oximetry), and cyanosis, none of which responds to efforts for oxygenation (a resuscitation bag connected to the ET tube and provision of manual ventilations). There may also be chest asymmetry, altered cardiac sounds (diminished, shifted, or muffled), a palpable liver and spleen, and subcutaneous emphysema. Infants on HFV may demonstrate an air leak by a sudden decrease in systemic pressure or an absence of chest movement (because of difficulty in auscultation of the chest with such modalities). The otherwise healthy full-term infant may exhibit only mild to moderate signs of respiratory distress. The presence of an air leak has been identified as contributing to the risk of an adverse developmental outcome in preterm infants (Laptook, O’Shea, Shankaran, et al, 2005).

Therapeutic Management

Diagnosis is confirmed by transillumination of the chest with a fiberoptic light and/or radiographic examination. In symptomatic infants, treatment is urgent. Evacuation of trapped air is accomplished by chest tube insertion into the pleural space through a small chest incision. The chest tube is then attached to continuous water-seal drainage. A dry suction control drainage system not requiring water is also available. In situations requiring infant transport, a pocket-sized Heimlich valve may be used until an appropriate drainage system can be established; the valve is not effective when fluid drainage is required. Needle aspiration serves as an emergency measure until a chest tube can be inserted. Pneumomediastinum seldom requires treatment, but pneumopericardium is managed by needle aspiration or pericardial tube drainage. The full-term newborn with a small tension pneumothorax may require only oxygen therapy and IV nutrition for a brief period if respiratory distress is not severe.

Nursing Care Management

The most important nursing function, which is most effective for early detection, is close observation for the possibility of an air leak in susceptible infants. Nurses maintain a high level of suspicion in (1) infants with RDS with or without positive pressure ventilation, (2) infants with meconium-stained amniotic fluid or MAS, (3) infants with radiographic evidence of interstitial or lobar emphysema, (4) infants who required resuscitation at birth, or (5) infants receiving CPAP or positive pressure ventilation. For infants at risk, needle aspiration equipment (30-ml syringe, three-way stopcock, and 23- to 25-gauge needles) should be at the bedside for emergency use.

The general nursing care of the infant with an extraneous air syndrome is the same as that for all high-risk neonates. Respiratory management is similar to that for infants with RDS. Assessing breath sounds frequently, monitoring the efficacy of gas exchange, and regulating oxygen therapy according to the infant’s needs are vital nursing functions. Attention to pain management with the procedure is vital in these preverbal and significantly stressed infants.

Therapeutic Management

Early recognition and management of conditions that contribute to or cause hypoxia and pulmonary vascular vasoconstriction are the primary goals in the prevention of PPHN. Additional treatment includes careful fluid regulation and evaluation of intravascular fluid volume. Supplemental oxygen reduces hypoxia and decreases pulmonary vasoconstriction. Assisted ventilation, often by HFV, is required if hypoxia is severe. Vasodilators, such as sildenafil (a phosphodiesterase [PDE5] inhibitor) or epoprostenol (prostacyclin), are sometimes prescribed to decrease PVR, thereby avoiding ECMO and NO. Sildenafil administered in intravenous or oral form has been shown to reduce PVR (hypertension) in neonates and improve oxygenation, but further controlled clinical trials are needed (Latini, Del Vecchio, De Felice, et al, 2008; Shah and Ohlsson, 2007b; Steinhorn, Kinsella, Pierce, et al, 2009).

Additional drug therapy used in the management of PPHN includes judicious use of sodium bicarbonate to maintain appropriate acid-base balance; volume expanders such as normal saline or lactated Ringer solution; and the vasopressors dopamine, dobutamine, and nitroprusside to increase systemic vascular resistance (Konduri, 2004). The use of inhaled NO has been successfully used to reverse pulmonary vascular vasoconstriction and is often attempted before other therapies such as ECMO (see Nitric Oxide, p. 354).

