#Case_11 How to improve my next post-thyroidectomy stridor if any?

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DrAmir0078

DrAmir0078

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Hi SDN Anesthesiologists,
I hope you are doing well. Last week, we had a total thyroidectomy case for a female - young.
Her thyroid was a bit moderate in size, she was Mallampati class 2/3 almost 3, upper left shift of larynx. It was not that difficult to Intubate.
I had used Ketamine + Thiopental + Atracurium and sevoflurane then Isoflurane for maintenance, beside multimodal analgesia during the case. She was also some sort of retrosternal extension.

At the time of extubation, Surgeons insisted to examine the vocal cords by DL - I tried to look at them, withdraw the tube, and they were mobile, extubation done with suction. (is it a custom to do it where you are?)
Patient was on Isoflurane and switched to Sevoflurane while before skin closure. She was fully awake before extubation (open her eyes and protrude her tongue), no changes in HR (prior Metoprolol given 15 minutes) nor blood pressure.
The problem is when extubated, she develops that inspiratory sound of stridor, and thought of laryngospasm - I applied positive pressure, jaw thrust and good Tidal volume, but in vain, even with propofol and sedation with Midazolan.
The patient was not relieving, although she was sedated, but the sound was very obvious.
Surgeons were saying of probability of tracheomalacia vs RLN injury, and with our Attending decided for emergency tracheostomy and prior rexploration.

While trying to prepare for tracheostomy, she was desaturating, upper 70s% and with jet like ventilation (I mean continuous ventilation manually by resvior bag - Rapid oscillating) and her PAW reached 28 to 32, we gave thiopental and Atracurium again (¿?) and patient went asleep, saturation went up to 92%.
Tracheostomy done, patient relieved and saturation returned to 98% - very brief desaturation.

During the event of stridor, I gave Dexamethasone and also gave 20 mg Laxis as I wad hearing crackles everywhere and feared of pulmonary edema. (passed urine)

After Tracheostomy, they tried to do suction, was clear and chest was clear.

Sent to ICU, some sedation, and put her on minimal PSV/Peep and after one hour she woke up like a charm and when we close the tracheostomy, she can talk and hear her voice!

What happened?
Laryngospasm?
Stridor?
Neuropraxia of RLN?

How do you manage?
What should've been done?

They sent her for ENT for evaluation of the vocal cords. She was discharged next day from ICU!

We don't have scoline - if it was laryngospasm - for a last resort !

What else?
One day an Attending, with a different case, he gave 300 mcg Adrenaline S.C and it works to relieve the stridor.

What is the best practice?

Thanks!
 
If the patient was wide awake it is unlikely laryngospasm. Any history that patient has tracheomalacia? Also doubtful IMO. Any reactive airway history?? Bronchospasm or asthma? Aspiration? Allergic reaction?

Good to think about the most common specific things that can happen immediately after thyroidectomy. 1. RLN injury and VC paresis although this shouldn't cause desaturation unless it was bilateral. 2. Hematoma. 3. Hypocalcemia from inadvertent removal of all the parathyroids is usually later in postop course, e.g. overnight or POD1.
 
Thanks Dr. Coffeebythelake,
There were no history of Asthma or reactive airways. I have tried to give multimodal analgesia from Paracetamol + Acupan and Ketolrac too. I noticed and discussed it with the surgeon of a weird skipping up HR when he manipulate and dissect retro-sternally by his finger, HR reaches 134 and once off, it was back to 86. I covered it with Metoprolol prior, just after excision.
One of our Attending when I discussed with him, he said "do not mix Thiopental + Atracurium, it has strong histamine release!" - well no Rocruronium- Esmeron available!
I didn't get hypertension episodes nor Tachycardia nor skin redness reflecting allergic reactions!
But, overheard the surgeon when was discussing the case with ENT, said" it was suspected of tracheomalacia"
I was monitoring the case from skin to skin, sitting at the head of the patient, it wasn't easy goiter, but how do I suspect as an Anesthesiologist a tracheomalacia?

Even the surgeon during the case told me, she is difficult and why you didn't off the case?
I didn't see a reason not to give!

coffeebythelake said:
If the patient was wide awake it is unlikely laryngospasm. Any history that patient has tracheomalacia? Also doubtful IMO. Any reactive airway history?? Bronchospasm or asthma? Aspiration? Allergic reaction?

