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At least 19 recordsLinked to original sources
PubMed1985

The long-term pulmonary sequelae of prematurity: the role of familial airway hyperreactivity and the respiratory distress syndrome.

Respiratory distress syndrome of the newborn, prematurity, and familial airway hyperreactivity may contribute to long-term pulmonary sequelae. We assessed the role of each by testing pulmonary function and airway reactivity in 11 prematurely born children who survived the respiratory distress syndrome and in 11 prematurely born children who had no neonatal respiratory disease, each of whom was paired with a sibling born at term. The subjects were between 7 and 12 years of age when studied. Airway reactivity was also assessed in their mothers. The group who had had the respiratory distress syndrome had higher ratios of residual volume to total lung capacity and lower values for forced expiratory volume in one second than did their siblings or normal controls (P less than 0.01). Expiratory flow was decreased in both groups born prematurely (P less than 0.02) and was related to neonatal exposure to oxygen (r = -0.71, P less than 0.02). The incidence of airway hyperreactivity was elevated in all groups, including the mothers. These data suggest that long-term pulmonary sequelae of the respiratory distress syndrome of the newborn are related to the disease, its treatment, or both, and to airway hyperreactivity. In prematurely born children without neonatal lung disease, the sequelae are related to airway hyperreactivity. The possibility of a relation between familial airway hyperreactivity and premature birth is suggested.

Airway Obstruction↗
PubMed2005

Vascular endothelial growth factor in preterm infants with respiratory distress syndrome.

Respiratory distress syndrome (RDS) secondary to surfactant deficiency is a common cause of morbidity and mortality in premature infants. Increasing evidence suggests that vascular endothelial growth factor (VEGF) may contribute to surfactant secretion and pulmonary maturation. However, differences in cord blood VEGF concentrations in infants with and without respiratory distress syndrome have not been reported. We hypothesized that premature infants with higher VEGF levels in cord blood had a lower risk of developing RDS. Cord blood samples were obtained from preterm infants born at 32 weeks of gestation or earlier. Infants were excluded if there was evidence of prenatal maternal infection or any infection within the first 3 days of life. Cord blood VEGF levels were measured using an enzyme-linked immunosorbent assay (ELISA). We found that neonates with clinically diagnosed RDS had a lower gestational age (GA), lower birth weight (BW), higher incidence of mechanical ventilation requirements, longer duration of mechanical ventilation, and lower Apgar scores at 1 and 5 min. Infants with RDS had significantly lower cord blood VEGF levels. GA, BW, premature rupture of membranes (PROM), and antenatal steroid treatment were not associated with changes in cord blood VEGF levels. The specificity of cord blood VEGF above 34 pg/ml for predicting the absence of RDS was 86%, the sensitivity was 53%, the positive predictive value was 84%, and the negative predictive value was 56%. Our data demonstrated that cord blood VEGF elevation was significantly correlated with an absence of RDS.

Apgar Score↗
PubMed1994

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.

Animals↗
PubMed2002

Surfactant proteins and genetic predisposition to respiratory distress syndrome.

Respiratory distress syndrome (RDS) is caused by surfactant deficiency at birth. The risk of RDS decreases from the gestational age of 24 weeks to full-term. Genetic and acquired factors additionally influence the risk of RDS. Surfactant deficiency in RDS is mainly caused by immaturity and a lack of differentiation of the alveolar epithelial cells involved in surfactant synthesis and secretion. A network of hormones and growth factors regulate perinatal development. Host-related factors, including the levels of expression of surfactant proteins (SP), modulate the responsiveness of growth factors. SP-A has roles in surface activity and regulatory roles particularly in innate immunity; SP-B is essential for the processing of surfactant and for the surface activity; SP-C has roles in surfactant metabolism and function; the regulatory roles of SP-D mainly pertain to innate immunity. The genetic variation of SP-A and SP-B genes and the risk of RDS have been studied. Both SP-A and SP-B associate with susceptibility to RDS. The association between the SP-A allele and genotypes and the risk of RDS is dependent on the SP-B genotype and significantly influenced by the degree of prematurity, antenatal glucocorticoid therapy, multiple birth, and birth order. The alleles/genotypes of SP-A, SP-C, or SP-D also associate with several other inflammatory lung and airway diseases. Rare mutations in SP-B or SP-C cause serious, often fatal lung diseases. Genetic and post-genomic research is likely to eventually result in new diagnostic applications and specific therapies for the prevention of respiratory failure and inflammatory lung diseases.

Embryonic and Fetal Development↗
PubMed2003

Plasma neutrophil lipocalin, elastase-alpha1-antitrypsin complex and neutrophil protease 4 in preterm infants with respiratory distress syndrome.

