Why is atelectasis dull to percussion (if one lobe will collapse, the intrapleural space above this part will increase, so it should be hyperresonant)? I understand the fact that there will be increase amount of tissue per volume, but what about increased intrapleural space?
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Atelectasis
Started by AlexBest96
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Why are you assuming the pleural space increases? The space doesn't really exist until you get a pleural effusion since it's only a potential space. The parietal pleural and pleural space will collapse around the visceral pleura.
Atelectasis is collapsed tissue/alveoli. You percuss over tissue it's going to be dull.
Wait, are you saying that the parietal pleura comes free from the chest wall and remains in contact with the now-smaller lung/visceral pleura?
If the lung gets smaller and the chest wall remains the same size, wouldn't you necessarily increase pleural space? Probably a minute change, all told, but minute changes run the whole show in respiration, no? The pleural space increases in volume slightly in order to generate the negative pressure that allows inspiration - you can't see it, but it's physiologically necessary.
That being said, unless a large volume of air enters the pleural space, I don't see why OP would expect hyperresonance.
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I'm not really sure what you're talking about, but I know the pleural space is not filled with air, nor does it fill with air in atelectasis.
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deleted87051
Are they seriously still teaching percussion? Useless IMO.
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deleted87051
The pleural space is the potential space between the visceral and parietal pleura. Under normal conditions it contains a scant amount of pleural fluid. If a larger collection of pleural fluid forms, it is called a pleural effusion. If air enters the pleural space, it is called a pneumothorax.
None of this has anything to do with atelectasis.
Both a pleural effusion and atelectasis will theoretically cause dullness to percussion. It is nonspecific. Better to get an ultrasound or a chest CT.
None of this has anything to do with atelectasis.
Both a pleural effusion and atelectasis will theoretically cause dullness to percussion. It is nonspecific. Better to get an ultrasound or a chest CT.
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like lobar consolidation, increase in the density of the space(since fluid is denser than lung tissue and air) will cause the sound to change to dullness.
Because there is no air there. You are seriously overthinking it, the purpose of percussion is to detect air. Collapsed lung has no air in it.
That's...kinda my point.
It doesn't fill with anything, that's why the pressure goes down during inspiration. Again, the scale for this change is tiny - you'd never appreciate it on any form of imaging or measurement that we have. For all practical purposes, it's irrelevant. But conceptually, the change exists both with inspiration and with lung collapse, which is what's tripping OP up.
It's natural for our brains to equate 'empty' with 'full of air', so when many people picture the pleural space getting larger, they basically picture a pneumothorax, which is inaccurate.
And what will fill the empty space between collapsed lung tissue and chest wall? Is it empty space (i.e. no air)? Thank you!)
Generally you don't get increased pleural space, you get reduced lung volumes (higher diaphragm when severe enough to cause a noticeable change). So nothing fills the space- it is still a potential space.
Again, you're conceptualizing it incorrectly. It's not empty space; it's nonexistent space.
I think op is referring to contraction atelectasis. OP , rationally thinking this could lead to both hyperesonence in the lateral most portions of the thoracic cavity if there is no plueral effusion, however it is still likely to lead to dullness to percussion centrally .
Even in that circumstance, which is what I was getting at above, the pleural space does not fill with air, and thus would not lead to hyperresonance. What more realistically happens is a very small net volume change, resulting in decreased pressure in that space, with any further decrease in lung volume resulting in increased inflation elsewhere in the lung and/or elevation of the diaphragm due to the pressure changes.
There is no air there, i am assuming that the increased negative pressue is likely to draw fluid at some point , still leading to effusion still as dullness as the end result on physical exam. However is there a possibility of a space opening up leading to hyperresonance? i would think it is possible.
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I mean, sure if they develop a pneumo, but otherwise even if a large 'empty' space opened up in the chest, without air inside it it would not be resonant. At that point, you're essentially talking about a vacuum (which is why it's not likely to develop on more than the micro scale, as those require a lot of force to maintain).
I don't know why you think that, but it doesn't matter. If there is, for example, a fibrotic mass causing contraction atelectasis, then it doesn't lead to anything occupying the pleural space. As an aside, I dispute that diagram's assertion that resorptive atelectasis is the most common. Given the commonality of pleural effusions, I think it's passive/compressive.
