Crazy OB case on call... appreciate icu input...

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jimbomd

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alright, so i am on ob call friday night at a large nyc public hospital to be kept nameless... where anything can, and does, happen. full board, in rm 5 is a 39 yo G5 at 33 weeks under observation for "thyroid storm." apparently a longstanding h/o hyperthyroidism, had been on ptu for a few years under good control, and stopped taking it a week prior to admission b/c some quack homeopath told her it was "bad for the baby." subsequently seen in clinic thurs. for tachycardia, palpitations, tremors, diaphoresis, etc. admitted for obs when found to be in thyroid storm. ptu and beta blockers started, she is doing fine.

so i am finally laying my head down to rest at about midnight friday, phone in the call room rings, nurse's frantic voice, the pt in rm 5 is coding! so i run my ass in there... ob residents attempting to bag, performing chest compressions. go to hob, pt's mouth full of thick, frothy white secretions. suction, no view. suction again, no view, hockey stick the tube in with a prayer. tube's in, no pulse, put paddles on, she's got a disorganized rhythm, looks like pea arrest. 2 rounds of epi/atropine, get a perfusing rhythm back. to the or for a super-stat section.

in or, l radial a-line, R IJ intro placed (used angiocath, got back what looked like pulsatile flow, transduced, with cvp 0f 21-22-- scary). baby delivered, apgars 1,5,8; baby intubated and off to nicu. ran o2/sevo, some versed/fentanyl, roc. hd stable through surgery; suctioned tube several times for thick frothy secretions coming back up.

back to recovery room, swanned, and tee performed. PA pressures in 50s/30s, funky looking waveform, unable to obtain wedge trace. tte performed, nl LV/RV function, severe TR/mild-mod MR, high PA pressures in 50s. no PE visible, no effusion, no RV septal bowing. cxr with b/l patchy opacities, looks like fluid overload vs. failure.

baby extubated 4 hrs following delivery, currently stable. mom extubated following day, moving extremities x4, localizing to pain, not following simple commands/interacting.

crazy case. according to the ob's, prior to the code called, she was talking normally, began to complain of dyspnea, got progressively worse, began to desat and became very agitated. was very combative, they tried to put a face mask and they were struggling with her until she lost mental status and they called it.

first things running through my head were PE, MI, ? amniotic fluid embolism (unlikely, as she was not laboring/postpartum). she was subsequently scanned and negative for pe, and troponins were mildly elevated (likely due to chest compressions) with no WMAs. then looking up hyperthyroidism and pulmonary hypertension and found a strong association between the two. now thinking it was a case of acute R heart failure in a pt with underlying undiagnosed pulmonary hypertension/valvular disease with desaturation and hypoxic arrest.

any critical care guys have some input?
 
A week of uncontrolled hyperthyroidism and the CV changes/stress of pregnancy likely combined to put your patient in this position. Given the abrupt course of your patient's event, I'd lean toward a sudden arrhythmia secondary to both the normal enlargement of the heart during pregnancy combined with the effects of the thyroid storm.

I would bet that the patient's cardiac dimensions were well above normal despite the preserved LV and RV SF's, laying the groundwork for an almost fatal arrythmia.

Otherwise blame it on the electrolytes.
 
Sounds like you covered everything.

Was the patient taking Ipodate as part of the anti thyroid regime?

Fluid restriction?
 
jimbomd said:
alright, so i am on ob call friday night at a large nyc public hospital to be kept nameless... where anything can, and does, happen. full board, in rm 5 is a 39 yo G5 at 33 weeks under observation for "thyroid storm." apparently a longstanding h/o hyperthyroidism, had been on ptu for a few years under good control, and stopped taking it a week prior to admission b/c some quack homeopath told her it was "bad for the baby." subsequently seen in clinic thurs. for tachycardia, palpitations, tremors, diaphoresis, etc. admitted for obs when found to be in thyroid storm. ptu and beta blockers started, she is doing fine.

