Hyaline membranes

Hyaline membranes

A fibrous layer that settles in the alveoli in RDS, and prevents oxygen from escaping from inhaled air to the bloodstream.

Patient discussion about Hyaline membranes

Q. HYALINE MEMBRANE DISEASE in pre-mature infants;what are the causes of it in pregnant women?

A. the cause of Hyaline Membrane disease is pre-mature birth. while the fetus develop, about in the 29th week a substance called surfactant is created in the lungs. this substance's function is to change the surface tension of the fluid in the lungs- therefore decreasing it's force. the surface tension tends to shrink the lungs and can cause the lungs to collapse. so a premature baby wouldn't be able to breath properly.

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References in periodicals archive ?
The acute/exudative phase is usually readily recognized by the presence of eosinophilic hyaline membranes, along with intra-alveolar edema, capillary congestion, and interstitial widening (Figure 1).
The clinical course and the documented complications, some of them defining AIDS, would be sufficient to explain the poor outcome but the autopsy opened an unexpected underworld: Kaposi sarcoma was confirmed in the stomach and colon but also in the esophagus and mediastinal lymph nodes (Figure 1(b)); Candida species was found in the anal canal, colon (Figure 1(c)), and lung, where hyaline membranes compatible with an acute respiratory distress syndrome were also seen (Figure 1(d)).
Diffuse alveolar damage (DAD) is a pathology term that describes the presence of alveolar fibrin, hyaline membranes and reactive epithelial cells within alveoli, with varied stages of inflammation.
RBCs and leukocyte infiltrates were seen in 13 and alveolar hyaline membranes in 9 cases.
The presence of viral inclusions in the lungs with interstitial inflammation, hyaline membranes, and giant cells is generally accepted as a diagnostic finding for CMV and MV pneumonia, respectively, despite the extent of virus-infected cells present.
The most common histopathologic finding was diffuse alveolar damage comprising intraalveolar edema, hyaline membranes, fibrin, and hemorrhage.
Microscopic findings have included interstitial infiltrates of mononuclear cells in the alveolar septa, congestion, septal and alveolar edema with or without mononuclear cell exudate, focal hyaline membranes, and occasional alveolar hemorrhage.
Radiologically, the early exudative phase shows bilateral and patchy ground-glass densities, corresponding to interstitial edema and hyaline membranes. The geographic distribution of the patchy ground-glass densities, together with areas of lobular sparing and lower lobe consolidation, serve as radiologic hallmarks.
(3) Procoagulation is a critical factor in DAD, as evidenced by the presence of fibrin-rich hyaline membranes, intra-alveolar fibrin, and in situ vascular thrombosis.
Pulmonary congestion with edema was note& but hyaline membranes had not formed (Figure A).
The pathologic stages of ALI/ARDS or diffuse alveolar damage can be divided into 3 subsequent and somewhat overlapping phases: (1) exudative phase, characterized by neutrophilic infiltrate, hemorrhage, and the accumulation of a protein-rich pulmonary edema; (2) fibroproliferative phase, including chronic inflammation, early fibrosis, resorption of hyaline membranes, and neovascularization; and (3) recovery phase, seen in surviving patients.