Respiratory distress syndrome (RDS) and chronic lung disease of prematurity (CLD) are associated with inflammation of the airways and interstitial tissue of the lung. It is hypothesized that RDS severity and the risk of developing CLD may be correlated with neutrophil gelatinase-associated lipocalin (NGAL), a marker of leucocyte activity, human elastase-alpha1-antitrypsin complex (HEAT) or free and complexed neutrophil protease 4 (NP4), markers of proteolytic enzyme secretion from granulocytes. Thirty-three preterm infants with RDS were enrolled in the study and plasma sampled between 3 and 14 days of life. NGAL, HEAT and NP4 concentrations varied widely in infants with RDS. Significant correlations between subsequent development of CLD and plasma concentrations of HEAT and NP4, respectively, were found on days 3-4 of life, p=0.006 and p=0.02, respectively.

Acute-Phase Proteins↗
PubMed1991

Effect of a single inflation of the lungs on oxygenation during total extracorporeal carbon dioxide removal in experimental respiratory distress syndrome.

Respiratory distress syndrome (RDS) was modelled in rabbits using pulmonary lavage to remove surfactant. The stability of the resulting pressure-volume hysteresis of the lungs in vivo was studied with the aid of whole-body plethysmography during apnoeic oxygenation made possible by total extracorporeal carbon dioxide removal. Systemic oxygen delivery was measured as a function of the constant airway pressure during apnoea. In 6 subjects a single brief inflation of the lungs to 3.5 kPa resulted in a doubling of both expired lung volume (volume above functional residual capacity) and arterial oxygen partial pressure at an airway pressure of 0.65 kPa. These rises were well maintained for 40 min following the inflation. In a further 6 subjects with RDS single inflations permitted optimum systemic oxygen transport to occur at the low airway pressure of 0.3 kPa, similar to the optimum airway pressure in 6 healthy control subjects. Where pressure-volume hysteresis is present in RDS it can be exploited during apnoeic oxygenation, and probably during high frequency ventilation, to improve oxygenation by the use of infrequent single inflations of the lungs.

Animals↗
PubMedDate not supplied

Current perspectives on the drug treatment of neonatal respiratory distress syndrome.

Respiratory distress syndrome (RDS) in preterm neonates is caused by a lack of alveolar surfactant, which leads to decreased pulmonary compliance and increased work of breathing. Effective therapy for RDS has reduced mortality at the expense of increasing the number of preterm survivors with chronic lung disease. Drugs such as corticosteroids, proterelin (thyrotropin-releasing hormone) and ambroxol have all been administered to mothers to promote fetal lung maturation, but of these only corticosteroids have been proven to be of benefit. The management of RDS includes assisted ventilation and surfactant replacement therapy. There are several surfactant preparations, some synthetic and others derived from animal lungs, and recent research has been directed at finding which, if any, is superior. The timing of the first dose has also been studied. Prophylactic surfactant administration within the first 15 minutes of life appears to be more efficacious than later treatment for very preterm babies, but could lead to some neonates being treated unnecessarily and perhaps being exposed to adverse effects. Newer treatments for neonates with RDS are aimed at reducing the pulmonary inflammation that occurs as a result of ventilatory barotrauma and oxygen toxicity. Superoxide dismutase, along with other antioxidants, may be beneficial as a free radical scavenger to reduce oxygen toxicity. Inhaled nitric oxide may reduce oxygen requirements by reducing ventilation-perfusion mismatching, and early treatment with corticosteroids may reduce pulmonary inflammation. All of these treatments are currently undergoing clinical trials.

Humans↗
PubMed1989

[Clinical and pathologic comparison of adult respiratory distress syndrome and infant respiratory distress syndrome].

The authors compared the clinical and pathological findings between adult respiratory distress syndrome (ARDS), and infant respiratory distress syndrome (IRDS). In ARDS, the most common causes were injury, infection, shock and acidosis. The clinical course was longer. The weight of the lungs increased markedly, the hyaline membrane formation in the alveoli was late in the clinical course, and the degree of edema in the interstitium of the lungs and microthrombosis within the blood vessels was more serious. The pathogenesis of ARDS was related to the activation of the complements and neutrophils by inflammation in which proteinase, oxygen radical, thromboxane, leukotriene and prostaglandin were released. Thus the endothelial cells of the blood vessels and capillary-alveoli membrane were damaged by these mediators. On the other hand, the main contributory factors of IRDS were suffocation of premature fetus by various reasons in the uterus and aspiration of meconium during delivery by the infant. The clinical course was shorter, alveolar hemorrhage and collapse were severe and hyaline membrane in alveoli was formed in early stage of the clinical course. Insufficiency of surfactant in premature fetus, damage of the surfactant system by hypoxia, aspiration of foreign materials and defect of the epithelial cells of infant were the pathogenic factors of IRDS, they resulted in increase of permeability of fluid and, as a result, led to pulmonary edema and atelectasis.

