Case today - thoughts?

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SexPanther

This could be a problem
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69 y/o male w/PMH chronic a-fib on propafenone/coumadin at home, HTN, COPD in the hospital for 18% TBSA burns to thorax and legs. Burn tissue has already been resected prior to scheduled procedure (skin graft) today. This hospitalization has been complicated by recurrent A-fib w/RVR for which he is on a dilt gtt along with PO metoprolol/amiodarone, hypoxic respiratory failure developing PNA and metabolic alkalosis.

Get to this dudes room this a.m. for transport and he is in ST/a-fib with rates of 140s-150s, BP holding steady. The diltiazem gtt is already maxed out so I have the nurse give his a.m. PO meds early and I give him 20mg dilt IV. I was very hesistant to give him a beta blocker IV due to the possibility of complete heart block from dual nodal blockade (surprised the arrythmia service had him on huge dose of PO metoprolol, as was the burn ICU team). Look at lytes and he's hypokalemic not yet repleted so I help nurse hang some K and Mag. 10 minutes later, he's back in NSR so all is good but it looked like we were gonna post-pone for a while.

Intra-op, things are going well. Oxygenating, ventilating, perfusing until.....his EtCO2 drops from 34 to 18 in seconds. My attending happens to be in the room and he's like "WTF." Wasn't sure either, took a look at his a-line and his BP was normotensive but then dropped precipitously w/in the next 30 seconds. He then developed hypoxemia with his SaO2 steadily dropping, no elevation in his Ppeak or Pmean. Flipped him onto 100%, bagged him w/o difficulty but sats and EtCO2 stayed low. I listened to BS while attending took care of BP; BS equal b/l. I then suctioned him well w/o improvement so we called for the bronch and a stat CXR. Bronchoscopy revealed a huge L mainstem mucous plug with ETT in good position; we cleaned him out thoroughly w/the bronch. CXR showed loss of airspace in L hemithorax w/o evidence of PTX, pulmonary edema etc. Added some recruitment maneuvers, and ultimately everything normalized.

So this guy plugged up and had a huge shunt leading to his hypoxemia which possibly contributed to the hypotension. Shunt usually (that I'm familiar with) doesn't cause low EtCO2 though and the timing of events is very curious: decreased EtCO2-->hypotension-->hypoxia. After thinking about this case and the events, I'm left thinking that something else was also in play, perhaps a PE that resolved on its own? Thoughts?

Ultimately, we were able to take our pt. back to the BICU on a t-piece and he was extubated this afternoon....looked great when I checked on him.
 
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69 y/o male w/PMH chronic a-fib on propafenone/coumadin at home, HTN, COPD in the hospital for 18% TBSA burns to thorax and legs. Burn tissue has already been resected prior to scheduled procedure (skin graft) today. This hospitalization has been complicated by recurrent A-fib w/RVR for which he is on a dilt gtt along with PO metoprolol/amiodarone, hypoxic respiratory failure developing PNA and metabolic alkalosis.

Get to this dudes room this a.m. for transport and he is in ST/a-fib with rates of 140s-150s, BP holding steady. The diltiazem gtt is already maxed out so I have the nurse give his a.m. PO meds early and I give him 20mg dilt IV. I was very hesistant to give him a beta blocker IV due to the possibility of complete heart block from dual nodal blockade (surprised the arrythmia service had him on huge dose of PO metoprolol, as was the burn ICU team). Look at lytes and he's hypokalemic not yet repleted so I help nurse hang some K and Mag. 10 minutes later, he's back in NSR so all is good but it looked like we were gonna post-pone for a while.

Intra-op, things are going well. Oxygenating, ventilating, perfusing until.....his EtCO2 drops from 34 to 18 in seconds. My attending happens to be in the room and he's like "WTF." Wasn't sure either, took a look at his a-line and his BP was normotensive but then dropped precipitously w/in the next 30 seconds. He then developed hypoxemia with his SaO2 steadily dropping, no elevation in his Ppeak or Pmean. Flipped him onto 100%, bagged him w/o difficulty but sats and EtCO2 stayed low. I listened to BS while attending took care of BP; BS equal b/l. I then suctioned him well w/o improvement so we called for the bronch and a stat CXR. Bronchoscopy revealed a huge L mainstem mucous plug with ETT in good position; we cleaned him out thoroughly w/the bronch. CXR showed loss of airspace in L hemithorax w/o evidence of PTX, pulmonary edema etc. Added some recruitment maneuvers, and ultimately everything normalized.

