Interesting case

[Radetzky]

Thought I’d post an interesting case I’ve had recently and hear some opinions as to how people would have approached it. Will post the case sequentially.

Some details changed to protect privacy.

30 yr old male had a MVR 10 years ago for infective endocarditis. Other medical hx is recent onset seizures for which he was started on Phenytoin 1 month ago.

He has come in with a 2 week history of worsening shortness of breath, cough and hemoptysis. He was hypotensive on arrival with BP 80/40 and exam by the ER physician heard right sided crackles, so has been treated with ceftriaxone and azithromycin for CAP and given 2L fluid for septic shock.

However he has deteriorated and you are called down to assist in the ER and find this man tachypneic at 40, saturating 85% on 15L via non rebreather, a blood pressure of 75/50 and peripherally shut down. He is drowsy but able to obey commands.

His venous blood gas shows ph 7, lactate 9, BD 25. Hb 16, WBC/plts normal, INR 3, APTT 80, Cr 3, CRP 40.

What are your thoughts at this stage and how would you approach? I shall provide any more info requested.

---

Members don't see this ad.

 

[jdh71]

Looks like he may need some resuscitation but would start some pressor and probably an endotracheal tube. Blood cultures, echo, ct of the chest and head. Need to expand out his MRSA coverage. Did he get a mechanical or bio prosthetic valve 10 years ago? Is he making urine and what is his K?

Smells like endocarditis to me from the doorway.

 

[deleted171991]

Thought I’d post an interesting case I’ve had recently and hear some opinions as to how people would have approached it. Will post the case sequentially.

Some details changed to protect privacy.

30 yr old male had a MVR 10 years ago for infective endocarditis. Other medical hx is recent onset seizures for which he was started on Phenytoin 1 month ago.

He has come in with a 2 week history of worsening shortness of breath, cough and hemoptysis. He was hypotensive on arrival with BP 80/40 and exam by the ER physician heard right sided crackles, so has been treated with ceftriaxone and azithromycin for CAP and given 2L fluid for septic shock.

However he has deteriorated and you are called down to assist in the ER and find this man tachypneic at 40, saturating 85% on 15L via non rebreather, a blood pressure of 75/50 and peripherally shut down. He is drowsy but able to obey commands.

His venous blood gas shows ph 7, lactate 9, BD 25. Hb 16, WBC/plts normal, INR 3, APTT 80, Cr 3, CRP 40.

What are your thoughts at this stage and how would you approach? I shall provide any more info requested.

Heart and lung on POCUS? WBC differential? Covid RNA? History of IVDU? This is septic/cardiogenic shock, until proven otherwise. Norepi, intubate, switch antibiotics, line up, go from there. ZERO extra fluids for now (that's not the correct treatment for either septic or cardiogenic shock). His AKI is from hypotension, most likely. I assume he's on heparin gtt. If not, his liver may be hit or he may have DIC.

Hemoptysis suggests congested pulmonary circulation. This may be an endocarditis that causes functional MS. He may also have pericardial fluid there; an echo of some kind is essential. The seizures may have been TIAs from emboli. This may also be Covid-19 (pulmonary microthromboses).

Beats me how anybody would put CAP, and not endocarditis or Covid-19, on top of their differential list, even on arrival.

 

[chocomorsel]

From where I am standing, everything should have a Covid19 differential and rule out.
Seen all those signs and symptoms on Covid19 patients. The bleeding too, but usually once they are on heparin. The labs for sure are common in Covid.
But of course keep Bacteria in mind as well.

 

[ThoracicGuy]

He needs an echo. Suspect MV or other cardiac issue here. High risk for recurrent endocarditis.

 

[Radetzky]

Ok answers and case progress

He had a mechanical valve and is warfarinised. Denies any IVDU.

K is 6 and the pt is anuric. WBC diff shows slightly elevated neutrophils, other cell lines normal.

Patient is intubated with covid precautions and commenced on norepi. Lined up and cultured. Covid PCR sent. Vancomycin added to antibiotic regime. Sent to the unit nursed in covid precautions.

Over the next couple of hours has progressive hypoxia with copious frothy secretions, which requires 15 of PEEP to settle. On 15 PEEP and 100% FiO2 with saturations of 90%. Any less PEEP is met with desaturation. Achieving 6ml/kg with a plateau of 35cmH20. CO2 70 mmHg.

Norepi has escalated to 1mcg/kg/min with a femoral art pressure of 60/30. Remains anuric with a pH of 6.9, lactate 10, base deficit 25.

