Effects Of Surfactant Replacement Therapy Research Articles

Surfactant Therapy for Respiratory Distress Syndrome in High- and Ultra-High-Altitude Settings.

ObjectiveThe objective of this study is to investigate the therapeutic effect of surfactant replacement therapy (SRT) on respiratory distress syndrome (RDS) in premature infants in the Qinghai-Tibet Plateau.Materials and MethodsThis multi-center retrospective cohort study collected and screened reasonable clinical data of 337 premature infants with RDS from 10 hospitals in the Qinghai-Tibet Plateau from 2015 to 2017. We grouped the cases by rationally analyzing their baseline characteristics, using logistic analysis to evaluate each factor's effect on the prognosis of the infants, and comparing the short-term improvement in blood gas and mortality after SRT treatment at different altitudes, in high-altitude (1,500–3,500 m) and ultra-high-altitude (3,500–5,500 m) groups.ResultsIndependent of altitude, the mortality rate of children with RDS in the SRT group was significantly lower than that of children in the non-SRT group (both P < 0.05). The effect of SRT on preterm infants with RDS in the high-altitude group [odds ratio (OR) = 0.44, 95% confidence interval (CI) = 0.22–0.87, P = 0.02] was better than that in the infants in the ultra-high-altitude group (OR = 0.26, 95% CI = 0.13–0.58, P < 0.01), with death rates of 34.34 and 49.71%, respectively. Similarly, after SRT, the improvement of PaO2/FiO2 and pH of children at high altitude was significantly better than those of children at ultra-high altitude (all P < 0.01).ConclusionsSRT plays a prominent role in curing infants with RDS in both high- and ultra-high-altitude regions, although with better effects at high rather than ultra-high altitude. This study provides a basis for further large-scale studies on SRT for RDS treatment at high altitudes.

Effect of surfactant replacement therapy in preterm with respiratory distress syndrome in low sources center Al-Zahraa teaching Hospital at Al-Najaf city-Iraq.

Background: Every year, 15 million premature babies are born around the world. Prematurity and its complications cause more than a million deaths each year, accounting for approximately a third of all newborn deaths globally. Respiratory failure due to Hyaline Membrane Disease (HMD) is one of the primary causes of preterm infant death and morbidity. Aims of the study: 1) To assess the outcome of surfactant therapy using INSURE method in the management of respiratory distress syndrome. 2) To define the cofounder that may associate with its failure. Methods: This is a cross sectional study was performed in Al Zahraa teaching hospital for maternity and children in a period between January till June 2021. All neonates (gestational age between 28-32 weeks) were enrolled in the study. All of them have been diagnosed as RDS depending on clinical signs (tachypnea, grunting, nasal flaring, and cyanosis, substernal and inter costal retractions) and radiological features (air bronchograms, increasing hypo-aeration, reticulogranular or ground glass opacification). All of them were included in this experiment after receiving SRT using the INSURE technique. The required dose of surfactant was drawn out from its ampoule into a sterile syringe and allowed to warm to room temperature. After endotracheal tube inserted the infant is positioned supine on a flat surface with head turned to one side. Results: A total number of 50 neonates with clinical and radiological signs of RDS were included in the study; 54% of the study was male compared to female 46%. INSURE method was successful in saving the life of 31 out of 50 (62%) of them. The mean birth weights in the failure group were 1180(± 334) grams was significantly lower than the success group 1485 (± 428) grams. This study also showed that the INSURE method was successful in 26 among 36(72%) neonates with gestational age ≥ 30 weeks while succeed in 4 among 14(28%) neonates with gestational age <30 weeks. The severity of RDS was significantly increased in the failure group than in success group (88.8% vs. 12.5%). Tachycardia is most common complication during surfactant replacement therapy (36%), bradycardia (28%) and de saturation (26%). Conclusion: INSURE method is good method in management of respiratory distress syndromethat associated with decreased need for mechanical ventilation & decreased neonatal mortality rate. This study shows that preterm neonates with lower birth weight, lower gestational age, lower Apgar score at 5 minutes, with severe RDS & with prolonged administration have increased risk for INSURE method failure. Tachycardia, bradycardia and de saturation are the main complications during surfactant giving. And enough ICU beds with good nursing care appropriate with number improving outcomes of preterm patient. Every patient was received surfactant echocardiogram must be done to him for risk of PDA.

