Case #3

[Bostonredsox]

76 year old female presents to hospital with mild chest pain and dyspnea. Treated on medical floor for a day or so with suspected pericarditis from a moderate sized pericardial effusion. symptoms eventually worsen, hypotension and JVD start to ensue, re-ECHOd, hemodynamically significant tamponade. Taken to OR, windowed, brought to MICU. Placed on Neo gtt with orders from CVS to keep the preload up and try and wean off pressor. Not on vent. Saturating well on 4L NC, sitting up 45 degress with significant orthonea but ok so long as not lying flat. Pericardial and pleural chest tubes in place with minimal output.

enter me on night shift.

Nurse calls, Neo is ,axed, MAP 47 but with poor waveform. Cuff map is 58.

Drop in fem art line. Good waveform. MAP 57, correlating with cuff. Ask her to connect CVP to the sublclavian line will i grab US. CVP 31, my US shows huge dilated IVC >3cm with no collapse on inspiration. Neck veins are massively distended. Huge hypocontracile RV. biatrial enlargement, LVEF 40ish. No recurrent effusion.

I ask for stat ABG/VBG/Lactate and renal panel. Oxygenating well, PaO2>200 n 6L. ScvO2 44%. Lactate up to 2.2 from 1.4. Cr up to 2.6 from 1.9, LFTs starting to rise. UOP is 50cc last 5 hours.

To me, Flow problem. tamponade, restrictive effusion, dilated RV...maybe a concurrent PE...but either way poor flow. Add dobutamine. Place Swan. RA around 30, PAP's 60/35...PCWP 30. Cardiac Index 1.4, CO 3.2. MAP stil 58-59. Gave small dose of lasix for the RV congestion and volume overload. Added vasopressin flat rate for the MAP. Titrated up dobutamine to CI >2.0 and SvO2 >55%.

Pt started to make urine a few hours later, pressures improved with maxed levo, 0.04 of vaso and 15 of dobutamine. Mildly tachy from the dobutamine but didnt want to go milrinone because of the renal failure.

So now shes better Im trying to think wtf is going on. Dilated RV on my echo, moreso than the initial preop one, and hypocontractile surely makes me think of acute massive PE. But with tamponade 12 hours ago and a trop of 1.5, MB of like 11....maybe RV failure from constriction?? Neither of those would explain the Wedge of 30 and her severe orthopnea...LV was mildly diminished but nothing compared to RV. Now the fib explains the biatrial enlargment but not the elevated LA pressures after the window was placed.

so on to morning....cards comes by for repeat echo. couples his measurements with my swan numbers. We do bedside LE....popliteal clot. presume at this point massive PE. window <24 hours ago rules him out for thrombolysis. Start heparin gtt. Plan for limited perfusion scan later today if respiratory status stays stable enough for her to tolerate it. Cards also points out, the huge LA and LV filling pressures and wedge near 30 are not explained by the suspected PE. His ef is 45-50. no segmental abnormalities. He does some other neat echo **** that I dont really understand, mitral inflows and whatever....and he concludes.....

Possible Massive PE given RV failure and + leg clot. But in addition.....Effusive Contrictive Pericarditis. Never heard of this before. EKG has no ST elevations at all and pt has no chest pain. So I am doing some reading on it now. Anyone else seen this before?

and as per our usual form, feel free to point out what I did wrong and things I may have missed or that you would have done differently.

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[sluggs]

I would think about an IVC filter. With the window and the "effusive constrictive pericarditis" there is a huge risk of bleed on the hep gtt. I am not a big filter fan, but seems like there is high risk of a sudden cessation of anticoagulation...
Sounds like lightening is striking twice on this poor patient..

 

[Hernandez]

Where is her cancer hiding at?

 

[alphaholic06]

Where is her cancer hiding at?

My thoughts exactly.

 

[jdh71]

I don't know. I think the PE, from the isolated DVT, likely initially missed, can explain almost everything that happened.

I don't know about all this extra Effusive Contrictive Pericarditis stuff. Which I'll need to read about.

I can't fault your management, but will take the time to underline for everyone, inclduing a reminder to myself, that PE is always the big hole in the thinking, the chink in the armor, and to always be on watch for it.

 

[souljah1]

Was her pericardial fluid sent for cytology? Agree that malignancy could be the common denominator here.

Your swan numbers (with their accompanying limitations) and echo findings (assuming the RV truly is blown out of proportion to the LV) aren't consistent with classic effusive-constrictive pericarditis - which basically demonstrates constrictive physiology despite draining the effusion. However, your echo is also not classic for massive PE -induced RV failure - where you'll see an apex occupying RV that is hypokinetic and ballooned along with septal bowing and a hypercontractile LV that is pancaked. I wonder if this is more of a Hickam's dictum as opposed to an Occam's razor example.

There exists the humbling possibility that your echo findings (and the cardiologist) are over calling the RV failure - which commonly occurs. If that were the case then all four chambers might be experiencing equalization in pressure (e.g. wedge = RA = RV mean, etc). If that were the case, then the popliteal clot could be a red herring - and this could all be constriction.

Also, re: pressor management of massive PE -> I like Epinephrine +/- Vaso (no Vaso receptors in pulmonary arteries) along with an additional inotrope. A little flolan gets thrown in once in a while as well.