Bedside echo done earlier and formal echo now obtained- no pericardial effusion, right ventricle significantly impaired with significant TR, poor views of LV and mitral valve, unable to comment.

CXR as attached (not the pts actual one, but representative).

Too unstable at this stage to obtain CT.

Next steps?

 

[WheezyBaby]

Ok answers and case progress

He had a mechanical valve and is warfarinised. Denies any IVDU.

K is 6 and the pt is anuric. WBC diff shows slightly elevated neutrophils, other cell lines normal.

Patient is intubated with covid precautions and commenced on norepi. Lined up and cultured. Covid PCR sent. Vancomycin added to antibiotic regime. Sent to the unit nursed in covid precautions.

Over the next couple of hours has progressive hypoxia with copious frothy secretions, which requires 15 of PEEP to settle. On 15 PEEP and 100% FiO2 with saturations of 90%. Any less PEEP is met with desaturation. Achieving 6ml/kg with a plateau of 35cmH20. CO2 70 mmHg.

Norepi has escalated to 1mcg/kg/min with a femoral art pressure of 60/30. Remains anuric with a pH of 6.9, lactate 10, base deficit 25.

Bedside echo done earlier and formal echo now obtained- no pericardial effusion, right ventricle significantly impaired with significant TR, poor views of LV and mitral valve, unable to comment.

CXR as attached (not the pts actual one, but representative).

Too unstable at this stage to obtain CT.

Next steps?

Pocus on IVC and hepatic veins? MV as high as I can get it without stacking, sacrifice lung protective vent settings for the time being. Intermittent bicarb amps, calcium bolus. Flolan. ECMO consult

 

[jdh71]

Ok answers and case progress

He had a mechanical valve and is warfarinised. Denies any IVDU.

K is 6 and the pt is anuric. WBC diff shows slightly elevated neutrophils, other cell lines normal.

Patient is intubated with covid precautions and commenced on norepi. Lined up and cultured. Covid PCR sent. Vancomycin added to antibiotic regime. Sent to the unit nursed in covid precautions.

Over the next couple of hours has progressive hypoxia with copious frothy secretions, which requires 15 of PEEP to settle. On 15 PEEP and 100% FiO2 with saturations of 90%. Any less PEEP is met with desaturation. Achieving 6ml/kg with a plateau of 35cmH20. CO2 70 mmHg.

Norepi has escalated to 1mcg/kg/min with a femoral art pressure of 60/30. Remains anuric with a pH of 6.9, lactate 10, base deficit 25.

Bedside echo done earlier and formal echo now obtained- no pericardial effusion, right ventricle significantly impaired with significant TR, poor views of LV and mitral valve, unable to comment.

CXR as attached (not the pts actual one, but representative).

Too unstable at this stage to obtain CT.

Next steps?

Needs CRRT. Another pressor. Heparin once INR settles some. And probably ECMO - an inhaled flolan trial with 4cc/kg (or maybe bi-level) is something you can try but with that pCO2 . . . I'm very intersted in the covid testing now

 

[bigtuna]

I think you need a TEE or PA cath at this juncture. Need to know if this is cardiogenic pulm edema or not. If cardiogenic pulm Edema -> likely heading to VVA ECMO. It not cardiogenic edema then prob looking at VV ECMO with RVAD support - something like protek duo. We have a high rate of RV failure in VV ECMO patients for ARDS. The ones going onto the ECMO with bad RV don't do well.

 

[WheezyBaby]

Needs CRRT. Another pressor. Heparin once INR settles some. And probably ECMO - an inhaled flolan trial with 4cc/kg (or maybe bi-level) is something you can try but with that pCO2 . . . I'm very intersted in the covid testing now

I don't think the decreased ventilation or the increased load on the RV with a change to bilevel would be wise here, but I'd be interested to hear your rationale

 

[jdh71]

I don't think the decreased ventilation or the increased load on the RV with a change to bilevel would be wise here, but I'd be interested to hear your rationale

You already are dealing with poor lung compliance, and anything you are going to try is likely going to decrease the ventilation. You try something different. It's a small chance things will look better, but you won't know without giving it a chance. Like I said "with that pCO2 . . ." it left the obvious pretty much unsaid. You add the flolan and improve the oxygenation, maybe you also improve your RV function. But I think given age and how things are going this is going to ECMO.

 

[chessknt]

Needs tee to see if a cardiac surgeon needs to be involved since this could all be downstream from a failed mitral valve. Get fem aline and cvc in preparation for Ecmo which is where this seems to be going assuming it is available. If not then pray there is something wrong with the valve that can be fixed and that he can come off bypass although it sounds like he can't survive a road trip to the or so he's screwed if no Ecmo around.