Adolescent↗
PubMed1996

Aerosolized surfactant in adults with sepsis-induced acute respiratory distress syndrome. Exosurf Acute Respiratory Distress Syndrome Sepsis Study Group.

BACKGROUND: Patients with acute respiratory distress syndrome (ARDS) have a deficiency of surfactant. Surfactant replacement improves physiologic function in such patients, and preliminary data suggest that it may improve survival. METHODS: We conducted a prospective, multicenter, double-blind, randomized, placebo-controlled trial involving 725 patients with sepsis-induced ARDS. Patients were stratified according to the risk of death at base line (indicated by their score on the Acute Physiological and Chronic Health Evaluation [APACHE III] index) and randomly assigned to receive either continuously administered synthetic surfactant (13.5 mg of dipalmitoylphosphatidylcholine per milliliter, 364 patients) or placebo (o.45 percent saline; 361 patients) in aerosolized form for up to five days. RESULTS: The demographic and physiologic characteristics of the two treatment groups were similar at base line. The mean (+/- SD) age was 50 +/- 17 years in the surfactant group and 53 +/- 18 years in the placebo group, and the mean APACHE III scores at randomization were 70.4 +/- 25 and 70.5 +/- 25, respectively. Hemodynamic measures, measures of oxygenation, duration of mechanical ventilation, and length of stay in intensive care unit did not differ significantly in the two groups. Survival at 30 days was 60 percent for both groups. Survival was similar in the groups when analyzed according to APACHE III score, cause of death, time of onset and severity of ARDS, presence or absence of documented sepsis, underlying disease, whether or not there was a do-not-resuscitate order, and medical center. Increased secretions were significantly more frequent in the surfactant group; the rates of other complications were similar in the two groups. CONCLUSIONS: The continuous administration of aerosolized synthetic surfactant to patients with sepsis-induced ARDS had no significant effect on 30-day survival, length of stay in the intensive care unit, duration of mechanical ventilation, or physiologic function.

Administration, Inhalation↗
PubMed1992

Respiratory timing in intubated neonates with respiratory distress syndrome.

Respiratory timing was studied in 100 babies ventilated for respiratory distress syndrome (RDS) during a brief period of continuous positive airway pressure. For the 76 spontaneously breathing babies the mean (SD) inspiratory and expiratory times were 0.31 (0.06) and 0.41 (0.12) seconds. Respiratory rate was predominantly modulated by expiratory time. The severity of RDS was the main influence on expiratory time.

Female↗
PubMed2000

Evolution of leukotriene B4, peptide leukotrienes, and interleukin-8 plasma concentrations in patients at risk of acute respiratory distress syndrome and with acute respiratory distress syndrome: mortality prognostic study.

OBJECTIVE: To compare the evolution of plasma concentrations of leukotriene (LT) B4, LTC4, LTD4, and interleukin (IL)-8 in patients with acute respiratory distress syndrome (ARDS) and in patients at risk of ARDS and to assess the value of these mediators in predicting mortality rate from ARDS. DESIGN: A case-control study comparing ARDS patients and patients at risk of ARDS as well as survivors and nonsurvivors with ARDS. SETTING: Hospital intensive care unit, laboratory, and department of hematology. PATIENTS: Twenty-one patients with ARDS and 14 patients at risk of ARDS. INTERVENTION: Arterial blood samples were collected on days 0, 1, and 5 after admission to the intensive care unit. MEASUREMENTS AND MAIN RESULTS: LTs were extracted, separated by high-pressure liquid chromatography and quantified by enzyme immunoassay. IL-8 was analyzed by ELISA. Plasma concentrations of LTB4 and LTC4 plus LTD4 were significantly higher in ARDS patients than in patients at risk of ARDS during the first 24 hrs. Concentrations of IL-8 were also higher in ARDS patients than in patients at risk throughout the study, although the differences between the two groups were only significant on day 5. Only the plasma concentration of LTB4 on day 1 was a marker of ARDS (72.2% sensitivity, 84.6% specificity). A logistic regression analysis showed that LTB4 and IL-8, on day 1, were markers of mortality rate in patients with ARDS (70.0% sensitivity, 87.5% specificity). CONCLUSIONS: LTs are elevated during the early phases of ARDS, whereas IL-8 increases throughout the study. The evaluation of LTB4 and IL-8 may be useful prognostic indices in patients with early phase ARDS after admission to the intensive care unit.

Biomarkers↗
PubMed2000

Inositol for respiratory distress syndrome in preterm infants.