Another approach to management of infants with pulmonary complications is the use of ECMO with a modified heart-lung machine. Blood is shunted from a catheter in the right atrium or right internal jugular vein by gravity to a servoregulated roller pump; pumped through a membrane lung and a small heat exchanger; and returned to the systemic circulation via a major artery, such as the carotid artery, to the aortic arch. A venovenous approach (femoral vein) may be used, thus avoiding the need to ligate the carotid artery. ECMO provides oxygen to the circulation and allows the lungs to rest. The goal of ECMO is to “buy time” for the severely injured lung to heal while effectively oxygenating major organ systems, including the brain, heart, kidneys, and lungs (Fig. 10-18).

ECMO is labor intensive and thus expensive. Technical malfunctions may occur, requiring frequent monitoring of the equipment and the patient’s response to treatment. Typically, two nurses, or a nurse and a perfusionist, are required as minimum staffing for the ECMO patient; more staff, including a respiratory therapist, are required in the acute phase. ECMO requires heparinization of the blood and blood circuit; for this reason it is not used in infants at less than 35 weeks of gestation, who are prone to intraventricular hemorrhage. Bleeding is one of the major complications associated with ECMO. Overall the need for ECMO has decreased with increased use of exogenous surfactant, inhaled NO, and HFV for neonatal hypoxemic respiratory failure (Konduri and Kim, 2009).

Nursing Care Management

The nursing care for PPHN is the same as for infants with severe respiratory difficulties and infants supported by mechanical ventilation and cardiovascular support. The infant with PPHN is often the sickest on the unit, depending on the causative factors and reaction to treatment. Because handling for any reason causes a decrease in arterial oxygen concentration, the nurse must weigh the stresses imposed by routine care against the risk of iatrogenic hypoxia. It is important to decrease noxious stimuli that cause hypoxia and to use clustered nursing interventions that keep nonsedated infants calm. Continuous monitoring of oxygenation, temperature, central venous pressure, vital signs, blood pressure, and acid-base balance decreases the need for physical manipulation and disturbance. Infants are further assessed for response to treatments, including IV therapy, fluids, electrolytes, and exogenous glucose.

Pathophysiology

The pathogenesis of BPD is complex and multifactorial. BPD begins with the immature lung that undergoes an initial injury leading to a chronic inflammatory process that results in recurrent injury and abnormal healing (Askin and Diehl-Jones, 2009a). A variety of mechanisms have been related to the initial injury: (1) prenatal infection (inflammatory process before birth), (2) mechanical ventilation (volutrauma, intubation), (3) supplemental oxygen (oxygen-derived free radicals), (4) increased pulmonary blood flow from PDA, or (5) postnatal infection.

The pulmonary changes are characterized by interstitial edema and epithelial swelling followed by thickening and fibrotic proliferation of the alveolar walls and squamous metaplasia of the bronchiolar epithelium. Areas of atelectasis and cystlike foci of hyperaeration are visible on radiographs between 10 and 20 days of life and persist for weeks; however, some infants may not demonstrate cystic foci. In addition, ciliary activity is paralyzed by high oxygen concentrations that interfere with the ability to clear the lung of mucus, thus aggravating airway obstruction and atelectasis. As the infant’s lungs begin healing, the process is altered, possibly by continuous high oxygenation, inadequate nutrition, or vitamin E deficiency, resulting in decreased surface for oxygen and carbon dioxide exchange. The overall results of this process are hypercarbia, hypoxemia, and subsequent inability to wean successfully from oxygen.

As survival of immature preterm infants (<28 weeks of gestation) increases, the occurrence of BPD also increases.

In addition to BPD, other diseases associated with similar radiographic findings include congenital heart disease and viral pneumonia caused by cytomegalovirus. There are no laboratory alterations that confirm a diagnosis; diagnosis is made on the basis of radiographic findings, oxygen therapy or positive pressure ventilation after 28 days, signs of respiratory distress, and a history of requiring mechanical ventilation in the first week of life for more than 3 days.