So this guy plugged up and had a huge shunt leading to his hypoxemia which possibly contributed to the hypotension. Shunt usually (that I'm familiar with) doesn't cause low EtCO2 though and the timing of events is very curious: decreased EtCO2-->hypotension-->hypoxia. After thinking about this case and the events, I'm left thinking that something else was also in play, perhaps a PE that resolved on its own? Thoughts?

Ultimately, we were able to take our pt. back to the BICU on a t-piece and he was extubated this afternoon....looked great when I checked on him.

Agree with your logic.
If a sdudden mucous plug caused the problem then I would think that you should have noticed some sudden change in airway pressure which appears to be not the case here.
I think the mucous was probably chronic and something more dramatic happened intraop that caused sudden decrease of cardiac output.
Could it be an air embolus? Or some other kind of embolus?
 
Agree with your logic.
If a sdudden mucous plug caused the problem then I would think that you should have noticed some sudden change in airway pressure which appears to be not the case here.
I think the mucous was probably chronic and something more dramatic happened intraop that caused sudden decrease of cardiac output.
Could it be an air embolus? Or some other kind of embolus?

I'm pretty sure it was some kind of embolus, air would definitely make sense as this was all around the time they started infiltrating the skin of his RLE. Or perhaps they dislodged a LE thrombus, he had been off of coumadin and heparin.
 
Sounds like acute obstructive shock to the Right ventricle, ie an embolus of sorts. Yet given that the patient has hx of COPD and recent burns to the chest indicating the possibility of inhalation injury and restrictive lung disease ( increased rate of atelectasis) the patient may infact have a diffusion impairment large enough to cause issues with CO2 diffusion in the case of mucuous plugging. Normally it would take greater than a 50% shunt to see changes in Co2 diffusion but in this case i would not rule out the possibilty of a large mucous plug causing this picture. Did you see a rise in your ET nitrogen? That would help with dx of air embolus.

He looked great when you saw him but what testing did he have and what were the results? PE CT? ECHO?
 
sudden hypoxia and decreased etco2 sounds like an embolus.
 
I'm pretty sure it was some kind of embolus, air would definitely make sense as this was all around the time they started infiltrating the skin of his RLE. Or perhaps they dislodged a LE thrombus, he had been off of coumadin and heparin.

Shoulda brought the TEE to the room and taken a look. 😀
 
Sounds like acute obstructive shock to the Right ventricle, ie an embolus of sorts. Yet given that the patient has hx of COPD and recent burns to the chest indicating the possibility of inhalation injury and restrictive lung disease ( increased rate of atelectasis) the patient may infact have a diffusion impairment large enough to cause issues with CO2 diffusion in the case of mucuous plugging. Normally it would take greater than a 50% shunt to see changes in Co2 diffusion but in this case i would not rule out the possibilty of a large mucous plug causing this picture. Did you see a rise in your ET nitrogen? That would help with dx of air embolus.

He looked great when you saw him but what testing did he have and what were the results? PE CT? ECHO?

Post-op, he continued to have tachypnea, dyspnea and CXR showed evidence of pulmonary edema. Decided to go with a TTE to assess LV/RV fxn, valves etc. Figured it may give us some indirect evidence of embolus as well as other valuable info. It showed grossly preserved LV and RV function on a limited study. Valves appeared normal, there was trace TR present. He had a mildly dilated aortic root. Doesn't sound like any indirect evidence of RV strain from embolus.

No CTA chest done due to concern of contrast nephropathy as well as lack of impact on decision making. He was back on his heparin gtt post-op and the burn ICU team had no desire to have a filter placed.
 
During my residency, I had a 2 month burn unit rotation. This situation is not uncommon in burn patients. Not a burn, then I would agree PE every time. But burn patients are a different animal. There would be two or three every month that would almost code because of mucous plugging. Go Figure!

Numb
 
During my residency, I had a 2 month burn unit rotation. This situation is not uncommon in burn patients. Not a burn, then I would agree PE every time. But burn patients are a different animal. There would be two or three every month that would almost code because of mucous plugging. Go Figure!

Numb

Interesting, thanks for the insight.

The other thing we considered was the mucous plug creating a ball-valve phenomena which could explain what happened. However, I would have expected to have elevated airway pressures and lack of expiratory breath sounds on the affected side. Neither of those were present.
 
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