Continuing Education Activity

Respiratory distress syndrome (RDS) represents a major cause of neonatal morbidity and mortality, primarily affecting premature infants due to surfactant deficiency and lung immaturity. The disorder results in alveolar collapse, reduced lung compliance, hypoxemia, and progressive respiratory failure shortly after birth. This course reviews the clinical features of RDS, including tachypnea, grunting, nasal flaring, retractions, cyanosis, and decreased air entry, and its diagnosis, which is supported by blood gas abnormalities and characteristic imaging findings.

This activity outlines the evidence-based pathophysiology, risk assessment, interpretation of imaging and blood gases, selection of respiratory support modalities, and surfactant administration strategies. Participants will also gain an understanding of the advances in fetal lung development, surfactant biology, genetics, and inflammatory mechanisms that have refined both preventive and therapeutic strategies, as well as current management that emphasizes antenatal corticosteroids, early noninvasive respiratory support, timely surfactant replacement, careful ventilation strategies, and comprehensive supportive care delivered through an interprofessional neonatal team. This activity for healthcare professionals is designed to enhance the learner's competence in identifying RDS, performing the recommended evaluation, identifying complications, and implementing an appropriate interprofessional approach when managing this condition to improve long-term outcomes for vulnerable preterm infants.

Objectives:

• Identify the pathophysiologic mechanisms that contribute to neonatal respiratory distress syndrome.
• Assess clinical findings to determine the disease severity in a patient with neonatal respiratory distress syndrome.
• Implement the management strategies of neonatal respiratory distress syndrome based on clinical factors.
• Collaborate with interprofessional team members to improve care coordination and outcomes in patients with neonatal respiratory distress syndrome.

Introduction

Respiratory distress syndrome (RDS) represents a common and serious condition among premature infants and arises from insufficient surfactant production that impairs lung function. The disorder remains a leading cause of neonatal morbidity and mortality worldwide, with the highest burden observed in infants born before 34 weeks of gestation. Surfactant deficiency promotes alveolar collapse, which reduces lung compliance and leads to hypoxemia and progressive respiratory failure.

Affected neonates typically develop signs of respiratory distress shortly after birth, including tachypnea, expiratory grunting, nasal flaring, and cyanosis. Early diagnosis depends on careful clinical evaluation, supported by characteristic radiographic findings and blood gas abnormalities. Management emphasizes surfactant replacement therapy and respiratory support, most commonly with continuous positive airway pressure, while mechanical ventilation serves as a rescue strategy for severe disease. Preventive interventions, particularly antenatal corticosteroid administration for mothers at risk of preterm delivery, have markedly reduced both incidence and severity. Optimal outcomes depend on coordinated interprofessional care involving neonatologists, nurses, respiratory therapists, and other healthcare professionals, along with a thorough understanding of RDS etiology, clinical presentation, and evidence-based treatment strategies to improve survival and limit complications in this vulnerable population.

Etiology

Neonatal RDS results from surfactant deficiency, either from inadequate production or functional inactivation in immature lungs. Prematurity influences both mechanisms and directly contributes to disease development.

Fetal Lung Development

A clear understanding of fetal lung development and surfactant production provides essential insight into the etiology of RDS. Fetal lung development progresses through embryonic, pseudoglandular, canalicular, saccular, and alveolar stages.[1]

During the embryonic period, the lung bud appears at 26 days as a ventral outpouching of the fetal esophagus.[2] Progressive penetration and division of the lung bud within the surrounding mesenchyme lead to the formation of the mainstem bronchi by 37 days, followed by branching into subsegmental bronchi by 48 days. Pulmonary vasculature develops concurrently, with the pulmonary artery arising from the sixth aortic arch by 37 days. The pseudoglandular stage begins near the fifth week of gestation and extends to the 16th week. Neuroepithelial cells, cartilage, ciliated cells, goblet cells, and basal cells form within the proximal pulmonary epithelium during this stage, while airway branching occurs 15 to 20 times by the 18th week of gestation.[2]

The canalicular stage spans from the 16th to approximately the 25th week and marks the development of the pulmonary acinus, the establishment of a blood–air barrier, and the initiation of surfactant production by type 2 cells, resulting in lungs capable of limited gas exchange. Capillary proliferation and bronchiolar growth progressively thin the mesenchyme, allowing fusion of capillary and respiratory epithelial basement membranes into a primitive blood–air barrier.[3] Lamellar bodies appear at 20 weeks within glycogen-rich cuboidal epithelial cells of the bronchioles, which subsequently differentiate into surfactant-producing type 2 cells.