Therapeutic Management

The first approach to management is prevention of the disorder in susceptible infants. Despite previous theorization that surfactant administration to preterm infants would eradicate BPD, studies so far have failed to show a significant decrease of BPD in infants less than 30 weeks receiving surfactant for prophylaxis or rescue (American Academy of Pediatrics, 2008). To reduce the risk of volutrauma when positive pressure ventilation is being used, maintain the lowest PIP necessary to obtain adequate ventilation, and use the lowest level of inspired oxygen to maintain adequate oxygenation. HFOV has been beneficial in reducing the risk of BPD, as has the administration of vitamin A (Shah, 2003). Fluid administration is carefully controlled and restricted. Drug or surgical intervention is indicated when there is significant shunting of blood through the PDA.

No specific treatment exists for BPD except to maintain adequate arterial blood gases with the administration of oxygen and to avoid progression of the disease. Corticosteroid (dexamethasone) therapy has been shown to benefit infants with BPD by decreasing the pulmonary inflammatory response and improving oxygenation and gas exchange, resulting in earlier weaning from mechanical assistance. However, with complications such as sepsis, hypertension, and hyperglycemia and an overall lack of decreased mortality in such infants, this therapy remains controversial. Other adverse effects of this long-acting, potent glucocorticoid have been reported: growth restriction, GI hemorrhage, and cardiomyopathy. In light of studies that show an increased incidence of periventricular leukomalacia, neuromotor abnormalities, CP, decreased cerebral cortical gray matter volume, and adverse long-term neurologic outcome, the benefits of this treatment may not outweigh the risks (American Academy of Pediatrics and Canadian Paediatric Society, 2002; Halliday, Ehrenkranz, and Doyle, 2009). Ongoing research is being done to determine whether an alternative dosing regimen of postnatal steroids can reduce the incidence of BPD without associated neurodevelopmental side effects (Onland, Offringa, De Jaegere, et al, 2009).

Weaning infants from oxygen is difficult and must be accomplished gradually. These infants do not tolerate excessive or even normal amounts of fluid well and have a tendency to accumulate interstitial fluid in the lungs, which aggravates the condition. Oral diuretics are used to control interstitial fluid. Nebulized or metered dose inhaler bronchodilators (albuterol) and inhaled steroids may be effective and promote improvement in infants with BPD. (See also Asthma, Chapter 32.) Oral electrolyte supplements are given to replace those lost with concurrent oral diuretics and renal water losses.

Growth and development are often delayed in infants with BPD, which is related in part to the difficulties in providing adequate nutrition and in part to the lack of normal sensory stimulation because of prolonged hospitalization. Children with BPD have metabolic needs far greater than those of the average infant. This can create a problem for the caregiver, who must meet the goals of adequate nutrition while avoiding overhydration, especially if the child is ill, eats poorly, or has cardiopulmonary instability. The infant may be further compromised by gastroesophageal reflux, a frequent complication in preterm infants. (See Chapter 33.) Adequate intake of protein is particularly important in preventing postnatal growth failure in LBW infants. Protein supplements may be necessary to ensure adequate intake.

Osteopenia may occur in infants with BPD and in preterm infants, with higher incidence among the infants with BPD, presumably because of low calcium and vitamin D intake secondary to the calciuric effects of diuretic therapy. Dietary supplementation with human milk fortifier, calcium and phosphorus, and vitamin D has reduced the incidence of osteopenia in preterm infants.

RSV prophylaxis with the monoclonal antibody palivizumab (Synagis) is effective in diminishing the complications of RSV. RSV is a common cause for hospitalization and death in growing preterm neonates, including those with BPD. Palivizumab is given intramuscularly to high-risk infants, does not interfere with immunizations, and has few side effects. Palivizumab is administered in a dose of 15 mg/kg once a month, usually beginning in October and ending in May. (See Respiratory Syncytial Virus, Chapter 32.)

Nursing Care Management

Infants with BPD expend considerable energy in their efforts to breathe; therefore it is important that they receive plenty of opportunities for rest and additional calories. Growth records provide clues to the need for change in their diets, and some infants require nutritional supplements. Because these infants tire easily and because large quantities of formula might compromise respiration, small, frequent feedings are better tolerated. Reducing environmental stimuli and subsequent hypoxia is an important aspect in the care of these infants. Close attention to the infant’s behavioral cues is important in the older infant with BPD because these cues may signal carbon dioxide retention.

