Doses Of Exogenous Surfactant Research Articles

Who Needs a Second Dose of Exogenous Surfactant?

To identify prenatal and postnatal risk factors associated with surfactant redosing. Retrospective, single-regional center study including all infants born from 24+0 to 31+6weeks of gestation in the Marche Region, Italy, and admitted to a single level III regional NICU from January 1, 2004, to February 28, 2021. Clinical factors associated with surfactant redosing were identified through logistic regression analysis. Of 1615 consecutive admissions, 662 infants were treated with exogenous surfactant: 462 (70%) received a single dose and 200 (30%) received more than 1 dose (25.5% two doses and 4.5% three doses). Risk of redosing was higher for infants born to mothers with hypertension in pregnancy (OR 3.95, P<.001), for small for gestational age (SGA) infants (OR 3.93, P<.001) and when the first surfactant dose was 100mg/kg instead of 200mg/kg (OR4.56/4.61, P<.001). Infants with greater GA, delayed first surfactant administration, and milder respiratory distress syndrome had reduced risk of redosing. Infants who required multiple surfactant doses had a higher rate of bronchopulmonary dysplasia and mortality, as well as longer duration of respiratory support than patients that received 1 dose. Hypertension in pregnancy and SGA status were found to be statistically and clinically significant predictors of surfactant redosing. Understanding the pathophysiology of these conditions requires further investigation.

Who needs a second dose of exogenous surfactant?

Who needs a second dose of exogenous surfactant?

A Case of Acute Lung Failure: Administration of Exogenous Surfactant As A Successful Treatment

We are describing a case of acute lung injury associated with uraemia and haemorrhagic shock. The treatment has consisted of the administration of repeated and equal doses of exogenous surfactant for 72 hours, starting within 48 hours from the beginning of the symptoms. A rapid improvement in the lung function has been detected, with consequent weaning from mechanical ventilation. The CT scan has confirmed the enhancement of atelectasis and hypoventilation. This case highlights the pivotal role of the administration of exogenous surfactant in selected cases of acute lung injury. If an anti-inflammatory effect is needed, we suppose that a repeated treatment with fractional dose is more effective.

Vascular endothelial growth factor (VEGF) in tracheal aspirates from preterm infants: effect of surfactant therapy

ObjectivesVascular endothelial growth factor (VEGF) regulates vascular endothelial cell differentiation and angiogenesis, and maturation of epithelial cells of the developing lungs. Different reports have described the role of VEGF in...

Metabolic precursors of surfactant disaturated-phosphatidylcholine in preterms with respiratory distress

Our objective was to study the metabolic precursors of surfactant disaturated-phosphatidylcholine (DSPC) in preterm infants with respiratory distress syndrome (RDS) on mechanical ventilation. We performed 46 DSPC kinetic studies in 23 preterms on fat-free parenteral nutrition and mechanical ventilation (birth weight = 1167 +/- 451 g, gestational age = 28.5 +/- 2.0 weeks). Eight infants received a simultaneous intravenous infusion of U(13)C-glucose and [16,16,16](2)H-palmitate, eight infants received U(13)C-glucose and (2)H(2)O, and seven received U(13)C-palmitate and (2)H(2)O. Surfactant DSPC kinetics were calculated from the isotopic enrichments of DSPC-palmitate from sequential tracheal aspirates and its metabolic precursors in plasma or urine. DSPC fractional synthesis rate (FSR) was 17 +/- 11, 21 +/- 16, and 15 +/- 6%/day from glucose, palmitate, and body water, respectively (P = 0.36). DSPC-FSR from U(13)C-glucose and (2)H(2)O were significantly correlated and yielded similar estimates (difference of -0.1 +/- 3%) (P = 0.91). The difference in the 15 infants receiving palmitate versus (2)H(2)O or palmitate versus glucose was +6.0 +/- 12%/day (P = 0.21). There was a significant correlation between DSPC-FSRs from plasma glucose and plasma FFA. The contribution of glucose versus palmitate to DSPC-FSR was 49 +/- 20% versus 51 +/- 20%, respectively. Plasma glucose and FFA showed similar contributions to DSPC-FSR in infants with RDS and fat-free parenteral nutrition. FSRs from (2)H(2)O or glucose were highly correlated.

