syncopal PE’s, gestalt, & sensationalism.

Want to know how to poke the EM FOAM bear? Make a sweeping generalization that we are “doing it wrong” that goes against the “first do no harm” mentality, while paradoxically potentially putting some patients in harms way…

Shortly after ACEP16 ended and many FOAMites was scrolling through their Twitter timelines, this paper popped up.

11 hospitals looked at 2,584 patients >18 years of age with a first time syncopal event lasting <1 minute, with obvious causes (seizure, trauma, stroke) excluded, as well as patients already on anticoagulation or with Afib. After all said and done, 560 were analyzed.

 

-330 had a low pretest probability via Wells scoring & negative d-dimer; thus PE ruled out.

-230 had high pretest probability, positive dimer, or both.

-180 under went CTPA, 49 underwent VQ (one died and had an autopsy)

-97 of these patients had a pulmonary embolism.

So, 97 of 2,584 total syncopal patients had a PE. (3.7%)

 

PE’s diagnosed by CT:

main artery: 30/72

lobar: 18/72

segmental: 19/72

subsegmental 5/72

 

so, we’ll say 42% (30/72) are “clinically relevant” PE’s . Thats 1.1% of all-comers.

 

Let’s dig in a bit more:

-80% of confirmed PE were 70 years of age or greater (46% over 80)

-11% had prior PE

-45% with PE had a respiratory rate >20breaths / min vs 7% without PE

-33% with PE had a heart rate >100 bpm vs 16.2% without PE

-36% with PE were hypotensive <110mm Hg systolic vs 22.9% without PE

-40% with PE had signs of DVT (leg swelling, redness, etc) vs 4.5% without PE

-20% with PE had active cancer vs 10% without PE

one patient died.

 

So while there are some pretty sensational headlines regarding this paper, it reminds me of a case & a podcast. I remember about 4 years ago, I had an elderly patient who syncopized after standing out of bed. But in the ED, she was tachycardic and I couldnt quite explain why. Something just felt off. She was in good healthy, and didnt seem particularly dry, so I sent a dimer. I then proceeded to get my behind chewed out because I sent a dimer on an elderly patient with clear orthostasis, and it was going to be positive since she was elderly, and we’re busy so it’ll ruin our throughput, yada yada yada. Turns out, she had a dimer in the thousands, and had a main artery PE.

About two years later, I heard this podcast on PE & gestalt.

Before bringing this full circle, a few concerns. I’m fairly certain that this will, at least short term, increase the use of dimers as a part of a syncopal work up, and probably for the “near syncopal” as well.  But what about age-adjusted dimers? A potential role can & should be seen here for those of us with concern enough to send a dimer, particularly if your gestalt dictates.  With 40% of these PE’s not being small, I think something is there, the question is, is it meaningful?  Better yet, is it worth chasing after that 1.1% ?   We do it for chest pain with troponins, we do it with lactics for infectious processes, why not age-adjusted dimers for syncope?  But is any of that actually good care?

 

Sadly, we’re still not exactly sure if we’ve benefitted the patients in this study by treating them since they were not followed for a prolonged period.

So where does this leave us? Well, I’ll leave up for you & your gestalt to decide.  I’m still trying to figure out if I actually helped that poor elderly woman.

Sono-guided ACLS

This study demonstrates what many of us have probably suspected – the absence of cardiac activity on ultrasound portends a grave diagnosis; but this study really is so much more.

Utilizing 20 sites across the US and Canada from May 2011-Nov 2014 looked at all nontraumatic in-ED and out of hospital cardiac arrests that arrived to the ED in either PEA or asystole, and whether or not POCUS demonstrated a potential role in resuscitation.

953 patients, 793 used for final analysis (106 not included due to resuscitation under 5 minutes, 8 patients DNR, 1 uninterpretable sono, 3 with incomplete timing data, 42 for no ACLS meds given) – had a cardiac sono at the “beginning and end of ACLS.” The primary outcome was percentage of patients that survived to hospital admission, with secondary outcomes of survival to discharge and ROSC. Unfortunately, neurologic intact survival was not evaluated. The treating EP’s were credentialed in POCUS at their local institutions and unblinded. Digital clips were reviewed by a single reviewer in a blinded fashion for agreement (which was deemed to be “substantial agreement”).

The data (numbers are percentage, such that “28.9” = the percentage of patients with cardiac activity on POCUS during the resuscitation who survived to admission):

 

Cutting to the chase, this study brings up a number of key points:

-PEA on the monitor may not necessarily be PEA, with a whopping 54% of patients having cardiac activity on POCUS

-asystole on the monitor may not be cardiac standstill, as 10% had cardiac activity on POCUS

– survival to admission with cardiac activity on POCUS is MUCH higher – 28.9% vs 7.2%, but….

– cardiac activity on POCUS for PEA/asystole portends only a 3.8% survival to discharge

-no cardiac activity = poor prognosis, 0.6% of patients survived (3 out of 530). With two of the three patients were Vfib at some point during EMS working on them.

-pericardial effusion was seen in 34 patients (4.3% of those in the final analysis). 15.3% of patients whom had a pericardiocentesis performed survived to discharge.