Adequate hydration is extremely important because a large amount of fluid are lost through respiration, and secretions must be thinned sufficiently to facilitate removal by suctioning. However, because BPD increases lung permeability, many infants are subject to pulmonary edema and require fluid restriction. Nurses must be alert to signs of both overhydration and underhydration, such as changes in weight, electrolytes, output measurements, and urine specific gravity and signs of edema.

Because the growing infant with BPD has a restricted fluid intake, has higher than average caloric requirements, and often requires many oral medications, the nurse is challenged by the complexity of care involved. Infants with BPD may become difficult or maladaptive feeders if they are aware of hunger yet compromised by not being able to eat fast enough to satiate that hunger because of the increased labor of breathing. Individualized nursing care aimed at decreasing oxygenation requirements during feedings, decreasing environmental stimuli, fortifying feedings, and providing more contact with a primary caregiver may facilitate the infant’s care. Feeding schedules should be individualized as much as possible. Oral medications that taste bad to the infant may be given at times separate from feedings to ensure that feeding time is pleasant. Adjustments to overall fluid administration requirements are made, taking into account that the oral medications are also fluids. Regurgitated medications and feedings need to be dealt with in regard to fluid and caloric needs and the amount of absorption of medication that occurs before emesis.

Parents are extremely anxious regarding the prognosis when their infant has BPD. In addition, the lengthy hospitalization interferes with parent-child relationships and deprives the infant of appropriate parental contact and stimulation. Nurses should encourage the parents to visit the infant and become involved in the routine care. The parents need to be informed regarding medical care, equipment, and procedures related to their infant and taught procedures such as suctioning and chest physiotherapy.

The older infant with BPD should have normal nurturing and developmental opportunities appropriate to the infant’s condition and abilities. Careful monitoring of physiologic and behavioral systems during any activity is necessary so that activity can be stopped before the infant becomes irritable or tired. Opportunities out of bed in an infant seat or on a floor mat with a nurse or physical or play therapist provide one-on-one interaction that can enhance the infant’s experience of the world and people.

Irritability has been associated with infants who have BPD, making their care often challenging and frustrating (see Developmental Outcome, p. 332). Some strategies to facilitate infant coping during prolonged hospitalization include (1) decreased number of unfamiliar caregivers, (2) increased access to parents, (3) predictability in schedule and caregivers, (4) consistency of care routines and practices, (5) pleasurable opportunities for play and socialization within physical tolerance, (6) adequate nutrition, and (7) uninterrupted rest cycles with diurnal variation to facilitate biologic rhythms. Parental involvement is critical because they are the one constant for the infant.

Sepsis

Sepsis, or septicemia, refers to a generalized bacterial infection in the bloodstream. Neonates are highly susceptible to infection as a result of diminished nonspecific (inflammatory) and specific (humoral) immunity, such as impaired phagocytosis, delayed chemotactic response, minimum or absent IgA and immunoglobulin M (IgM), and decreased complement levels. Because of the infant’s poor response to pathogenic agents, there is usually no local inflammatory reaction 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.

Although the mortality from sepsis has diminished, the incidence has not. Nursery epidemics are not infrequent, and the high-risk infant has a four times greater chance of developing septicemia than does the normal neonate. The frequency of infection is almost twice as great in male infants as in females and also carries a higher mortality for males. Other factors increasing the risk of infection are prematurity, congenital anomalies or acquired injuries that disrupt the skin or mucous membranes, invasive procedures such as placement of IV lines and ET tubes, administration of total parenteral nutrition, and nosocomial exposure to a number of pathogens in the NICU. Thorough hand washing is the single most important infection control measure in the NICU. Proper handling of formula and supplies such as syringes and gavage tubes is also vital to prevent infection.

Breast-feeding has a protective effect against infection and should be promoted for all newborns. It is of particular benefit to the high-risk neonate. Colostrum contains agglutinins that are effective against gram-negative bacteria. Human milk contains large quantities of IgA and iron-binding protein that exert a bacteriostatic effect on Escherichia coli. Human milk also contains macrophages and lymphocytes that promote a local inflammatory reaction.