Good to think about the most common specific things that can happen immediately after thyroidectomy. 1. RLN injury and VC paresis although this shouldn't cause desaturation unless it was bilateral. 2. Hematoma. 3. Hypocalcemia from inadvertent removal of all the parathyroids is usually later in postop course, e.g. overnight or POD1.
Click to expand...
 
The surgeon puts some needles in the neck and uses a probe that beeps when the recurrent laryngeal nerve is stimulated. This is when they are dissecting out the thyroid. I tube with sux and don't paralyze the patient with any long acting afterwards.

Why switch from iso to sevo? Seems unnecessary.

Opening eyes does not mean an awake patient. I had a patient once who opened eyes to voice but still obstructed and desatted after extubation. It was an older man who had a 6 hour robot prostate in trendelenburg position.

Like coffee I think that an awake patient would not laryngospasm. And tracheomalacia happens if you're intubated for a long time, not a 1-2 hour surgery. It wouldn't get better overnight.

Why didn't you reintubate instead of traching? I feel like stridor right after this kind of surgery is a nerve problem. Probably vocal cord paresis vs swelling as inspiratory makes me think upper airway. Probably should slow down the breathing
 
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GassYous said:
The surgeon puts some needles in the neck and uses a probe that beeps when the recurrent laryngeal nerve is stimulated. This is when they are dissecting out the thyroid. I tube with sux and don't paralyze the patient with any long acting afterwards.

Why switch from iso to sevo? Seems unnecessary.

Opening eyes does not mean an awake patient. I had a patient once who opened eyes to voice but still obstructed and desatted after extubation. It was an older man who had a 6 hour robot prostate in trendelenburg position.

Like coffee I think that an awake patient would not laryngospasm. And tracheomalacia happens if you're intubated for a long time, not a 1-2 hour surgery. It wouldn't get better overnight.

Why didn't you reintubate instead of traching?
Click to expand...
Yes, prior to the decision of tracheostomy, we re-intubate (didn't mention it? My apologies)!

That fancy monitoring doesn't exist!

I switched from irritating longer duration Isoflurane to better rapid recovery (wearing off) Sevoflurane.

It was inspiratory sound with jaw thrust and face mask.

I was feared aspiration too, I did gentle suction prior to extubation.

I feel, I didn't quite managed the event with what I have available, so questioning how to improve it!

Do you think, if I used sc adrenaline would change the outcome?

Our attending was more into re-intubation and tracheostomy.
 
Was patient moving air and maintaining sats despite stridor before propofol and midaz?
 
This happened to me in residency too and the best and safest move is to reintubate. I'm not sure that I would trach this patient if I have a secure airway but I would let them chill in the icu for a day or so and reevaluate for extubation.
 
Hello DrAmir.
For what i gather from your posts is that you operate in an environment with limited resources (which is to be expected). However despite this, your (or your attendings) anesthetics are often complicated or going in different directions needlessly.
I would advise you to keep your anesthetic as simple as possible: use the less agents you possibly can, don't change between different agents (iso/sevo) to eliminate variables. I would not do a laryngoscopy before extubation: it's not the right time and is low yield (as proven in this case).
Rapid desaturation post extubation is almost certainly mechanical: residual paralysis, laryngospasm or laryngeal nerve injury. In the case presented my bet is on nerve injury so i would have reintubated send to icu and have ENT reevaluate later for extubation.
 
Well, this is the thing!
If we re-intubate, why would do tracheostomy!?
Would rather - next time if I am in charge - tell them to send the patient to the ICU and re-evaluate over there!
PAW after Intubation with 6.5 mm (prior 7.5 mm) - no 7 mm available - was 25 cmH2O.
Even though, sending to the ICU should've been wiser!
I agree.
GassYous said:
This happened to me in residency too and the best and safest move is to reintubate. I'm not sure that I would trach this patient if I have a secure airway but I would let them chill in the icu for a day or so and reevaluate for extubation.
Click to expand...
 
Hello Dr.dhb,
Yes, I do work in limited resources in Iraq as you know.
Personally, I don't like to examine the vocal cords, it looks outdated and dangerous with what we have.
After the surgery was almost done, anaesthetic agents were stopped, and the patient was reversed - I depend on verbal command, opening eyes, tongue out - no TOF./ - and with tidal volume is achieved direct laryngoscopy was done. The endotracheal tube was deflated and removed slowly, and the vocal cords were mobile!
So, examining the vocal cords with DL puts the patient at risk too, (I gave metoprolol, and was well on multimodal analgesia), it is yet the sympathetic stimulation or the pain of the incision vs DL, suction itself is irritating, so all of these and I have to look at the cords to see their mobility!