The saccular stage occurs from approximately the 24th to the 32nd week of gestation and involves the formation of terminal saccules and respiratory bronchioles with walls thick enough for gas exchange, supporting potential extrauterine viability in the setting of prematurity.[3] The alveolar stage begins at 32 weeks, characterized by the septation of the respiratory bronchioles and the formation of alveoli, which increase the gas-exchange surface area. By term age, the lungs contain approximately 50 to 150 million alveoli.

Surfactant

Pulmonary surfactant lines the inner surface of mature alveoli. During fetal development, alveoli remain filled with fetal lung fluid and do not participate in gas exchange. Surfactant production begins around 20 weeks of gestation within alveolar type 2 cells. The surfactant complex consists primarily of lipids, including 70% to 80% phospholipids, along with 10% protein and 10% neutral lipids. Four surfactant-associated proteins comprise the complex: SP-A, SP-B, SP-C, and SP-D. SP-A and SP-D regulate pulmonary inflammatory responses, SP-B supports lamellar body formation and SP-C processing, and SP-C works with SP-B to enhance surfactant deposition and function by reducing surface tension.[4][5][6]

Surfactant synthesis begins with phospholipid production in the endoplasmic reticulum of type 2 cells, followed by transfer through the Golgi apparatus into lamellar bodies. The surfactant lipoprotein complex assembles within lamellar bodies at the apical surface of type 2 cells and enters the alveoli through exocytosis. Elastic recoil of the chest wall and lung parenchyma, combined with surface tension at air–fluid interfaces, generates forces within the lung.

The surfactant-lipoprotein complex lowers surface tension in small airways and alveoli, preventing alveolar collapse and limiting interstitial fluid entry into the airspaces.[7] Type 2 cells reabsorb secreted surfactant from the alveoli, recycling molecules through endocytosis into multivesicular bodies and lamellar bodies to maintain the surfactant pool.[8] Preterm infants demonstrate both reduced surfactant quantity and decreased functional activity related to compositional differences.

Genetics

Genomic research has identified genetic and nongenetic factors that contribute to susceptibility to RDS.[9] Abnormal lung development pathways now represent emerging therapeutic targets, with growing emphasis on genomic influences and personalized treatment strategies. Higher rates of RDS among monozygotic twins compared with dizygotic twins, along with familial clustering, support a genetic predisposition.[10]

Genetic surfactant protein deficiencies may produce varying disease severity. Rare autosomal recessive mutations in the SP-B gene cause severe neonatal RDS with progression to respiratory failure.[11] Mutations in the SP-C gene affect approximately 0.1% of the population and typically present later with interstitial lung disease. Neonatal RDS is also associated with deletions in ATP-binding cassette subfamily A member 3. Approximately 4% of the population carries this deletion, although the incidence of fatal RDS within this group remains unknown.[12][13]

Epidemiology

As the most common cause of respiratory distress in premature infants, RDS occurs in about 24,000 infants born in the United States annually. RDS is also the most common complication of prematurity, leading to significant morbidity in late preterm neonates and even mortality in very low birth weight infants. The exact definition of RDS is imprecise, thus requiring a careful analysis of statistical data. 