Here's a good question for you -> What if, in the setting of metastatic cancer (e.g. adeno) you are highly suspicious of a PE in a patient with acute dyspnea, hypoxemia, and hemodynamic derangements associated with a ballooning RV and septal bowing. You do a PE-protocol CT scan and it is negative for clot; and then you do a V/Q scan and it shows multiple segmental V/Q mismatches -> what could it be? What gives you multiple perfusion defects that aren't seen on CT scan?

 

[jdh71]

Was her pericardial fluid sent for cytology? Agree that malignancy could be the common denominator here.

Your swan numbers (with their accompanying limitations) and echo findings (assuming the RV truly is blown out of proportion to the LV) aren't consistent with classic effusive-constrictive pericarditis - which basically demonstrates constrictive physiology despite draining the effusion. However, your echo is also not classic for massive PE -induced RV failure - where you'll see an apex occupying RV that is hypokinetic and ballooned along with septal bowing and a hypercontractile LV that is pancaked. I wonder if this is more of a Hickam's dictum as opposed to an Occam's razor example.

There exists the humbling possibility that your echo findings (and the cardiologist) are over calling the RV failure - which commonly occurs. If that were the case then all four chambers might be experiencing equalization in pressure (e.g. wedge = RA = RV mean, etc). If that were the case, then the popliteal clot could be a red herring - and this could all be constriction.

Also, re: pressor management of massive PE -> I like Epinephrine +/- Vaso (no Vaso receptors in pulmonary arteries) along with an additional inotrope. A little flolan gets thrown in once in a while as well.

Here's a good question for you -> What if, in the setting of metastatic cancer (e.g. adeno) you are highly suspicious of a PE in a patient with acute dyspnea, hypoxemia, and hemodynamic derangements associated with a ballooning RV and septal bowing. You do a PE-protocol CT scan and it is negative for clot; and then you do a V/Q scan and it shows multiple segmental V/Q mismatches -> what could it be? What gives you multiple perfusion defects that aren't seen on CT scan?

Good stuff souljah. I've only seen one constriction case in all of fellowship and even then as a consultant (cards had lost their damn minds and put a chest tube in a constriction effusion and now wanted our help getting the tube out) but I think perhaps you are looking at this right running the numbers.

I never did get around to reading about the effusion constriction stuff today - was busy putting out fires in my clinic and the lab.

And I'll bite on your question. What?

 

[souljah1]

Lab fires are serious business.

A history of metastatic cancer plus RV strain with a negative PE protocol CT and a + VQ scan should make you think about microscopic pulmonary tumor emboli. Have seen two cases in the last year, one of which was an autopsy.

 

[Hernandez]

You're on a roll today, good posts soul....

 

[ORL10]

If it was a PE you would think there might be more signifcant respiratory distress (taking into account I didn't see the patient). I guess my assumption would be a big PE causing signficant RV dysfunction associated with hypotension is frequently accompanied by respiratory distress.

An infrequent complication after pericardiotomy is myocardial stunning, with significant pulmonary edema, and cardiogenic shock. Why was the RV affected >> than LV function, don't know maybe already some underlying RV dysfunction previously?

Shenoy M., Dhar S., Gittin R., Sinha A., Sabado M. Pulmonary edema following pericardiotomy for cardiac tamponade. Chest. 1984;86:647&#8211;648.

 

[jdh71]

If it was a PE you would think there might be more signifcant respiratory distress (taking into account I didn't see the patient). I guess my assumption would be a big PE causing signficant RV dysfunction associated with hypotension is frequently accompanied by respiratory distress.

An infrequent complication after pericardiotomy is myocardial stunning, with significant pulmonary edema, and cardiogenic shock. Why was the RV affected >> than LV function, don't know maybe already some underlying RV dysfunction previously?

Shenoy M., Dhar S., Gittin R., Sinha A., Sabado M. Pulmonary edema following pericardiotomy for cardiac tamponade. Chest. 1984;86:647–648.

patients

they be tricky

heh

 

[souljah1]

You're on a roll today, good posts soul....

Thanks, Hernandez.

 

[Bostonredsox]

thanks for the posts.

I asked for epi given poor perfusion and hypotension, was overruled by CTS attending.

Cytology was negative for malignancy.

Formal US of legs was negative for clot. Either our US threw the clot to the lung....or we saw something else. Ill admit I am novice at LE US.

I read up on the Eff Cons Peri. To me it fits. We removed the effusion, and she then behaved like a restrictive pericarditis pt. She was better when I left yesterday morning. Levo off, vaso almost off and dobut down to 5. They were getting a V/Q that afternoon. Im on again tomorrow Il try and fill in more details.

 

[VentdependenT]

Ive never heard of any of this stuff before. if this was EC pericarditis nothing would get better with window. never the less pt did better so whatever you did didnt kill her, make her worse, or perhaps, made her better.

 

[VentdependenT]

Good case anyways and good management, as is the M.O. for boston.

 

[Bostonredsox]

Thanks vent.

V/q was negative. She was weaned off all pressors and tropes. Pleural and pericardial chest tubes were pulled. Diuresis well over last 24 hours or so. Transferred to stepdown.

Crazy case.

 

[bigtuna]

Occasionally patients with pre-existing RV failure related to PAH decompensate after draining pericardial effusions:

http://www.ncbi.nlm.nih.gov/pubmed/18414173

This is probably due to acute worsening of RV dilatation leading to LV compression.


Your swan numbers obviously do not look like PAH but perhaps you witnessed a similar phenomenon.