How would you examine the vocal cords in such limited resources?

Honestly, it is like a trauma to me, I have been giving anesthesia for lots of such cases without an issue!
What was missed at my side?



dhb said:
Hello DrAmir.
For what i gather from your posts is that you operate in an environment with limited resources (which is to be expected). However despite this, your (or your attendings) anesthetics are often complicated or going in different directions needlessly.
I would advise you to keep your anesthetic as simple as possible: use the less agents you possibly can, don't change between different agents (iso/sevo) to eliminate variables. I would not do a laryngoscopy before extubation: it's not the right time and is low yield (as proven in this case).
Rapid desaturation post extubation is almost certainly mechanical: residual paralysis, laryngospasm or laryngeal nerve injury. In the case presented my bet is on nerve injury so i would have reintubated send to icu and have ENT reevaluate later for extubation.
Click to expand...
 
We stopped allowing surgeons to look at the cords post-op about 20 years ago. There's very little reason to do this (if they cut the nerve, it's too late - it's already cut) and you're doing something very stimulating at the end of the procedure that will just get you into trouble.

If they have to have their look, absolutely do not back off on agents, narcs, etc. Extubate under direct vision - if they cough at all, they're not deep enough. Once they're done looking, then turn off all your agents and allow the patient to awaken.
 
That what we did, we have awaited like 20 minutes - she had an earlier propofol and midazolan + the sound continued despite.

We could've wait longer, but how long longer?

I am with re-intubation and sent to ICU for re-evaluation!

Why to tracheostomy her, even if she had tracheomalacia / injury - well may be to facilitate ENT to look at her VC later, why? Can't they do it with tube in?

They re-explored the field immediately before tracheostomy, no hematoma and they removed the drain they put it earlier.

I just don't get it!
dhb said:
If this was post extubation then i would not have reintubated and would have waited for complete emergence.
Click to expand...
 
jwk said:
We stopped allowing surgeons to look at the cords post-op about 20 years ago. There's very little reason to do this (if they cut the nerve, it's too late - it's already cut) and you're doing something very stimulating at the end of the procedure that will just get you into trouble.

If they have to have their look, absolutely do not back off on agents, narcs, etc. Extubate under direct vision - if they cough at all, they're not deep enough. Once they're done looking, then turn off all your agents and allow the patient to awaken.
Click to expand...
I wished if I had narcotics handy and esmolol - it is common sense. DL them and they are awake - is irritating, stimulating and painful, but what to do?
When it works, it does, but when not, it is trouble!
 
DrAmir0078 said:
Hi SDN Anesthesiologists,
I hope you are doing well. Last week, we had a total thyroidectomy case for a female - young.
Her thyroid was a bit moderate in size, she was Mallampati class 2/3 almost 3, upper left shift of larynx. It was not that difficult to Intubate.
I had used Ketamine + Thiopental + Atracurium and sevoflurane then Isoflurane for maintenance, beside multimodal analgesia during the case. She was also some sort of retrosternal extension.

At the time of extubation, Surgeons insisted to examine the vocal cords by DL - I tried to look at them, withdraw the tube, and they were mobile, extubation done with suction. (is it a custom to do it where you are?)
Patient was on Isoflurane and switched to Sevoflurane while before skin closure. She was fully awake before extubation (open her eyes and protrude her tongue), no changes in HR (prior Metoprolol given 15 minutes) nor blood pressure.
The problem is when extubated, she develops that inspiratory sound of stridor, and thought of laryngospasm - I applied positive pressure, jaw thrust and good Tidal volume, but in vain, even with propofol and sedation with Midazolan.
The patient was not relieving, although she was sedated, but the sound was very obvious.
Surgeons were saying of probability of tracheomalacia vs RLN injury, and with our Attending decided for emergency tracheostomy and prior rexploration.

While trying to prepare for tracheostomy, she was desaturating, upper 70s% and with jet like ventilation (I mean continuous ventilation manually by resvior bag - Rapid oscillating) and her PAW reached 28 to 32, we gave thiopental and Atracurium again (¿?) and patient went asleep, saturation went up to 92%.
Tracheostomy done, patient relieved and saturation returned to 98% - very brief desaturation.

