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.

Improving Outcomes, Mythbusting, Pulmonary

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.

Cardiology, Improving Outcomes, Mythbusting, Neurology

Chronic viral infection & Coronary disease.

Are you openly ignoring a cardiac risk factor that is in the ballpark of smoking or early family history?   Even after controlling for numerous factors, well controlled HIV has a significantly higher cardiovascular MORTALITY rate – with an adjusted rate ratio of 1.53, while poorly controlled patients even moreso, with an adjusted rate ratio of 3.53, according to this paper.  It should be noted that this is one of several papers looking into HIV as a risk factor for early cardiac disease and death.

It is important to realize the limitations of our tools that we have at our disposal.  For instance, PERC and HEART are not validated in an HIV population.

I suspect many if not all chronic viral infections will portray a similar trend. It is already seen in HepC, albeit to a lesser extent. It will be interesting to see if the new age HepC drugs decrease the known risk of increased coronary artery disease and cerebrovascular disease after treatment.


Class Warfare – Ortho Follow-up Style.

This paper is glimpse into the sad realities brought about by the class warfare unveiled by the current US public/private insurance system.

They looked at all 102 Dallas-Fort Worth orthopaedic groups. All groups were called twice from a patient discharged from the ED with an ankle fracture who utilized a standardized script- one call saying they were uninsured, another saying they had either private insurance or medicaid. All in all, 204 calls were made (59 private, 43 medicaid, 102 uninsured).

Success rate for ability to make a follow up appointment:

83.1% for privately insured

81.4% for uninsured

14% for medicaid callers

Controlling for paired calls to same practice, an uninsured caller had almost a 6x higher rate of follow up than medicaid callers. Also despicable is that the uninsured had to bring a median of $350 to their first appointment (less than 2% were asked to bring $100 or less) – or, 48% more than the usual total payment collection from a privately insured patient ($236), and 273% more than the usual payment collected from medicaid ($128).

Want more heinous activity? 48% of uninsured patients were directed to the ED when they asked where they could go.

Wait, you want more? Of the ortho practices that appeared on medicaids list of practices accepting new patients:

15 of 38 told callers they did not accept medicaid

11 said they did not treat ankles

9 had non-working numbers

3 actually scheduled an appointment

Less than 10% of medicaid patients were able to secure an appointment with ortho practices that were on medicaid’s list of providers accepting new patients! Either their database needs updating, or the practices are outright lying. Given the difference in payments between the uninsured, private patients, and medicaid patients, I suspect the problems lay on the side of the individual practices.

Emergency Medicine- the front lines and safety net.


Chronic opiate use leads to worse surgical outcomes

No surprises here. This study looks at outcomes after major elective abdominal surgery ~500 patients on chronic opiates vs ~1900 opioid naive patients from a single center from 2008-2014.

9.2% higher costs, 12.4% longer LOS (5.9 vs 5.2 days), higher complication rate (20% vs 16%), more readmits (10% vs 6%), without a difference to discharge destination (home, SNF, etc).

On one hand, you play the hand youre given – you help the patient the best way you can. But, what if that means you detox them first? It will be interesting to see if some providers go to that extreme. Especially if they (or hospitals) are not reimbursed at a higher rate to take on the added risk / LOS / bounceback rates. I know of orthopaedics refusing surgery based on a patients weight – I can envision a scenario in which the (currently) heavily-stigmatized opiate addicted patient is deemed unfit for non-emergent surgery so that facilities and providers retain their “5 star” ratings for various non-emergent surgical procedures to gain the insurance dollars of the “educated consumer”.

Sigh. This is quite the ethical pickle.

Next question – does this spill into EM? Should we withhold 1-2 doses of opiates for fear of worse outcomes? A perforated viscous seems like a good indication for opiates if ever there was one.

Cardiology, Critical Care, Improving Outcomes

Brady arrest? Go Full Bore.

Do you believe in full bore medicine?

(hat tip to SMACCdub for that line)

This paper puts those thoughts under the microscope a bit, and challenges us to think ahead and be prepared.

They looked at all OHCA from 2006 to 2012 with initial brady/asystolic arrests to determine if they may benefit from pre-hospital pacing, and to look at survival rates associated with various rhythms. Clear non-cardiac causes (trauma, drowning, respiratory, neurologic, suicide) were excluded.

7925 OHCA in the Netherlands

less non-cardiac (6681 patients)

less those without EKGs (~500 patients)

less ~3000 patients with VF/VT (now at 2643 patients)

less those with normo/tachycardia and those with pacers previously placed (~300 patients)


This leaves us with 2333 brady/asystolic (idioventricular, junctional, sinus brady, 3rd degree with/without escape, asystole) patients – or, about 30% of their OHCA.

Unwitnessed arrest still protends a poor outcome, with survival about 0.5%. However, for witnessed arrests, they report 4% survival for idioventricular / junctional arrests and 6.8% for sinus brady arrests. This seems consistent with prior studies. However, for a study trying to determine whether or not pacing is beneficial, their pace rates were quite low. They paced 11 of 220 sinus brady patients and 41 of 452 idioventricular / junctional patients, with a delay of 30.1 and 16.5 minutes to pacing respectively – with an electrical capture rate of 55% and 70% to boot.  Esssentially, they can’t answer the question “Does pacing help” with such a care gap.

So, why is this? For sinus brady, maybe patients are hanging in the 40’s-50’s and felt to be quasi-stable. Maybe its the angst of floating a pacer. Perhaps the lengthy delay for sinus brady is giving atropine, then giving it again… and maybe again- akin to pressor-angst for sepsis (giving a 4th, 5th, and 6th liter rather than starting pressors or a central line).  I imagine there is a mental barrier – whether it be not thinking about pacing or passing the buck (“I’ll let the ICU figure it out.”). The evolution of the ED-ICU model (and perhaps UPMC’s cardiac arrest unit) may be the best place to look at this type of “full bore” medicine and whether or not it would be beneficial.

But for now, there is a large gap in care. Bradycardic arrests represent about 10% of arrests, have a reasonable survival rate, and are (potentially) suboptimally managed – and you have the tools to potentially improve an outcome.  We can not say whether or not pacing is futile care for this condition.

Until then, go full bore. Your patients & their families deserve it until pacing is demonstrably shown to not be beneficial in bradycardic arrests.

Improving Outcomes, Improving Throughput, Mythbusting, Pediatrics, Pediatrics, Pediatrics

SCI still rare in kids.

This paper demonstrates that once again, kids are quite durable.

The authors looked at 3701 patients under 19 years old evaluated for a cervical spine injury. Of the 44 patients with clinically significant cervical spine injury (CSI), 32 had plain films, none of which missed an injury.

32 out of 3701… or 0.86%

-There were ZERO patients under two years old with a CSI

Here is the caveat- one injury begets another. Of the 32 patients with CSI, ten (31%) had multiple lesions, with plain films not identifying all lesions in 4 patients. Given that, I think its fair to say CT (or admission for MRI) is warranted once an abnormality is found.

In summary, relevant cervical injuries in kids are rare (<1%), and plain films are a reasonable screening tool. CT is once again rarely needed, but beware since one injury seemingly begets another. I pretty much agree with the authors on this one,

Our calculated 100 % sensitivity (90% on PECARN, finding 168 of 186 CSI) does come with a large confidence interval and it should be expected that plain films sensitivity for CSI is likely lower in clinical practice. However, the small risk of missed injuries from plain films must be balanced against the increased risk of malignant trans- formation from performing CT scans on all children with suspected CSI.