Necrotizing Enterocolitis

NEC is an acute inflammatory disease of the bowel with increased incidence in preterm and other high-risk infants; it is most common in preterm infants. Because the signs are similar to those observed in many other disorders of the newborn, nurses must constantly be aware of the possibility of this disease.

Patent Ductus Arteriosus

PDA is a common complication of severe respiratory disease in preterm infants. It occurs in the majority of preterm infants under 1200 g (2.6 lb), and the incidence diminishes in direct relationship to increasing birth weight. During fetal life the ductus remains patent through the vasodilatory action of prostaglandin, which is produced by the placenta and circulated to the fetus. Postnatally the increase in oxygen tension has a constricting effect on the ductus, but it may reopen in preterm infants in response to the lowered oxygen tension associated with respiratory impairment.

Lack of ductal smooth muscle in preterm infants also prolongs patency of the ductus arteriosus. Functional closure occurs usually within 3 to 4 days, but complete anatomic closure with fibrosis and permanent sealing of the lumen may take up to 2 to 3 weeks.

Anemia

Preterm infants tend to develop anemia that is more severe and appears earlier than in more mature infants. It may be a result of hemorrhage during pregnancy or labor and delivery (loss of placental integrity, anomalies of the umbilical cord, fetomaternal hemorrhage), hemorrhage during the neonatal period (ICH, visceral trauma), or blood disorders (hemolytic disease, thrombocytopenia). Anemia may also be iatrogenic from blood withdrawn in the NICU for laboratory tests. Physiologic characteristics of prematurity tend to contribute to the development of anemia (i.e., a decreased red blood cell mass at birth, a drop in the production of hemoglobin, and shortened survival time of red blood cells). This lag in hematopoiesis during continued growth results in physiologic anemia, probably as a consequence of diminished erythropoietin values.

Fortunately, even VLBW infants are able to accommodate the GI absorption of iron required for their high needs. Iron is supplied in iron-fortified formulas or iron supplements as both a preventive and therapeutic measure. Transfusions with packed red blood cells are often required for severe anemia, usually for replacement of blood loss from iatrogenic measures. At 4 to 12 weeks of age, “physiologic anemia” reaches a peak, at which time infants sometimes display signs that suggest true anemia.

Polycythemia

The current definition of polycythemia is a venous hematocrit of 65% or more (Sarkar and Rosenkrantz, 2008). With a hematocrit above 65%, blood flow becomes increasingly sluggish and hyperviscous, resulting in hypoperfusion of organs. Polycythemia may result from in utero twin-to-twin transfusion and maternal-fetal transfusion, delayed cord clamping or stripping of the umbilical cord, maternal diabetes, or intrapartum asphyxia. The small-for-gestational-age infant is the most at risk for polycythemia; increased red blood cell consumption of glucose further predisposes the infant to hypoglycemia. Infants with polycythemia have a high incidence of cardiopulmonary distress symptoms (PPHN, cyanosis, and apnea), seizures, hyperbilirubinemia, and GI abnormalities.

Appropriate therapy for correcting metabolic disturbances (e.g., hypoxia, hypoglycemia, and hyperbilirubinemia) is implemented. Lowering blood viscosity by partial plasma exchange transfusion may be considered in symptomatic cases.

Retinopathy of Prematurity

Although often discussed in relation to respiratory dysfunction, retinopathy of prematurity (ROP) is a disorder involving immature retinal vasculature. Formerly known as retrolental fibroplasia, ROP is a term used to describe retinal changes observed in preterm infants. The incidence and severity of the disease correlates with the degree of the infant’s maturity—the younger the gestational age, the greater the likelihood of the development of ROP, with extremely preterm infants being the group most at risk. However, cases have been documented of ROP in full-term infants who received no oxygen therapy (Korones, 2003).