During the event of stridor, I gave Dexamethasone and also gave 20 mg Laxis as I wad hearing crackles everywhere and feared of pulmonary edema. (passed urine)

After Tracheostomy, they tried to do suction, was clear and chest was clear.

Sent to ICU, some sedation, and put her on minimal PSV/Peep and after one hour she woke up like a charm and when we close the tracheostomy, she can talk and hear her voice!

What happened?
Laryngospasm?
Stridor?
Neuropraxia of RLN?

How do you manage?
What should've been done?

They sent her for ENT for evaluation of the vocal cords. She was discharged next day from ICU!

We don't have scoline - if it was laryngospasm - for a last resort !

What else?
One day an Attending, with a different case, he gave 300 mcg Adrenaline S.C and it works to relieve the stridor.

What is the best practice?

Thanks!
Click to expand...
albuterol nebulizer via facemask after extubation
sounds like airway reactivity
thats why it got better with epi the next time
lots of people who dont have diagnosed asthma can have airway reactivity when you put a tube in the trachea
 
academic.oup.com

Post-thyroidectomy tracheomalacia: minimal risk despite significant tracheal compression

AbstractBackground. Tracheomalacia is a feared complication of goitre surgery, but considered rare in the Western World. This study aimed to estimate the r
academic.oup.com academic.oup.com

it seems the existence of post thyroid tracheomalacia is hotly debated.

Anyway, my principle is why make a hole in the neck when you’ve got a perfectly good one in the cords.

I also try nebulised adrenaline in most cases of post extubation stridor
 
Did you reverse at all?
Without tof you really don't know where you are with paralysis.

Why do you give metoprolol and wish you had esmolol? I have basically never given a beta blocker to such a patient.

Why give midaz for an elective case such as this? Again no one gives this unless extremely anxious.

You might have to tell us exact doses and times of each to help tease this out.

From your post trache findings it doesn't sound like rln or tracheomalacia.

You do have visual capnography and o2 monitor for inhaled and exhaled? Were you actually bagging her with 100%fio2?because it may have been o2 supply or leak or just inadequate bvm? I dont know...
Very hard to say.
 
This could have been just transient trauma to the recurrent nerves or some swelling around them that resolved. Probably the tracheostomy could have been delayed and you could have reintubated the patient and left her a few hours on the vent then attempt extubation later.
If the surgeon injected local anesthesia in the thyroid bed this could be the cause too.
 
the most likely diagnosis is still most likely. its either laryngospasm or bronchospasm.

your story points toward laryngospasm, but there are some details that is confusing.

you mention you delivered good tidal volume? was there End tidal CO2?
"The problem is when extubated, she develops that inspiratory sound of stridor, and thought of laryngospasm - I applied positive pressure, jaw thrust and good Tidal volume, but in vain, even with propofol and sedation with Midazolan."

if you have good tidal volume, and assuming there is good EtCO2, thats probably not any of the things you listed. Good tidal volume + good EtCO2 waveform should bring up saturation..

perhaps your team didnt wait long enough??

I would never trach someone who is ventilatable and then got a Tube and is still ventilatable.
 
Planktonmd said:
This could have been just transient trauma to the recurrent nerves or some swelling around them that resolved. Probably the tracheostomy could have been delayed and you could have reintubated the patient and left her a few hours on the vent then attempt extubation later.
If the surgeon injected local anesthesia in the thyroid bed this could be the cause too.
Click to expand...
If I am in charge - next time as Anesthesiologist, I will re-intubate if all measure failed and sent to the ICU and re-evaluate after few hours and ENT team at the bedside!
Many thanks Sir
 
anbuitachi said:
the most likely diagnosis is still most likely. its either laryngospasm or bronchospasm.

your story points toward laryngospasm, but there are some details that is confusing.

you mention you delivered good tidal volume? was there End tidal CO2?
"The problem is when extubated, she develops that inspiratory sound of stridor, and thought of laryngospasm - I applied positive pressure, jaw thrust and good Tidal volume, but in vain, even with propofol and sedation with Midazolan."

if you have good tidal volume, and assuming there is good EtCO2, thats probably not any of the things you listed. Good tidal volume + good EtCO2 waveform should bring up saturation..

perhaps your team didnt wait long enough??