so i am finally laying my head down to rest at about midnight friday, phone in the call room rings, nurse's frantic voice, the pt in rm 5 is coding! so i run my ass in there... ob residents attempting to bag, performing chest compressions. go to hob, pt's mouth full of thick, frothy white secretions. suction, no view. suction again, no view, hockey stick the tube in with a prayer. tube's in, no pulse, put paddles on, she's got a disorganized rhythm, looks like pea arrest. 2 rounds of epi/atropine, get a perfusing rhythm back. to the or for a super-stat section.

in or, l radial a-line, R IJ intro placed (used angiocath, got back what looked like pulsatile flow, transduced, with cvp 0f 21-22-- scary). baby delivered, apgars 1,5,8; baby intubated and off to nicu. ran o2/sevo, some versed/fentanyl, roc. hd stable through surgery; suctioned tube several times for thick frothy secretions coming back up.

back to recovery room, swanned, and tee performed. PA pressures in 50s/30s, funky looking waveform, unable to obtain wedge trace. tte performed, nl LV/RV function, severe TR/mild-mod MR, high PA pressures in 50s. no PE visible, no effusion, no RV septal bowing. cxr with b/l patchy opacities, looks like fluid overload vs. failure.

baby extubated 4 hrs following delivery, currently stable. mom extubated following day, moving extremities x4, localizing to pain, not following simple commands/interacting.

crazy case. according to the ob's, prior to the code called, she was talking normally, began to complain of dyspnea, got progressively worse, began to desat and became very agitated. was very combative, they tried to put a face mask and they were struggling with her until she lost mental status and they called it.

first things running through my head were PE, MI, ? amniotic fluid embolism (unlikely, as she was not laboring/postpartum). she was subsequently scanned and negative for pe, and troponins were mildly elevated (likely due to chest compressions) with no WMAs. then looking up hyperthyroidism and pulmonary hypertension and found a strong association between the two. now thinking it was a case of acute R heart failure in a pt with underlying undiagnosed pulmonary hypertension/valvular disease with desaturation and hypoxic arrest.

any critical care guys have some input?

Yeah crazy indeed. If you state that she had some undiagnosed valve dz and pulm htn then she prob had a weaker than nml myocardium esp with the pg since it is working harder. And Im sure she was getting generous amts of crystalloids on the floor. If it indeed was acute right failure as you think maybe she was beta blocked to much which aggrevated her valve dz and decreased c/o then compensated by increasing catacholamines increasing as well when she became sob initially and prob anxious with increased symp tone all increasing vascular resistance and impedance against the beta blocked myocardium. plus she was in a hypermetabolic state with her increase BMR d/t hyperthyroidism and increased VO2 causing her to desat faster when her regurg exacerbated. then she crumped.



Or maybe if it was long standing myocardium issues she may have been cathecholamine depleted and with the weak heart blocked to much became hypotensive.

Who knows, interesting case though, just had several lectures on thyroid storm, this def. helps me put it more into clinical perspective. Thanks.
 
Most things are covered here but I find it rather interesting as to how fast it all came about. If it was not a PE then I would have expected a more progressive clinical picture unlike this one which seems to be quite abrupt. Was the pt really doing just fine, talking and acting normal, and then all of a sudden became dyspneic and SOB with CP?

What type of scan was performed when looking for the possible PE? VQ scan or CTscan?
 
Hyperthyroidism can present with non-perfusing rhythms.
 
militarymd said:
Hyperthyroidism can present with non-perfusing rhythms.

YEs true, But I am having trouble explaining the pulsatile nature of the IJ except that there was an acute increase in pulm pressure with TR. An Mi is possible but unlikely at her age (but not totally). Was she hyperthermic?

Right now, I would have my $$ on two diagnosis. 1) acute CHF caused by thyroid storm leading to dilated heart with TR and to a lesser degree MR due to the thicker left ventricle.
2) PE
 
thanks for the replies guys; appreciate the input.

am off this weekend (thankfully, as i needed some serious recovery time from my call), but discussed this lady with my friend on in the sicu today.

so on further review... she did have a dilated cardiomyopathy per the official attending read of the echo, with severe TR and mod MR. EFs were normal. No ipodate, and she was not on fluid restriction (getting 100 /hr of LR) prior to code. noyac, a ct angio was done which was neg for pe. i know this can miss smaller, peripheral pe's, but one that would present so quickly and dramatically would have to be hard to miss.

i agree with many of your thoughts... dilated cardiomyopathy combined with TR and physiologic changes of pregnancy, in addition to thyroid storm and crazy elevated sympathetic tone, could easily set the stage for arrhvthmia, acute R heart failure, arrest.

possible excess fluid administration, frothy white junk in ETT, cxr afterward looking wet, echo, high cvp (pulsatile R IJ--- scared the poop out of me), high R filling pressures... seems to fit.

fascinating case, though. good thing i kept notes for the inevitable m&m. and buffed all my notes in the chart for the lawyers.

so be very careful with hyperthyroid pregnant ladies!!!