The most significant risk factors for RDS are prematurity and low birth weight. Other risk factors include white race, male gender, late preterm delivery, maternal diabetes, perinatal hypoxia and ischemia, and delivery in the absence of labor.[14] The incidence of RDS increases with decreasing gestational age at delivery. In one study of babies born between 2003 and 2007 at various National Institute of Child Health and Human Development (NICHD) Neonatal Research Network centers, 98% of babies born at 24 weeks of gestation had RDS, while at 34 weeks of gestation, the incidence was 5%, and less than 1% at 37 weeks of gestation.[15]

Pathophysiology

Neonatal RDS is caused by surfactant deficiency, especially in patients with immature lungs. A surfactant deficiency increases surface tension in the small airways and alveoli, thereby reducing the compliance of the immature lung. The delicate balance of pressures at the air-fluid interface is essential to prevent the collapse or filling of the alveolus with fluid. The pathophysiology of RDS can be described using Laplace's law, denoted as the equation:

P=2T/R (where P is pressure, T is surface tension, and R is the radius)

Laplace's law describes the relationship between the pressure difference across the interface between 2 static fluids and the surface shape. As the surface tension increases at the alveolar level, the amount of pressure required to maintain alveolar shape increases. With reduced surfactant production, atelectasis develops throughout the lung, impairing gas exchange.

Widespread, repeated atelectasis eventually damages the respiratory epithelium, triggering a cytokine-mediated inflammatory response. As pulmonary edema develops as a result of the inflammatory response, increasing amounts of protein-rich fluid from the vascular space to leak into the alveoli, which further inactivate surfactant.[16][17] Furthermore, many infants with RDS require mechanical ventilation, which may have deleterious effects on the lung.

Overdistension of the alveoli during positive pressure ventilation leads to further damage and inflammation. Besides, oxidative stress, generated both by high oxygen tensions from mechanical ventilation and by inflammatory processes within the lung, also promotes the conversion of surfactant into an inactive form through protein oxidation and lipid peroxidation.[18][19][20] Thus, RDS can cause hypoxemia through alveolar hyperventilation, diffusion abnormality, ventilation-perfusion mismatch, intrapulmonary shunting, or a combination of these mechanisms. This hypoxemia and tissue hypoperfusion ultimately lead to increased cellular anaerobic metabolism, resulting in lactic acidemia.

Histopathology

Historically, neonatal RDS was known as hyaline membrane disease, owing to an eosinophilic membrane that lines the distal airspaces, usually terminal bronchioles or alveolar ducts, in autopsies of neonates with RDS. Macroscopically, lung tissue from infants with RDS appears similar to hepatic tissue with a ruddy appearance. The hyaline membrane mentioned above is composed of fibrin, cellular debris from lung epithelium, red blood cells, and leukocytes. Microscopic histological examination may also reveal pulmonary tissue with few dilated alveoli among diffuse areas of atelectasis.[21]

History and Physical

The infant with neonatal RDS is often born prematurely and presents with signs of respiratory distress, usually immediately after delivery, or within minutes of birth. The infant may present with decreased breath sounds and possibly diminished peripheral pulses. Upon clinical examination, such neonates have signs and symptoms of increased work of breathing, including tachypnea, expiratory grunting, nasal flaring, retractions (subcostal, subxiphoid, intercostal, and suprasternal), and use of accessory muscles, as well as cyanosis and poor peripheral perfusion. Auscultation reveals uniformly decreased air entry. In untreated RDS, the symptoms will progressively worsen over 48 to 72 hours towards respiratory failure, and the infant may become lethargic and apneic.[22] The infant may also develop peripheral extremity edema and decreased urine output.

Evaluation

Since the definition of neonatal RDS is imprecise, prompt diagnosis and treatment require an overall assessment of prenatal and delivery history to identify perinatal risk factors, clinical presentation, radiographic findings, and evidence of hypoxemia on blood gas analysis. The clinical presentation consists of nonspecific respiratory symptoms, including tachypnea, nasal flaring, grunting, retractions, and cyanosis, with decreased air entry on auscultation; therefore, diagnosis typically requires additional diagnostic testing. 