I would never trach someone who is ventilatable and then got a Tube and is still ventilatable.
Click to expand...
I applied Larson maneuver aka laryngospasm notch with PPV for more than 10 minutes and had good vT and never desaturated. I gave propofol, didn't work, gave midazolam (patient was anxious) - that sound kept me astonished ! - I gave even Dexamethasone / Laxis (Feared of Pulmonary edema)
Called the Attending, he holds the mask again, gave 5 mg Diazepam (he said will be fine and sleep) - it didn't work... Sound kept worry us all and no desaturation !
Surgeon called ENT for tracheostomy, this idea approved by all as a decision.
We re-intubate her easily, but smaller tube and we got now desaturation - chest was full of crypitation coarse ones...
PAW was 25 - 28 and sat was going down fast, and with my jet like ventilation as I said continuous rapid oscillation of the reservoir bag with 150 ml vT and very rapid and PAW won't exceed 32 - 35, we could bring the saturation to 92% and they then tracheostomy her, and surgeon said "please do suction as her chest is full of crypitation" - they found nothing (was my Laxis worked? I gave 10 mg 15 minutes apart at the beginning of event) and her saturation came up to 98% !

I am so confused!

Sent to ICU, she was Ok and fine next hour and discharged to the ward next day!

Why we couldn't break the laryngospasm?
But, we didn't manage the stridor well with neb adrenaline, or SC adrenaline (I have no idea of its rule?). Even if it was stridor, no desaturation, what the worst outcome?
Is it wiser to wait? Or re-intubate?

I am full!
 
Possible that she develops negative pressure pulmonary edema after a laryngospasm.

I would take bronchospasm off of the differential, as it is unlikely to cause audible stridor
 
Hork Bajir said:
Possible that she develops negative pressure pulmonary edema after a laryngospasm.

I would take bronchospasm off of the differential, as it is unlikely to cause audible stridor
Click to expand...
I thought of it, that is why I gave laxis.
No morphine available nor old school (digoxine), except Oxygen, and Laxis!
 
if the patient did not have tracheomalacia walking in, they don’t have it now (and unless an adult gives a hx of not being able to sleep supine for their entire life, they do not have clinically significant tracheomalacia).

if you have stridor, it is an upper airway problem, and thus unlikely bronchospasm.

if you do not have bronchospasm and hemodynamic changes it is unlikely mast cell mediated and does not need epi

if you have a soft neck it is not mass/compression.

if you are easily moving air prior to paralysis, unlikely laryngospasm.

if you have an asleep patient it is not paradoxical vocal cord dysfunction (well, almost certainly not)

if you have had recent surgical manipulation near the innervation of the cords, and the above issues are not the problem, THIS almost certainly is.

if you have coarse breath sounds you have a problem at the alveolar interface, c/w NPPE.

The unifying diagnosis is obstruction at the level of the cords causing NPPE (negative pressure pulmonary edema). The question is if iatrogenic (surgical cord disfunction) or intrinsic (patient inhaled against closed glottis).

For love or money you could not get me to agree to trach this patient.

I respect you so much for coming here to share, and your dedication to learning. As others have said, most of the anesthetics you post are too clever by half. I understand that you are executing your attending’s plans the majority of the time, but when you are planning and executing your own anesthetic, remember that simple and clean is generally safer and more elegant.
 
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repititionition said:
if the patient did not have tracheomalacia walking in, they don’t have it now (and unless an adult gives a hx of not being able to sleep supine for their entire life, they do not have clinically significant tracheomalacia).

if you have stridor, it is an upper airway problem, and thus unlikely bronchospasm.

if you have a soft neck it is not mass/compression.

if you are easily moving air prior to paralysis, unlikely laryngospasm.

if you have an asleep patient it is not paradoxical vocal cord dysfunction (well, almost certainly not)

if you have had recent surgical manipulation near the innervation of the cords, and the above issues are not the problem, THIS almost certainly is.

if you have coarse breath sounds you have a problem at the alveolar interface, c/w NPPE.

The unifying diagnosis is obstruction at the level of the cords causing NPPE (negative pressure pulmonary edema). The question is if iatrogenic (surgical cord disfunction) or intrinsic (patient inhaled against closed glottis).

For love or money you could not get me to agree to trach this patient.

