A 60 year old woman, known for COPD, shows up short of breath and hypotensive.
The clip goes thru a series of views of the IVC and the heart.
What do you see?
Answer and further case data coming soon!
A 60 year old woman, known for COPD, shows up short of breath and hypotensive.
The clip goes thru a series of views of the IVC and the heart.
What do you see?
Answer and further case data coming soon!
So I get an early morning call from a really good ER guy informing me of a likely ICU admission: a young guy (30’s) with a bilateral pneumonia and fever whom he suspected might get worse before he got better. He’s given him some fluids and started ceftriaxone and azithromycin. Sounds good to me. Sold. I tell him I’ll come take a look as soon as I roll into work (we do home call).
An hour or so later I head to the ED and see a him, in bed at 30 degrees or so with nasal prongs, maybe a little tachypneic but certainly not in severe distress and not particularly toxic. The nurse informs me that his temperature was apparently 40 degrees. The CXR (I’ll try to put it up soon) shows bilateral infiltrates, more predominant in the lower two thirds of the lung fields. WBC is 14, lactate 2.3.
So this guy had been short of breath for about 2 weeks, having some cough and localized left sided pain associated with movement, cough and pressure. The cough was non-productive. As I was getting this history (yup, generally bedside ultrasound is simultaneous with history-taking for me), this is what I see:
(parasternal long axis)
(parasternal short axis)
(right lower costal margin)
(you can see this in most of the lung fields)
He has no past medical history or notable family history, drinks occasional wine, has not traveled of late and works as an electrician. He is active and played soccer – the last time a few weeks ago. He came to the ED for dyspnea, but had still been able to go up several flights of stairs, albeit with more dyspnea than he normally would have.
check back tomorrow and let’s see what happens!
If you haven’t read Part 1, get the story and the cool clips here first: http://wp.me/p1avUV-ce
So the polls are in! So far at least, 58% of you would blast away with full dose lytics, 26% with MOPETT-style half-dose, 10% content with heparin, and 5% would go for a PA catheter directed lysis.
So 90% would lyse this patient. I’m glad to hear that, because in my opinion, more patients should be lysed than I see being done around me.
What did I do? I went for the half-dose lytics, with an excellent result. Within a few hours she was much less dyspneic, BP was up to 110-120 systolic, and though RV dysfunction persisted, it was mostly resolved by the next day. I think it is important to note that I had a long chat with her, explaining the risk of intracerebral hemorrhage, which I quoted as being less than 2%. She opted for thrombolysis with the idea of averting cardiopulmonary limitation given her active lifestyle.
I think the physiological rationale for half-dose lytics is good, since, unlike when used for arterial lysis (coronary or cerebral) the entire dose will pass through the lungs. One could argue that the clot burden is larger, but the resolution seen in MOPETT and in the dozen or so cases I’ve lysed (no intracerebral bleeds yet), rapid resolution of RV dysfunction supports a sufficient response. I’ve yet to give – but am ready and willing – a “rescue” top-up 2nd half dose if the first hasn’t worked.
I think the other important point in this case is the importance of bedside ultrasound in the assessment of all shock patients. Although I have no doubt whatsoever that my competent colleague would have come to the diagnosis of PE, it may have been minutes to hours later, possibly after having to begin pressors for a lack of response to fluids. I won’t hypothesize what might have happened in that time. Maybe nothing, maybe not.
She went home a few days later.
This is why the blind administration of fluid resuscitation is a growing pet peeve of mine. Two litres in sepsis? Ok, probably, but not every shock is sepsis… I think that in 2014, going on 2015, with virtually all ERs and ICUs equipped with an ultrasound, there is no place for the empiric bolus. It takes all of 5 seconds to look at an IVC, and another 15 to get an idea of cardiac function in most patients. Like a famous corporation says:
Opinions, rants and rotten tomatoes welcome!
So I’m walking to the ED to reassess a COPD’er that was on BiPAP, and one of the ED docs sees me in passing and says – “I might have a case for you, she’s on her 3rd litre and still a bit hypotensive…I’ll let you know.” So I re-route and decide to take a look right away, because I’m never fond of shock NYD.
So here is this woman in her 50’s, BP is 93/67, RR 22 and moderately dyspneic. She has been increasingly so for a few days without infectious symptoms. The X-ray is clear and her labs unremarkable aside from a lactate at 3.3 mmol/l. She is moderately overweight but quite active. Non=smoker without any cardiorespiratory known illness and on no medications.
Here is what we see on ultrasound-enchanced physical examination:
So, what do you see?
