Clinical scenario-What would you do?

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DocSpy332

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Hello sdn! I would appreciate your clinical judgment on the following scenario:

Setting: Resident in small regional hospital covering floors and ICU.

Patient:
80M w/ h/o Parkinson, COPD (w/ home oxygen/baseline 2L), using BPAP at nights, CHF p/w SoB. Patient communicates only by single words and head nodding. VSS (afebrile, 125/75, 89, 92%). Initial PE reveals diminished BS over R lung base, inflamed/erythematous RLE, o/w unremarkable (or baseline), not fluid overloaded. CBC, CMP, BNP wnl (or baseline). VBG: pH=7.35, PaCO2=68, HCO3=37 (baseline). CXR reveals R pleural effusion. Chest CT confirms R pleural effusion and shows R ventricular enlargement. Patient undergoes thoracentesis with drainage of clear fluid. Sent for analysis (pending). New CXR shows improvement on R pleural effusion. Pt reports feeling better. RLE treated as infx per primary.

O/N event:
On-call resident called at bedside b/c patient is "acting differently". A couple hours earlier nursing staff placed off BPAP b/c pt didn't tolerate it. On PE: VSS (130/84, 94, 94%), but pt has short (less than 5 seconds) spells of agonal breathing and then returns to baseline. He is trying to explain that something is wrong and he is pointing at his chest and mouth. When questioned about CP he is shaking his head negatively. STAT Trops, EKG, VBG, CXR ordered. Pt placed back on BPAP.
15 minutes later:
Trops wnl, EKG at baseline.
CXR: R pleural effusion is worsening again
VBG: pH=7.45, PaCO2=48, HCO3=35
Sats: >90% no drops

Visited pt again: Pt now has definitely agonal breathing, using accessory muscles, while VS show hypertension (145/98) and tachycardia (123bpm). Sats still >90%.

What would be your next step in this scenario given that PE is very likely but he also has worsening R pleural effusion s/p thoracentesis? Would you be worried about hemothorax?

p.s.: If I am missing any pertinent info let me know

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Bedside POCUS? You can even do bedside ultrasound of the effusion to assess/confirm.
Arterial blood gas?
Did they leave a pigtail cath/place a chest tube to monitor for drainage?
Were any of the labs back for the fluid? Shouldn't take more than 6-12 hours to at least confirm transudate vs exudate. Also, did fluid appear infectious or clear? Was it bloody?
If the effusion is coming back THAT quickly; He needs another chest tube. Hell, I'd say do a bedside ultrasound and get a chest tube in either by yourself or with GS help.
 
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If your clinical question is should we anticoagulate, then I'd say no. Should we get a ct pe? I dont think so since I still wont anticoagulate given concern for hemotorax. Usually reaccumulation of the effusion this quickly I've only seen (in my humbly limited experience) is hepatic hydrothorax, malignant and hemo. I think we need a little more data, but this is someone I would transfer to a higher acuity of care if on the gmf while we do further workup. When they are tachy and has ams, did he have a fever then? Are you convinced enough that this cellulitis was cellulitis or was it a clot or edema from adhf? How much effusion was seen on the initial upright cxr?
 
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Examine the patient. Look at the neck veins, feel the extremities (is this high blood pressure all SVR? Blood pressure is not perfusion), EKG, echo (if they are willing to do it to evaluate RV strain), ABG, troponin, BNP, CT PE protocol.

What did the Thora fluid look like? Was the lung clearly reexpanded or was the effusion just gone? Recurrence of effusion could be related to PE, pulmonary infarction, etc. Separately, the fluid may have been there chronically, so he may just be filling up a chronic space and becoming intravascularly dry. Alternatively, it could be hemothorax, fortunately the CT PE protocol will be able to give you some sense of the density in hounsfield units of the fluid.

If the patient has a PE and evidence of some sort of hemodynamic compromise (not just pressure, but perfusion) then you could always just bring the patient to IR for catheter directed thrombolysis. Moreover, if the leg is more along the lines of a DVT, you should have a diagnosis of VTE before placing the ivc filter.
 
Why are you getting troponins....


Waste of his blood
 
Why are you getting troponins....


Waste of his blood
If it's a PE, a positive troponin will help to convince IR to take the patient for catheter directed thrombolysis as it is a negative prognostic finding. Especially if RV dysfunction is present.

