Pulmonary Hyaline Membranes and Vascular Anomalies of the Lung

PEDIATRICS ◽  
1963 ◽  
Vol 32 (6) ◽  
pp. 1094-1097
Author(s):  
C. BOZIC

We have described an infant who died on the third day of life with typical hyaline membrane disease in all portions of the lung perfused by the pulmonary artery. The inferior portion of the left lower lobe, which was separately perfused by three aberrant vessels from the aorta, was emphysematous and had no hyaline membranes. It seems likely that the inequalities in oxygenation of the lung played a role in the localization of the disease.

PEDIATRICS ◽  
1967 ◽  
Vol 39 (5) ◽  
pp. 791-792
Author(s):  
FORREST H. ADAMS ◽  
ADEL EL-SALAWY

A very interesting brief case report, entitled "Pulmonary Hyaline Membranes and Vascular Anomalies of the Lung," was published in Pediatrics by Bozic. This case is commonly referred to as the "Lausanne baby" and is used by many to support the hypothesis that hyaline membrane disease is primarily related to reduced pulmonary blood flow. Although there are good reasons from observations in both man and animal to implicate reduced pulmonary blood flow as an important factor in the pathophysiology of hyaline membrane disease, we do not believe the "Lausanne baby" can be used to support this hypothesis.


2019 ◽  
Vol 30 (1) ◽  
pp. 154-155
Author(s):  
Ambria S Moten ◽  
Abbas E Abbas

Abstract It has been previously suggested that lung tissue remains viable without blood supply from the pulmonary artery (PA). However, our experience demonstrates otherwise. We present 2 cases of accidental left lower lobe PA occlusion during upper lobectomy causing ischaemic changes to the remaining lung tissue. Both patients became septic secondary to necrosis of infarcted lung and required completion pneumonectomy. Development of collateral circulation to bypass the occluded PA may occur but is often insufficient to support the affected lung tissue. Unless the patient is medically unfit, resection of the ischaemic lung should be undertaken.


PEDIATRICS ◽  
1968 ◽  
Vol 42 (1) ◽  
pp. 204-205
Author(s):  
Jan Rokos ◽  
Oonjai Vaeusorn ◽  
Richard Nachman ◽  
Mary Ellen Avery

In analyzing the evidence for the role of prematurity and the significance of added stress in the pathogenesis of hyaline membrane disease, it seems pertinent to examine the occurrence of the disease in twins. Were prematurity alone the determinant of the likelihood of developing the disease, one would expect the disease to occur in both twins. If perinatal stress were a significant factor in the pathogenesis of the disease, then Twin B should have it more commonly than Twin A. A greater incidence in Twin B has been cited by several investigators in reviews of their experience with the disease. Crosse See Table in the PDF file. found hyaline membranes in 8.4% of liveborn autopsied twins delivered first, and in 15.1% of the second born.1


PEDIATRICS ◽  
1983 ◽  
Vol 72 (2) ◽  
pp. 170-175
Author(s):  
Susan Beckwitt Turkel ◽  
John R. Mapp

Since it was first described several years ago, yellow bilirubin staining of the pulmonary membranes in neonatal hyaline membrane disease has apparently become more common. In a retrospective study of neonatal autopsy experience, it was found that as more of the premature infants survived longer, yellow hyaline membrane disease was a more frequent finding, increasing from 7% of all newborns having hyaline membrane disease at autopsy in 1970 to 50% in 1980. In comparing 499 cases with eosinophilic hyaline membranes with 168 cases of yellow membranes, newborns with bilirubin staining of the pulmonary membranes were found to be more premature (P < .02), had smaller autopsy weight (P < .002), and survived longer (P < .00001). When multiple clinical parameters were compared between a group of infants with yellow membranes and a group of infants with pink membranes who were matched for gestational age, year of birth, and length of survival, no differences were found between the two groups. No correlation was found between kernicterus and yellow staining of the pulmonary hyaline membranes in the first years of the study, but there was a strong correlation in the last 5 years, coincident with the increase in the rate of yellow hyaline membrane disease found at autopsy. The gross bilirubin staining of the brain was the secondary type of kernicterus, not toxic bilirubin encephalopathy. The observation of bilirubin staining in the lung and in the brain correlates with prolonged survival in some very small premature infants. This does not appear to be a manifestation of bilirubin toxicity, but rather a marker of prior tissue damage.


1984 ◽  
Vol 18 ◽  
pp. 390A-390A
Author(s):  
M B Escobedo ◽  
R L Boyd ◽  
C Cipriani ◽  
M Montes ◽  
T Kuehl ◽  
...  

PEDIATRICS ◽  
1963 ◽  
Vol 32 (5) ◽  
pp. 940-941
Author(s):  
JACK LIEBERMAN

Clara M. Ambrus et al, in their report on the fibrinolysin system in Hyaline-Membrane Disease (Pediatrics, 32:10, 1963) studied the plasminogen-activator content of the lungs by utilizing human fibrin as substrate. With their methods they appear to have found normal levels of this activator in the lungs of infants dying with hyaline-membrane formation, and therefore could not confirm my earlier observations of a lack of such activity in this condition. Inasmuch as I used a bovine-fibrin substrate in my studies, Ambrus suggests that the difference in our results may be due to the difference in substrate.


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