Gender-related efficacy of pulmonary surfactant in infants with respiratory distress syndrome: A STROBE compliant study.

Whether gender influences the efficacy of exogenous pulmonary surfactant (PS) for replacement therapy in newborns with respiratory distress syndrome (RDS) has not been well studied yet.Retrospective cohort study design. Data on PS therapy including blood gas, oxygenation function parameters, and therapy results were collected and analyzed from 370 infants diagnosed with RDS in 20 hospitals of the Northwest China Neonatal Collaboration from January 2011 to December 2011.Female infants were more sensitive to PS treatment than males. In multivariate analysis, when adjusted for other variables, an increased initial dose of surfactant significantly reduced mortality risk (OR = 0.98, 95%CI [0.96, 0.99], P = .002). An interaction between gender and initial dose of PS was observed. In male infants, an increased initial dose of surfactant was correlated with reduced mortality risk (OR = 0.97, 95%CI [0.96, 0.99], P = 0.005), while in female infants, we failed to found a relationship between the initial dose of surfactant and the risk of mortality (OR = 0.99, 95%CI [0.96, 1.02], P = .543). Moreover, the effect of surfactant replacement therapy was better for female infants than male infants at initial PS doses <130 mg/kg.Gender influences the efficacy of PS treatment. An increased initial dose of PS should be used in RDS therapy for male infants.

Effects of exogenous surfactant on the non‐heart‐beating donor lung graft in experimental lung transplantation – a stereological study

The use of non-heart-beating donor (NHBD) lungs may help to overcome the shortage of lung grafts in clinical lung transplantation, but warm ischaemia and ischaemia/reperfusion injury (I/R injury) resulting in primary graft dysfunction represent a considerable threat. Thus, better strategies for optimized preservation of lung grafts are urgently needed. Surfactant dysfunction has been shown to contribute to I/R injury, and surfactant replacement therapy is effective in enhancing lung function and structural integrity in related rat models. In the present study we hypothesize that surfactant replacement therapy reduces oedema formation in a pig model of NHBD lung transplantation. Oedema formation was quantified with (SF) and without (non-SF) surfactant replacement therapy in interstitial and alveolar compartments by means of design-based stereology in NHBD lungs 7 h after cardiac arrest, reperfusion and transplantation. A sham-operated group served as control. In both NHBD groups, nearly all animals died within the first hours after transplantation due to right heart failure. Both SF and non-SF developed an interstitial oedema of similar degree, as shown by an increase in septal wall volume and arithmetic mean thickness as well as an increase in the volume of peribron-chovascular connective tissue. Regarding intra-alveolar oedema, no statistically significant difference could be found between SF and non-SF. In conclusion, surfactant replacement therapy cannot prevent poor outcome after prolonged warm ischaemia of 7 h in this model. While the beneficial effects of surfactant replacement therapy have been observed in several experimental and clinical studies related to heart-beating donor lungs and cold ischaemia, it is unlikely that surfactant replacement therapy will overcome the shortage of organs in the context of prolonged warm ischaemia, for example, 7 h. Moreover, our data demonstrate that right heart function and dysfunctions of the pulmonary vascular bed are limiting factors that need to be addressed in NHBD.