 

[WheezyBaby]

Any thoughts on the PTT? I'm assuming that's presentation lab and not s/p any therapies. APLA and PMV thrombosis? Just trying to tie in the PTT. Could just be sepsis/DIC-related with pseudonormal platelets from where they should be acute phase elevated

 

[deleted171991]

Ok answers and case progress

He had a mechanical valve and is warfarinised. Denies any IVDU.

K is 6 and the pt is anuric. WBC diff shows slightly elevated neutrophils, other cell lines normal.

Patient is intubated with covid precautions and commenced on norepi. Lined up and cultured. Covid PCR sent. Vancomycin added to antibiotic regime. Sent to the unit nursed in covid precautions.

Over the next couple of hours has progressive hypoxia with copious frothy secretions, which requires 15 of PEEP to settle. On 15 PEEP and 100% FiO2 with saturations of 90%. Any less PEEP is met with desaturation. Achieving 6ml/kg with a plateau of 35cmH20. CO2 70 mmHg.

Norepi has escalated to 1mcg/kg/min with a femoral art pressure of 60/30. Remains anuric with a pH of 6.9, lactate 10, base deficit 25.

Bedside echo done earlier and formal echo now obtained- no pericardial effusion, right ventricle significantly impaired with significant TR, poor views of LV and mitral valve, unable to comment.

CXR as attached (not the pts actual one, but representative).

Too unstable at this stage to obtain CT.

Next steps?

Here's my take.

To me, this is still Covid-19 vs endocarditis, and those two have different treatments, so a diagnosis is essential. Massive PE would have also been in the game, had this not developed over 2 weeks. My money is on Covid, based on the history and clinical picture, although the severe septic shock is atypical.

So how would one diagnose, absent a Covid-19 test (which could be false negative) and CT? One idea is the TEE that has been mentioned; I think ruling out endocarditis is a must. I wouldn't place a PAC (it won't help much, and will not distinguish between myocarditis- and endocarditis-related left heart/valve dysfunction). My number 1 tool would be a lung ultrasound. If I see subpleural echodensities, that's Covid-19 until proven otherwise.

Regardless which one it is, I would add a second pressor, instead of going crazy on the norepi. He really needs better peripheral perfusion beyond anything else. If this is from Covid-19, he may have a chance with early ECMO (although I am not optimistic about that pulmonary circulation). If this is from endocarditis, he may be toast. Regardless of the diagnosis, the prognosis is pretty poor, absent a miracle (remdesivir?).

I would also try some steroids at this point, after we rule out endocarditis (or confirm Covid).

 

[deleted171991]

Any thoughts on the PTT? I'm assuming that's presentation lab and not s/p any therapies. APLA and PMV thrombosis? Just trying to tie in the PTT. Could just be sepsis/DIC-related with pseudonormal platelets from where they should be acute phase elevated

It's probably either DIC or Covid/shock-related liver failure. I wouldn't correct that PTT, for multiple reasons.

He may have phenytoin-induced APLA though, but that doesn't come with thrombosis. Or he may have seized from APLA in the first place. Still the whole picture smells of coronavirus, which can give the same disseminated thromboses.

Very interesting case, by the way.

 

[psychbender]

TEE can really shed some light on what is going on here. I am a bit biased, in that much of my ICU time is spent in the CCU/CVICU setting, but I have seen mitral valve endocarditis present in much the same way, when there is a very large regurgitant jet directed towards the right pulmonary veins. This leads to unilateral cardiogenic pulmonary edema, severe RV dysfunction, and congestive hepatopathy, and downstream classic cardiogenic shock. If this is the case, then jacking up the afterload isn't going to improve peripheral perfusion, and you may actually need an inodilator and volume removal to assist the failing RV, and decrease PVR/SVR. Monitoring the heart as these changes are made in real-time can let you know if you are on the right track, or just messing things up further.

 

[dingdong28]

What about the patient's liver function tests, mostly the ALT, ALP and direct bilirubin? LDH? ESR? Procalcitonin, although we already know the lactic acid is high?

I'm surprised there isn't a left shift with the patient's neutrophils. I know I've seen increased bands, metamyelocytes, myelocytes, and even promyelocytes with toxic granulation in several patient's at our hospital with positive COVID. I'm going to take a shot in the dark and would think you'd expect a left shift if this patient had endocarditis? I would guess performing a CBCDF and monitoring the differential daily (hopefully your lab performs manual differentials) would help for a COVID rule out/in.