Chest Radiography

Chest radiographic findings pathognomonic of RDS include homogeneous lung disease with diffuse atelectasis, classically described as having a ground-glass reticulogranular appearance with air bronchograms, as well as low lung volumes (see Image. Respiratory Distress Syndrome). The air-tissue interface formed between microalveolar collapse in the background with the air-filled larger airways in the foreground creates the classic appearance of air bronchograms.

Arterial Blood Gas Analysis

Arterial blood gas analysis may show hypoxemia that responds to increased oxygen supplementation and hypercapnia. Serial blood gases may show worsening respiratory and metabolic acidosis, including lactic acidemia, in infants with worsening RDS.

Lung ultrasound (LUS) has emerged as a superior diagnostic modality with higher sensitivity and specificity than chest x-ray.[23] LUS can accurately grade RDS severity, reduce misdiagnosis rates, and guide treatment decisions, including surfactant administration.[23][24] Quantitative lung ultrasound demonstrates the highest diagnostic accuracy among available tools for personalizing RDS management.[24]

Other Investigations

An echocardiogram may reveal a patent ductus arteriosus, which may complicate the clinical course of RDS. Complete blood counts may show evidence of anemia and abnormal leukocyte counts, suggesting infection. In some cases, an evaluation for underlying infectious etiologies may be necessary, including blood, cerebrospinal fluid, and tracheal cultures (when appropriate).

Treatment / Management

Management Overview

The goals of optimal management of neonatal RDS include decreasing incidence and severity using antenatal corticosteroids, followed by optimal management using respiratory support, surfactant therapy, and overall care of the premature infant. Therapeutic strategies include:

• Antenatal corticosteroids
• Monitoring oxygenation and ventilation
• Assisted ventilation of the neonate
• Exogenous surfactant therapy
• Supportive care, including thermoregulation, nutritional support, fluid and electrolyte management, and antibiotic therapy [25][26] 

Monitoring Oxygenation and Ventilation

Serial blood gas monitoring may be necessary to optimize oxygenation and ventilation. Ideally, neonates undergo blood gas monitoring with an umbilical or peripheral arterial catheter placed under sterile technique. The partial pressure of arterial oxygen (PaO₂) on an arterial blood gas is maintained between 50 and 80 mm Hg, the partial pressure of arterial carbon dioxide (PaCO₂) is maintained between 40 and 55 mm Hg, and the pH is greater than 7.25. 

Noninvasive pulse oximetry is now the standard of care to monitor oxygen saturation (SaO₂). Unclear higher limits often limit the utility of pulse oximetry, since PaO₂ could be significantly higher at SaO2 levels above 95%. Noninvasive capnography and transcutaneous carbon dioxide monitoring are used as adjuncts for monitoring ventilation.

Assisted Ventilation of the Neonate

The goals of assisted ventilation are to reduce atelectasis by providing a constant distending positive airway pressure. The current preferred strategy is the early initiation of continuous positive airway pressure (CPAP) with selective surfactant administration.[27] In most institutions, noninvasive modalities are preferred over invasive ventilation, as they reduce mortality and the risk of bronchopulmonary dysplasia compared with invasive ventilation alone or with surfactant.[28][29] 

Continuous Positive Airway Pressure 

Nasal CPAP is an initial intervention in preterm infants with RDS or risk of RDS without respiratory failure. Multiple modalities are available for CPAP delivery, including ventilator-derived CPAP and a less expensive bubble CPAP device. Infants who received CPAP fared as well as infants who received prophylactic surfactant therapy along with mechanical ventilation in the SUPPORT trial (Surfactant Positive Airway Pressure and Pulse Oximetry Randomized Trial), and those who received early CPAP had a reduced need for surfactant therapy.[30] Also, the incidence of bronchopulmonary dysplasia decreased with CPAP use.[25] The goals of treatment include keeping SpO2 between 90% and 95% and PaCO₂ between 45 and 65 mm Hg.

Noninvasive Respiratory Support

Nasal Intermittent Positive Pressure Ventilation (NIPPV) appears superior to CPAP alone for decreasing extubation failure and the need for intubation in preterm infants, but is not cost- or safety-wise superior.[31] The primary difference between NIPPV and CPAP is that NIPPV requires a ventilator to provide positive-pressure ventilation. In contrast, CPAP may use a less expensive device, eg, bubble CPAP, to deliver the appropriate pressures.

