Transient Tachypnea of the Newborn
Transient Tachypnea of the Newborn
Transient tachypnea of the newborn (TTN) is a self-limiting condition involving a mild degree of respiratory distress. TTN is the result of a delay in clearance of fetal lung liquid leading to transient pulmonary edema. In the past, respiratory distress was thought to be a problem of relative surfactant deficiency, but it is now characterized by an airspace-fluid burden secondary to the inability to absorb fetal lung liquid. It usually occurs within a few hours of birth and resolves over a 48- to 72-hour period. It occurs in approximately 1% of live term births, and its incidence is higher in males than females (Jha & Makker, 2020).
Pathophysiology
Most newborns make the transition from fetal to newborn life without incident. During fetal life, the lungs are filled with a serous fluid because the placenta, not the lungs, is used for nutrient and gas exchange. During and after birth, this fluid must be removed and replaced with air. An infant born by cesarean birth is at risk of having excessive pulmonary fluid as a result of not having experienced all of the stages of labor. Passage through the birth canal during a vaginal birth compresses the thorax, which helps remove the majority of this fluid. Surgical births bypass the lessening of lung fluid for the newborn, causing an increased risk of TTN. Pulmonary circulation and lymphatic drainage remove the remaining fluid shortly after birth. TTN occurs when the liquid in the lung is removed slowly or incompletely. The excess lung fluid results in decreased pulmonary compliance. Tachypnea develops to compensate for the increased workload of breathing associated with reduced compliance.
Nursing Assessment
Astutely observe the newborn with respiratory distress because TTN is a diagnosis of exclusion. Initially, it might be difficult to distinguish this condition from RDS or group B streptococcal pneumonia, because the clinical picture is similar. However, the symptoms of TTN rarely last more than 72 hours. If symptoms progress beyond 72 hours, further investigation into another cause should be considered (Martin & Rosenfeld, 2019).
HEALTH HISTORY AND PHYSICAL EXAMINATION
Review the perinatal history for contributing factors. TTN is commonly seen in newborns whose mothers have been heavily sedated in labor or have gestational diabetes or newborns who have been born via cesarean birth without labor. Also check the history for evidence of a prolonged labor, fetal macrosomia, inadequate initial resuscitation, breech births, rapid labor and birth, infants experiencing hypothermia, infants born before 38 weeks’ gestation, and maternal asthma and smoking. These factors are associated with a higher incidence of TTN.
Closely assess the newborn for signs of TTN. Within the first few hours of birth, observe for tachypnea, expiratory grunting, mild intercostal retractions, decreased breath sounds due to reduced air entry, labored breathing, nasal flaring, crackles on auscultation, and mild cyanosis. Mild to moderate respiratory distress is present by 6 hours of age with respiratory rates as high as 100 to 140 breaths per minute (Fanaroff & Fanaroff, 2019). Also inspect the newborn’s chest for hyperextension or a barrel shape. Auscultate breath sounds, which may be slightly diminished secondary to reduced air entry.
LABORATORY AND DIAGNOSTIC TESTING
To aid in the diagnosis, a chest x-ray or lung ultrasound may be done. These usually reveal mild symmetric lung hyperaeration and prominent perihilar interstitial markings and streaking. These findings correlate with lymphatic engorgement of retained fetal fluid. In addition, an arterial blood gas (ABG) assessment is important to ascertain the degree of gas exchange and acid–base balance. It typically demonstrates mild hypoxemia, mildly elevated CO2 level, and a normal pH (Kenner et al., 2019).
Nursing Management
Management of TTN is supportive. As the retained lung fluid is absorbed by the infant’s lymphatic system, the pulmonary status improves. Nursing management focuses on providing adequate oxygenation and determining whether the newborn’s respiratory manifestations appear to be resolving or persisting. Provide supportive care while the retained lung fluid is reabsorbed. Administer intravenous (IV) fluids and/or gavage feedings until the respiratory rate decreases enough to allow safe oral feeding. Withhold oral feedings until the respiratory status has improved. Provide supplemental oxygen via a nasal cannula or oxygen hood to maintain adequate oxygen saturation. Maintain a neutral thermal environment with minimal stimulation to minimize oxygen demand.
Provide ongoing assessment of the newborn’s respiratory status. As TTN resolves, the newborn’s respiratory rate declines to 60 breaths per minute or less; cyanosis, nasal flaring, and grunting sounds resolve; the oxygen requirement decreases; the ABG values return to the normal range; bilateral breath sounds demonstrate good air entry; and the chest x-ray shows resolution of the perihilar streaking. Provide reassurance and progress reports to the parents to help them cope with this crisis.
