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Results for “HYALINE MEMBRANE DISEASE”

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At least 19 recordsLinked to original sources
PubMed1977

[Recent acquisitions in hyaline membrane disease].

Hyaline membrane disease is an important factor in the postnatal mortality of prematures. Its pathogenesis is examined. Prematurity, maternal diabetes, and caesarean section are seen as predisposing causes. Delayed biochemical maturation of the lung (shown by a low lecithin-sphyngomyelin ration in the amniotic fluid and probably caused by hypophyseal-adrenal insufficiency) results in an absence of surfactant. Labour stimulates its production by massive release of endogenous cortisol. The part played by betamethasone and other substances in prophylaxis is discussed. It is felt that, at present, the availability of preformed tensioactive factors alone can achieve the decidedly improved prognosis required in so serious a disease.

Female↗
PubMed1990

Childhood pulmonary function following hyaline membrane disease.

Hyaline membrane disease per se is not associated with abnormal lung function or increased nonspecific airway reactivity in childhood or adulthood. Very-low-birth-weight infants who survive almost routinely in neonatal ICUs are at risk, however, for developing airflow obstruction and having airway hyperreactivity as children, and for having recurrent bouts of wheezing, cough, and respiratory infections. Neonates who develop BPD have the greatest risk of abnormal pulmonary function as children. Continued research into the prevention of premature birth and into the causes of neonatal lung injury, combined with improvements in the neonatal ICU and follow-up treatment, will undoubtedly contribute to improvement in the clinical course of premature infants.

Bronchial Provocation Tests↗
PubMedDate not supplied

Chevalier Jackson Lecture: In quest of the prevention of hyaline membrane disease.

Hyaline membrane disease or respiratory distress syndrome of prematurely born infants is more common in males, in Caucasians, has a familial predisposition, and is associated with maternal diabetes and delivery by cesarean section before the onset of labor. Now known to be the sequel of surfactant deficiency, it can be predicted prenatally by assay of amniotic liquid for surface active materials produced by the fetal lung. Deficiency of adequate surfactant synthesis or secretion can result in low levels of lecithins and other phospholipids in amniotic liquid. Lung maturation can result in low levels of lecithins and other phospholipids in amniotic liquid. Lung maturation can be accelerated if labor or elective delivery can be deferred at least 24 hours. Glucocorticoids given to the mother cross the placenta and enter fetal lung tissues; specific receptors exist in the lung which permit glucocorticoids to promote cell differentiation and surfactant synthesis precociously. Clinical trials support the efficacy and lack of short-term toxicity of glucocorticoids in human pregnancy after 28 weeks gestation in the event of premature onset of labor. Maternal toxemia, infection or illness which may be aggravated by glucocorticoids may contraindicate prenatal treatment. Postnatally endogenous glucocorticoids accelerate lung maturation, and further administration confers no additional benefit.

Animals↗
PubMed1990

[Problems posed by the development of exogenous surfactants for the treatment of hyaline membrane disease].

The hyaline membrane disease (HMD) is a respiratory distress occurring at birth of some premature infants, attributed to an endogenous pulmonary surfactant deficiency. The present treatments are iatrogenic and inefficient for the most diseased infants. The exogenous surfactant supplementation intends to give to the baby formulations playing in vivo the role of the natural surfactant. The research developed for the formulation and the diffusion of these exogenous surfactants have to solve physicochemical problems but also of industrial production and of safety use. In spite of their adequate physicochemical and pharmacological properties, surfactants of natural sources, for industrial grounds, are not still distributed at a large scale. The efficiency of artificial surfactants is variable, and the use of non-biodegradable molecules in several preparations let to safety problems. The development of new types of artificial surfactants, more efficient and safe, implies a better knowledge of the physico-chemical mechanisms intervening in the pulmonary surfactant dynamics.

Chemical Phenomena↗
PubMed1984

Pulmonary epithelial permeability in hyaline-membrane disease.

