Neonatal RDS question for pulmonologists

[BlackNDecker]

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Someone help me connect the dots here...

Decreased surfactant --> Increased surface tension ---> Increased collapsing pressure

Accompanied by:

Decreased ventilation w/ vasoconstriction ---> endothelial necrosis ---> fibrinous exudate and cellular debris ---> hyaline membrane dz ---> Increased collapsing pressure(via increased elastance)

Ok, so this makes sense, BUT pathologically characterized by dilated respiratory bronchioles & alveolar ducts 😕

 

[AJM]

Moving to the Peds forum...
(Adult pulmonologists don't deal with neonatal lung disease....)

 

[DropkickMurphy]

As I understand it (and I'll do some research to make sure) but I've understood the dilation of brochioles (which is notable on chest X-ray as the reticulogranular pattern that plays an important role in staging IRDS) to be a result of air trapped in the bronchioles surrounded by collapsed and consolidated non-aerated alveolar lung parenchyma . Granted I haven't been in a NICU since I graduated from my RT training in 2001, but I do believe this is correct.

I've never heard of alveolar dilation being a feature of IRDS....where did you hear about it occuring in this setting?

 

[pedsid]

I also though that it was characterized pathologically by the presence of hyaline ... it's been a couple years since path ... but I think that's true. Not a whole lot will cause lung tissue to fill up with hyaline. ... remember something about apple-green bifrengance (sp?) on path.

 

[BlackNDecker]

As I understand it (and I'll do some research to make sure) but I've understood the dilation of brochioles (which is notable on chest X-ray as the reticulogranular pattern that plays an important role in staging IRDS) to be a result of air trapped in the bronchioles surrounded by collapsed and consolidated non-aerated alveolar lung parenchyma . Granted I haven't been in a NICU since I graduated from my RT training in 2001, but I do believe this is correct.

I've never heard of alveolar dilation being a feature of IRDS....where did you hear about it occuring in this setting?

First off, thanks for the response 👍

I got this from 2 sources:
Goljan's Rapid Review - Pathology
Dudek's HY Systems - Lung

So DEFINITELY the alveoli are collapsed, correct? So the air is trapped somewhere between the alveolar ducts and the terminal bronchioles? Is it typical for any of the conducting airways to collapse as well further up?

I also though that it was characterized pathologically by the presence of hyaline ... it's been a couple years since path ... but I think that's true. Not a whole lot will cause lung tissue to fill up with hyaline. ... remember something about apple-green bifrengance (sp?) on path.

Definitely characterized by hyaline...if you look at the second pathway in my original post you will see it. BUT...apple-green birefringence is characteristic of congo red staining of amyloid. I am not familiar with this in relation to hyaline?

 

[fishmonger69]

Someone help me connect the dots here...

Decreased surfactant --> Increased surface tension ---> Increased collapsing pressure

Accompanied by:

Decreased ventilation w/ vasoconstriction ---> endothelial necrosis ---> fibrinous exudate and cellular debris ---> hyaline membrane dz ---> Increased collapsing pressure(via increased elastance)

Ok, so this makes sense, BUT pathologically characterized by dilated respiratory bronchioles & alveolar ducts 😕

the only reason i can think of that 'pathologically' the alveoli and bronchioles might be dilated is that they are filled with inflammatory and proteinaceous material (as the inflammatory process continues membranes become 'leaky', worsening the condition). however, you are correct that all of this is caused because the alveoli collapse secondary to increased surface tension (p=2t/r) because of surfactant deficiency.

i think you understand the process, so just drop that last line and move on to the next paragraph in your studies 🙂

 

[BlackNDecker]

the only reason i can think of that 'pathologically' the alveoli and bronchioles might be dilated is that they are filled with inflammatory and proteinaceous material (as the inflammatory process continues membranes become 'leaky', worsening the condition). however, you are correct that all of this is caused because the alveoli collapse secondary to increased surface tension (p=2t/r) because of surfactant deficiency.

i think you understand the process, so just drop that last line and move on to the next paragraph in your studies 🙂

Cool man...this is a constant problem of mine

 

[drv]

I think you have understood the whole process.

o DEFINITELY the alveoli are collapsed, correct? So the air is trapped somewhere between the alveolar ducts and the terminal bronchioles?

your argument is correct. I am not a pathologist or neonatologist. This is my view. I tried to read Avery's Diseases of the Newborn, 8th edition, Nelson and manual of neonatal care.This is what i understood.

In RDS alveolar and respiratory bronchiole dilatation is never a characteristic feature( some air trapping possible but mostly ducts and bronchioles are filled with fluid leaked from cappilaries and oedema). If this dilatation develop extensively, it suggets development of bronchopulmonary dysplasia/ chronic lung disease which will appear as late complication of RDS( we had one case like this in our NICU recently).

 

[pedsid]

First off, thanks for the response 👍

I got this from 2 sources:
Goljan's Rapid Review - Pathology
Dudek's HY Systems - Lung

So DEFINITELY the alveoli are collapsed, correct? So the air is trapped somewhere between the alveolar ducts and the terminal bronchioles? Is it typical for any of the conducting airways to collapse as well further up?



Definitely characterized by hyaline...if you look at the second pathway in my original post you will see it. BUT...apple-green birefringence is characteristic of congo red staining of amyloid. I am not familiar with this in relation to hyaline?

Yep you're right ... that's my diclaimer about a few years out of path 🙂 ...

 

[kickazzz2000]

Someone help me connect the dots here...

Decreased surfactant --> Increased surface tension ---> Increased collapsing pressure

Accompanied by:

Decreased ventilation w/ vasoconstriction ---> endothelial necrosis ---> fibrinous exudate and cellular debris ---> hyaline membrane dz ---> Increased collapsing pressure(via increased elastance)

Ok, so this makes sense, BUT pathologically characterized by dilated respiratory bronchioles & alveolar ducts 😕

As air is forced out of the collapsed microatelectatic alveoli, they dilate the broncholes and ducts.