High-Flow Nasal Cannula

Heated, humidified high-flow nasal cannulas (HFNC) are also used in some centers as an alternative to CPAP to provide positive-pressure ventilation for neonates with RDS. As reported in a clinical trial by Roberts et al, HFNC was inferior to CPAP.[32] 

Mechanical Ventilation

Patients who do not respond to CPAP develop respiratory acidosis (pH <7.2 and PaCO₂ >60-65 mm Hg), hypoxemia (PaO₂ <50 mm Hg or FiO₂ >0.40 on CPAP), or severe apnea and are managed with endotracheal intubation and mechanical ventilation. The goals of mechanical ventilation include providing adequate respiratory support while balancing the risks of barotrauma, volutrauma, and oxygen toxicity. Time-cycled pressure-limited ventilation is the preferred initial mode of ventilation in preterm infants with RDS. High-frequency oscillatory ventilation (HFOV) and high-frequency jet ventilation (HFJV) are often used as rescue modalities when high conventional ventilator support is required or when concerns about pulmonary air leaks arise. Other strategies include the use of high-frequency ventilation empirically in extremely preterm infants to minimize lung injury. 

Exogenous Surfactant Therapy

Surfactant replacement therapy is the mainstay intervention for RDS, significantly reducing neonatal mortality and morbidity.[33][34] Surfactant hastens recovery and decreases the risk of pneumothorax, interstitial emphysema, intraventricular hemorrhage (IVH), bronchopulmonary dysplasia, and neonatal mortality in the hospital and at 1 year. However, neonates who receive surfactant for established RDS have an increased risk of apnea of prematurity.

The magnitude of surfactant’s beneficial effect strongly depends on the timing of administration, with earlier administration after birth yielding better outcomes.[35] However, prophylactic surfactant is not currently recommended as it may increase the risk of lung injury or death and could expose some neonates to unnecessary treatment.[33] The optimal approach is early rescue surfactant therapy administered to infants receiving CPAP when specific thresholds are met.[35]

According to European census guidelines, the surfactant is administered to immature babies with FiO₂ greater than 0.3 and mature babies with FiO₂ greater than 0.4. Currently, no clinically significant advantages have been identified in using one type over another when used in similar doses, including:

• Beractant: This is a modified natural surfactant prepared from minced bovine lungs with the additives.
• Poractant alfa: This surfactant is a modified natural surfactant derived from minced porcine lung extract.
• Calfactant: This surfactant is a natural surfactant obtained from lavaging calf lung alveoli and contains 80% phosphatidylcholine with only 1% protein.
• Synthetic surfactant: Clinical trials are ongoing.[36]

Surfactant is administered either by standard endotracheal intubation, which requires an experienced practitioner, or by less invasive surfactant administration (LISA) techniques, eg, aerosolized nebulized surfactant preparations, laryngeal mask, pharyngeal instillation, and thin intratracheal catheters.[37][38][39][40][41] The standard technique of surfactant administration by endotracheal intubation and mechanical ventilation may result in transient airway obstruction, pulmonary injury, pulmonary air leak, and airway injury.[42][43] 

Emerging evidence suggests that the LISA technique is associated with lower rates of bronchopulmonary dysplasia, death, and mechanical ventilation compared with surfactant administration via endotracheal intubation.[44] Still, further investigations are required to establish the LISA technique as the preferred method of surfactant administration in place of endotracheal intubation. If the neonates maintain adequate respiratory drive with FiO₂ less than 0.3, it should be planned to stop surfactant and switch to CPAP. Oxygen saturation (>90%), thermoregulation (36.5 °C to 37.5 °C), and the status of fluid and nutrition should be monitored.