Neonatal hyaline-membrane disease is complicated by pulmonary edema, yet left atrial pressures are normal. Alveolar-capillary-membrane permeability may therefore be increased. To assess pulmonary epithelial permeability, we measured the pulmonary clearance and half-life of aerosolized 99mTc-diethylenetriamine pentacetate (99mTc-DTPA) on 31 occasions in 15 intubated premature infants with hyaline-membrane disease. Three infants with respiratory failure due to other diseases were studied on four occasions. All studies of infants with hyaline-membrane disease that were performed in the first 72 hours of life demonstrated a biphasic clearance curve with a rapid-phase half-life of 1.6 +/- 0.6 minutes (mean +/- S.D.). As these infants recovered, the curve became monophasic with a half-life of 56.0 +/- 32.1 minutes. Two infants remained dependent on oxygen and ventilator support and had persistent biphasic curves with a rapid-phase half-life of 1.5 +/- 0.7 minutes. All infants without hyaline-membrane disease had monophasic curves with a half-life of 65.4 +/- 33.6 minutes. Using a similar technique, we observed that newborn lambs and piglets have a monophasic pulmonary clearance of 99mTc-DTPA (114 +/- 59 minutes in lambs and 52.5 +/- 16.3 minutes in piglets). We conclude that the lungs of neonates with hyaline-membrane disease are abnormally permeable to small solutes and that this abnormality persists in infants with subsequent chronic lung disease.

Aerosols↗
PubMed1997

Pulmonary function in infants with neonatal chronic lung disease with or without hyaline membrane disease at birth.

We studied whether neonatal chronic lung disease (NCLD), hyaline membrane disease (HMD) and differences in ventilatory support affected pulmonary function during the first year of life, in 65 infants born prematurely. The relationship between body weight and oxygen consumption (V'O2) was also analysed. The study comprised 14 infants without cardiorespiratory disease, 19 infants with HMD but without NCLD, 9 infants with NCLD without prior HMD, and 23 infants with NCLD following HMD. At 6 and 12 months corrected postnatal age, static respiratory system compliance (Crs) was measured by weighted spirometry and the functional residual capacity by closed circuit helium dilution (FRCHe) combined with assessment of ventilation distribution from the mixing index (MI). Ventilatory support during the first 5 days of therapy was quantified from peak inspiratory pressure (PIP), mean airway pressure (MAP) and fractional inspiratory concentration of oxygen (FI,O2). Infants with NCLD had a shorter duration of gestation and lower birth weight than those without NCLD (Wilcoxon, p=0.002 and p=0.001, respectively). Pulmonary function at 6 and 12 months corrected age was not different between NCLD infants with or without HMD at birth. Infants with NCLD had lower Crs and MI than those without NCLD (analysis of variance (ANOVA), p<0.011), but their FRCHe was not different. V'O2 adjusted for body weight was comparable in the four groups. PIP and FI,O2 were higher (Wilcoxon, p<0.01) in the NCLD infants than in those with HMD alone, but MAP was not different. Except for FI,O2, these indices were not different among the infants with NCLD. We conclude that birth weight is the major determinant of the development of neonatal chronic lung disease. At 6 and 12 months corrected age, the abnormal pulmonary function is not associated with prior hyaline membrane disease.

Birth Weight↗
PubMed1975

Studies on the prevention of respiratory distress syndrome of infants due to hyaline membrane disease with plasminogen.

Hyaline membrane disease (HMD) is leading single cause of death of newborn, premature infants. The "hyaline membranes" consist chiefly of fibrin. The clinical manifestation of HMD is the respiratory distress syndrome (RDS). Infants with RDS were treated with urokinase-activated human plasmin in a previous clinical trial. Survival rate was increased in the plasmin treated group as compared to the placebo recipients. However, cost and difficulty in the preparation of the enzyme made this treatment impractical. We, as well as others, have shown the premature infants lack serum plasminogen; thus they are unable to develop effective fibrinolysis and are defenseless against pulmonary fibrin deposition. Therefore, plamsinogen was tested as a possible preventive agent in RDS due to HMD. In a double blind, randomized study, infants between 1 and 2.5 kg birth weight received plasminogen or placebo shortly after birth, and were then followed for development of RDS. After 100 infants were entered into the study, the code was broken and results were evaluated to assure safety of the procedure. Among the 100 infants, 51 received placebo, 49 received plasminogen. Among the infants who received placebo, seven developed mild, and ten developed severe respiratory distress; of these ten, five died with histopathologically documented HMD. Two infants died from causes other than HMD. Among the 49 infants treated with plasminogen, 13 developed mild and three developed severe respiratory distress. There was no death due to HMD. Two deaths were due to other causes. Factors placing the infant at risk from HMD (degree of prematurity, sex, cesarean section, bleeding episodes during pregnancy, maternal diabetes) were found to be evenly distributed between control and treated groups. Since completing the first phase of the study, data of an additional 277 infants has become available. Although the code was not broken in this series, a preliminary look at mortality data in comparison with mortality data of the first series of 100 (in which the code was broken) suggests that preventive activity of plasminogen has been maintained in the second phase of the study.