As a lab guy, the high PTT would have me a little nervous without being able to explain why it's so high. Would a d-dimer and fibrinogen be useful in this case, especially with the possibility of DIC? I believe a d-dimer is also elevated in COVID patients, although elevated for other reasons as well. Were you able to obtain urine for a UA, even though the patient is anuric?

Sorry for the interjection since I'm not a CC physician. This is a really cool read and I'm always interested in how lab testing can play a role in helping you all.

 

[deleted171991]

You may love this, @dingdong28 : as an intensivist, before ordering a lab, I wonder if it will change my management. If not, why waste money, labor, and possibly blood?

The D-dimer will be high in everything (Covid, endocarditis, thrombosis etc.). There is a value in obtaining a fibrinogen, because it could be repleted. But do I want to? Right now, that coagulopathy serves me very nicely, since I am afraid of thrombosis on the valve and in the microcirculation. If it's thrombotic DIC, what can I do, except give therapeutic heparin?

Yes, the UA may be nice for a differential diagnosis. Still it wouldn't change my management. That kidney needs perfusion, regardless whether that's a prenal (most likely) or intrarenal process.

ESR would confirm what the CRP is already suggesting: big time systemic inflammation. LDH is non-specific. The transaminases are worth obtaining; albumin, too. Procalcitonin is useful to decide when to stop antibiotic treatment, not when/if to start it. Etc.

What would be worth proving is the cytotoxic phase of Covid (IL-6 etc.), especially if plasma exchange or IL-6 antagonists are available.

 

[bigdan]

Questions:
1. Any fever or sick contacts?
2. What is lymphocyte count?
3. Procal?

This entire presentation could be cardiogenic shock from pannus/acute thrombus formation over mitral inflow.

 

[Radetzky]

Good discussion

So commenced CVVHDF. Despite trying various things on the vent not able to get CO2 down much further. Flolan trialled without obvious improvement (in sats or hemodynamics). There was concern that flolan might worsen any cardiogenic pulmonary oedema through raised capillary pressures. Thoughts on this guys?

Vaso added to try boost systemic pressure and RV perfusion as well as Milrinone to try increase forward flow and decrease PVR. Gave calcium boluses as well. This resulted in some improvement but MAP still 60. Fluid removal 100 per hour commenced on CVVHDF.

ALT 1000, bilirubin elevated, albumin mildly decreased, fibrinogen mildly decreased. Procalcitonin was some indeterminate number. Interestingly community INRs in the last month were sub therapeutic despite wife confirming pt was compliant with coumadin. Anybody want to take a guess as to why?

First set of covid testing negative. Lymphocytes normal. No sick contacts.

TEE obtained which shows thrombus on prosthetic mitral valve causing complete obstruction during a part of diastole. PA pressures near systemic, severely impaired RV function, mildly depressed LV.

Next steps?

 

[bigdan]

...or dehiscence or leaflet failure (or whatever.

TEE
CT surgery
I’m a Swan user, so I’d place one

 

[Radetzky]

You may love this, @dingdong28 : as an intensivist, before ordering a lab, I wonder if it will change my management. If not, why waste money, labor, and possibly blood?

The D-dimer will be high in everything (Covid, endocarditis, thrombosis etc.). There is a value in obtaining a fibrinogen, because it could be repleted. But do I want to? Right now, that coagulopathy serves me very nicely, since I am afraid of thrombosis on the valve and in the microcirculation. If it's thrombotic DIC, what can I do, except give therapeutic heparin?

Yes, the UA may be nice for a differential diagnosis. Still it wouldn't change my management. That kidney needs perfusion, regardless whether that's a prenal (most likely) or intrarenal process.

ESR would confirm what the CRP is already suggesting: big time systemic inflammation. LDH is non-specific. The transaminases are worth obtaining; albumin, too. Procalcitonin is useful to decide when to stop antibiotic treatment, not when/if to start it. Etc.

What would be worth proving is the cytotoxic phase of Covid (IL-6 etc.), especially if plasma exchange or IL-6 antagonists are available.

How would you prove CRS associated with covid and what would be your threshold for IL6i? Honest q because I don’t know.

 

[bigdan]

Ah.
You were typing while I was.

CT surgery consult

 

[jdh71]

There was concern that flolan might worsen any cardiogenic pulmonary oedema through raised capillary pressures. Thoughts on this guys?

Sure. Makes physiologic sense. By helping the RV put more blood from pre cap to post cap against the end of the line MV goombah could very easily worsening the post cap pressures leading to more pulmonary edema.