Respiratory Distress Syndrome
Despite many medical advancements, newborns are still at risk for a deadly condition that robs them of their first breaths, respiratory distress syndrome (RDS). RDS is caused by a developmental deficiency in surfactant synthesis accompanied by lung immaturity and hypoperfusion. Surfactant keeps the air sacs in the lungs from collapsing and allows them to inflate easily. Without surfactant, the alveoli collapse at the end of expiration. RDS is characterized by compromised lung expansion, poor gas exchange, hypoperfusion, and ventilatory failure. Since the link between RDS and surfactant deficiency was discovered more than 30 years ago, tremendous strides have been made in understanding the pathophysiology and treatment of this disorder. The introduction of prenatal steroids to accelerate lung maturity and the development of synthetic surfactant can be credited with the dramatic improvements in the outcomes of newborns with RDS.
RDS affects up to 25,000 infants born alive in the United States annually. The incidence declines with degree of maturity at birth. It occurs in 50% of preterm newborns of less than 28 weeks’ gestation, 30% of those born at 28 to 34 weeks, and less than 5% of those born after 34 weeks (Pramanik, 2020). Intensive respiratory care, usually with continuous positive airway pressure (CPAP) or another noninvasive respiratory support, may be necessary.
Pathophysiology
Lung immaturity and surfactant deficiency contribute to the development of RDS. Surfactant is a complex mixture of phospholipids and proteins that adheres to the alveolar surface of the lungs. Anatomically, the immature lung cannot support oxygenation and ventilation because the alveolar sacs are insufficiently developed, causing a deficient surface area for gas exchange. Physiologically, the amount of surfactant is insufficient to prevent collapse of unstable alveoli. Surfactant forms a coating over the inner surface of the alveoli, reducing the surface tension and preventing alveolar collapse at the end of expiration. In the affected newborn, surfactant is deficient or lacking, and this deficit results in stiff lungs and alveoli that tend to collapse, leading to diffuse atelectasis (Fig. 24.2).
The work of breathing is increased because increased pressure similar to that required to initiate the first breath is needed to inflate the lungs with each successive breath. Hypoxemia and acidemia result, leading to vasoconstriction of the pulmonary vasculature. Right-to-left shunting occurs, and alveolar capillary circulation is limited, further inhibiting surfactant production. As the disease progresses, fluid and fibrin leak from the pulmonary capillaries, causing hyaline membranes to form in the bronchioles, alveolar ducts, and alveoli. Hyaline membranes produce a glassy appearance in the lung membranes, apparent on x-rays. These membranes further decrease gas exchange. These factors decrease the total surface area of the gas exchange membrane. The end result is hypoxemia, acidemia, and worsening respiratory distress. A vicious cycle is created, compounding the problem (Dyer, 2019).
Nursing Assessment
Nursing assessment focuses on keen observation to identify the signs and symptoms of respiratory distress. In addition, assessment aids in differentiating RDS from other respiratory conditions, such as TTN or group B streptococcal pneumonia.
HEALTH HISTORY AND PHYSICAL EXAMINATION
Review the history for risk factors associated with RDS. These include preterm birth, perinatal asphyxia regardless of gestational age, neonatal sepsis, previous birth of an infant with RDS, cesarean birth in the absence of preceding labor (due to the lack of thoracic squeezing), male gender, perinatal asphyxia, cold stress, and maternal diabetes (produces high levels of insulin which inhibit surfactant production). It is believed that each of these conditions has an impact on surfactant production, thus resulting in RDS in the full-term infant (Martin et al., 2019).
TAKE NOTE!
Prolonged rupture of membranes, fetal growth restriction, gestational hypertension, maternal heroin addiction, and use of prenatal corticosteroids reduce the newborn’s risk for RDS because of the physiologic stress imposed on the fetus. Chronic stress experienced by the fetus in utero accelerates the production of surfactant before the 35th week of gestation and thus reduces the incidence of RDS at birth.
The newborn with RDS usually demonstrates signs at birth or within a few hours of birth. Observe the infant for expiratory grunting, shallow breathing, nasal flaring, chest wall retractions (Fig. 24.3), see-saw respirations, and generalized cyanosis. Auscultate the heart and lungs, noting tachycardia (rates above 150 to 180 bpm), fine inspiratory crackles, and tachypnea (rates above 60 breaths per minute). Use the Silverman–Anderson index assessment tool to determine the degree of respiratory distress. The index involves observation of five features, each of which is scored as 0, 1, or 2 (Fig. 24.4). The higher the score, the greater the respiratory distress. A score over 7 suggests severe respiratory distress.
LABORATORY AND DIAGNOSTIC TESTING
The diagnosis of RDS is based on the clinical picture, a lung ultrasound or x-ray, and ABGs that show hypoxemia and acidosis. A chest x-ray reveals hypoaeration, underexpansion, and a “ground glass” pattern. Other lab tests are done to rule out infection and sepsis as a cause of the respiratory distress (Chowdhury et al., 2019).
