Neonatal respiratory distress syndrome and surfactant therapy; a brief review.
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Abstract:
Several randomized clinical trials have now documented a beneficial effect of surfactant replacement in established neonatal respiratory distress syndrome (RDS). These results have been obtained with surfactant isolated from animal lungs or human amniotic fluid. Treatment with exogenous natural surfactant usually reverses the clinical course of severe RDS, reduces the incidence of serious complications including bronchopulmonary dysplasia, and improves survival rate. Prophylactic surfactant treatment at birth reduces the incidence of severe RDS in very premature babies; this effect has been documented with natural as well as synthetic surfactant preparations. Increased incidence of patent ductus arteriosus was reported in one series of RDS patients treated with modified bovine surfactant, but otherwise no adverse effects have been observed.Keywords:
Bronchopulmonary Dysplasia
Surfactant therapy
Ductus arteriosus
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Surfactant deficiency has come to be understood as equivalent clinically to lung immaturity, except in situations of extreme prematurity or lung hypoplasia. Thus, surfactant deficiency and the diagnosis respiratory distress syndrome (RDS) have been applied quite uniformly to preterm infants with respiratory distress who have no other identifiable problems. While the diagnosis can be made more specific by assay of surfactant phospholipid composition (12), such measurements are seldom made in clinical practice. Perinatal discussions of the premature with respiratory distress also have been focused toward surfactant by the availability of multiple tests of “lung maturation” based on the assay of surfactant components in amniotic fluid (19). While surfactant is necessary for normal lung function, adequate surfactant is not sufficient to assure normal gas exchange in the preterm. There are no simple ways to separate surfactant deficiency states clearly from other aspects of lung development, such as airway development, alveolarization, and the development of the pulmonary vasculature in the preterm infant. The anatomic data of Hislop et al. (13) and Langston et al. (22) indicate a considerable variability in the number of alveoli in the preterm infant at each gestational age, resulting in large differences in potential gas exchange surfaces in different infants. Airway development also differs between infants of comparable gestational ages, as is evident clinically by susceptibility to the development of pulmonary interstitial emphysema. Assuming that surfactant treatments for RDS fully correct the surfactant deficiency, a realistic expectation based on animal studies (16), surfactant treatments should be useful in the near future to eliminate the surfactant deficiency component of lung immaturity syndromes. Any residual lung disease can then be better characterized.
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Surfactant therapy has revolutionized neonatal care and is used routinely for preterm infants with respiratory distress syndrome. Recent investigation has further elucidated the function of surfactant-associated proteins and their contribution toward surfactant and lung immune defense functions. As the field of neonatology moves away from intubation and mechanical ventilation of preterm infants at birth toward more aggressive use of nasal continuous positive airway pressure, the optimal timing of exogenous surfactant therapy remains unclear. Evidence suggests that preterm neonates with bronchopulmonary dysplasia and prolonged mechanical ventilation also experience surfactant dysfunction; however, exogenous surfactant therapy beyond the first week of life has not been well studied. Surfactant replacement therapy has been studied for use in other respiratory disorders, including meconium aspiration syndrome and pneumonia. Commercial surfactant preparations currently available are not optimal, given the variability of surfactant protein content and their susceptibility to inhibition. Further progress in the treatment of neonatal respiratory disorders may include the development of "designer" surfactant preparations.
