Clinical Question

  1. I had my first case of negative pressure pulmonary edema yesterday. 26 YO for a knee scope, declined SAB and LE block, she requested a general and due to her GERD/heartburn, I chose GA with ETT. I did a RSI without difficulty and the case proceded without incident. During emergance, she seemed to have a bit of difficulty coordinating her breathing, and had a couple of MINOR episodes of desaturation as I woke her up. Eventually, I extubated her when reflexive but due to her continued coughing she never truely followed commands. Her sat was 98% with evidence of good exchange occuring immediatly. Upon arrival in PACU, her sats were 89% and we placed her on a simple mask at 10 liters with sats improving to 93-95%. She had fairly severe crackles throuout and 10 mg of lasix improved things immediatly. A CXR showed a PE picture and improved over the next couple of hours. When thinking about her ETT, there was a fair amount of frothy pink sputum present. Should have sent alarm bells off sooner I guess. She was discharged home a number of hours later, happy and feeling fine. I'm looking for possible explainations. Anyone care to comment?
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  2. 20 Comments

  3. by   Tenesma
    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...
  4. by   deepz
    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
  5. by   Tenesma
    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)
  6. by   deepz
    Quote from Tenesma
    ....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
  7. by   keermie
    Quote from deepz
    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.
  8. by   Tenesma
    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
  9. by   deepz
    Quote from Tenesma
    .... I challenge you to find in the anesthesia literature....

    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
  10. by   Athlein1
    "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.
    Last edit by Athlein1 on Mar 17, '04
  11. by   Trauma Tom
    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".

    Quote from Tenesma
    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
  12. by   nilepoc
    Quote from deepz
    **** the literature. Not every clinical observation gets written up. Where do you get these ideas?

    Physician, correct thy own misconceptions.

    deepz
    Hey Deepz, try and participate in a kind manner. This is not a pissing match.
    Last edit by nilepoc on Mar 17, '04
  13. by   Tenesma
    deepz... my point regarding the literature is as follows: if it is a common event that patients develop NNPE while intubated (as experienced by you and Keermie) then surely it should be in textbooks, or at least in case reports... but it isn't. and every clinical observation that can further our field, help others in similar situations, SHOULD be written up.

    so back to my original points
    1) Original poster's patient didn't have NNPE
    2) correct management is PEEP and not diuretics
    3) it can only happen with a closed glottis, not with an ETT (no matter how hard somebody bites on it)

    I know however, that many instructors (even MDAs) perpetuate this myth - and it just isn't true...
  14. by   WntrMute2
    Quote from Tenesma
    deepz... my point regarding the literature is as follows: if it is a common event that patients develop NNPE while intubated (as experienced by you and Keermie) then surely it should be in textbooks, or at least in case reports... but it isn't. and every clinical observation that can further our field, help others in similar situations, SHOULD be written up.

    so back to my original points
    1) Original poster's patient didn't have NNPE
    2) correct management is PEEP and not diuretics
    3) it can only happen with a closed glottis, not with an ETT (no matter how hard somebody bites on it)

    I know however, that many instructors (even MDAs) perpetuate this myth - and it just isn't true...
    Well I have to admit, the MDA running the recovery room informed me of her diagnosis after seeing a chest X-ray and she ordered the lasix. I'm not sure that applying CPAP in this instance whould have been as effective as the lasix which worked in minutes. (Yes I know obout the vasodilatory properties but whatever the MOA, it worked rapidly and completly).

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