– only 15 patients received lytics for suspected PE, with only one (6.7%) surviving to discharge. (which was almost the MORTALITY rate of PEAPETT)

 

Whew. This is a lot to digest. Let’s just say that ultrasound helps you tease out a spectrum of disease and further characterizes what you are dealing with. I’m looking at POCUS in codes as a risk stratification tool. Is there a prolonged time without cardiac activity without a potentially reversible causes? Might want to consider calling it earlier since survival to discharge is abysmally low. And sheesh… 1 out of 25 cardiac arrests had a pericardial effusion??? Wow. Time to brush up on those pericardiocentesis skills.

Caveats- this was done by EP’s credentialed for POCUS, so they’re likely more talented than the rest of us.  Dont let that scare you though, rather, this.  Perhaps seeing cardiac movement on ultrasound lends a “bridge to hope” and the team puts in a more-heroic-than-usual effort.

And of course, this also leads to more questions- of those 28.9% with cardiac activity that survive to admission, what if they are brought straight to the cath lab? Or started on ECMO? Would this potentially alter survival rates and neurologically intact survival in meaningful ways? Time shall tell.  Until then, cut that KT window, pick up the probe, and have your TPA & long pericardiocentesis needle ready.

How do you PE part 2

Last PE post, we discussed PEITHO, TOPCOAT, MOPPETT, and the lysis of massive and submassive PEs.  So what do we do for the un-submassive and unmassive PEs?

     The Outpatient Treatment of Pulmonary Embolism (OTPE) study compared outpatient vs inpatient treatment of low-risk patients with acute PE.  Patients were treated with lovenox bridge to coumadin either as outpatient or inpatient (171 v. 168 patients). Patients were followed for 90 days, with follow up calls at days 1-7, 14, 30, 60, 90.  Only 1 outpatient developed a recurrent VTE, two outpatients developed “major bleeding” within 2 weeks – both IM hematomas.  Neither recurrent VTE or major bleeding between the two groups was statistically significant.  Likewise, one person in each group died from non-VTE and nontreatment-related causes. 99% of participants completed the Press-Ganey, satisifaction survey with 92% of outpatients and 95% of inpatients being satisfied or very satisfied with their care.  As for bounce backs?  Readmissions, ED visits, and PMD visits were similar in the two arms.  The total number of home nursing visits was higher among outpatients (14% vs 6% of patients), but the mean time spent in the hospital was obviously greater for inpatients (3.9 days vs 0.6 days).

     I question whether or not outpatient treatment at most facilities would be >90% satisfied, but certainly intriguing.  Gazing into my crystal ball, I suspect the day will come when we are either admitting & providing lytics, or discharging from the ED on Xarelto / Pradaxa / other.  For PE risk score, you may use Hestia or PESI .

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Outpatient versus inpatient treatment for patients with acute pulmonary embolism: an international, open-label, randomised, non-inferiority trial. PMID: 21703676

How do you PE?

We have MOPETT, PEITHO, and now, TOPCOAT.

    MOPETT looked at 121 patients, and found that tpa led to a decrease in pulmonary hypertension (22 vs 8 mm Hg) at 28 month follow up, and a decreased LOS (2.2 vs 4.9 days). This drew some backlash and claims that there was an unusually high incidence of pulmonary HTN in this trial.

    PEITHO looked at 1,005 patients, with “intermediate risk” which they defined as RV strain on echo or CT, plus a positive troponin. Patients were randomized to weight based tenecteplase as a bolus + standard anticoagulation vs standard anticoagulation only. Essentially, death at 7 & 30 days were similar – 1.2% vs 1.8% (lytics vs no lytics) at 7 days and 2.4% vs 3.2% at 30 days (lytics vs no lytics). Stroke at 7 days was 2.4% in the lytic treatment arm vs 0.2% without lytics, while hemodynamic compromise defined as persistent hypotension, pressor requirements, intubation and CPR, was higher in the no lytics group (1.6% vs 5%). They make no mention of pulmonary hypertension at follow up. So really, the patient has a 3% chance of death either way.

    Now, there is TOPCOAT. Normotensive patients with PE and RV strain (either on echo or BNP), were given either tenecteplase bolus + standard anticoagulation or standard anticoagulation only. The study, unfortunately, enrolled only 83 patients, with 40 receiving tenecteplase. 16 non-lytic patients vs 6 lytic patients had an adverse outcome, defined as death, shock, intubation, major bleeding within 5 days, recurrent PE, poor functional capacity (RV dysfunction + dyspnea at rest or exercise intolerance), or an SF36 Physical component score <30 at 90 day follow up. Basically, since only 1 patient died and 2 required intubation of the 16 non-lytic patients, the main difference here is functional capacity and quality of life. More on SF36 here: http://www.sf-36.org, though it is essentially a composite score measuring quality of life).

    For submassive PE’s, the general trend is that a shared decision will need to be made: mortality is essentially the same, 2-3%, no matter the treatment. Would they rather it be from PE or from its treatment, but knowing that they have a chance at better quality of life months to years down the line? There are potential legal landmines on either side of this discussion. Document well, my friends!

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Unusually high incidence of pulmonary hypertension in MOPETT trial. PMID: 23764652

Moderate pulmonary embolism treated with thrombolysis (from the “MOPETT” Trial). PMID: 23102885

Fibrinolysis for patients with intermediate-risk pulmonary embolism. PMID: 24716681

Treatment of submassive pulmonary embolism with tenecteplase or placebo: cardiopulmonary outcomes at three months (TOPCOAT): Multicenter double-blind, placebo-controlled randomized trial. PMID: 24484241