An Extremely Low-Birthweight Infant Who Has Scrotal Discoloration

### Prenatal History: ### Birth History: ### Hospital Course: The infant had respiratory distress syndrome that required mechanical ventilation and three doses of exogenous surfactant; he was extubated to nasal continuous positive airway pressure on the eighth postnatal day. Additionally, he received three doses of prophylactic indomethacin during the first 72 hours after birth. His ductus arteriosus was closed upon completion of indomethacin treatment. He was treated with cefotaxime and ampicillin for the first eight postnatal days for culture-negative presumed sepsis. Within the first 24 hours of birth, he received dopamine, an insulin infusion to treat hyperkalemia, and nitric oxide for 36 hours due to refractory hypoxemia. His nutritional requirements were delivered with total parenteral nutrition; enteral feedings had not been started. He did not receive postnatal steroids. Nine days after birth, he developed inguinal and scrotal discoloration (Fig. 1). These findings were associated with hypotension (mean arterial pressure, 20 mm Hg), decreased urine output (0.13 mL/kg per hour), hypothermia (core body temperature of 96.4°F [35.8°C]), and five episodes of …

Economic outcome for intensive care of infants of birthweight 500–999 g born in Victoria in the post surfactant era

Objective: To determine the incremental cost of improving the outcome for extremely low birthweight (ELBW, birthweight 500–999 g) infants born in Victoria after the introduction of exogenous surfactant (the post surfactant era). Methodology: This was a geographically determined cohort study of ELBW children in Victoria, Australia of consecutive livebirths born in three distinct eras: (i) 1979–80 (n= 351); (ii) 1985–87 (n= 560); and (iii) 1991–92 (n= 429). Exogenous surfactant was first used in Victoria in March, 1991. The consumption of nursery resources per livebirth, and the survival and sensorineural disability rates at 2 years of age for each era were investigated. Utilities were assigned as follows: 0 for dead, 0.4 for severe disability, 0.6 for moderate disability, 0.8 for mild disability, and 1 for no disability. Utilities were multiplied for more than one disability. Dollar costs were assumed to be $1470 ($A 1992) per day of assisted ventilation, and one dose of exogenous surfactant was assumed to be equivalent to one third of a day of assisted ventilation. Cost‐effectiveness (additional costs per additional survivor or life‐year gained) and cost‐utility (additional costs per additional quality‐adjusted survivor or life‐year gained) ratios were calculated for the pre‐surfactant era (1985–87 vs 1979–80), and for the post surfactant era (1991–92 vs 1985–87). Results: Considering only the costs incurred during the primary hospitalization, cost‐effectiveness and cost‐utility ratios were lower (i.e. economically better) in the post surfactant era than in the pre‐surfactant era (pre‐surfactant vs post surfactant; S7040 vs$4040 per life year gained; $6700 vs$5360 per quality‐adjusted life year gained). Both ratios fell with increasing birthweight. In contrast with the pre‐surfactant era, cost‐utility ratios were less favourable than cost‐effectiveness ratios in the post surfactant era. With costs for long‐term care of severely disabled children added, both cost ratios were higher in the post surfactant era. Conclusion: The incremental cost during the primary hospitalization of improving the outcome for ELBW infants has fallen in the post surfactant era.

Distribution of a Second Dose of Exogenous Surfactant in Rabbits with Severe Respiratory Failure