 

[jdh71]

The guy obviously needs the cold steel for the MV. Chance to cut, chance to cure. But he’s sick AF. Why did he have such a catastrophic anticoagulation failure. And he’s been working on the MV clot for awhile I suspect with that seizure. How BIG was the RV? It’s function was no good but was it big? This does bring up the prospect of antiphospholipid syndromes even CAPS.

 

[WheezyBaby]

Good discussion

So commenced CVVHDF. Despite trying various things on the vent not able to get CO2 down much further. Flolan trialled without obvious improvement (in sats or hemodynamics). There was concern that flolan might worsen any cardiogenic pulmonary oedema through raised capillary pressures. Thoughts on this guys?

Vaso added to try boost systemic pressure and RV perfusion as well as Milrinone to try increase forward flow and decrease PVR. Gave calcium boluses as well. This resulted in some improvement but MAP still 60. Fluid removal 100 per hour commenced on CVVHDF.

ALT 1000, bilirubin elevated, albumin mildly decreased, fibrinogen mildly decreased. Procalcitonin was some indeterminate number. Interestingly community INRs in the last month were sub therapeutic despite wife confirming pt was compliant with coumadin. Anybody want to take a guess as to why?

First set of covid testing negative. Lymphocytes normal. No sick contacts.

TEE obtained which shows thrombus on prosthetic mitral valve causing complete obstruction during a part of diastole. PA pressures near systemic, severely impaired RV function, mildly depressed LV.

Next steps?

Pheny increased warfarin metabolism, MV thrombus, cardiogenic shock, liver failure, therapeutic INR

Surprised they tolerated going on circuit with those MAPs much less UFing

The worsening edema is a concern with flolan but worth a trial in a patient like that.

Give lytics

 

[deleted171991]

Hemoptysis suggests congested pulmonary circulation. This may be an endocarditis that causes functional MS.

TEE obtained which shows thrombus on prosthetic mitral valve causing complete obstruction during a part of diastole. PA pressures near systemic, severely impaired RV function, mildly depressed LV.

This is not to show how smart I am (because I am not that smart).

This is to show the young padawans how much history and knowledge of physical exam and pathophysiology of symptoms/disease matter. Do your H&P's, on every ICU patient, and dig some more every day when you see them.

 

[Radetzky]

This is not to show how smart I am (because I am not that smart).

This is to show the young padawans how much history and knowledge of physical exam and pathophysiology of symptoms/disease matter. Do your H&P's, on every ICU patient, and dig some more every day when you see them.

When I started in critical care I naively thought I didn’t have to bother so much with history and physical anymore because I had all these nice numbers in front of me to tell me exactly what I needed.

How foolish was I. I soon realised the ability to take a good history was more important than ever, otherwise you get lost in a sea of data points.

 

[Radetzky]

The guy obviously needs the cold steel for the MV. Chance to cut, chance to cure. But he’s sick AF. Why did he have such a catastrophic anticoagulation failure. And he’s been working on the MV clot for awhile I suspect with that seizure. How BIG was the RV? It’s function was no good but was it big? This does bring up the prospect of antiphospholipid syndromes even CAPS.

I don’t have exact dimensions for you. But its significantly dilated and causing septal flattening

Surprised they tolerated going on circuit with those MAPs much less UFing

Was a concern. However reasoning was that given TEE findings, including what I’ve mentioned above, cardiac output might actually improve with volume removal

 

[bigtuna]

...or dehiscence or leaflet failure (or whatever.

TEE
CT surgery
I’m a Swan user, so I’d place one

totally agree with the PA cath - especially if you can't get a TEE done immediately. That would have pretty well cinched the diagnosis - at least gotten off the track of covid, etc. Did CT surgery take to the OR? I think its either that or VA ECMO to try to stabilize first. TPA risky and low chance of working

 

[dingdong28]

You may love this, @dingdong28 : as an intensivist, before ordering a lab, I wonder if it will change my management. If not, why waste money, labor, and possibly blood?

The D-dimer will be high in everything (Covid, endocarditis, thrombosis etc.). There is a value in obtaining a fibrinogen, because it could be repleted. But do I want to? Right now, that coagulopathy serves me very nicely, since I am afraid of thrombosis on the valve and in the microcirculation. If it's thrombotic DIC, what can I do, except give therapeutic heparin?

Yes, the UA may be nice for a differential diagnosis. Still it wouldn't change my management. That kidney needs perfusion, regardless whether that's a prenal (most likely) or intrarenal process.

ESR would confirm what the CRP is already suggesting: big time systemic inflammation. LDH is non-specific. The transaminases are worth obtaining; albumin, too. Procalcitonin is useful to decide when to stop antibiotic treatment, not when/if to start it. Etc.