Birth Weight↗
PubMed1976

Pulmonary changes in neonatal sepsis to group B beta-hemolytic Streptococcus: relation of hyaline membrane disease.

The radiographic changes of hyaline membrane disease were seen in seven of eight infants with group B beta-hemolytic streptococcal sepsis. Hyaline membranes were found throughout the lungs of all six infants who were examined after death. The most striking finding was the presence of group B streptococci within the membranes of five infants. Streptococci were so numerous in one instance that they comprised the bulk of the membrane. Another infant uas thought to have classical hyaline membrane disease until numerous group B streptococci were found within the membranes when lung sections were examined with special stains. No other organisms were identified within the membranes of any infant. These findings suggest that infection with group B streptococcus may cause a syndrome clinically and radiologically indistinguishable from hyaline membrane disease.

Female↗
PubMed1976

Air embolus following pulmonary interstitial emphysema in hyaline membrane disease.

Two cases of hyaline membrane disease are presented complicated by severe, interstitial emphysema and resulting in death from air embolus. This is consistent with the experimental evidence of other investigators that shows that such an air embolus may be more common complication of hyaline membrane disease than previously expected.

Embolism, Air↗
PubMed1987

Use of total inspiratory pressure-volume curves for determination of appropriate positive end-expiratory pressure in newborns with hyaline membrane disease.

Thirty newborns with hyaline membrane disease were treated by mechanical ventilation with individualized appropriate positive end-expiratory pressure (APEEP) from inspiratory pressure-volume curves of the total respiratory system. APEEP was started before H24 in group 1 (19 patients), and after H24 in group 2 (11 patients). Until APEEP, the 2 groups had classical PEEP levels (lower than 0.8 kPa) either without or with incomplete improvement in arterial hypoxia. The mean APEEP of each group was greater than classical PEEP (p less than 0.001). In group 1 the time of exposure to FiO2 greater than 0.4 was shorter (23.8 +/- 13.7 h) than in group 2 (88.6 +/- 56.9 h) (p less than 0.001) and rapid improvement in blood gas exchanges was seen in group 1 compared to group 2 that was independent of the severity of the disease. Tolerance was excellent. APEEP ventilation started before H24 is of special interest in the management of newborns with severe alveolar injury.

Hemodynamics↗
PubMed2001

Hyaline membrane disease in a term neonate.

Hyaline membrane disease is primarily a disorder of preterm infants. Its occurrence in term infants is very uncommon and therefore may escape attention. We describe a term infant who developed severe respiratory distress soon after birth. Diagnosis of hyaline membrane disease was revealed at autopsy.

Anti-Bacterial Agents↗
PubMed1993

Evaluation of complement activation in premature newborn infants with hyaline membrane disease.

Fifteen premature newborns with hyaline membrane disease causing acute respiratory distress were evaluated for complement activation. A high intrapulmonary right-to-left shunt and marked arterial-alveolar oxygen difference indicated the severity of the respiratory failure. Twenty preterm healthy infants served as controls. Total haemolytic activity, plasma concentrations of complement components and regulatory proteins (C3, C4, C1-inhibitor, factors H and I) as well as activation products (C3a, C3dg, C1rsC1-inhibitor, C3b(Bb)P) gave no evidence of significant complement activation. Functional activity of the ubiquitous regulatory protein C1-inhibitor was significantly reduced without impact on classical pathway activation. These data suggest that, in contrast to the adult form of respiratory distress syndrome, the low-pressure pulmonary oedema characterising hyaline membrane disease is not mediated by activation of the complement system.

Biomarkers↗