In addition to immaturity, numerous factors have been implicated in the etiology of ROP, including hyperoxemia and hypoxemia, hypercarbia and hypocarbia, PDA, apnea, intralipid administration, IVH, infection, vitamin E and A deficiency, prenatal infection, exposure to light, and genetic factors (Askin and Diehl-Jones, 2009b). Previously considered an iatrogenic disease related to hyperoxia, ROP is now believed to be a complex disease of prematurity with multiple causes and therefore difficult to completely prevent.

Perinatal Hypoxic-Ischemic Brain Injury

Hypoxic-ischemic brain injury, or hypoxic-ischemic reperfusion injury, is the most common cause of neurologic impairment observed in term and preterm infants. The brain damage usually results from asphyxia before, during, or after delivery. Ischemia and hypoxemia may occur simultaneously, or one may precede the other. The fetal brain is somewhat protected against mild hypoxic events but may be damaged when there is a decrease in cerebral blood flow, systemic blood pressure, and oxygen and nutrients such as glucose. Subsequent reperfusion after the event may further result in bleeding of the fragile capillaries and tissue ischemia.

Hypoxic-ischemic encephalopathy (HIE) is the resultant cellular damage from hypoxic-ischemic injury that causes the clinical manifestations observed in each case. Such clinical manifestations are variable and may be mild, moderate, or severe. In some infants little or no residual damage may be observed. In general, hypoxia that is severe enough to cause HIE will also damage other organs such as the liver, kidneys, myocardium, and GI tract (Verklan, 2009; Hankins, Koen, Gei, et al, 2002). In the preterm infant HIE may occur in conjunction with IVH. As a consequence of prematurity and general organ and system immaturity, the preterm infant may also suffer hypoxic-ischemic brain damage in the neonatal period as a result of altered cerebral blood flow, systemic hypotension, and decreased cellular nutrients (blood glucose and oxygen).

The site of the hypoxic-ischemic injury varies according to the infant’s gestational age. In the full-term infant the primary ischemic damage is parasagittal cerebral injury with cortical necrosis (deeper region of the brain). In the preterm infant the primary ischemic lesion is in the white matter near the ventricles, or periventricular, with resultant periventricular leukomalacia (Volpe, 2008).

Intraventricular Hemorrhage

Germinal matrix–intraventricular hemorrhage is known by a variety of terms according to the locus of bleeding: intraventricular hemorrhage, periventricular hemorrhage, and subependymal-intraventricular hemorrhage. Most authorities use the term intraventricular hemorrhage (IVH) to describe this disorder, which is responsible for a significant percentage of seriously ill infants and neonatal mortality. The incidence of IVH ranges from 20% to 25% of VLBW infants (McCrea and Ment, 2008). IVH is extremely common in preterm infants, especially ELBW and VLBW infants less than 32 weeks of gestation; the degree of neonatal immaturity correlates with the incidence of hemorrhage, and subsequent neurologic handicap is not uncommon.

Intracranial Hemorrhage

ICH in neonates, although manifested in the same ways as those described in older children, occurs with different frequencies and different degrees of severity.

Neonatal/Perinatal Stroke

Neonatal stroke is reported to occur in 1 in 4000 live term births (Nelson and Lynch, 2004). Neonatal stroke has been defined to encompass all ischemic and hemorrhagic events that affect the venous and arterial distribution of blood supply from early gestation to the first 28 days of life (Golomb, Cvijanovich, and Ferriero, 2006). Perinatal stroke refers to strokes that occur between 28 weeks of gestation and the first 7 days of life, primarily as a result of altered arterial blood flow and ischemia (Nelson and Lynch, 2004). Fetal stroke may occur as early as 8 weeks’ gestation (Kirton and deVeber, 2009).

Neonatal stroke is the second leading cause of seizures in term neonates and may be caused by arterial, thrombotic, or ischemic events that result in altered brain blood flow and infarction. Neonatal stroke is more predominant in males, and there is an increased tendency toward left-sided involvement. Known risk factors for neonatal and perinatal stroke include the presence of maternal and/or fetal factor V Leiden, antiphospholipid, and prothrombin factors (Curry, Bhullar, Holmes, et al, 2007; Simchen, Goldstein, Lubetsky, et al, 2009). Cerebral palsy, motor deficits, epilepsy, and language deficits, and visual deficits may occur as a result of neonatal stroke (Kirton and deVeber, 2009).