Bronchopulmonary Dysplasia
Surfactant therapy
Meconium aspiration syndrome
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Introduction and aim
Surfactant replacement is a corner stone therapy for respiratory distress syndrome (RDS) and has been shown to be both safe and efficacious for premature infants. The aim of this study was to assess the immediate changes in lung mechanics caused by administration of two different natural surfactants. Secondary aim of this study was to determine the relationship between initial lung mechanics and occurrence of bronchopulmonary dysplasia (BPD).Method
Preterm infants who wereResults
10 premature infants were studied. Mean gestational age was 28.4 ± 1.6 (26–31) weeks and mean birth weight was 955 ± 155 (710–1250) g. Five infants received beractant and the other five received poractantalpha. The alteration of lung mechanics after surfactant administration was summarized in Table 1.Conclusion
Surfactant therapy significantly reduced the resistance and improved the lung compliance. These effects were not directly related to the type of surfactant administered.Bronchopulmonary Dysplasia
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Our objective was to determine if preterm infants with respiratory distress syndrome who develop bronchopulmonary dysplasia have abnormalities in surfactant phospholipids and/or function. Tracheal aspirate samples obtained from preterm infants with respiratory distress syndrome on days 1, 3–5, 7–10, 14–17, 21–24 and 27–30 were analyzed for total phospholipids and phospholipids fractions by determination of total phospholipid phosphorus and thin layer chromatography, respectively. Surfactant properties were assessed with captive bubble surfactometer. Sixteen out of 56 (29%) infants died during the first 30 d of life. Infants who died were more immature, required more ventilatory support and had a surfactant with lower surface‐tension‐reducing properties than infants who survived ( p < 0.05). Surviving infants were divided into group I (no bronchopulmonary dysplasia at 27–30 d, n = 25) and group II (with bronchopulmonary dysplasia at 27–30 d, n = 15). No significant differences in concentrations of surfactant phospholipids nor measurements of surface tension were noted among groups of infants. Surfactant therapy after birth was associated with a significant increase in concentrations of total phospholipids, lecithin, phosphatidylinositol and lower surface‐tension measurements at 3–5 d of age among surviving infants ( p < 0.01). Abnormalities in concentrations of surfactant phospholipids or surfactant function could not be demonstrated during the first month of life among preterm infants with respiratory distress syndrome who develop bronchopulmonary dysplasia.
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Several randomized clinical trials have now documented a beneficial effect of surfactant replacement in established neonatal respiratory distress syndrome (RDS). These results have been obtained with surfactant isolated from animal lungs or human amniotic fluid. Treatment with exogenous natural surfactant usually reverses the clinical course of severe RDS, reduces the incidence of serious complications including bronchopulmonary dysplasia, and improves survival rate. Prophylactic surfactant treatment at birth reduces the incidence of severe RDS in very premature babies; this effect has been documented with natural as well as synthetic surfactant preparations. Increased incidence of patent ductus arteriosus was reported in one series of RDS patients treated with modified bovine surfactant, but otherwise no adverse effects have been observed.
Bronchopulmonary Dysplasia
Surfactant therapy
Ductus arteriosus
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The rationale for surfactant therapy in premature infants is presented, along with a discussion of the characteristics of surfactant and a review of clinical trials of surfactant for the prevention and treatment of neonatal respiratory distress syndrome (RDS). RDS is a major complication of prematurity, affecting up to 40,000 infants in the United States and Canada annually. Poor lung compliance due to a functional or quantitative deficiency of surfactant causes progressive collapse of the lungs. Surfactant, a mixture of phospholipids, neutral lipids, and proteins synthesized by pneumocytes during gestation, reduces surface tension and stabilizes alveoli, which increases lung compliance and decreases the work of breathing. Mammalian, human, and artificial surfactants are being investigated for use in premature infants. Several controlled trials of exogenous surfactant therapy have demonstrated reductions in mortality and pulmonary air-leak phenomena and improved gas exchange, but these results are not seen consistently, and no significant reductions in bronchopulmonary dysplasia have been observed. Surfactant has no appreciable toxicity, although the potential for immunogenicity exists. Typical doses range from 60 mg to 200 mg/kg administered endotracheally either before the first breath or after development of RDS. Surfactant is a safe investigational agent that appears promising for the prevention and treatment of neonatal RDS, although additional clinical trials with long-term follow-up are needed to determine its true efficacy.
