Negative Pressure Pulmonary Edema in outpatient setting

[Ignatius J]

Just a case from the other day....

Had a NPPE from a big dude biting down on his LMA. Actually had to give some sux to get it out.

What is your threshold for sending these folks home? Just curious to get some opinions....

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[caligas]

Ooh. Id have to admit that one. How did you dx the pulmonary edema? (I assume crackles and low sat)

 

[sevoflurane]

How do you know he had NPPE? It is not due to biting down on a tube, it's do to forceful negative pressure against a closed glottis (laryngospasm).
Did you get a chest x-ray? Did you see pink frothy stuff come out the tube?

The last one I had I direct admitted to the ICU. She got some lasix and D/C'd late the next day.

 

[sevoflurane]

Funny thing is that this obese female requested me for her next case... guess what? She laryngospasmed on me AGAIN (despite all my efforts to avoid it)... but no NPPE.

She went home with a letter to present to her next anesthesiologist.

 

[gasdoc77]

Just a case from the other day....

Had a NPPE from a big dude biting down on his LMA. Actually had to give some sux to get it out.

What is your threshold for sending these folks home? Just curious to get some opinions....

I've had a young healthy female that developed it and I put her on non-invasive bipap, lasix, observed and discharged that day. I've also had a very young peds patient (dental) at an outpatient center that I rode with in the back of an ambulance and personally bagged until I handed over care at the local peds hospital to be admitted. I always take it on a case by case basis and don't think there is a right or wrong answer.

 

[drccw]

How do you know he had NPPE? It is not due to biting down on a tube, it's do to forceful negative pressure against a closed glottis (laryngospasm).
Did you get a chest x-ray? Did you see pink frothy stuff come out the tube?

The last one I had I direct admitted to the ICU. She got some lasix and D/C'd late the next day.

Forceful negative pressure against a closed tube (i.e. completely obstructed due to biting) can also cause NPPE....

I've seen it once...

drccw

 

[sevoflurane]

Forceful negative pressure against a closed tube (i.e. completely obstructed due to biting) can also cause NPPE....

I've seen it once...

drccw

Ahh... Never thought of it that way, but it makes sense. Same physiology.

 

[Ignatius J]

How do you know he had NPPE? It is not due to biting down on a tube, it's do to forceful negative pressure against a closed glottis (laryngospasm).
Did you get a chest x-ray? Did you see pink frothy stuff come out the tube?

The last one I had I direct admitted to the ICU. She got some lasix and D/C'd late the next day.

Sevo and caligas,

You're right. It was a presumptive diagnosis, but pretty textbook by my clinical judgment. Case went fine w/o issue and he had no prior medical history. But again, big strong 30M.

It was the end of the anesthetic. After getting the LMA out with sux, he woke up and immediately I saw pink, frothy sputum. Sats about 90% on 10L face tent. Lungs sounded wet. Amazingly enough, no real tachypnea or distress.

Also, no CXR or even CPAP/vents at this surgery center. But boy is it nice!

 

[nimbus]

To answer the original question, if they can maintain a room air saturation greater than 90%, I would feel okay sending them out. Otherwise they need to be admitted with supplemental O2.

 

[Ignatius J]

To answer the original question, if they can maintain a room air saturation greater than 90%, I would feel okay sending them out. Otherwise they need to be admitted with supplemental O2.

Nimbus, appreciate the tidbit. Thats exactly what I did. Extra watch time + lasics + family counseling + orders to not send pt home until sats were > 90% on RA. Luckily, case was in the morning and not the end of the day. Unfortunately, the story continued from there and I'll go into that in a bit. About to start a case.

 

[OB1🤙]

FYI Lasix isn't recommended for NPPE.

 

[fakin' the funk]

Sats about 90% on 10L face tent. Lungs sounded wet. Amazingly enough, no real tachypnea or distress.

Usually that kind of oxygen requirement buys somebody an ICU, maybe a stepdown.

Some math for the juniors: 10L facetent is probably something like 60% FiO2. SpO2 of 90% is something like a PaO2 of 60 mmHg. So, PaO2/FiO2 = 60/0.6 = 100. A severe oxygenation impairment. Acute lung injury. Something like a 30-40% shunt fraction.