I respect you so much for coming here to share, and your dedication to learning. As others have said, most of the anesthetics you post are too clever by half. I understand that you are executing your attending’s plans the majority of the time, but when you are planning and executing your own anesthetic, remember that simple and clean is generally safer and more elegant.
Click to expand...
Nice summary of issues at hand. Of course the pt. didn’t need a trach but sometimes you are at thewhim of the surgeon or attending or whoever.
 
I gotta be honest i dont tell other docs anything unless i want them to intervene ans help me or the patient right now.

There isn't enough in this for me to ask the surgeon to trache the patient. Once intubated that trumps or at least equals an acute trache. There is no extra benefit. We know this from trache man albeit different settings.

So all told i like reps explanation but either way reintubate and chill in icu til tomorrow then cuff leak and yank it...

This is the problem with involvement of other physicians. Procedure bias. Everyone only knows how to do interventions. No one is trained to observe... Sometimes all you need time.

Ultimately you did good work and no harm to patient so kudos to you and team
 
repititionition said:
if the patient did not have tracheomalacia walking in, they don’t have it now (and unless an adult gives a hx of not being able to sleep supine for their entire life, they do not have clinically significant tracheomalacia).

if you have stridor, it is an upper airway problem, and thus unlikely bronchospasm.

if you do not have bronchospasm and hemodynamic changes it is unlikely mast cell mediated and does not need epi

if you have a soft neck it is not mass/compression.

if you are easily moving air prior to paralysis, unlikely laryngospasm.

if you have an asleep patient it is not paradoxical vocal cord dysfunction (well, almost certainly not)

if you have had recent surgical manipulation near the innervation of the cords, and the above issues are not the problem, THIS almost certainly is.

if you have coarse breath sounds you have a problem at the alveolar interface, c/w NPPE.

The unifying diagnosis is obstruction at the level of the cords causing NPPE (negative pressure pulmonary edema). The question is if iatrogenic (surgical cord disfunction) or intrinsic (patient inhaled against closed glottis).

For love or money you could not get me to agree to trach this patient.

I respect you so much for coming here to share, and your dedication to learning. As others have said, most of the anesthetics you post are too clever by half. I understand that you are executing your attending’s plans the majority of the time, but when you are planning and executing your own anesthetic, remember that simple and clean is generally safer and more elegant.
Click to expand...

Agree. Inspiratory stridor -> extrathoracic. In this case, the likely diagnosis is nerve paresis to the cords. Variable extrathoracic obstruction -> treat by decreasing ventilation so that you get less airway collapse. Midaz was okay, you can given some opioids and keep airway open with cpap.
 
repititionition said:
if the patient did not have tracheomalacia walking in, they don’t have it now (and unless an adult gives a hx of not being able to sleep supine for their entire life, they do not have clinically significant tracheomalacia).

if you have stridor, it is an upper airway problem, and thus unlikely bronchospasm.

if you do not have bronchospasm and hemodynamic changes it is unlikely mast cell mediated and does not need epi

if you have a soft neck it is not mass/compression.

if you are easily moving air prior to paralysis, unlikely laryngospasm.

if you have an asleep patient it is not paradoxical vocal cord dysfunction (well, almost certainly not)

if you have had recent surgical manipulation near the innervation of the cords, and the above issues are not the problem, THIS almost certainly is.

if you have coarse breath sounds you have a problem at the alveolar interface, c/w NPPE.

The unifying diagnosis is obstruction at the level of the cords causing NPPE (negative pressure pulmonary edema). The question is if iatrogenic (surgical cord disfunction) or intrinsic (patient inhaled against closed glottis).

For love or money you could not get me to agree to trach this patient.

I respect you so much for coming here to share, and your dedication to learning. As others have said, most of the anesthetics you post are too clever by half. I understand that you are executing your attending’s plans the majority of the time, but when you are planning and executing your own anesthetic, remember that simple and clean is generally safer and more elegant.
Click to expand...
I am so thankful for your all valuable explanation and giving in experience to this case.
This is my avenue to vent cases from where I am, and I respect your all opinions, it helps a lot. I am not alone with my thoughts.
I will try my best to keep it simple and go with the flow.
 