BACKGROUND: Inositol is an essential nutrient required by human cells in culture for growth and survival. Inositol promotes maturation of several components of surfactant and may play a critical role in fetal and early neonatal life. OBJECTIVES: To assess the effectiveness/safety of supplementary inositol in preterm infants with RDS in reducing adverse neonatal outcomes. SEARCH STRATEGY: Medline, Embase, and Reference Update Databases were searched in August 1997 using key words: inositol and infant-newborn and random allocation or controlled trial or randomized trial (RCT). The reference lists of identified RCTs, personal files and Science Citation Index were searched. Unpublished additional information was obtained from the authors of one RCT published in abstract form. SELECTION CRITERIA: All randomized controlled trials of inositol supplementation to preterm infants with a control group that received a placebo or no intervention were included. Outcomes of interest were bronchopulmonary dysplasia (BPD), death, BPD or death, retinopathy of prematurity (ROP), intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), and sepsis. DATA COLLECTION AND ANALYSIS: Data on neonatal outcomes were abstracted independently by the two researchers and any discrepancy was resolved through consensus. Revman was used for analysis of the data. MAIN RESULTS: Four reports of three RCTs were identified. One report was a duplicate publication. The outcome of death or bronchopulmonary dysplasia was reported in two trials, and was found to be significantly reduced (RR 0.56, 95% CI 0.42, 0.77; RD -0.215, 95% CI -0.323, -0.107). The outcome of death was reported in two trials and was found to be significantly reduced (RR 0.48, 95% CI 0.28, 0.80; RD -0.131, 95% CI -0.218, -0.043). Retinopathy of prematurity, stage 4 or needing therapy, was reported in two trials, and was found to be significantly reduced (RR 0.09, 95% CI 0.01, 0.67; RD -0.078, 95% CI -0.128, -0.027). Intraventricular hemorrhage, grade III-IV, was significantly decreased (RR 0.55, 95% CI 0.32, 0.95; RD -0.090, 95% CI -0.170, -0.010). Neither sepsis nor necrotizing enterocolitis outcomes were increased. When a secondary analysis was done excluding a study published in abstract form, the results differed only in that there was a significant reduction in retinopathy of prematurity, any stage (RR 0.53, 95% CI 0.29, 0.97; RD -0.082, 95% CI -0.159,-0.005). REVIEWER'S CONCLUSIONS: Inositol supplementation results in statistically significant and clinically important reductions in important short-term adverse neonatal outcomes. A multi-center RCT of appropriate size is justified to confirm these findings.

Dietary Supplements↗
PubMed2003

Variable tissue expression of transferrin receptors: relevance to acute respiratory distress syndrome.

Acute respiratory distress syndrome (ARDS) is associated with altered plasma and lung iron chemistry. Iron can promote microbial virulence and catalyse pro-oxidant reactions, thereby contributing to the oxidative stress that characterises the syndrome. Therefore, the expression of ferritin and transferrin receptors (TfR) were sought in the lungs and hearts of rodents treated with lipopolysaccharide (LPS), and measurements of TfR and ferritin protein expression were taken from lung biopsy specimens from patients with ARDS and appropriate controls. TfR messenger ribonucleic acid (mRNA) was significantly upregulated in the lungs and significantly downregulated in the hearts of rats 4 h after LPS. Ferritin mRNA levels (light and heavy chains) remained unaltered. Protein TfR levels were significantly upregulated in lungs and downregulated in hearts 4 h post-LPS. Ferritin protein levels were significantly downregulated in lungs compared to baseline values but were unaltered in hearts. Nonhaem iron levels were increased in lungs and decreased in hearts, and iron-regulatory-protein activity increased in hearts but not lungs. TfR protein levels were significantly increased in lung biopsies from patients with ARDS compared to controls. Transferrin receptors are upregulated in rodent lungs during inflammation but are downregulated in the heart. Transferrin receptor protein levels were significantly increased in the lungs in clinical acute respiratory distress syndrome. These findings have implications for the pathogenesis of acute respiratory distress syndrome, especially in relation to the role of iron as a mediator of oxidative stress.

Adult↗
PubMed1999

Management of patients with acute respiratory distress syndrome.

Acute respiratory distress syndrome is a complex clinical syndrome of respiratory failure that presents a challenge to every critical care team. Since the first clear description by Ashbaugh et al more than 30 years ago, much has been learned about the pathophysiologic process that occurs within the lungs after they suffer either a direct or indirect injury. Unfortunately, little success has been achieved in improving outcomes; however, hope is on the horizon. Current research evaluating optimal ventilator management, ECMO, the use of inhaled nitric oxide, and other experimental management strategies will hopefully combine to produce improved outcomes.

Critical Care↗