Clinical findings of severe amniotic fluid aspiration pneumonia and effects of surfactant replacement therapy

Purpose: Severe aspiration of the amniotic fluid is known to cause fatal respiratory distress in neonates. We conducted this study to investigate the clinical findings of severe amniotic fluid aspiration pneumonia (AFAP) in neonates and the effect of pulmonary surfactant replacement therapy (SRT). Methods: Retrospective analysis of medical records was conducted on 28 patients who received ventilator care due to severe AFAP in a neonatal intensive care unit over a 7-year period (2000-2006). Patients whose amniotic fluid was contaminated with meconium were excluded. Results: A large number of cases were term infants (82.1%) and infants born by caesarean section (85.7%), and the 1and 5-min Apgar scores of these patients were 6.5±1.2 and 7.5±1.3, respectively. Soon after birth, the amount of amniotic fluid sucked out from airway below the vocal cord was 16.0±10.1 mL. All patients received SRT with a modified bovine-derived surfactant (120 mg/kg/dose), and one dose was administered in most cases (75%). Compared with pre-SRT, the oxygenation index (8.0±9.6 vs. 18.9±7.3) according to ventilator care was a significant improvement at 12 h after SRT (P<0.001). Furthermore, most cases showed radiological improvement for aeration at 12 h post-treatment. Many cases (46.4%) had cardiorespiratory complications, but their final outcomes were excellent (survival rate, 96.4%). Conclusion: AFAP may be an important cause of serious respiratory distress in near-term and term infants, and SRT seems to be an effective adjuvant therapy in mechanically ventilated neonates with severe AFAP. (Korean J Pediatr 2009;52: 429-434)

Treatment of Premature Calves with Clinically Diagnosed Respiratory Distress Syndrome

Respiratory distress syndrome (RDS) has been reported previously in premature calves. However, there have been no published data on the effect of surfactant replacement therapy in the treatment of premature calves with RDS. Surfactant replacement therapy added to the standard treatment for premature calves clinically diagnosed with RDS would increase the viability of the calves. Twenty-seven premature calves with clinically diagnosed RDS. Twenty calves were instilled intratracheally with bovine lung surfactant extract and provided with standard treatment for RDS (surfactant group). Seven calves were given only standard care for RDS without surfactant therapy and placed in the control group. Standard treatment for newborn calves with RDS includes warming, administration of intranasal oxygen, fluid replacement, administration of antibiotics, and immunoglobulin solution. Arterial blood samples were collected from the calves at 3 observation points, the first just before treatment (hour 0) and at 2 hours (hour 2) and 24 hours (hour 24) after treatment was started to determine if ventilation was adequate, improving, or deteriorating. Blood gases, pH, bicarbonate, and lactate concentrations were measured. In the surfactant group, mean partial pressure of oxygen significantly increased at hours 2 and 24. Mean partial pressure of carbon dioxide decreased and mean arterial blood pH increased at hour 24 in the surfactant group compared with the control group (P < .05). Of the 20 calves in the surfactant group, 12 survived and 8 died. All 7 calves in the control group died. The results of this study suggest that surfactant replacement therapy may reduce neonatal deaths in premature calves with clinically diagnosed RDS.

New developments in neonatology: less severe retinopathy of prematurity?

To determine the effects of surfactant replacement therapy (SRT), high-frequency oscillatory ventilation (HFOV), and general improvements in quality of care on the incidence of severe retinopathy of prematurity (ROP). Retrospective comparison of the incidence and severity of ROP in two groups of preterm infants admitted to our neonatal intensive care unit (NICU) in two consecutive 5-year periods (1986-1995) and screened for ROP. During the second study period, natural surfactant was introduced in the treatment of respiratory distress syndrome (RDS) and HFOV was used for treatment of respiratory insufficiency of any origin. The effects of these developments and general improvements on the incidence of severe ROP were analyzed with stepwise logistic regression. The overall incidence of ROP from 1986-1990 was not significantly different from the incidence of ROP from 1991-1995. The incidence of severe ROP (ROP stage 3 or greater) was significantly lower in the second period (15.7% versus 6.4%, P=.015). For infants <1000 g, the incidence of overall ROP was increased significantly during the second study period (47.6% versus 60.1 %, P=.045), although the incidence of severe ROP remained unchanged. Only SRT was associated with a decreased risk for severe ROP; HFOV and general improvements in quality of care had no influence on the outcome. In patients with RDS, the incidence of severe ROP decreased significantly during the second period. Of the recent new developments in neonatology, only SRT was associated with a decreased risk for severe ROP.