Maybe your interventional radiologists are more aggressive than the ones I've dealt with, though.
 
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It takes 30 seconds to do a diagnostic thora and see if it is a hemothorax. If the fluid was clear before and now is grossly bloody you have an answer. Even if they had a bloody malignant effusion in the initial tap sending a BF HCT will give you the quickest answer.
 
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This is an old man with fairly advanced COPD and probably under-diagnosed severity CHF who is having acute respiratory failure. His R effusion may be chronic and it is very unlikely whoever drained it measured pleural pressures and may have tried to drain too much fluid off his trapped lung and he simply had reaccumulation. Hemothorax is also possible but would probably intubate first if he is agonal breathing assuming it is within his code status. Really doubt this is a PE because recurrent pleural effusion makes no sense in that scenario. If it was he should be offered heparin gtt not cath-directed lysis which is of very dubious value in most circumstances but especially in an 80 year old who would be forced to lay flat in bed for a day.

Hopefully code status has been discussed--he appears to be near end of life so dragging him through this acute event until the next one happens is of questionable value.
 
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If it's a PE, a positive troponin will help to convince IR to take the patient for catheter directed thrombolysis as it is a negative prognostic finding. Especially if RV dysfunction is present.

Maybe your interventional radiologists are more aggressive than the ones I've dealt with, though.
but you haven't made any diagnosis and this isn't an ACS. I get trops/BNP after diagnosing a PE, not before. The most likely scenario is you'll have a troponin of 0.22 and no diagnosis. This isn't an NSTEMI.
 
but you haven't made any diagnosis and this isn't an ACS. I get trops/BNP after diagnosing a PE, not before. The most likely scenario is you'll have a troponin of 0.22 and no diagnosis. This isn't an NSTEMI.
I am 100% okay acknowledging that you are smarter and more focused with your lab orders. But what's the downside?

I got the troponin, which didn't give me the diagnosis (neither did the EKG but we got that anyway), but he also went down to CT, so we got our diagnosis (or ruled out PE). Im curious. Would you prefer getting lower extremity ultrasound and a d-dimer so that you can be more targeted in the CT PE order?

This seems to be a very medicine vs surgery thing. Medicine prides themselves on only getting the optimal labs, and I respect that, because in routine care, its more cost effective. It seems to me that this patient is not doing well, though. Heck, he may be dead by the time the diagnosis is made and the troponin is ordered. And then it results. And then you call IR.
 
I am 100% okay acknowledging that you are smarter and more focused with your lab orders. But what's the downside?

I got the troponin, which didn't give me the diagnosis (neither did the EKG but we got that anyway), but he also went down to CT, so we got our diagnosis (or ruled out PE). Im curious. Would you prefer getting lower extremity ultrasound and a d-dimer so that you can be more targeted in the CT PE order?

This seems to be a very medicine vs surgery thing. Medicine prides themselves on only getting the optimal labs, and I respect that, because in routine care, its more cost effective. It seems to me that this patient is not doing well, though. Heck, he may be dead by the time the diagnosis is made and the troponin is ordered. And then it results. And then you call IR.
This guy isnt in any shape to leave the floor if he is agonal breathing. ABCs-if he is full code he needs his airway protected. He is 80+ years old with advanced chronic disease and shouldn't be full code but if he wants to die on a vent that's his right.

I don't know what about this case is screaming PE to anyone. He isn't having hypoxia or new hypercapnia. His HR is up but he is also in respiratory distress. He had a thoracentesis earlier in the day-hemothorax vs pulm edema makes more sense to me.

I think your local culture seems to be to call ir for every bad PE. That is great for maximum billing but the reality is that heparin works well for most and in those it doesnt ecmo is better.
 
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I am 100% okay acknowledging that you are smarter and more focused with your lab orders. But what's the downside?

I got the troponin, which didn't give me the diagnosis (neither did the EKG but we got that anyway), but he also went down to CT, so we got our diagnosis (or ruled out PE). Im curious. Would you prefer getting lower extremity ultrasound and a d-dimer so that you can be more targeted in the CT PE order?