What would be worth proving is the cytotoxic phase of Covid (IL-6 etc.), especially if plasma exchange or IL-6 antagonists are available.

I greatly appreciate and respect your mindset as far as ordering lab tests for your patients. That goes for everybody who may be reading this. I will say it's interesting to see how different physician's practice medicine as far as lab tests are concerned: Some order everything so they have everything readily available to them and some order what may only be necessary and will add-on testing or order more if needed.

I felt as though a lot of those tests I mentioned were going to be somewhat unhelpful since they're nonspecific towards a certain diseases. I guess the fibrinogen could have also been useful if we had no history of the patient's anticoag history. Since your PT/PTT results are based off of the patient's ability to form a clot, the elevated time would be something a good MLT/MLS would identify and run a fibrinogen based off of the clot curve.

I was going to mention some of the cytotoxic COVID testing, but know that those take a few days to come back. My shop went live with the Abbott ID NOW for covid testing. There's a run read in the pathology forum about the ID NOW testing platform, in addition to my description of actually performing the test and various lab directors who are very involved with the testing.

Now I do have a question about the CRP/ESR: Why are they often ordered together? I know they're useful as inflammation markers and the ESR can be useful in identifying other tumor markers, autoimmune diseases and such. Are they ordered together for confirming the status of inflammation? Are they like peanut butter and jelly, they're just good together?

Thank you very much for the detail. I know it's hard to grasp one's appreciation through a computer but I really do appreciate it.

Thank you everybody for the awesome discussion!

I'm going to go off topic for just a brief moment and hopefully this is all right: This week is national lab week and I know that we celebrate a lot of professions in healthcare for a week at a time, but the lab is often the forgotten department in healthcare. If you can reach out to the lab manage at your facility and if you have any kind words for your lab and pathology staff, I guarantee the lab staff would whole-heartedly and genuinely appreciate whatever you have to say (hopefully nothing too negative). One of the IM residents at my facility did this for me back in December after an MTP. I won't lie, I got a little teary eyed and definitely made my week. It was unfortunate that the patient didn't make it in the end (it was a solid 14 hour MTP). I still have his email tacked to my wall in my office. I'll be looking at my mailbox to see if any of our intensivists sends an email to our lab staff (and I'll know they must have seen this post!)

 

[deleted171991]

totally agree with the PA cath - especially if you can't get a TEE done immediately. That would have pretty well cinched the diagnosis - at least gotten off the track of covid, etc. Did CT surgery take to the OR? I think its either that or VA ECMO to try to stabilize first. TPA risky and low chance of working

One can't get off the Covid track with PAC.

Microthromboses in the pulmonary circulation -> increased PA pressures (same as in chronic LV failure).
Myocarditis with decreased EF -> increased PCWP.

The thing that gets off the covid track is a well-done lung ultrasound. It's unlikely to have a patient this sick without the typical subpleural lung lesions.

I've treated endocarditis patients, and I have never floated a Swan in them. Not because I don't know how to use one, but because echo (including TEE every few days) is enough for me. (Plus PAC is valuable for exactly one thing - PA pressures - and having a foreign body in a bacteremic bloodstream is not doing the patient any favors).

This patient is a classical example why PAC is almost worthless for the left heart. He had increased PCWP due to MS, not LV failure. The PCWP has gone the way of CVP and IVC diameter long time ago, in my mind, no offense.

 

[psychbender]

The patient is a classical example why PAC is almost worthless for the left heart. He had increased PCWP due to MS, not LV failure. The PCWP has gone the way of CVP and IVC diameter long time ago, in my mind, no offense.

And yet, it doesn't seem to be going away from the minds of surgeons and cardiologists any time soon. "His PAD is over 20, we need to diurese him!" Shoot me now.

 

[deleted171991]

And yet, it doesn't seem to be going away from the minds of surgeons and cardiologists any time soon. "His PAD is over 20, we need to diurese him!" Shoot me now.

That may be because most increases in PA pressures (which the PAC does measure correctly) are due to decompensated LV failure (type 2 PHTN), which should be treated with diuresis.

That doesn't change the fact that the PAC predisposes people to thinking in numbers, AKA knee-jerk/bad medicine.

 

[bigtuna]

One can't get off the Covid track with PAC.

Microthromboses in the pulmonary circulation -> increased PA pressures (same as in chronic LV failure).
Myocarditis with decreased EF -> increased PCWP.

The thing that gets off the covid track is a well-done lung ultrasound. It's unlikely to have a patient this sick without the typical subpleural lung lesions.