GassYous said:
Agree. Inspiratory stridor -> extrathoracic. In this case, the likely diagnosis is nerve paresis to the cords. Variable extrathoracic obstruction -> treat by decreasing ventilation so that you get less airway collapse. Midaz was okay, you can given some opioids and keep airway open with cpap.
Click to expand...
I am at the edge - next October I will be a fourth year resident, can't make a full decision - at least I was although blamed for Laxis !
I don't know if I had opioid handy and gave without informing, would ended up with more "blaming".
Thanks for all your support. I grew up here.
 
for all those sayings its nerve paresis... he extubated the patient and took a look at teh cords and they were mobile. this pushes nerve paresis down on my differential. more likely to be some degree of laryngospasm.
 
anbuitachi said:
for all those sayings its nerve paresis... he extubated the patient and took a look at teh cords and they were mobile. this pushes nerve paresis down on my differential. more likely to be some degree of laryngospasm.
Click to expand...

Awake patients don't laryngospasm
 
anbuitachi said:
for all those sayings its nerve paresis... he extubated the patient and took a look at teh cords and they were mobile. this pushes nerve paresis down on my differential. more likely to be some degree of laryngospasm.
Click to expand...
So mobile with laryngospasm then 🤔:shrug:
 
Angus Avagadro said:
Outside of anecdotal efficacy, any downside of a trial of Calciun Chloride? I might have considered that.
Click to expand...

I mean it might be effective if laryngospasm was due to hypocalcemia and tetany. I wouldn't fumble around for that stick of calcium chloride in this situation.
 
As an ENT reading this post, a few thoughts:

1. Examination of the vocal cords immediately after extubation with a couple of hours of GA is pretty much useless. Patients are too groggy to follow complex commands to assess vocal fold function and if you are looking with a rigid laryngoscope, you are instrumenting an airway that is probably edematous and reactive from a couple of hours of surgeons pushing on it. Benefit is low and risk of laryngospasm is high.

2. If the patient's trachea wasn't compromised by the goiter pushing on it, it's not worse after the goiter is removed. I agree with article above, tracheomalacia after thyroidectomy doesn't really seem to exist in adults even with massive long-standing goiters.

3. Tracheostomy at this point seems very ill-advised. After re-intubation, patient could've been transferred to ICU, sort out any post-op issues (hypocalcemia, make sure any local wears off, etc), and then a controlled extubation with ENT at bedside to immediately assess vocal fold function fiberoptically. VC function cannot be assessed with tube still in place. If one is available, an airway exchange catheter can be placed prior to extubation (popular in North America is the Cook Medical brand) and can act as a bougie for re-intubation if necessary and can be hooked up to a ventilator. Only trach if the ENT exam confirms bilateral cord paralysis. If there was still stridor after extubation with bilateral cord mobility, needs a bronch and evaluation for tracheomalacia.

4. If the ENT says the cords were moving, RLN paresis very unlikely to be the cause of the stridor, unless the stridor was related to local anesthesia (no idea why that would be used around the nerves in a case like this). Neural recovery after RLN injury takes at least weeks and more often 2-3 months. Plus, as someone mentioned above, stridor really only occurs with bilateral RLN injury (unless the larynx is grossly edematous from prolonged surgery), and I think the story of bilateral RLN injury causing airway collapse and then suddenly reversing in a few days makes no sense.

I suspect from the story that the surgeons asking for you to do a DL at the end of the case prompted laryngospasm. You asked about treating the stridor with with nebulized or systemic epinephrine, wouldn't really work if the cause of the stridor was anything but laryngeal edema (anaphylaxis, infection, venous obstruction, etc). If your differential is RLN injury vs. laryngospasm, both of those are structural causes of airway obstruction that will not be greatly improved with epinephrine.
 
Last edited:
Newtwo said:
I gotta be honest i dont tell other docs anything unless i want them to intervene ans help me or the patient right now.

There isn't enough in this for me to ask the surgeon to trache the patient. Once intubated that trumps or at least equals an acute trache. There is no extra benefit. We know this from trache man albeit different settings.

So all told i like reps explanation but either way reintubate and chill in icu til tomorrow then cuff leak and yank it...

This is the problem with involvement of other physicians. Procedure bias. Everyone only knows how to do interventions. No one is trained to observe... Sometimes all you need time.

Ultimately you did good work and no harm to patient so kudos to you and team
Click to expand...
no harm? the patient was trached for what sounds like asthma..
 
images.jpeg.jpg
 
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