This seems to be a very medicine vs surgery thing. Medicine prides themselves on only getting the optimal labs, and I respect that, because in routine care, its more cost effective. It seems to me that this patient is not doing well, though. Heck, he may be dead by the time the diagnosis is made and the troponin is ordered. And then it results. And then you call IR.
I would have sent him for EKG (rhythm vs ACS), CTPE, get cultures and an abg, everything else is basically useless in the acute setting. Lytes, trop, BNP, aren't going to add anything to your workup, delay actual medical care for him, and probably result in a bunch of additional tests and consults he doesn't need.
 
Re expansion edema? Probably not though. He would be hypoxic with that most likely. He would probably be hypoxic with a lot of the aforementioned stuff above. Interesting that he was in such distress with accessory use but no hypoxia
 
This is an old man with fairly advanced COPD and probably under-diagnosed severity CHF who is having acute respiratory failure. His R effusion may be chronic and it is very unlikely whoever drained it measured pleural pressures and may have tried to drain too much fluid off his trapped lung and he simply had reaccumulation. Hemothorax is also possible but would probably intubate first if he is agonal breathing assuming it is within his code status. Really doubt this is a PE because recurrent pleural effusion makes no sense in that scenario. If it was he should be offered heparin gtt not cath-directed lysis which is of very dubious value in most circumstances but especially in an 80 year old who would be forced to lay flat in bed for a day.

Hopefully code status has been discussed--he appears to be near end of life so dragging him through this acute event until the next one happens is of questionable value.

This guy isnt in any shape to leave the floor if he is agonal breathing. ABCs-if he is full code he needs his airway protected. He is 80+ years old with advanced chronic disease and shouldn't be full code but if he wants to die on a vent that's his right.

I don't know what about this case is screaming PE to anyone. He isn't having hypoxia or new hypercapnia. His HR is up but he is also in respiratory distress. He had a thoracentesis earlier in the day-hemothorax vs pulm edema makes more sense to me.

I think your local culture seems to be to call ir for every bad PE. That is great for maximum billing but the reality is that heparin works well for most and in those it doesnt ecmo is better.

I think this summarizes most of my thoughts.

One could raise the question - Why therapeutically drain a pleural effusion in a stable patient with CHF, unless it was new and there was concern for malignancy or a parapneumonic effusion? Most people don't do bedside pleural manometry, but in the setting of a likely chronic effusion one can do a poor man's manometry with the tubing from the thoracentesis kit by holding it vertical, and can stop pulling fluid when the pleural pressure falls to zero. Then the re-accumulation from the trapped/entrapped lung can be avoided and one doesn't have to go down this rabbit hole, because there is no utility in draining it dry.

Additionally, when you say "worsening R pleural effusion" do you mean worse than before the tap, or just re-accumulation after the tap? The concern for hemothorax could be valid. Re-expansion edema would probably be discernible from effusion on chest imaging.

And @DocSpy332 when you say "sats > 90%" are you also saying the FiO2 on the BiPAP was unchanged? It may not take a lot to cause respiratory distress in a patient with an already disadvantaged diaphragm from severe COPD. There are a lot of clarifications required, and I wonder if OP is going to come back to this thread and give us updates.
 
This guy isnt in any shape to leave the floor if he is agonal breathing. ABCs-if he is full code he needs his airway protected. He is 80+ years old with advanced chronic disease and shouldn't be full code but if he wants to die on a vent that's his right.

I don't know what about this case is screaming PE to anyone. He isn't having hypoxia or new hypercapnia. His HR is up but he is also in respiratory distress. He had a thoracentesis earlier in the day-hemothorax vs pulm edema makes more sense to me.