I've treated endocarditis patients, and I have never floated a Swan in them. Not because I don't know how to use one, but because echo (including TEE every few days) is enough for me. (Plus PAC is valuable for exactly one thing - PA pressures - and having a foreign body in a bacteremic bloodstream is not doing the patient any favors).

This patient is a classical example why PAC is almost worthless for the left heart. He had increased PCWP due to MS, not LV failure. The PCWP has gone the way of CVP and IVC diameter long time ago, in my mind, no offense.

I'm not an expert in lung ultrasound. My understanding is that the subpleural echodensities that are thought characteristic of covid correlate to the subpleural ground glass opacities seen on CT. But can you reliably differentiate Covid from pulm edema when you have a cxr that looks like the one that was posted. I can guarantee that CT would be diffuse GGO's and I have seen a couple Covid patients that look like that. I guess if there were small pleural effusions that would point more to a cardiogenic edema problem but i'm not sure that's enough to make the call for certain.

I don't think a PA cath is any worse in a bacteremic pt than the central line and HD cath they undoubtedly have.

Anyway - I agree TEE is the way to go but I have worked in places where you might not get a stat TEE done the same day.

 

[psychbender]

That may be because most increases in PA pressures (which the PAC does measure correctly) are due to decompensated LV failure (type 2 PHTN), which should be treated with diuresis.

That doesn't change the fact that the PAC predisposes people to thinking in numbers, AKA knee-jerk/bad medicine.

Key word being 'most.' To a hammer, everything is a nail. Agree with the knee-jerk comment. Some of the consultants with whom I work pick a number and threshold, and want to make management decisions based off just that, rather than the whole clinical picture, ignoring anything that points to an alternate diagnosis.

 

[ShockIndex]

I would get him a priest...

 

[Radetzky]

One can't get off the Covid track with PAC.

Microthromboses in the pulmonary circulation -> increased PA pressures (same as in chronic LV failure).
Myocarditis with decreased EF -> increased PCWP.

The thing that gets off the covid track is a well-done lung ultrasound. It's unlikely to have a patient this sick without the typical subpleural lung lesions.

I've treated endocarditis patients, and I have never floated a Swan in them. Not because I don't know how to use one, but because echo (including TEE every few days) is enough for me. (Plus PAC is valuable for exactly one thing - PA pressures - and having a foreign body in a bacteremic bloodstream is not doing the patient any favors).

This patient is a classical example why PAC is almost worthless for the left heart. He had increased PCWP due to MS, not LV failure. The PCWP has gone the way of CVP and IVC diameter long time ago, in my mind, no offense.

im familiar with lung uss for effusions, b lines etc. not too familiar with the appearance of the subpleural echodensities. Do you have any examples of what these look like?

 

[deleted171991]

im familiar with lung uss for effusions, b lines etc. not too familiar with the appearance of the subpleural echodensities. Do you have any examples of what these look like?

Lung Ultrasound findings in COVID 19 - Critical Care Sonography

Text Genevieve Carbonatto Specific examination ultrasound findings in COVID 19 are not unique to the disease. Lung findings include pleural line irregularities, pleural thickening, B lines and consolidations. What is striking is the remarkably similar distribution of lung pathology from...

www.criticalcare-sonography.com

Lung Ultrasound in COVID-19

Medical Education video on performing and interpreting lung ultrasound in suspected SARS-CoV-2 (COVID-19) patients

litfl.com

Combatting COVID19 - Is Lung Ultrasound an Option?

Cian McDermott and Rachel Liu take us through how ultrasound can be used in the diagosis and prognostication of Covid 19 patients #FOAMed

www.stemlynsblog.org

Features of lung ultrasound in COVID 19 infection - Critical Care Sonography

Text Genevieve Carbonatto Literature is coming out on the lung ultrasonography of novel coronavirus. This is a summary of the literature so far The features of lung ultrasound are not specific for COVID 19 pneumonitis or pneumonia but highly suggestive in patients presenting with a history...

www.criticalcare-sonography.com

 

[jdh71]

I don't think lung US is actually really that helpful in CVOD19. Some critical care docs like to slap an US on everything. YMMV.

 

[deleted171991]

I don't think lung US is actually really that helpful in CVOD19. Some critical care docs like to slap an US on everything. YMMV.

I don't disagree. Though some (Italian, I think) intensivists have reported being able to follow the progression of disease by doing daily lung ultrasounds.

I was just pointing out that it would have been useful in this particular patient, absent a reliable Covid test (most of them have a high false-negative rate) and chest CT. And US is more useful than a PAC, provided that one can get decent windows (even a subxyphoid view will tell one more than the PAC).