In the first clip, we see a large, dilated IVC with little variation – despite the dyspnea, making it a more significant finding – according to the Effort-Variation Index (http://wp.me/p1avUV-9k). This automatically implies there will be some pathology (unless iatrogenically very volume loaded) to be found downstream.
In the second clip, you have a hyperdynamic and underfilled LV and a dilated, poorly contractile RV. In the absence of cardiopulmonary disease and in an active patient, this is highly suggestive of an acute process, namely pulmonary embolism.
On further questioning she had done a new yoga stretching class as a possible endothelial-damaging process.
So what did I do? Get a STAT angioscan:
What would you do next?
I’ll tell you what I did tomorrow, and hopefully have some good bloody arguments!
PS for awesome talks by amazing speakers, don’t forget to register for CCUS 2015!!! For more info: http://wp.me/p1avUV-aU and register at www.ccusinstitute.org!
Ok, so in the process of doing a little bedside ultrasound teaching, I was scanning this lady in the ER who was being worked up for urosepsis. She had been previously a little hypotensive, apparently, and had gotten some fluid boluses, but was not looking quite comfortable with a BP of about 90 systolic.
So her IVC was pretty normal, about 10-12 mm with visible respiratory variation.
Then I saw something funny in the parasternal views (short axis at the level of the aortic valve)…
Hint: as I scanned around the patient for the possible cause of this, I noted a pressure bag hanging with an empty bag of NS (argh! NS!)… Really empty. I mean, not a drop left in the tubing…
This is iatrogenic air embolism. You can see the bulk of the air is in the RA (left side of the screen), and air bubbles make it into the RV (inflow-outflow) at the top, and some into the PA (curving to the bottom right).
This is not elegant. There is always some air in the drip chamber, so, especially on a pressure bag, an IV bag can’t be allowed to be totally empty…
When we agitate saline to do a bubble study, you get a few seconds of bubble persistence. In this case, two separated examinations about 10 minutes apart revealed little or no change.
Fortunately for the patient, the amount if air is not really enough to cause pulmonary vascular obstruction, as you generally need upwards of 150cc to cause an arrest, and, as we can see by the normal IVC/RV, there was no evidence of even pulmonary hypertension. I left her in the left lateral decubitus position and she remained monitored, recovering uneventfully. I’ll review the management of venous air embolism in the next post!
Here is another clip, a bit of a reverse and hybrid parasternal short axis view but for some reason gave me the best images:
So here is an awesome clip from an ICU colleague of mine, Lorraine Law. She was managing a post arrest (elderly woman who collapsed at home and was resuscitated but remaining in profound shock) case using bedside ultrasound and came across this pathology:
video courtesy of Lorraine Law & Shirish Shantidatt
what do you think?
scroll below for my thoughts…
So the clip starts with a subxiphoid 4 chamber view that clearly shows a massively dilated RV with a hyperdynamic and underfilled LV.
[For the hemodynamic novices, remember that the ventricles are kind of like roommates who share a pericardium. Especially in acute scenarios, if one gets overloaded, the other will have to give way, until the pressure equilibrates. If the process is exceedingly slow, they can do some renovations and stretch the pericardium, but this takes likely weeks. In this case, the elevated PAP overloads the RV and the RVDP > LVDP, resulting in decreased diastolic filling, which in turn drops the stroke volume/cardiac output/MAP.]
We can see that the RV TAPSE (tricuspid valve excursion towards apex) is really minimal, supporting an acute or acute on chronic process.
The clip then shows a long axis view of the IVC with echogenic material, most likely thrombus, with a to and fro motion, going in and out of the RA. Wow. You don’t see this very often. The only thing preventing further travel is actually the fact that the cardiac output is so low due to massive embolism so that the flow can in fact barely carry the clots forward anymore at this point, similar to the sluggish IVC clip I put up a few months ago (http://wp.me/p1avUV-5t).
The most likely diagnosis is pulmonary embolism, and thrombolysis is indicated. Unfortunately despite my colleague’s timely diagnosis, the clot burden was likely too much, and despite thrombolysis, the patient passed away of intractable shock. One can imagine that the TPA actually has to make it to the lungs, and with such a degree of obstruction, it is likely that very little actually got to the pulmonary vasculature…
Unfortunate case, but quite impressive images.
A crazy thought, using hindsight and with the luxury of knowing the fatal prognosis: intracardiac (RV) TPA bolus? Small spinal needle? Anyone bold enough? Food for thought if (when) I see one like this…
Really quite impressive images. A couple of weeks ago I admitted a pretty young patient after a successful resuscitation due to massive pulmonary embolism. Immediately after ROSC in emergency department, he was transported to the cath-lab where TPA bolus was administered directly through a PA cathether. In ICU we continued the infusion. In less than 24 hours we obtained a relative hemodynamic stability and discontinued all the vasopressors, but the case remains unfortunate because despite therapeutic hypothermia the post-anoxic damage was so severe that led to cerebral death declaration two days later.