(oh, and she's currently extubated, hd stable, no pressors/inotropes. head ct shows poss anoxic brain injury; she is moving all extremities, grimacing/reacting to pain, but not following commands. baby is ok).
 
Armchair quarterback here.

With thyroid storm, I think she should have been receiving all available therapies...including iodine in whatever form.

LR at 100 cc/hr is an awful lot of sodium for someone who is not bleeding.
 
my bad... she was getting sski... 3 drops tid.

and i know about the fluid... ob's tend to do stuff without thinking.
 
Noyac said:
YEs true, But I am having trouble explaining the pulsatile nature of the IJ except that there was an acute increase in pulm pressure with TR. An Mi is possible but unlikely at her age (but not totally). Was she hyperthermic?

Right now, I would have my $$ on two diagnosis. 1) acute CHF caused by thyroid storm leading to dilated heart with TR and to a lesser degree MR due to the thicker left ventricle.
2) PE

The precipitating event/arrythmia and subsequent conversion preceded placement of the IJ central access. In the presence of severe TR, I would expect (and have seen) pulsatile IJ waveforms. An MI would be highly possible given her comorbidities, but given her abrupt decompensation, I would still bet on a non-perfusing rhythm. The MR and TR most likely were already present given the severity of her condition.

I would love to know what dimensions were recorded for her heart.
 
UTSouthwestern said:
I would love to know what dimensions were recorded for her heart.

Also, "normal RV/LV function" in the setting of regurgitant lesions is not necessarily normal.
 
UTSouthwestern said:
The precipitating event/arrythmia and subsequent conversion preceded placement of the IJ central access. In the presence of severe TR, I would expect (and have seen) pulsatile IJ waveforms. An MI would be highly possible given her comorbidities, but given her abrupt decompensation, I would still bet on a non-perfusing rhythm. The MR and TR most likely were already present given the severity of her condition.

I would love to know what dimensions were recorded for her heart.

I agree with the non-perfusing rhythm due to the enlarged heart but what comorbidities are you thinking about that would lead to an MI at 39 yo? I know the thyroid storm (tachycardia) and all but that is all that was discribed. Am I missing something?

On a side note. When the first plane hit the world trade center on 9/11 I was rolling a pt to the OR with a 12" knife sticking out of his chest and moving with every heart beat. I induced him and stuck a cordis in his R IJ. The pulsatile pressure of the IJ was impressive to say the least. If the blood had been any more red I would have sworn I was in the carotid but it was dark enough to know it had to be venous. The knife was through and through the the R ventricle. He went home in 2 days.
 
Noyac said:
I agree with the non-perfusing rhythm due to the enlarged heart but what comorbidities are you thinking about that would lead to an MI at 39 yo? I know the thyroid storm (tachycardia) and all but that is all that was discribed. Am I missing something?

On a side note. When the first plane hit the world trade center on 9/11 I was rolling a pt to the OR with a 12" knife sticking out of his chest and moving with every heart beat. I induced him and stuck a cordis in his R IJ. The pulsatile pressure of the IJ was impressive to say the least. If the blood had been any more red I would have sworn I was in the carotid but it was dark enough to know it had to be venous. The knife was through and through the the R ventricle. He went home in 2 days.

Sometimes I miss the crazy **** I used to see at Parkland. Not a lot, but sometimes.

DCM of pregnancy is another possibility.
 
UTSouthwestern said:
Sometimes I miss the crazy **** I used to see at Parkland. Not a lot, but sometimes.

DCM of pregnancy is another possibility.


I'm with you UT 😉
 
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