Supportive Care

Preterm infants with apnea of prematurity may require caffeine therapy. Caffeine can also be administered to preterm infants younger than 28 weeks of gestation with extremely low birth weight (BW <1000 g) to increase respiratory drive and enhance the use of CPAP. A low incidence of bronchopulmonary dysplasia and earlier extubation in preterm infants who received caffeine was noted compared to placebo.[45]

Optimal fluid and electrolyte management is critical in the initial course of RDS. Some neonates may require volume resuscitation using crystalloids as well as vasopressors for hypotension. Furthermore, the overall care of a preterm infant includes optimizing thermoregulation, providing nutritional support, administering blood transfusions for anemia, treating a hemodynamically significant PDA, and administering antibiotic therapy as necessary.

Personalized Medicine Approach

RDS exhibits substantial heterogeneity requiring individualized management based on physiopathology and actual patient needs.[24] Simple clinical algorithms cannot adequately address the complexity of RDS treatment. Precision medicine strategies that utilize lung ultrasound, advanced oxygenation metrics, and surfactant assays enable personalized decisions on surfactant administration timing and respiratory support escalation.[24]

Differential Diagnosis

Multiple conditions can cause neonatal respiratory distress and require differentiation from RDS, including transient tachypnea of the newborn, pulmonary air leak disorders such as pneumothorax and pneumomediastinum, neonatal pneumonia, meconium aspiration, persistent pulmonary hypertension of the newborn, and broader categories such as cyanotic congenital heart disease and interstitial lung disease.[22]

Infants with transient tachypnea of the newborn experience delayed resorption of fetal lung fluid and develop marked tachypnea shortly after birth, with symptoms that typically improve within 24 hours. Chest radiography demonstrates perihilar streaking consistent with interstitial edema and lacks the diffuse reticulogranular ground glass pattern characteristic of RDS.

Pulmonary air leak syndromes, including pneumothorax and pneumomediastinum, often present with respiratory distress and have a more acute onset. Clinical findings may include asymmetric chest expansion and diminished breath sounds on the affected side. Chest radiography may reveal hyperlucent regions when air accumulation reaches a significant degree. Pulmonary interstitial emphysema primarily affects mechanically ventilated infants and produces respiratory symptoms later than expected for RDS, with chest radiographs showing cystic lucencies from air trapped in perivascular tissues.

Neonatal bacterial pneumonia, particularly caused by Group B Streptococcus, frequently mimics RDS clinically and radiographically, prompting empiric antibiotic therapy and respiratory support. Infants with cyanotic congenital heart disease may exhibit similar respiratory symptoms, although chest radiographs lack diffuse reticulogranular ground glass changes and instead reflect the specific underlying anatomic defect.

Prognosis

The prognosis for infants treated with antenatal corticosteroids, appropriate respiratory support, and exogenous surfactant therapy is excellent. Mortality is now less than 10%, with some studies reporting survival rates as high as 98% in settings with advanced neonatal care. This contrasts sharply with outcomes in low-income countries, where limited access to interventions results in substantially higher mortality among premature infants with RDS, in some cases approaching 100%.[46]

With adequate ventilatory support alone, endogenous surfactant production eventually begins, and RDS typically improves within 4 to 5 days as surfactant synthesis increases and postnatal diuresis occurs. In contrast, untreated severe disease can lead to profound hypoxemia in the early days of life, resulting in multiorgan failure and death.

Advances in modern management, including surfactant therapy and gentle ventilation strategies, have dramatically improved survival for preterm infants with RDS. Nonetheless, survivors remain at risk for chronic lung disease, particularly bronchopulmonary dysplasia, especially among those requiring prolonged mechanical ventilation or high oxygen exposure. The shift from routine intubation toward CPAP-first approaches, with selective surfactant administration using less invasive techniques, represents a paradigm change aimed at reducing ventilator-induced lung injury while preserving therapeutic effectiveness. Noninvasive surfactant administration techniques, including aerosolization or atomization, may play an increasingly important role in future management.[33]

Complications

Complications of neonatal RDS are mainly related to the clinical course of RDS and the long-term outcomes of neonates. While surfactant therapy has decreased the morbidity associated with RDS, many patients continue to have complications during and after the acute course of RDS.