Since you're at a freestanding ASC I assume you just called EMS and had the pt taken to an ED? Or if the surgeon has admitting privileges, direct to a stepdown/ICU? Or, if it was early in the day, lasix + observation?

 

[dhb]

If available NIPPV is a better treatment than lasix...

 

[Ignatius J]

If available NIPPV is a better treatment than lasix...

Yes. Understand Lasix isnt the treatment as it can cause metabokic alkalosis with respiratory compensation in the setting of hypoxia. It is controversial but there are some case reports hinting to benefit. With limited tools (no access to NIPPV), I thought the benefits of a small dose outweighed the risks.

 

[sevoflurane]

FYI Lasix isn't recommended for NPPE.

Yeah... there has been a great deal of debate over lasix administration in NPPE. Some anecdotal reports stating that overzealous administration of lasix can cause hypovolemia that can go unrecognized. Personally, I leave it up to the ICU doc taking charge.

People are still doing it though:

Her PACU course was significant for a persistent productive cough with white mucous and she was placed on 100% FIO2 non-rebreather for comfort. A chest X-ray (Figure 1A) revealed moderate pulmonary edema. She was admitted to the surgical intensive care unit (SICU) overnight for monitoring with the presumed diagnosis of negative pressure pulmonary edema and was given one dose of intravenous furosemide 20 mg. She was weaned to room air overnight. On post-operative day (POD) 1, her chest X-ray showed mild improvement (Figure 1B). She was advanced to a regular diet and was transferred to the floor. She was discharged home on POD 2.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3919040/

Published October, 2013

 

[sevoflurane]

Sevo and caligas,

You're right. It was a presumptive diagnosis, but pretty textbook by my clinical judgment. Case went fine w/o issue and he had no prior medical history. But again, big strong 30M.

It was the end of the anesthetic. After getting the LMA out with sux, he woke up and immediately I saw pink, frothy sputum. Sats about 90% on 10L face tent. Lungs sounded wet. Amazingly enough, no real tachypnea or distress.

Also, no CXR or even CPAP/vents at this surgery center. But boy is it nice!

I've been through this scenario a total of 3 times in my career. One of the 3, I was a resident responding to a code in outpatient pacu: The kid ended up in asystole, then resuscitated but unfortunately he ended up with an anoxic brain injury post T&A. Settled out of court.

The other 2 times have been in PP and I knew exactly what it was when it was happening. The key is early sux. The longer you wait, the more pulmonary edema is going to enter the lungs and the harder it will be to get the patient D/C'd early.

Igantius... it sounds like you didn't let it progress very far, or the patient didn't generate such negative pressures to cause serious impairment.
Good job man!

edit...

one of mine (the female mentioned earlier), had it happen during a D&C with an LMA.... and she was a difficult airway. The difficult AW part with a mouth full of frothy sputum that wouldn't stop was a real problem.

 

[sevoflurane]

forget the glidescope with copious frothy sputum... got lucky with a #4 intubating LMA.

 

[jwk]

The other 2 times have been in PP and I knew exactly what it was when it was happening. The key is early sux. The longer you wait, the more pulmonary edema is going to enter the lungs and the harder it will be to get the patient D/C'd early.

This is indeed the key - and why I never saw a case of NPPE my first 15 years of practice. This was pre-LMA days - it was either a mask or ETT. Pretty much ANY sign of laryngospasm would buy you a quick dose of sux. 10-20mg is often all that is needed, and most of the time they don't stop breathing. Biting the tube generally wasn't an issue back then either because everyone got an oral airway. Now we see too much expensive dentition, but that wasn't the case in my first gig. A soft bite block still works great though.

 

[urge]

I would use the same pacu discharge criteria that you use for any case.

The question is whether they fail to pass the criteria. Then, you need to send that patient where nippv is available.

I would give lasix. You cannot have much edema when you are dry as a Pringle.

 

[OB1🤙]

http://journals.lww.com/anesthesiology/fulltext/2011/02000/questioning_diuretic_use_in_acute.40.aspx

 

[urge]

http://journals.lww.com/anesthesiology/fulltext/2011/02000/questioning_diuretic_use_in_acute.40.aspx

That letter is only an opinion. They don't cite any evidence for or against. They even say they use diuretics in their hospital.

The question in matter is how does NPPE resolve?

Does the fluid evaporate? Does it get resorbed? Both? Is it just magic?