This is correct. It's like people are thinking of this as a closed system with respect to volume. It's not. The diaphragm moves up, the mediastinum moves over, or the aerated lung hyperexpands. Those are all lower energy ways to compensate as opposed causing the pleura surfaces to separate.
i suppose I understand that contents will shift to compensate for the loss in volume. I am just thinking outloud that the shift in it self would theoretically change the resonance of the lungs, and not necessarily to lead to dullness, is it also possible to have an edge case where the compensatory shift is maxed out or is that just incompatible with life.
I think if we include all of the postop atelectasis, etc., under the resorptive category, that's where it starts to get more common.
Like I said in an earlier post, people have a tendency to equate 'empty' with 'air-filled', which is, I think, OP's original confusion. I find that thinking of all systems as a sort of dynamic equilibrium helps...so if lung collapses, pleural space increases, but as soon as THAT happens, intrapleural pressure decreases, leading to volume shifts from the remaining lung and/or diaphragm. The net volume change of the pleural space is microscopic, reflected more by the pressure effects than by any visible increase in the pleural space itself.
I suppose if you happen to be able to detect the relatively hyperexpanded lung that's nearby the atelectatic lung, then yeah, it might be hyperresonant. That's purely hypothetical, though, and not at all practical or realistic.
Entire lungs go down in the setting of central bronchial occlusion, like with mucus plugging. And while there's frequently a concomitant pleural effusion, the atelectasis isn't causal. Between diaphragmatic elevation, mediastinal shift, and the collapsed lung, there are plenty of structures to fill the hemithorax.
Yep. It's what I was trying to get at, too, when I said..
Right, or put another way, the volume change in the pleural space is, at most, transient, lasting only long enough for other structures to compensate. Just like there's an instantaneous moment of zero velocity when an object is thrown against gravity.
percussion heh
Definitely has to be passive/compressive atelectasis. Essentially every inpatient has that after lying on their back long enough. Heck, I did a CT-guided lung biopsy a few days ago and over several scans, I saw the passive atelectasis gradually build up as gravity performed its magic.
Also, of note, that text mentioned that "airless ... collapsed portion of lung tissue" is radiolucent. Uh, it's radioopaque because loss of air = increased density, and increased density = more radioopaque.
Then again, leave it to a chiropractor to **** it up (yes, the author is a chiro).
When I see your avatar on my phone, I always think it's a B/W photo of a guy with a mustache and a monocle.
I think people are overestimating the actual volume change in atelectasis. Remember that the surface area of your lungs is the size of a tennis court crammed into your thoracic cavity. With atelectasis, you are just collapsing the alveoli so you can collapse an entire lobe’s worth and it’s really not that appreciably smaller. The change in density is quite apparent on imaging or under the microscope though because the resolution is so much larger. I guess when looking at the cut surface I can kind of tell when there’s atelectasis (vs say pneumonia, compared to normal it’s obvious) but if I’m just looking at a lung on the table without feeling the weight I don’t really know what the smaller airways have going on.
This doesn't make sense to me. Sure, I understand the concept that for the most part, the volume change is smaller scale than most people are picturing (in fact, I pointed that out in my first post), but I disagree that you could collapse an entire lobe's worth and not appreciate a difference. This is why you see shifts with large scale atelectasis - because it's an appreciable size change in the lung, but it takes only an unappreciable size change of the pleural space to create a powerful pressure differential (which, in turn, pulls the diaphragm up and/or the mediastinum over, or induces hyperinflation elsewhere in the lung).
Yes, it causes a shift that you can detect on imaging, but to OP's question, no it doesn't create a giant pocket of air between the lung and the chest wall such that theres any confusion as to why you get dullness to percussion.
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deleted87051
I’ve only ever diagnosed atelectasis by CXR, chest CT or direct visualization in an open chest. Never by percussion or auscultation. I don’t think anyone else does either.
I understand that, and in fact posted as such multiple times already in this thread. I still object to the phrasing in your last post, which I think was imprecise to the point of inaccuracy. But glad to see we don't disagree on the actual physiology at play, just wording!
