Clinical Question

two things: it doesn't sound like pulmonary edema... and you don't treat negative pressure pulmonary edema with lasix... it is treated with positive pressure ventilation (CPAP ideally) until the symptoms resolve

1) NPPE (negative pressure pulmonary edema) in your setting is seen after laryngospasm... you have to have very noticeable laryngospasm in order to create the kind of negative intrathoracic pressures that will lead to fluid extravasating into the pulmonary bed. In fact, your patient would have been apneic, would have turned cyanotic and you probably would have had to reintubate or give succinylcholine and positive pressure mask for a bit....
it doesn't sound like any of this happened.

2) frothy sputum can be attributed to many things - in a young woman with a good heart more likely to be just over-production of secretions or a recent cold that she didn't tell you about.

3) the reason you don't treat with lasix: negative pressure pulmonary edema is a reversible event that goes away with improvement of intrathoracic pressure and provision of supplemental oxygen and positive airway pressure for a few hours.... unless you have evidence that you also have left ventricular failure leading to pulmonary overload, then you should be improving left ventricular funtion.... Giving lasix would imply that you felt this patient was volume overloaded, and I can tell you that even if you gave a 26 year old 6 liters of volume for a knee scope - they will no go into pulmonary failure (given that they are otherwise healthy). Lasix is not the appropriate drug (even though if you look at the non-anesthesia literature - it seems that everybody treats weird CXR with lasix now-adays). If she had any symptomatic relief after lasix administration it probably was due to the pulmonary vasodilation that you get with lasix initially --- so in the future, if you think somebody should be diuresed, but you don't want to expose them to the risks of a non-reversible drug - you can always try turning on TNG and that will provide you with the same result that lasix will in the short run, without exposing them to dehydration/polyuria/possible nephrotoxicity/ototoxicity..

4) the reason this patient improved: supplemental oxygenation and good self-reinflation of her lungs (remember that atelectasis in a supine/semi-supine CXR can look like pulmonary edema).

just a few thoughts...

As Tenesma says, laryngospasm will precede negative pressure induced PE; so will a patient biting the ET shut upon emergence. You don't mention either episode before the desats began, so I'm left to wonder why you choose to call it negative pressure induced PE in the first place?

deepz

actually... i have been reviewing medical cases re: ?NPPE and ETT tubes, and it turns out that it is impossible to create enough negative intrathoracic pressure with an ETT being bitten, primarily because it is nearly impossible to get a perfectly closed system (there will always be a little leak in the ETT)

Actually ... wrong. Having seen the phenomenon on a number of occasions in strong young male patients, I can assure you that it can and does occur.

deepz

I second this. It is a primary reason I usually choose an oral airway vs nasal airway, as I have seen this numerous times. The population, a young athletic male, is especially predisposed due to wild wake ups and strength. In my experience, CPAP or reintubation with PP are essential.

ok

in order to get negative pressure pulmonary edema you need to create between 100 and 200mmHg of negative pleural pressure (this was studied in animals and correlated with humans) ... and this can only be achieved in a strong patient who has a COMPLETELY closed system: ie: glottis is closed... An intubated patient does not have a COMPLETELY closed system for two reasons: the cuff is hardly ever a perfect seal AND the ETT can't be completely sealed closed with biting - try it, take an ETT and bite on it - then have a friend connect you to an ambubag and have him bag - air will still pass no matter ho hard you bite (of course it might be difficult to bag due to the increased compliance, but it is still possible).

while i am sure you guys have been practicing anesthesia for a long time, I would suggest that your comments of seeing negative pressure pulmonary edema numerous times is a bit of an exaggeration - and I challenge you to find in the anesthesia literature (don't use the medical ICU literature though - cause they have no clue) ANY case reports of negative pressure pulmonary edema in the setting of an intubated patient...

i am not trying to start a tempest - just trying to correct some misperceptions

**** the literature. Not every clinical observation gets written up. Where do you get these ideas?

Physician, correct thy own misconceptions.

deepz

"Negative pressure pulmonary edema is a complication of acute and chronic upper-airway obstruction that is likely underrecognized and misdiagnosed by anesthesiologists" (Sulek, Complications in Anesthesiology, 1996)

Indeed.

Actual case scenario described to me: extremely healthy male, competitive endurance athlete at collegiate level, for minor outpatient procedure. Woke up like a wild guy, all over the table. Subsequently developed classic NPPE with classic treatment - PEEP and tincture of time. Didn't even miss a day of practice. True story...told by an MDA.

I must say as a future SRNA how refreshing it is to come to this board and see CRNA's and MDA's discussing their clinical experiences and exchanging their views and experiences that can only enhance the relationship between the professions as opposed to the idle chatter that seems occur at times as to who is "better" or who has been doing it "longer".