I would expect a good amount of it to be resorbed and having a higher oncotic pressure in blood should probably speed that up. There you go. Same level of evidence that these letter writers provided. I should send this to be published.

Either that or magic.

 

[Ignatius J]

Usually that kind of oxygen requirement buys somebody an ICU, maybe a stepdown.

Some math for the juniors: 10L facetent is probably something like 60% FiO2. SpO2 of 90% is something like a PaO2 of 60 mmHg. So, PaO2/FiO2 = 60/0.6 = 100. A severe oxygenation impairment. Acute lung injury. Something like a 30-40% shunt fraction.

Since you're at a freestanding ASC I assume you just called EMS and had the pt taken to an ED? Or if the surgeon has admitting privileges, direct to a stepdown/ICU? Or, if it was early in the day, lasix + observation?

I would much rather monitor in my PACU than call EMS directly on PACU arrival. I've only had 2 cases now, but from my experience, NPPE improves relatively quickly with treatment and observation.

I've been through this scenario a total of 3 times in my career. One of the 3, I was a resident responding to a code in outpatient pacu: The kid ended up in asystole, then resuscitated but unfortunately he ended up with an anoxic brain injury post T&A. Settled out of court.

The other 2 times have been in PP and I knew exactly what it was when it was happening. The key is early sux. The longer you wait, the more pulmonary edema is going to enter the lungs and the harder it will be to get the patient D/C'd early.

Igantius... it sounds like you didn't let it progress very far, or the patient didn't generate such negative pressures to cause serious impairment.
Good job man!

edit...

one of mine (the female mentioned earlier), had it happen during a D&C with an LMA.... and she was a difficult airway. The difficult AW part with a mouth full of frothy sputum that wouldn't stop was a real problem.

Appreciate the kind words. It was a little frustrating as I can't think of anything egregious that I did wrong, but I do not want to be in denial about a complication either. I think my take home points are giving sux early and often in acute postoperative airway obstruction and like another poster said, treating these on a case by case basis.

 

[urge]

It was a little frustrating as I can't think of anything egregious that I did wrong, but I do not want to be in denial about a complication either.

You let the patient wake up with the LMA in. Have you ever had one placed? I don't consider it a good thing.

 

[deleted171991]

My guess is that the patient did not "wake up" with the LMA in place, as much as he went through stage II with the LMA in place, was stimulated by OR personnel and bit down on the tube. With a strong dude, even a bite block doesn't help.

In situations like this, I just give some propofol fast, enough so that the dude stops biting, then take out the LMA. Never had a NPPE, though.

 

[fakin' the funk]

Yes. Understand Lasix isnt the treatment as it can cause metabokic alkalosis with respiratory compensation in the setting of hypoxia.

That's not why. You don't get a contraction alkalosis causing any degree of compensatory respiratory acidosis after just a single dose of lasix. Even people getting massively, aggressively diuresed don't really develop a compensatory respiratory acidosis, not clinically significant anyway. I know the book says they might...but they don't. Usually they get alkalotic and a dose or two of acetazolamide sorts that out. But this is after days of aggressive diuresis.

I think those objecting are saying you're going to cause, or unmask, hypovolemia.

 

[OB1🤙]

Alveolar fluid is cleared by pulmonary lymphatics, and not by resorption back across the capillary into the blood directly. I invite you to propose a mechanism by which a loop diuretic improves this lymphatic drainage.

 

[urge]

Alveolar fluid is cleared by pulmonary lymphatics, and not by resorption back across the capillary into the blood directly. I invite you to propose a mechanism by which a loop diuretic improves this lymphatic drainage.

So easy.

Where do lymphatics drain? Central Veins perhaps?

Wouldn't having a low CVP help drain the lymphatic system?

 

[OB1🤙]

So you're saying that when you give lasix for NPPE, it's to decrease CVP?

This in a patient whose lymphatic drainage at whatever their CVP is (i.e. normal) was sufficient to keep the alveoli dry?

Um, OK. I just don't agree with you.

 

[deleted171991]

I think time beats lasix, in a normovolemic healthy patient.

 

[urge]

So you're saying that when you give lasix for NPPE, it's to decrease CVP?

This in a patient whose lymphatic drainage at whatever their CVP is (i.e. normal) was sufficient to keep the alveoli dry?