Nursing Management
If untreated, RDS will worsen. However, it can be a self-limiting disease, with respiratory symptoms declining after 72 hours. This decline parallels the production of surfactant in the alveoli (Halim et al., 2019). The newborn needs supportive care until surfactant is produced. Several therapies for established RDS include conventional mechanical ventilation, which is avoided if possible; CPAP or positive end-expiratory pressure (PEEP) to prevent volume loss during expiration; and surfactant therapy. The use of exogenous surfactant replacement therapy to stabilize the newborn’s lungs until postnatal surfactant synthesis matures has become a standard of care but is not necessarily evidence-based. Knowledge of the surfactant proteins and lipids produced by the epithelial II cells was critical in the development of surfactant replacement preparations used to treat RDS, which enabled widespread use of these preparations used to prevent and treat RDS. This preparation has dramatically improved morbidity and mortality in preterm infants (Hussain & Marks, 2019; Norwitz et al., 2019).
Despite recent advances in the perinatal management of neonatal RDS, controversies still exist. Strong evidence exists for the role of a single course of prenatal steroids in RDS prevention, but the potential benefit and long-term safety of repeated courses are unclear. A Cochrane review concluded that the incidence of RDS was reduced in infants born before 48 hours and between 1 and 7 days of treatment of mothers with antenatal corticosteroids, but not those born before 24 hours of administration (Sotiriadis et al., 2018). Many practices involved in preterm neonatal stabilization at birth are not evidence-based, including oxygen administration and positive-pressure lung inflation, and they may at times be harmful. Surfactant replacement therapy is crucial in the management of RDS, but the best preparation, optimal dose, and timing of administration at different gestations are not always clear. Respiratory support in the form of mechanical ventilation may also be lifesaving, but it can also cause lung injury, and protocols should be directed at avoiding mechanical ventilation whenever possible by using nasal CPAP or nasal ventilation. For newborns with RDS to experience the best outcomes, it is essential that they have optimal supportive care, including maintenance of a normal body temperature, proper fluid management, good nutritional support, and support of the circulation to maintain adequate tissue perfusion (Resnik et al., 2019).
As recommended, care of the newborn with RDS is primarily supportive and requires a multidisciplinary approach to obtain the best outcomes. Therapy focuses on improving oxygenation and maintaining optimal lung volumes. Expect to transfer the newborn to the neonatal intensive care unit (NICU) soon after birth. Apply the basic principles of newborn care, such as thermoregulation, cardiovascular and nutritional support, normal glucose level maintenance, and infection prevention, to achieve the therapeutic goals of reducing mortality and minimizing lung trauma.
Anticipate the administration of surfactant replacement therapy, prophylactically or as a rescue approach. With prophylactic administration, surfactant is given soon after birth, thus providing replacement surfactant before severe RDS develops. Rescue treatment is indicated for newborns with established RDS who require noninvasive respiratory support and supplemental oxygen. It is typically given within 2 hours after birth and repeated again at 4 hours. The earlier the surfactant is administered, the better the effect on gas exchange. Following surfactant administration, the newborn must be closely monitored, and preparation for reduced need for oxygenation and respiratory support must be anticipated (Martin, 2020).
Administer the prescribed oxygen, nitrous oxide, or room air concentration via nasal cannula. Anticipate the need for ventilator therapy, which has greatly improved in the past several years, with significant advances in conventional and high-frequency ventilation therapies (Fig. 24.5). Recent studies show no difference in outcomes for newborns who received early treatment with high-frequency oscillatory ventilation compared with those receiving conventional mechanical ventilation. They are both equally effective in prevention of bronchopulmonary dysplasia (BPD) without being associated with increased mortality or brain damage (Martin, 2020). Although mechanical ventilation has increased survival rates, it is also a contributing factor to BPD, pulmonary hypertension, and ROP (Cunningham et al., 2018).
In addition, support the newborn with RDS using the following interventions:
Continuously monitor the infant’s cardiopulmonary status via invasive or noninvasive means (e.g., arterial lines or auscultation, respectively).
Monitor oxygen saturation levels continuously; assess pulse oximeter values to determine oxygen saturation levels.
Closely monitor vital signs, acid–base status, and ABGs.
Administer broad-spectrum antibiotics if blood cultures are positive.
Provide fluids and vasopressor agents as needed to prevent or treat hypotension.
Test blood glucose levels and administer dextrose as ordered for prevention or treatment of hypoglycemia.
Cluster caregiving activities to avoid overtaxing and compromising the newborn.