Acute complications of positive-pressure ventilation or invasive mechanical ventilation include air-leak syndromes, eg, pneumothorax, pneumomediastinum, and pulmonary interstitial emphysema. Also, an increase in the incidence of intracranial hemorrhage and patent ductus arteriosus is observed in very low birth weight infants with RDS, although independently linked to prematurity itself. 

Bronchopulmonary dysplasia is a chronic complication of RDS. The pathophysiology of bronchopulmonary dysplasia involves both arrested lung development and lung injury and inflammation. In addition to surfactant deficiency, the immature lung of the premature infant has decreased compliance, decreased fluid clearance, and immature vascular development, which predispose the lung to injury and inflammation and further disrupt the normal development of alveoli and the pulmonary vasculature. Also, oxidative stress from hyperoxia secondary to mechanical ventilation, and the premature lung's decreased antioxidant capacity, both contribute to further lung damage by increasing TGF-β1 and other proinflammatory cytokines.[47]

Neurodevelopmental delay is another complication of RDS, especially with infants who received mechanical ventilation long-term.[48] The incidence of cerebral palsy was also increased in infants with RDS, with decreasing incidence as gestational age increased. The length of time on mechanical ventilation correlates with increased rates of both cerebral palsy and neurodevelopmental delay.

Deterrence and Patient Education

While the goal of preventing preterm birth altogether continues to be investigated, RDS can be reduced by the administration of antenatal corticosteroids. Administration of antenatal corticosteroids significantly reduces the incidence of RDS and the need for mechanical ventilation. The use of antenatal corticosteroids decreased the incidence of RDS in a review of 21 studies and 4083 infants, and reduced neonatal and fetal deaths in a review of 3627 infants across 13 studies.[49] Antenatal corticosteroids have also been shown to reduce infant mortality and periventricular leukomalacia. Notably, no statistically significant increase in maternal mortality was noted with antenatal corticosteroid administration.

The beneficial effect of antenatal corticosteroid use after 34 weeks of gestation is controversial due to limited information on long-term developmental outcomes.[50] Maternal antenatal corticosteroids are recommended for possible preterm delivery in the next 7 days between 23 and 34 weeks of gestation.[51] Some institutions offer antenatal corticosteroids at 22 weeks of gestation if delivery is anticipated within the next week. Despite multiple interventions targeting various etiologies, the goal of preventing preterm birth remains elusive.

Enhancing Healthcare Team Outcomes

Neonatal RDS represents a major cause of morbidity and mortality in premature infants and results primarily from surfactant deficiency and lung immaturity. Affected neonates develop impaired lung compliance, hypoxemia, and progressive respiratory failure shortly after birth, often presenting with tachypnea, retractions, grunting, and cyanosis. Clinical features overlap with several other neonatal respiratory conditions, making accurate diagnosis dependent on careful history, laboratory evaluation, and imaging. Evidence-based management emphasizes antenatal corticosteroids, early noninvasive respiratory support, timely surfactant administration, and vigilant supportive care to reduce complications and improve survival.

Optimal care for neonatal RDS depends on coordinated interprofessional practice. Physicians, general practitioners, and advanced practitioners establish a diagnosis, define goals of care, and guide respiratory and medical management while addressing comorbidities such as air-leak syndromes, patent ductus arteriosus, pulmonary hypertension, and sepsis. Neonatal nurses provide continuous monitoring, thermoregulation, and family-centered care, while respiratory therapists manage complex ventilation strategies across disease severity. Pharmacists support safe medication use, surfactant therapy, and nutritional planning. Effective communication and care coordination among all team members enhances patient safety, supports long-term outcomes, and ensures consistent, patient-centered care from delivery room stabilization through NICU discharge and follow-up.

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Disclosure: Priyam Pattnaik declares no relevant financial relationships with ineligible companies.

Disclosure: Kehinde Adebisi declares no relevant financial relationships with ineligible companies.

Disclosure: Brian Lee declares no relevant financial relationships with ineligible companies.