Um, OK. I just don't agree with you.

Was sufficient before the alveoli was flooded.

Sure, if you leave it alone it will clear eventually. But by your hands off approach you wouldn't need NIPPV either. It will clear. Might need to transfer the pt to a hospital while you wait.

 

[deleted171991]

Alveolar fluid is cleared by pulmonary lymphatics, and not by resorption back across the capillary into the blood directly.

Why not? If alveolar fluid can get back into the interstitium, from where it's drained by the lymphatics, why wouldn't it get back into the alveolar capillaries, too, if pressure gradients are favorable? Since the initial blood-interstitium transport was passive, along pressure gradients, why wouldn't it work the other way round?

On the other hand, lowering the intravascular hydrostatic pressures by making the patient hypovolemic is not a good strategy in my book either.

 

[urge]

Since I know most of you cannot think for yourselves and are only able to regurgitate stuff you have read, here you go.

 

[deleted171991]

"While the pulmonary lymphatics serve as one of the most important means of removal of pulmonary edema fluid, they are not the only route of removal. Fluid may also be reabsorbed by means of the pulmonary vasculature. If this were the case lung transplants would not be possible since the pulmonary lymphatics are interrupted on the donor lung and not reanastomosed."

However, let me repeat myself: lowering CVP by inducing hypovolemia, in a normovolemic otherwise-healthy patient, does not sound like the best answer. I like the NIPPV or wait-and-see answers much better.

The reason Lasix is not proven to make a difference might be the same for which incentive spirometry does not really change the speed of outcome either: neither of them augments the passive flow between the pulmonary interstitium and lymphatics or capillaries enough.

 

[Ignatius J]

That's not why. You don't get a contraction alkalosis causing any degree of compensatory respiratory acidosis after just a single dose of lasix. Even people getting massively, aggressively diuresed don't really develop a compensatory respiratory acidosis, not clinically significant anyway. I know the book says they might...but they don't. Usually they get alkalotic and a dose or two of acetazolamide sorts that out. But this is after days of aggressive diuresis.

I think those objecting are saying you're going to cause, or unmask, hypovolemia.

You highlighted the reason why I gave the lasics. One small dose won't cause a significant alkalosis. Not sure I buy the "unmasking hypovolemia" but that's just me.

 

[OB1🤙]

Since I know most of you cannot think for yourselves and are only able to regurgitate stuff you have read, here you go.

View attachment 184556

Yes, if CVP is high, it will impede lymphatic drainage.

We're talking about patients with normal CVP.

You sound mad. Not sure why.

 

[urge]

However, let me repeat myself: lowering CVP by inducing hypovolemia, in a normovolemic otherwise-healthy patient, does not sound like the best answer. I like the NIPPV or wait-and-see answers much better.

That's fine. I don't disagree with that approach if you think the diuretic will be detrimental. That's a clinical call.

My beef is with the idea that a diuretic has no effect on pulmonary edema.

 

[OB1🤙]

"While the pulmonary lymphatics serve as one of the most important means of removal of pulmonary edema fluid, they are not the only route of removal. Fluid may also be reabsorbed by means of the pulmonary vasculature. If this were the case lung transplants would not be possible since the pulmonary lymphatics are interrupted on the donor lung and not reanastomosed."

However, let me repeat myself: lowering CVP by inducing hypovolemia, in a normovolemic otherwise-healthy patient, does not sound like the best answer. I like the NIPPV or wait-and-see answers much better.

I'll concede that direct alveolar to capillary fluid movement is possible then. But in normal people, this isn't what happens.

 

[Ignatius J]

You let the patient wake up with the LMA in. Have you ever had one placed? I don't consider it a good thing.

Wasn't the plan. This was a case of a patient "getting light" by a bed transfer at the end of the case (at 1.1 MAC w/ narcs on board no less).

I think when to pull LMAs is a topic of debate. I've seen it work great both ways.

 

[OB1🤙]

If you think a diuretic has a clinically meaningful effect on noncardiogenic pulmonary edema by means of lowering of venous pressure (in a patient with a normal venous pressure) that's your call. I just don't agree.

People can think about the physiology and decide for themselves what they think is plausible.

 

[urge]

You sound mad. Not sure why.

Not really. Arguing is a sport.