Place the newborn in the prone position to optimize respiratory status and reduce stress.
Perform gentle suctioning to remove secretions if present to maintain a patent airway.
Assess level of consciousness to identify intraventricular hemorrhage.
Monitor x-ray studies to detect atelectasis or air leak.
Provide a neutral thermal environment to reduce metabolic and oxygen demands.
Provide sufficient calories via gavage and IV feedings.
Maintain adequate hydration and assess for signs of fluid overload.
Provide information to the parents about treatment modalities; give thorough but simple explanations about the rationales for interventions and provide support.
Encourage the parents to participate in care
Despite recent advances in the perinatal management of neonatal RDS, controversies still exist. Strong evidence exists for the role of a single course of prenatal steroids in RDS prevention, but the potential benefit and long-term safety of repeated courses are unclear. A Cochrane review concluded that the incidence of RDS was reduced in infants born before 48 hours and between 1 and 7 days of treatment of mothers with antenatal corticosteroids, but not those born before 24 hours of administration (Sotiriadis et al., 2018). Many practices involved in preterm neonatal stabilization at birth are not evidence-based, including oxygen administration and positive-pressure lung inflation, and they may at times be harmful. Surfactant replacement therapy is crucial in the management of RDS, but the best preparation, optimal dose, and timing of administration at different gestations are not always clear. Respiratory support in the form of mechanical ventilation may also be lifesaving, but it can also cause lung injury, and protocols should be directed at avoiding mechanical ventilation whenever possible by using nasal CPAP or nasal ventilation. For newborns with RDS to experience the best outcomes, it is essential that they have optimal supportive care, including maintenance of a normal body temperature, proper fluid management, good nutritional support, and support of the circulation to maintain adequate tissue perfusion (Resnik et al., 2019).
As recommended, care of the newborn with RDS is primarily supportive and requires a multidisciplinary approach to obtain the best outcomes. Therapy focuses on improving oxygenation and maintaining optimal lung volumes. Expect to transfer the newborn to the neonatal intensive care unit (NICU) soon after birth. Apply the basic principles of newborn care, such as thermoregulation, cardiovascular and nutritional support, normal glucose level maintenance, and infection prevention, to achieve the therapeutic goals of reducing mortality and minimizing lung trauma.
Anticipate the administration of surfactant replacement therapy, prophylactically or as a rescue approach. With prophylactic administration, surfactant is given soon after birth, thus providing replacement surfactant before severe RDS develops. Rescue treatment is indicated for newborns with established RDS who require noninvasive respiratory support and supplemental oxygen. It is typically given within 2 hours after birth and repeated again at 4 hours. The earlier the surfactant is administered, the better the effect on gas exchange. Following surfactant administration, the newborn must be closely monitored, and preparation for reduced need for oxygenation and respiratory support must be anticipated (Martin, 2020).
Administer the prescribed oxygen, nitrous oxide, or room air concentration via nasal cannula. Anticipate the need for ventilator therapy, which has greatly improved in the past several years, with significant advances in conventional and high-frequency ventilation therapies (Fig. 24.5). Recent studies show no difference in outcomes for newborns who received early treatment with high-frequency oscillatory ventilation compared with those receiving conventional mechanical ventilation. They are both equally effective in prevention of bronchopulmonary dysplasia (BPD) without being associated with increased mortality or brain damage (Martin, 2020). Although mechanical ventilation has increased survival rates, it is also a contributing factor to BPD, pulmonary hypertension, and ROP (Cunningham et al., 2018).
In addition, support the newborn with RDS using the following interventions:
Continuously monitor the infant’s cardiopulmonary status via invasive or noninvasive means (e.g., arterial lines or auscultation, respectively).
Monitor oxygen saturation levels continuously; assess pulse oximeter values to determine oxygen saturation levels.
Closely monitor vital signs, acid–base status, and ABGs.
Administer broad-spectrum antibiotics if blood cultures are positive.
Provide fluids and vasopressor agents as needed to prevent or treat hypotension.
Test blood glucose levels and administer dextrose as ordered for prevention or treatment of hypoglycemia.
Cluster caregiving activities to avoid overtaxing and compromising the newborn.
Place the newborn in the prone position to optimize respiratory status and reduce stress.
Perform gentle suctioning to remove secretions if present to maintain a patent airway.
Assess level of consciousness to identify intraventricular hemorrhage.
Monitor x-ray studies to detect atelectasis or air leak.
Provide a neutral thermal environment to reduce metabolic and oxygen demands.
Provide sufficient calories via gavage and IV feedings.
Maintain adequate hydration and assess for signs of fluid overload.
Provide information to the parents about treatment modalities; give thorough but simple explanations about the rationales for interventions and provide support.
Encourage the parents to participate in care