Light microscopic and ultrastructural study of the adverse effects of oxygen therapy on the neonate lung.
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Alterations of lung tissues were evaluated in 74 infants with respiratory distress who received respirator therapy and high concentrations of oxygen for varying durations. Infant survival ranged from 3 hours to 135 days. Sequential pathologic changes were revealed to be an exudative reaction superimposed upon the early stages of typical hyaline membrane disease. This merged with and was eventually replaced by a reparative fibroproliferative response that was most pronounced in those infants who survived for the longest period of time. This response appeared causally related to the development of pulmonary complications of interstitial fibrosis, emphysema, obliterative bronchiolitis and cystic bronchiolectasis. Correlative ultrastructural studies disclosed generalized capillary endothelial damage in early stages of oxygen therapy, interstitial edema and alteration of alveolar cells attributed to the toxic effects of oxygen. Proliferation of type 2 alveolar cells with incorporation of hyaline membranes into septal walls was a notable feature of the reparative reaction and appeared significant in the subsequent development of interstitial fibrosis. (+info)
Pulmonary complications of oxygen therapy.
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Three cases of the neonatal respiratory distress syndrome are described. The babies were treated by prolonged oxygen given by intermittent positive pressure respiration after endotracheal intubation. Two of the infants died and at necropsy the lungs in both cases were consolidated. Both showed widespread haemorrhagic exudate and interstitial oedema. Early organization of the exudate was apparent in one case. The third infant survived but developed a similar exudative condition and a ;honeycomb' lung. It is suggested that many of the changes found in the lungs of these cases could be attributed to the toxicity of oxygen. (+info)
Comparison of birth weight-gestation distribution in cases of stillbirth and neonatal death according to lesions found at necropsy.
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The birth weight/gestation distribution of a large series of cases of perinatal death has been analysed according to the lesion (or lesions) present at necropsy. Among the lesions associated with low gestation babies dying with hyaline membranes have a much higher mean birth weight for gestation than either the babies with intraventricular haemorrhage or "no cause found." Among infants dying of intrapartum asphyxia or cerebral birth trauma it was found that those who were stillborn with trauma had, at term, a significantly higher mean birth weight than the control livebirths, and that, at all gestations, the stillbirths with trauma were, on average, heavier than the babies dying neonatally with this lesion. Cases of intrapartum asphyxia were smaller than the stillbirths with trauma, but those dying during the second stage of labour were larger than those dying during the first stage.Cases of intrauterine pneumonia-that is, stillbirths and first-day deaths-were also shown to be larger for length of gestation than cases of extrauterine pneumonia-that is, deaths between the second and the 28th day. The cases with haemorrhagic pneumonia, however, were, at least at term, smaller than the cases of extrauterine pneumonia, and cases of massive pulmonary haemorrhage showed evidence of growth retardation at all gestations. (+info)
A fatal case of Legionnaires' disease originating in Scotland.
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A 21-year-old female died in May 1976 from a pneumonic illness presenting with a right pleural effusion. Histopathology showed florid hyaline membrane disease of the left lung only, and focal pneumonitis in the lower lobe. Further investigations carried out by the Center for Disease Control, Atlanta, Georgia, showed that this patient had Legionnaires' disease infection, the first indigenous case diagnosed in Scotland. Post-mortem examination showed features differing from those in other published cases. (+info)
Localization of plasminogen activator in neonatal lung in the presence of hyaline membrane disease.
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A case is described in which Todd's method (1959) for the histological localization of plasminogen activator was applied to neonatal lung tissue obtained at (unsuccessful) open cardiac massage. This was localized around small pulmonary veins, usually at some distance from the hyaline membrane. (+info)
Coagulation studies in massive pulmonary haemorrhage of the newborn.
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Coagulation studies were performed on two newborn infants with fatal massive pulmonary haemorrhage. The first showed a reduced level of plasma fibrinogen with defective thrombin-fibrinogen reaction, corrected by protamine, and defective thromboplastin generation. In the second case, a premature infant, the fibrinogen level was normal but there was a severe defect in thromboplastin generation with evidence of an inhibitor. A relationship between the pulmonary haemorrhage and coagulation defects is suggested but not established. (+info)
Adrenocorticotropic hormone cells and immunoreactive beta-endorphin cells in the human pituitary gland: normal and pathologic conditions studied by the peroxidase-labeled antibody method.
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The comparative immunohistochemical localization of adrenocorticotropic hormone (ACTH) and beta-endorphin-like immunoreactivity (referred to as beta-endorphin) was studied in 16 human anterior pituitary glands from 6 normal adults, 4 normal fetuses, 1 stillborn infant, 2 anencephalic infants, 1 adult with Crooke's hyaline degeneration, and 2 patients with pituitary adenomas associated with Cushing's syndrome. Mirror sections were used in order to enable precise comparison of the same cells on the two consecutive tissue sections. In these normal and pathologic human anterior pituitary glands, ACTH and beta-endorphin were mostly localized in the same cells. In the normal adult pituitary glands, however, some ACTH cells were negative for beta-endorphin; and in one of the pituitary adenomas, some tumor cells were positive for only one hormone (beta-endorphin). These data suggest concomitant production of ACTH and beta-endorphin in the same cells and support the production of precursor molecules for these two hormones. The significance of ACTH-positive, beta-endorphin-negative normal cells and beta-endorphin-positive, ACTH-negative tumor cells is also discussed. (+info)
Measurement of amniotic fluid surfactant.
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Measurement of the production of surfactant is the most direct means of prenatally assessing fetal pulmonary maturity. We review assays which have evolved for measuring surfactant, classifying them into two general categories: biochemical quantitation and biophysical measurements. Biochemical quantitation assays include the amniotic fluid lecithin/sphingomyelin ratio and quantitation of lecithin and other surfactant phospholipids. Biophysical measurements include measurement of surface-tension-lowering ability of extracts of amniotic fluid lipid and evaluation of surface-tension-related properties such as foam stability and microviscosity. Assays of surfactant are subject to certain pre-analysis sources of variation over which the analyst has no control, such as variability in total in vivo amniotic fluid volume, incomplete in vivo mixing of surfactant with amniotic fluid, and presence of contaminating blood or meconium. We also examine other factors such as centrifugation speed and time, and storage of the amniotic specimen before analysis. These factors can dramatically affect analyses, and must be carefully controlled by the analyst. In general, both biochemical and biophysical approaches to surfactant analysis are useful diagnostically. When properly performed, both approaches give results that correlate well, both with each other and with clinical outcome. Because "mature" and "immature" values overlap, none of the assays can completely eliminate false predictions, whether of fetal maturity or fetal immaturity. (+info)