Thanks Marco, very interesting. There is a recent study on catheter directed thrombolysis in PE reviewed at PulmCCM:(http://pulmccm.org/main/2014/randomized-controlled-trials/catheter-directed-thrombolysis-submassive-pe-better-heparin-rct/)
A physiological point about PE resuscitation is the relative inefficiency of CPR, as both venous return and LV filling is severely limited, so systemic perfusion is even worse than the usually poor output during chest compressions…
Thanks for reading!
The point about the possible inefficiency of CPR is crucial in my opinion. The patient I brought as example had a witnessed cardiac arrest (he called EMS when in respiratory distress) and CPR without interruption from the beginning, nevertheless he resulted in brain death declaration.
I remember very clearly a 43-year-old woman that 3 years ago had a massive PE in the OR shortly after a long lumbar vertebral stabilization. We admitted her to ICU after more than 80 minutes of CPR, a bolus of rTPA and with severe hemodynamic instability. RV was extremely dilated. When she eventually regained stability I had little hope about her neurological recovery, but surprisingly she was extubated the following day and last year she returned to our 12-months post-ICU follow-up showing perfect recovery.
I think that systemic and cerebral perfusion during “obstructive” cardiac arrests such as massive PE is very difficult to asses with current technology. A couple of times I was tempted to check it with trans cranial doppler, but usually there’s too much confusion during CPR.
When I was a resident I witnessed to a iatrogenic cardiac arrest in a patient with advanced monitoring that led to an interesting publication: http://www.researchgate.net/publication/10832333_Cerebral_perfusion_pressure_and_cerebral_tissue_oxygen_tension_in_a_patient_during_cardiopulmonary_resuscitation
Wow, very interesting cases. What fortune to have been able to record that data, as obviously getting that in during CPR would be almost impossible. TCD, at least after ROSC, could be contributory… Another option is using NIRS, which I’ll be working with this summer.
As has been discussed in a previous post (http://wp.me/p1avUV-7T), patients with sub-massive PE (hypoxic, tachycardic, some troponin rise, etc…but no hypotension) remain in a grey zone, which is, to me , a dubious situation at best – their mortality can be up to 15%, morbidity likely more. Everyone agrees the low-risk patients don’t need thrombolysis, and everyone pretty much agrees that the patient in shock needs it. There is data out there suggesting that some patients clearly benefit from thrombolysis despite not being in shock, in good part relating to avoiding chronic pulmonary hypertension and its consequences.
The issue for many clinicians is that they have a “stable” patient in front of them, and they are considering giving them a drug that can potentially give them a bleed in the head and leave them dead or crippled. Many shy away from this. Part of this is cultural, because the same docs probably wouldn’t hesitate giving the drug to a lateral or posterior MI, which is not likely to kill you, or even leave you a cardiac cripple (just to be clear, I’m not advocating against thrombolysis in these cases, just trying to find a parallel), but since the AHA guidelines say to do it and everyone else does it, there’s no trepidation. It is the standard of care. For most of us acute care clinicians who do not do outpatient medicine, if the patient survives and gets discharged home, chalk one up in the win column. But, as has become clear in recent years with the post-critical illness syndromes, morbidity can be just as important as mortality, especially in the younger patients. Kline et al (Chest, 2009) showed how almost 50% of “submassive PE” patients treated with anticoagulation alone had dyspnea or exercise intolerance at 6 months. They only had a 15% improvement in their pulmonary artery pressures (mean 45 mmhg).
What are the real risks? Pooling the data together gives a value around 2% with a spread between 0.8% and 8%, more or less. This represents each patient’s inherent risk of bleeding, as well as some of the inconsistencies with post-thrombolysis anticoagulation (safest to aim for 1.5-2 x PTT baseline in the first 48h).
The MOPETT trial which, as a #FOAMite you have certainly come across, showed that a half-dose of TPA was highly effective, and they felt it might be possible to go lower. The physiological beauty in that is that, unlike other sites we thrombolyse with full dose TPA, the lungs get 100% of the TPA (coronary artery gets maybe 5%, brain gets 15%). Mind you, of course, the culprit clot/artery obviously doesn’t get 100%, but much, much more (if we figure that you need about 50% vascular area occlusion to cause RV dysfunction) TPA per “clot” than other pathologies. One can argue that anatomically, there is a greater clot burden than coronary or arterial thrombolysis, which may offset this somewhat. However, the date was quite clear in this trial that the therapy was effective, and the bleeding was none.