Exacerbation of influenzavirus pneumonia by intranasal administration of surfactant in a mouse model.

Although surfactant-secreting type II alveolar cells have been shown to be damaged during influenzavirus pneumonia, little is known about the effects of surfactant replacement therapy. We have developed a mouse influenza model, in which viral infection can be localized to the upper respiratory tract or to both the upper and lower respiratory tract depending on the volume (rather than infectious dose) of intranasal inocula of influenzavirus. In this model, only mice infected with a large inocula die with massive infection in the lung. Using this model, we unexpectedly found that intranasal administration of surfactant dramatically exacerbated influenzavirus infection causing fatal disease even in mice inoculated with a small inocula. This exacerbation resulted from enhancement of intrabronchial and intraalveolar spread of virus, as confirmed by immunohistochemical detection of viral antigen in lungs. Assuming this experimental model in mice recapitulates naturally occurring disease in humans, extreme caution is warranted in surfactant-replacement treatment of influenzavirus pneumonia in humans.

Surfactant decreases pulmonary vascular resistance and increases pulmonary blood flow in the fetal lamb model of congenital diaphragmatic hernia

Introduction: Experiments using animal models of neonatal respiratory distress syndrome have shown a decrease in pulmonary vascular resistance (PVR) with surfactant replacement, whereas studies with the lamb model of congenital diaphragmatic hernia (CDH) have demonstrated improvement in oxygenation and lung mechanics with this therapy. The aim of the present study was to measure the effects of surfactant replacement therapy on the pulmonary hemodynamics of the lamb model of CDH. Methods: Ten lambs with surgically created CDH and five control lambs were instrumented at term, with the placental circulation intact. Ultrasonic flow probes were positioned around the main pulmonary artery and the common origin of the left and right pulmonary arteries to record total lung and main pulmonary artery blood flow. Catheters were inserted to record systemic, pulmonary, and left atrial pressure. Five CDH animals received 50 mg/kg of surfactant by tracheal instillation just before delivery. All 15 animals were then ventilated for 4 hours. Results: Correcting the surfactant deficiency in the CDH lamb resulted in a significant increase in pulmonary blood flow, a decrease in PVR, and a reduction in right-to-left shunting. These improvements in hemodynamics were associated with a significant improvement in gas exchange over 4 hours. Conclusion: The fetal lamb model of CDH has elevated PVR in comparison to controls. Prophylactic surfactant therapy reduces this resistance and dramatically increases pulmonary blood flow while reducing extrapulmonary shunt. A surfactant deficiency may be partially responsible for the persistent pulmonary hypertension in neonates with CDH.

Acute effects of synthetic surfactant replacement on pulmonary blood flow in neonatal respiratory distress syndrome.

To assess the acute effects of surfactant replacement therapy on the pulmonary blood flow in neonatal respiratory distress syndrome (RDS), 23 distressed infants were studied before and for 1 hour after either synthetic surfactant instillation (n = 13) or endotracheal suctioning (n = 10). Doppler ultrasound was used to measure blood flow velocity and flow velocity integral, representing volumetric flow, of the left pulmonary artery branch, ductal left-to-right shunt, and ascending aorta. Surfactant instillation increased the left pulmonary artery and ductal shunt flow velocity and flow velocity integral for 1 hour in 10 of 13 treated infants, whereas no change was found after endotracheal suctioning. There was a significant (P < 0.05) correlation between the changes in the pulmonary artery and ductal flow values at 1 hour after surfactant treatment. The mean increase during 1 hour after treatment in the pulmonary artery flow ranged from 15 to 25% and in the ductal left-to-right shunt from 28 to 33%. No change in the aortic flow or heart rate was found in either group. Our results thus suggest that synthetic surfactant therapy may acutely increase pulmonary blood flow and ductal left-to-right shunting in infants with RDS.