I think your local culture seems to be to call ir for every bad PE. That is great for maximum billing but the reality is that heparin works well for most and in those it doesnt ecmo is better.
Agreed that airway protection is most important. I would've probably intubated if goals of care were discussed and he was full code.
If your clinical question is should we anticoagulate, then I'd say no. Should we get a ct pe? I dont think so since I still wont anticoagulate given concern for hemotorax. Usually reaccumulation of the effusion this quickly I've only seen (in my humbly limited experience) is hepatic hydrothorax, malignant and hemo. I think we need a little more data, but this is someone I would transfer to a higher acuity of care if on the gmf while we do further workup. When they are tachy and has ams, did he have a fever then? Are you convinced enough that this cellulitis was cellulitis or was it a clot or edema from adhf? How much effusion was seen on the initial upright cxr?
I don't know. Again, I'd say screw the fancy imaging studies; look at the heart with an US. If you see RV massively enlarged and the septum is basically collapsing the L ventricle...and elevated DDimer? You have your answer. If you think there's a hemothorax; again, use an US at bedside and look for it. Pleural effusions are probably the easiest thing to see with US and takes 5 minutes. And you can tap and answer your question that way.
I would have sent him for EKG (rhythm vs ACS), CTPE, get cultures and an abg, everything else is basically useless in the acute setting. Lytes, trop, BNP, aren't going to add anything to your workup, delay actual medical care for him, and probably result in a bunch of additional tests and consults he doesn't need.

And that's still not the best approach. CT PE required creatinine levels and consent along with transport, etc etc. If it's a massive/saddle emboli that's causing shock; you'd never get him to the CT in time. If you're concerned about that; you use an US. A diagnostic US will tell you what's going on faster than a CT PA will. Hell, an EKG will also give you the RV strain you're looking for.

Also, why cultures? What infection would possibly cause someone to deteriorate that fast? Unless you wiped your ass and stuck it in his SVC, you won't get any answers for at least 6 hours...with the best diagnostic tests for cultures.

My only question is how fast labs are done. I know some fancy hospitals have bedside labs that can be done quickly ie FS.
 
Pleural effusion rapidly reaccumulating within a few hours after thora is most likely iatrogenic hemothorax. Needle insertion site probably not lateral enough and didn't use vascular ultrasound beforehand. Probably the only thing useful on labs would be significant hemoglobin drop and he needs chest tube and possible OR pending GOC and securing airway. Don't know why you would think PE if he has an obvious finding on CXR to explain his respiratory distress... Doubt there is any real need for CT and could decompensate rapidly while going to scan.
 
I wonder if OP is defining “agonal” differently than me? Might intubate based on how he looks to me. The assessment is fairly “secret sauce” for me and I can’t exactly give you my recipe.

Was he particular dyspnic on presentation? He wasn’t “overloaded” as above. I have no real problems with the thora. Never put a chest tube in what might be a heart failure effusion. Heart failure effusions can reaccumulate really fast. Not totally convinced just having fluid back explains symptoms.

RV was big early on and probably would have gotten formal echo early but if it hadn’t been done yet this guy need an US on his chest now. PoC is the future of medicine. Better start getting facile with it now. And if RV looks like garbage I would eventually CT PA once stabilized.

I’d also sneak a needle on a syringe into the fluid to see if it looks like blood. Hgb can take a bit to drop. My training on bleeding wa that the initial hgb is always wrong (unless it is very very right! Ha!)
 
I wonder if OP is defining “agonal” differently than me? Might intubate based on how he looks to me. The assessment is fairly “secret sauce” for me and I can’t exactly give you my recipe.

Was he particular dyspnic on presentation? He wasn’t “overloaded” as above. I have no real problems with the thora. Never put a chest tube in what might be a heart failure effusion. Heart failure effusions can reaccumulate really fast. Not totally convinced just having fluid back explains symptoms.

RV was big early on and probably would have gotten formal echo early but if it hadn’t been done yet this guy need an US on his chest now. PoC is the future of medicine. Better start getting facile with it now. And if RV looks like garbage I would eventually CT PA once stabilized.

I’d also sneak a needle on a syringe into the fluid to see if it looks like blood. Hgb can take a bit to drop. My training on bleeding wa that the initial hgb is always wrong (unless it is very very right! Ha!)
The "but the Hgb is unchanged" argument in hemorrhage is quite annoying, it seems to somehow flip all medical school teaching about how bleeding works on its head as soon as one becomes a resident (or even higher).
 
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The "but the Hgb is unchanged" argument in hemorrhage is quite annoying, it seems to somehow flip all medical school teaching about how bleeding works on its head as soon as one becomes a resident (or even higher).

It really only works well in chronic bleeding. The medical school approach.

In acute bleeding it a pretty tricky deal as it’s such a snapshot. And if the hgb is really low on a snapshot you are already pretty far behind the “8 ball”. And then we replace with PRBCs instead of whole blood which makes repeat checks also more nuanced.
 
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