 

[ShockIndex]

So, any update on our friend with alien blood, refractory obstructive cardiogenic shock, and multisystem organ failure? I’m sure CT surgery was tripping all over themselves in the rush to the OR to fix that MV, no?

I detect 3 morals to this story:

First, patients with prosthetic valves presenting with refractory shock need a TEE early. Hence the value of critical care and cardiac anesthesiologists with advance perioperative ultrasound “skilz.” Knowing that this guy has a trashed valve is vital for peri-operative planning and prognosis determination if he is deemed to be a poor operative candidate (I suspect he is).

Second, Dilantin is a ****ty first-line anticonvulsant for most seizure disorders. It has more side-effects than Keppra when used emergently for status and more drug-drug interactions when used in the sub-acute environment. Think twice before using this drug - we are no longer in the ‘80s and MJ is dead.

Third - patients on Coumadin are not normal and seeing that drug on a med list is God warning you. Listen to her. At least look up the drug-drug interactions or call a damn pharmacist before prescribing any new medication to patients taking rat poison.

 

[MoMoGesiologist]

One can't get off the Covid track with PAC.

Microthromboses in the pulmonary circulation -> increased PA pressures (same as in chronic LV failure).
Myocarditis with decreased EF -> increased PCWP.

The thing that gets off the covid track is a well-done lung ultrasound. It's unlikely to have a patient this sick without the typical subpleural lung lesions.

I've treated endocarditis patients, and I have never floated a Swan in them. Not because I don't know how to use one, but because echo (including TEE every few days) is enough for me. (Plus PAC is valuable for exactly one thing - PA pressures - and having a foreign body in a bacteremic bloodstream is not doing the patient any favors).

This patient is a classical example why PAC is almost worthless for the left heart. He had increased PCWP due to MS, not LV failure. The PCWP has gone the way of CVP and IVC diameter long time ago, in my mind, no offense.

The surgeons/fellows/residents/ED docs love checking the IVC and then asking me to check it as the intensivist. Drives me effing crazy. No, the hypotensive pt with the collapsible IVC on 100% FiO2 and so edematous their hands and feet look like balloons doesnt need more fluids! Stop looking at ONE thing and just go back to basics

 

[deleted547339]

The surgeons/fellows/residents/ED docs love checking the IVC and then asking me to check it as the intensivist. Drives me effing crazy. No, the hypotensive pt with the collapsible IVC on 100% FiO2 and so edematous their hands and feet look like balloons doesnt need more fluids! Stop looking at ONE thing and just go back to basics

Not to mention that there’s no good data on ivc diameter in the chronic setting. Come into the ED in shock? Sure, probably has diagnostic data. Two weeks into the hospitalization? Who TH knows?

 

[Radetzky]

So.. unfortunately CT surgery only available in another hospital and patient too unstable to put in the back of an ambulance.

Decided to proceed with chemical thrombolysis.

24 hours later repeat TEE shows near complete resolution of thrombus. Vaso off. Norepi down to 0.15mcg/kg/min. Continues on Milrinone. FiO2 down to 40%. Lactate on the way down.

 

[Radetzky]

Yes, people seem to forget that IVC diameter does not equal IVC pressure

 

[jdh71]

So.. unfortunately CT surgery only available in another hospital and patient too unstable to put in the back of an ambulance.

Decided to proceed with chemical thrombolysis.

24 hours later repeat TEE shows near complete resolution of thrombus. Vaso off. Norepi down to 0.15mcg/kg/min. Continues on Milrinone. FiO2 down to 40%. Lactate on the way down.

do what you gotta do sometimes

 

[ShockIndex]

Yes, people seem to forget that IVC diameter does not equal IVC pressure

And, that CVP is a poor measure of volume responsiveness.

Nice job with the case. Did you go with 100 mg TPA over 2 hours or wt. based TPA or TNKase?

 

[WheezyBaby]

And, that CVP is a poor measure of volume responsiveness.

Nice job with the case. Did you go with 100 mg TPA over 2 hours or wt. based TPA or TNKase?

Lexicomp apparently actually offers dosing specific to this, says 1 mg/hr for 25 hr. Seems light for obstructive shock though

 

[deleted171991]

So.. unfortunately CT surgery only available in another hospital and patient too unstable to put in the back of an ambulance.

Decided to proceed with chemical thrombolysis.

24 hours later repeat TEE shows near complete resolution of thrombus. Vaso off. Norepi down to 0.15mcg/kg/min. Continues on Milrinone. FiO2 down to 40%. Lactate on the way down.

I almost suggested this earlier, catheter-guided, then I thought it could be darn high-risk for the cerebral circulation. Glad it worked.