Ok, so let’s get to the PIETHO. 1000 patients, TPA+heparin vs heparin alone in normotensive but intermediate risk patients. So, first question is how was that risk defined? Patients needed to have echocardiographic/CT signs of RV dysfunction AND a positive troponin. Interestingly enough, onset of symptoms was up to 15 days before randomization…not exactly early treatment, and unfortunately there is no information about the actual time to thrombolysis or subgrouping. The results were as one could imagine. The combined endpoint of death or hemodynamic decompensation was 2.6% in the thrombolytic group vs 5.6% in the anticoagulation. I’m not a fan of combined endpoints. Hemorrhagic stroke was 2.0% vs 0.2%. Their conclusion? Exercise caution. Hmmm…not much of a step forward. Basically tells us what we know. It helps the hemodynamics, but you can bleed. They do re-affirm that bleeding is more likely in the over-75.
What do we REALLY need to figure out?
1. echographic risk stratification – at least into moderate and severe RV dysfunction.
2. longer term outcomes (hopefully PIETHO has a follow-up study in the pipeline, since they had good numbers).
3. a point-of-care study – time is of the essence, and may have an impact on dosage. IMHO thrombolysis should be done within a few hours of presentation at most.
4. further dosage data – 1/2? 1/3? 1/4? small boluses q1h until RV function improves?
I wish I could do it, but community hospitals don’t have the ideal setup, nor do I have a research team that can handle something of this scale. But surely someone can!
It won’t change my practice. I will continue to offer thrombolysis in select cases, especially the younger patients, who obviously have a lower risk of bleeding, and stand to benefit the most, as pulmonary hypertension can be crippling. I know I’d take the risk of bleeding when I see 50% dyspnea/exercise intolerance two years down the road…
Finally, bedside ultrasound to anyone with dyspnea/hypoxia should be a standard of care for every acute care physician. No ifs, ands or buts, no exception. Waiting for a CT angio or formal (read daytime hours) echocardiogram is, to me, unacceptable. If you, a friend or family member were in that ER bed, would you trust a physical examination and a CXR to rule out the need for an immediate intervention? I wouldn’t, not my own, and not even Dr. Bates’, Dr. DeGowin’s or Dr. Sapira’s, or all three combined.
Kline JA, Steuerwald MT, Marchick MR, Hernandez-Nino J, Rose GA. Prospective evaluation of right ventricular function and functional status 6 months after acute submassive pulmonary embolism: frequency of persistent or subsequent elevation in estimated pulmonary artery pressure. Chest 2009;136:1202e1210.
Guy Meyer, M.D., Eric Vicaut, M.D., Thierry Danays, M.D., Giancarlo Agnelli, M.D., Cecilia Becattini, M.D., Jan Beyer-Westendorf, M.D., Erich Bluhmki, M.D., Ph.D., Helene Bouvaist, M.D., Benjamin Brenner, M.D., Francis Couturaud, M.D., Ph.D., Claudia Dellas, M.D., Klaus Empen, M.D., Ana Franca, M.D., Nazzareno Galiè, M.D., Annette Geibel, M.D., Samuel Z. Goldhaber, M.D., David Jimenez, M.D., Ph.D., Matija Kozak, M.D., Christian Kupatt, M.D., Nils Kucher, M.D., Irene M. Lang, M.D., Mareike Lankeit, M.D., Nicolas Meneveau, M.D., Ph.D., Gerard Pacouret, M.D., Massimiliano Palazzini, M.D., Antoniu Petris, M.D., Ph.D., Piotr Pruszczyk, M.D., Matteo Rugolotto, M.D., Aldo Salvi, M.D., Sebastian Schellong, M.D., Mustapha Sebbane, M.D., Bozena Sobkowicz, M.D., Branislav S. Stefanovic, M.D., Ph.D., Holger Thiele, M.D., Adam Torbicki, M.D., Franck Verschuren, M.D., Ph.D., and Stavros V. Konstantinides, M.D., for the PEITHO Investigators*, Fibrinolysis for Patients with Intermediate- Risk Pulmonary Embolism, N Engl J Med 2014;370:1402-11.
Mohsen Sharifi, MDa,b,*, Curt Bay, PhDb, Laura Skrocki, DOa, Farnoosh Rahimi, MDa, and Mahshid Mehdipour, DMDa,b, “MOPETT” Investigators, Moderate Pulmonary Embolism Treated With Thrombolysis (from the “MOPETT” Trial), Am J Cardiol 2012
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