 

[urge]

Wasn't the plan. This was a case of a patient "getting light" by a bed transfer at the end of the case (at 1.1 MAC w/ narcs on board no less).

Don't do that.

1.1MAC is too light.

Why would you transfer with the LMA in? Is production pressure at your place so high that the patient must emerge in the hallway while you push the bed to PACU?

 

[Ignatius J]

Don't do that.

1.1MAC is too light.

Why would you transfer with the LMA in? Is production pressure at your place so high that the patient must emerge in the hallway while you push the bed to PACU?

We were in a sloppy lateral position. This was the easiest way for a transfer. I don't think you can blanket it by saying 1.1 is too light to pull an LMA either.

I think you're taking this away from the original topic.

 

[Numbex]

Lasix is a pulmonary vasodilator. I would expect it to, all things being equal, lower PCWP. Those two things seem adaptive effects in NPPE. NPPE is a disorder of pulmonary capillary permeability. Anything that increases alveolar pressure or decreases capillary pressure is helpful in decreasing edema and thus shunt in this situation. I give lasix for less significant reasons than NPPE so this idea that one small dose will cause metabolic alkalosis and thus apnea seems silly to worry about.

 

[pgg]

You let the patient wake up with the LMA in. Have you ever had one placed? I don't consider it a good thing.

There's nothing wrong with removing an LMA in an awake patient at the end of the case. It's not a traumatic experience.

 

[stonemd]

With LMA in you should have a bite block inplace to prevent patient from biting and occluding the airway. Usually a rolled up 4x4 will suffice.

I regularly leave LMAs in and have pacu remove them. In fact we have done 3000+ tonsils with flexible LMAs and find patients have less hypoxia/spasm postop as well as shorter pacu stays as compared to tracheal tubes. After seeing the results we think why take out a good airway in an anesthesthetized patient. Lots of different approaches but this certainly works well at our center.

 

[Ignatius J]

With LMA in you should have a bite block inplace to prevent patient from biting and occluding the airway. Usually a rolled up 4x4 will suffice.

I regularly leave LMAs in and have pacu remove them. In fact we have done 3000+ tonsils with flexible LMAs and find patients have less hypoxia/spasm postop as well as shorter pacu stays as compared to tracheal tubes. After seeing the results we think why take out a good airway in an anesthesthetized patient. Lots of different approaches but this certainly works well at our center.

Agree with leaving them in to PACU. The LMAs in my residency would have taken a snapping turtle to clamp them down. Fair point, and something that I could do different to prevent this, although I haven't ever seen someone use a bite block with an LMA.

 

[risnwb]

With LMA in you should have a bite block inplace to prevent patient from biting and occluding the airway. Usually a rolled up 4x4 will suffice.

I regularly leave LMAs in and have pacu remove them. In fact we have done 3000+ tonsils with flexible LMAs and find patients have less hypoxia/spasm postop as well as shorter pacu stays as compared to tracheal tubes. After seeing the results we think why take out a good airway in an anesthesthetized patient. Lots of different approaches but this certainly works well at our center.

I usually skip the bite block and yank em when they have somewhere around .3 Mac, and pop in an oral airway if they are obstructing a little. Seems to work great, and I'm ready to transfer to stretcher as soon as drapes come down. Patients usually open their eyes while nurse is placing monitors in PACU. Not sure I see the benefit of leaving it in place if they will breathe fine without it...



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[urge]

There's nothing wrong with removing an LMA in an awake patient at the end of the case. It's not a traumatic experience.

I think the patient with NPPE would disagree.

 

[urge]

With LMA in you should have a bite block inplace to prevent patient from biting and occluding the airway. Usually a rolled up 4x4 will suffice.

I regularly leave LMAs in and have pacu remove them. In fact we have done 3000+ tonsils with flexible LMAs and find patients have less hypoxia/spasm postop as well as shorter pacu stays as compared to tracheal tubes. After seeing the results we think why take out a good airway in an anesthesthetized patient. Lots of different approaches but this certainly works well at our center.

The thought of having a tonsil emerge in PACU with nurses being the overseer gives me angina.

 

[pgg]

I think the patient with NPPE would disagree.

Laryngospasm is a result of messing with the patient during stage 2. That can occur with the LMA in or out.

Or are you really suggesting that LMAs must be removed deep?