Diagnosis with MRI and venography is most accurate because head ultrasonography may be negative with an ischemic event; the electroencephalogram may be normal (Golomb, Cvijanovich, and Ferriero, 2006).

Because neonatal stroke can only be diagnosed retrospectively, it is important for the nurse to be vigilant for apnea or seizure activity in the first year of life, the time when clinical manifestations will appear.

Neonatal Seizures

Seizures in the neonatal period are usually the clinical manifestation of a serious underlying disease. The most common cause of seizures in the neonatal period (for term and preterm infants) is HIE secondary to perinatal asphyxia (Volpe, 2008). Although not life threatening as an isolated entity, seizures constitute a medical emergency because they signal a disease process that may produce irreversible brain damage. Consequently, it is imperative to recognize a seizure and its significance so that the cause, as well as the seizure, can be treated (Box 10-11).

Infants of Diabetic Mothers

Before insulin therapy, few women with diabetes were able to conceive; for those who did, the mortality rate for both mother and infant was high. The morbidity and mortality of infants of diabetic mothers (IDMs) have been significantly reduced as a result of effective control of maternal diabetes and an increased understanding of fetal disorders. However, the offspring of diabetic mothers are at risk for a large number of congenital anomalies. Central nervous system anomalies such as anencephaly, spina bifida, and holoprosencephaly occur at rates 10 times higher than any other population of mothers (Gabbe, Niebyl, and Simpson, 2007). Cardiac anomalies such as ventriculoseptal defects are increased fivefold in IDMs, and sacral agenesis and caudal regression occur almost exclusively in IDMs (Gabbe, Niebyl, and Simpson, 2007). Because infants born to women with gestational diabetes mellitus are at risk for many of the same complications as IDMs, the following discussion includes both types of infants.

Critical Thinking Exercise—Infant of a Diabetic Mother

The severity of the maternal diabetes affects infant survival. Several factors determine the severity: duration of the disease before pregnancy; age of onset; extent of vascular complications; and abnormalities of the current pregnancy such as pyelonephritis, diabetic ketoacidosis, pregnancy-induced hypertension, and noncompliance. The single most important factor influencing fetal well-being is the mother’s normoglycemic status. Reasonable metabolic control that begins before conception and continues during the first weeks of pregnancy can prevent malformation in an IDM. Elevated levels of hemoglobin A_1c during the first trimester appear to be associated with a higher incidence of congenital malformations.

Drug-Exposed Infants*

Maternal Infections

The range of pathologic conditions produced by infectious agents is large, and the difference between the maternal and fetal effects caused by any one agent is also great. Some maternal infections, especially during early gestation, can result in fetal loss or malformations because the fetus’s ability to handle infectious organisms is limited and the fetal immunologic system is unable to prevent the dissemination of infectious organisms to the various tissues.

Not all prenatal infections produce teratogenic effects. Furthermore, the clinical picture of disorders caused by transplacental transfer of infectious agents is not always well defined. Some microbial agents can cause remarkably similar manifestations, and it is not uncommon to test for all when a prenatal infection is suspected. This is the so-called TORCHS complex, an acronym for:

To determine the causative agent in a symptomatic infant, perform tests to rule out each of these infections. The O category may involve testing for several viral infections (e.g., hepatitis B, varicella zoster, measles, mumps, HIV, human papillomavirus, and human parvovirus). Although this acronym has received substantial criticism because it does not cover the entire spectrum of congenital infections (Klein, Baker, Remington, et al, 2006), it is still used in clinical settings. Bacterial infections are not included in the TORCHS workup, since they are usually identified by clinical manifestations and readily available laboratory tests. Gonococcal conjunctivitis (ophthalmia neonatorum) and chlamydial conjunctivitis have been significantly reduced by prophylactic measures at birth. (See Chapter 8.) HIV infection is discussed in Chapter 35. The major maternal infections, their possible effects, and specific nursing considerations are outlined in Table 10-11.

Key Points

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