Newborn infants with respiratory distress who fail to respond to surfactant treatment receive a second dose of surfactant. The effect of this strategy on the distribution of surfactant to the lung is unknown. We therefore investigated the distribution of the first (100 mg/kg body weight) and second dose (50 mg/kg body weight) of surfactant (Alveofact) in lung-lavaged rabbits (n = 6). We used 141Ce- and 103Rn-labeled microspheres that were mixed with the first and second dose of surfactant, respectively. Arterial PO2 increased from 5.7 +/- 1.1 to 10.6 +/- 2.0 kPa (p < 0.05) (mean +/- SD) after the first and from 20.1 +/- 3.8 to 30.1 +/- 2.5 kPa (p < 0.05) after the second dose. Thereafter the rabbits were killed, and the lungs were cut into 200 pieces. The radioactivity of Ce and Rn microspheres was measured and distribution histograms were obtained. Histograms of the first, second, and the total dose of surfactant showed similar nonuniform distribution. Correlation coefficients of the Ce and Rn radioactivity in the different lung lobes widely ranged per lung lobe per rabbit. In addition, the percentage of the number of lung pieces that received an amount of surfactant that was less than the calculated endogenous surfactant pool decreased from 12.5 +/- 3.2% to 8.5 +/- 3.0% (p < 0.05) after the first and second dose, respectively. This indicates that the second dose was directed both to areas that initially received surfactant and to areas that were still surfactant-deficient. The surfactant-deficient areas were aerated after this second dose, resulting in a further rise in PO2.(ABSTRACT TRUNCATED AT 250 WORDS)

In Vivo Studies of Aerosolized Exogenous Surfactant

Exogenous surfactant administration is currently being investigated in patients with the adult respiratory distress syndrome CARDS). Several animal studies and recent clinical experience suggest that this therapy has promise. Currently, the optimal method of delivery is unknown. Both instillation of large doses of exogenous surfactant as well as aerosolization with small quantities of surfactant deposited in lung tissue have been evaluated. Both methods of delivery have significantly improved lung function in animal models of lung injury and are currently being evaluated in multicenter clinical trials. From the animal model of lung injury in which injury was induced by repetitive saline lung lavage, it has been shown that aerosolized surfactant was, in some cases, superior to instilled surfactant. With improvements in technology resulting in increased aerosolized surfactant deposition within lung tissue, consistent improvements in physiologic parameters have been shown suggesting a dose-response phenomeno...

The fate of exogenous surfactant in neonates with respiratory distress syndrome.

Respiratory distress syndrome (RDS) in newborn neonates is characterised by deficient secretion of surfactant from type III alveolar cells. Administration of surfactant to airways acutely decreases the degree of respiratory failure and increases the survival rate in neonates with RDS. Clinically available surfactants are lipid extracts derived from animal lung lavage or from whole lung. Synthetic surfactants contain phospholipids or additional spreading agents. An optimal exogenous surfactant would be efficacious, nontoxic and nonimmunogenic, resistant to oxidants and proteolytic agents, widely available at reasonable cost and manufactured with little batch-to-batch variability. Surfactant has been instilled into the airways as a bolus infusion through the endotracheal tube. In addition, surfactant may be given by aerosolisation or continuous infusion into the airways. Suggested dosages range from 50 to 200 mg/kg. Exogenous surfactant is cleared from the epithelial lining fluid (ELF) mainly by alveolar epithelial cells, although alveolar macrophages and the central airways may also contribute to clearance of the drug. Only small quantities of surfactant actually enter the blood stream. A significant fraction of surfactant is taken up, processed, and secreted back into the alveolar space by type II alveolar cells. This process is termed recycling. Phosphatidylglycerol, given to small premature neonates as a component of exogenous human surfactant, has an apparent pulmonary half-life of 31 +/- 3 hours (n = 11). The apparent pulmonary half-life of the main surfactant component dipalmitoyl phosphatidylcholine is 45 hours (n = 3) and that of surfactant protein A is about 9 hours (n = 4). A relationship between the dose of exogenous surfactant and its concentration in the ELF has been demonstrated. Some neonates with RDS respond poorly to surfactant therapy. The reasons for this include insufficient levels of surfactant in the ELF, uneven distribution of exogenous surfactant, inability of exogenous surfactant to enter the metabolic pathways, inhibition of surface activity by plasma-derived proteins, or inactivation of surfactant as a result of proteases, phospholipases, or oxygen free radicals. In addition, surfactant therapy may be ineffective in neonates with respiratory failure caused by factors other than surfactant deficiency. The efficacy of exogenous surfactant can be improved by increasing the dosage of surfactant and by administration of surfactant very early in respiratory failure.