Pulmonary hemodynamics after synthetic surfactant replacement in neonatal respiratory distress syndrome

To evaluate the acute effects of surfactant replacement therapy on pulmonary circulation in neonatal respiratory distress syndrome, we studied 25 infants before and for 1 hour after either synthetic surfactant administration (n = 15) or endotracheal suctioning (n = 10). The noninvasive Doppler method was used to estimate systolic pulmonary artery pressure from tricuspid regurgitant flow velocity and to measure blood flow velocity of the left-to-right shunt through the ductus arteriosus. Pulmonary artery pressure decreased significantly within 15 minutes after surfactant administration and remained low throughout the study period, whereas suctioning did not change pulmonary artery pressure levels. No changes in systemic pressure were found in either group. Velocity of the ductal left-to-right shunting increased and remained elevated for 1 hour only in surfactant-treated infants. In addition, right-to-left ductal shunting disappeared in four infants after surfactant administration. Our data thus indicate that administration of synthetic surfactant to infants with respiratory distress syndrome reduces pulmonary vascular resistance, resulting in a decrease in pulmonary artery pressure and an increase in ductal flow velocity.

Surfactant therapy of newborn rabbits impairs lung macrophage bactericidal activity.

Because in vitro studies indicate that pulmonary alveolar macrophages (PAM's) filled with phospholipid vesicles have depressed microbicidal capacity, we tested the intrapulmonary bactericidal activity of newborn PAM's after surfactant treatment. Term newborn rabbits received intratracheally either homologous surfactant or one of two artificial phospholipid vesicle preparations followed by pulmonary aerosol infection with group B streptococci (GBS). Four hours after lung infection, phagocytic killing of GBS was reduced by 70-90% in animals treated with the homologous and one of the artificial surfactants compared with untreated animals or animals that received intrapulmonary injections of the surfactant vehicle (P less than 0.02). The other artificial phospholipid preparation decreased intrapulmonary inactivation of GBS by 30-40% compared with the controls. The phospholipid vesicles in the three preparations were avidly ingested and processed by newborn PAM's. The diminished in vivo killing of GBS was not attributed to decreased viability or phagocytic behavior of the PAM's toward GBS. The bactericidal defect that was evident in the newborn PAM's appeared related to the uptake of large phospholipid vesicles in the preparations rather than to the phospholipid content of the surfactants themselves. When in vitro conditions that stimulated the alveolar environment were used, the natural surfactant preparation promoted GBS proliferation, whereas the artificial preparations did not. Our findings indicate that surfactant administration reduces the bactericidal activity of neonatal PAM's. We conclude that additional investigations are needed to ascertain the effect of surfactant replacement therapy on lost defenses of the lung.

“SURFACTANT REPLACEMENT THERAPY” IN SURFACTANT DEPLETED RABBITS: LUNGFUNCTION, SURVIVAL AND BIOCHEMICAL ASPECTS

To study the effects of surfactant replacement therapy in Respiratory Distress Syndrome we induced surfactant deficiency in adult artificially ventilated (FiO2 1.0) rabbits by lung lavage. 19 Animals received natural sheep surfactant intratracheal, 6 served as controls.Results: In all surfactant treated animals PaO2 rose instantaneously from 11.31±5.00 to 37.78±13.40 kPa (mean±S.D.) (p<0.01). PaCO2 did not change significantly neither did dynamic lungcompliance. 9 Of the 19 surfactant treated animals were succesfully weaned off the ventilator. Static lung compliance was 1.07±0.30 in surviving, 0.71±0.08 in non-surviving (p<0.05) and 0.33±0.09 ml/cm H2O/kg bodyweight in controls (p<0.01). Phospholipid content of the lamellar body fraction, isolated from lung tissue increased from 0.97±0.33 to 2.50±0.10 μmol/g wet weight in the surfactant treated animals.Conclusion: Surfactant replacement results in an instantaneous rise in PaO2. This rise is not associated with a change in dynamic lung compliance, however static lung compliance is improved after surfactant replacement. Phospholipid analysis of the lamellar body fraction indicates that the administered surfactant phospholipids seem to be incorporated by the lamellar bodies of the type II alveolar cells.