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Respiratory distress syndrome (RDS) is a syndrome caused by pulmonary insufficiency especially in premature infants. It is due to lack of alveolar surfactant along with structural immaturity of the lung. Although recent advances in the management of RDS, it is still a major cause of morbidity and mortality in premature infants. Surfactant replacement therapy is crucial in the management of RDS. Exogenous lung surfactant can be either natural or synthetic. Natural surfactant is extracted from animal sources such as bovine or porcine. Synthetic surfactant is manufactured from compounds that mimic natural surfactant properties. Until recently, natural surfactant extracts would seem to be the more desirable choice. Two basic strategies for surfactant replacement have emerged: prophylactic or preventive treatment, in which surfactant is administered at the time of birth or shortly thereafter to infants who are at high risk for developing RDS from surfactant deficiency; and rescue or therapeutic treatment, in which surfactant is administered after the initiation of mechanical ventilation in infants with clinically confirmed RDS. At least 100 mg/kg of phospholipid is required, but there are pharmacokinetic and clinical data suggesting that 200 mg/kg has a better clinical outcome. Recent recommended method is ‘INSURE’ (Intubate SURfactant Extubation) technique. After installation of pulmonary surfactant, reducing the high peak and fluctuations in oxygen saturation are important since these are associated with an increased incidence of retinopathy of prematurity. Non-invasive ventilatory support can reduce the adverse effects associated with intubation and mechanical ventilation, such as bronchopulmonary dysplasia.
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Objective Treatment of preterm infants with respiratory distress syndrome (RDS) with exogenous surfactant has greatly improved clinical outcome. Some infants require multiple doses, and it has not been studied whether these large amounts of exogenous surfactant disturb endogenous surfactant metabolism in humans. We studied endogenous surfactant metabolism in relation to different amounts of exogenous surfactant, administered as rescue therapy for RDS. Design Prospective clinical study. Setting Neonatal intensive care unit in a university hospital. Patients A total of 27 preterm infants intubated and mechanically ventilated for respiratory insufficiency. Interventions Infants received a 24-hr infusion with the stable isotope [U-13C]glucose starting 5.3 ± 0.5 hrs after birth. The 13C-incorporation into palmitic acid in surfactant phosphatidylcholine (PC) isolated from serial tracheal aspirates was measured. Infants received either zero (n = 5), one (n = 4), two (n = 15), or three (n = 3) doses of Survanta (100 mg/kg) when clinically indicated. Measurements and Main Results Using multiple regression analysis, the absolute synthesis rate (ASR) of surfactant PC from plasma glucose increased with 1.3 ± 0.4 mg/kg/day per dose of Survanta (p = .007) (mean ± sem). The ASR of surfactant PC from glucose was increased by prenatal corticosteroid treatment with 1.3 ± 0.4 mg/kg/day per dose corticosteroid (p = .004), and by the presence of a patent ductus arteriosus with 2.1 ± 0.7 mg/kg/day (p = .01). Conclusion These data are reassuring and show for the first time in preterm infants that multiple doses of exogenous surfactant for RDS are tolerated well by the developing lung and stimulate endogenous surfactant synthesis.
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Surfactant-replacement therapy is a life-saving treatment for preterm infants with respiratory distress syndrome, a disorder characterized by surfactant deficiency. Repletion with exogenous surfactant decreases mortality and thoracic air leaks and is a standard practice in the developed world. In addition to respiratory distress syndrome, other neonatal respiratory disorders are characterized by surfactant deficiency, which may result from decreased synthesis or inactivation. Two of these disorders, meconium aspiration syndrome and bronchopulmonary dysplasia, might also be amenable to surfactant-replacement therapy. This paper discusses the use of surfactant-replacement therapy beyond respiratory distress syndrome and examines the evidence to date.
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Several recent reports have documented the efficacy of surfactants replacement therapy in the neonatal respiratory distress syndrome (RDS). The surfactants tested in these trials were obtained from animal lungs or human amniotic fluid. In general, such natural preparations seem to be superior to entirely synthetic surfactants, although promising results have recently been obtained in animal experiments with artificial surfactant based on isolated apoproteins and synthetic phospholipids. Furthermore, surfactant replacement therapy seems to be more effective when the exogenous material is administered at birth, before the first breath, than when surfactant is instilled into the airways after a period of ventilation. This discrepancy may be due to maldistribution of the exogenous material, or to the rapid development of epithelial lesions in the immature lung, with leakage of surfactant-inhibiting proteins into the airspaces. A transient beneficial response to surfactant replacement may also be due to circulatory problems, especially reversal of the shunt through a patent ductus arteriosus, with overloading of the lung circulation leading to pulmonary oedema and recurrent respiratory failure. Additional, properly randomized clinical trials are required to evaluate the benefits and potential hazards of surfactant replacement therapy in neonatal RDS.
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